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Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis
Sars- COV-2 Serological
Antigens & Monoclonal Antibody
https://www.bmj.com/content/336/7651/1006.short  
Research
Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis
BMJ 2008; 336 doi: https://doi.org/10.1136/bmj.39537.939039.BE (Published 01 May 2008)Cite this as: BMJ 2008;336:1006

John Victor Peter, physician1,  
Preeta John, lecturer2,  
Petra L Graham, lecturer3,  
John L Moran, senior consultant4,  
Ige Abraham George, lecturer5,  
Andrew Bersten, professor6

Correspondence to: J L Moran john.moran@adelaide.edu.au
Accepted 14 March 2008
Abstract
Objective To systematically review the efficacy of steroids in the prevention of acute respiratory distress syndrome (ARDS) in critically ill adults, and treatment for established ARDS.

Data sources Search of randomised controlled trials (1966-April 2007) of PubMed, Cochrane central register of controlled trials, Cochrane database of systematic reviews, American College of Physicians Journal Club, health technology assessment database, and database of abstracts of reviews of effects.

Data extraction Two investigators independently assessed trials for inclusion and extracted data into standardised forms; differences were resolved by consensus.

Data synthesis Steroid efficacy was assessed through a Bayesian hierarchical model for comparing the odds of developing ARDS and mortality (both expressed as odds ratio with 95% credible interval) and duration of ventilator free days, assessed as mean difference. Bayesian outcome probabilities were calculated as the probability that the odds ratio would be ≥1 or the probability that the mean difference would be ≥0. Nine randomised trials using variable dose and duration of steroids were identified. Preventive steroids (four studies) were associated with a trend to increase both the odds of patients developing ARDS (odds ratio 1.55, 95% credible interval 0.58 to 4.05; P(odds ratio ≥1)=86.6%), and the risk of mortality in those who subsequently developed ARDS (three studies, odds ratio 1.52, 95% credible interval 0.30 to 5.94; P(odds ratio ≥1)=72.8%). Steroid administration after onset of ARDS (five studies) was associated with a trend towards reduction in mortality (odds ratio 0.62, 95% credible interval 0.23 to 1.26; P(odds ratio ≥1)=6.8%). Steroid therapy increased the number of ventilator free days compared with controls (three studies, mean difference 4.05 days, 95% credible interval 0.22 to 8.71; P(mean difference ≥0)=97.9%). Steroids were not associated with increase in risk of infection.

Conclusions A definitive role of corticosteroids in the treatment of ARDS in adults is not established. A possibility of reduced mortality and increased ventilator free days with steroids started after the onset of ARDS was suggested. Preventive steroids possibly increase the incidence of ARDS in critically ill adults.

Introduction
The acute respiratory distress syndrome (ARDS) is a life threatening condition with mortality rates of about 40-60%.1 2 The pathophysiological basis of acute respiratory distress syndrome—excessive and protracted inflammation characterised by increased vascular permeability and extravasation of plasma and leucocyte infiltration1—is often systemic, resulting in multiorgan dysfunction and death. Treatment strategies, with the exception of low tidal volume mechanical ventilation,3 have had little impact on outcomes. Since inflammation is thought to contribute to the pathogenesis of ARDS1 it is rational to explore modulating therapies for this inflammation, provided the adverse effect of such treatment is not excessive. Corticosteroids, potent anti-inflammatory agents, and immunomodulators, which exert inhibitory effects in several stages of the inflammatory cascade,4 would seem to be a logical choice for treatment of ARDS. Clinical outcomes in trials on the role of steroids in ARDSw1-w5 have varied, however, and two recent systematic overviews on the efficacy of steroids in ARDS have reached opposite conclusions: “current evidence does not support a role for corticosteroids in the management of ARDS in either the early or late stages . . .”5 and “prolonged glucocorticoid treatment substantially and significantly improves meaningful patient-centred outcome variables, and has a distinct survival benefit . . .”6 Thus the therapeutic status of steroids in ARDS is unclear. We assessed whether steroids are associated with mortality benefit in adults with ARDS. We also determined the effect of steroids on infections and duration of ventilator free days and the role of steroids in preventing the development of ARDS in critically ill adults.

Methods
We selected randomised controlled trials in critically ill patients that evaluated steroid treatment compared with no steroid treatment to reduce the incidence of ARDS or to improve the outcome from ARDS. Only trials reporting mortality, incidence of ARDS, or data on ventilation were included. We excluded studies reporting only physiological end points (improvements in gas exchange), descriptive or retrospective cohort studies, studies in children, and studies reporting the use of steroids in fat embolism syndrome. Our search had no language restrictions. We classified trials into two groups: preventive steroid treatment in critically ill patients to decrease the development of ARDS, and steroid treatment started after the onset of ARDS.

Search strategy and quality assessment
We carried out an electronic search for the period 1966 to April 2007 through Medline, the Cochrane central register of controlled trials, the Cochrane database of systematic reviews, the American College of Physicians Journal Club, the health technology assessment database, and database of abstracts of reviews of effects. We restricted the search to studies on adults and used the search terms “ARDS”, “adult respiratory distress syndrome”, “acute respiratory distress syndrome”, “non-cardiogenic pulmonary edema”, “respiratory insufficiency”, “systemic inflammatory response syndrome”, “shock lung”, “respiratory failure”, “lung injury”, “septic shock”, “sepsis”, AND “steroids”, “corticosteroids”, “prednisolone”, “methyl prednisolone”, “hydrocortisone” AND “randomized controlled clinical trials”, “controlled trials” and “randomized trials”. We reviewed the abstracts of trials generated by the electronic search and retrieved trials pertaining to steroids in ARDS and sepsis for a more detailed evaluation. To identify additional trials we examined review articles, including a Cochrane systematic review on pharmacological therapies in ARDS.7 In addition three investigators hand searched the American Journal of Respiratory and Critical Care Medicine, Chest, Critical Care Medicine, European Respiratory Journal, Lancet, New England Journal of Medicine, Intensive Care Medicine, and Thorax. The hand search included an electronic or manual search of the table of contents as well as abstracts of conference proceedings of the various societies published in these journals.

Two investigators extracted predefined data from included studies into standardised data abstraction forms. Quality assessment of these studies was done unblinded by three investigators using a 10 point scoring system (table 1⇓) modified from a previous meta-analysis.9 When differences in scoring existed, a consensus was reached. Extracted data were reviewed and verified by two investigators before analysis.

Outcome measures
The primary outcome was hospital mortality or survival to hospital discharge. This end point was difficult to determine, however, as mortality was also reported at 14 to 60 days after the onset of ARDS. The hazard ratio would have been the optimum metric for mortality effect10 but was found to be impractical because of the variability in reporting. As the hazard ratio may be approximated from the odds ratio,11 we chose the odds ratio as an appropriate metric for the mortality effect. We considered several secondary end points a priori: year of study completion, ventilator free days, improvements in lung injury score, incidence of ARDS in critically ill patients after preventive treatment, and steroid related complications, particularly new infections, pneumonia, hyperglycaemia, and neuromuscular dysfunction. Because of selection bias in trial reporting12 assessable secondary end points were incidence of ARDS in critically ill patients after preventive treatment with steroids, number of patients developing new infections or pneumonia, number of ventilator free days, and year of study completion.

Definitions
ARDS was defined after the 1994 American-European consensus definition13; we retrieved earlier studies to establish consistency with this definition. Secondary infections were defined generally as a positive culture from a normally sterile site. As the time span of the studies was 20 years, we anticipated revisions of the definitions for secondary infections—for example, the use of quantitative cultures in more recent years. The duration of ventilator free days was defined as the number of days patients were alive and breathing without assistance during the 28 days after onset of ARDS, and was presented in the studies as mean (standard deviation) days.

Statistical analysis
We used Bayesian random effects models14 to assess the effect of steroids compared with control on mortality, proportion of patients who developed ARDS, new infections, and pneumonia, expressed as odds ratios with 95% credible intervals. These methods were most appropriate for the binary outcome data reported since some studies had small sample sizes and the normality assumptions associated with commonly used (frequentist) meta-analysis techniques were not appropriate. Furthermore, Bayesian methods allowed heterogeneity to be adequately incorporated into the analysis. We used a model for summary statistics to assess the overall mean difference (steroid treatment minus placebo) in the number of ventilator free days. We calculated Bayesian outcome probabilities as the probability that the odds ratio was 1 or more or the mean difference was 0 or more. A probability of 50% suggests a null effect whereas a probability of at least 90% signifies harm for the odds ratio analyses, but benefit (increase in ventilator free days) for the mean difference analysis; and a probability of less than 10% indicates benefit for the odds ratio analyses and harm (decrease in ventilator free days) for the mean difference analysis. We also used Bayesian metaregression14 to determine the relation between the odds of mortality and time to treatment in ARDS, total dose of steroids, and year of study completion. The slope (β) with 95% credible intervals and the probability that β was 0 or more are presented. We presented heterogeneity as the standard deviation between studies. For all analyses a standard deviation close to 0 indicates little heterogeneity, whereas for the odds ratio meta-analyses a standard deviation of more than 1 might be considered to reflect substantial heterogeneity. Similarly, for the mean difference analysis, a standard deviation greater than, for example, 10 might be considered to indicate substantial heterogeneity. Publication bias was not formally assessed, as the two subgroups each had fewer than 10 studies.15

We analysed the data with WinBUGS16 using three simultaneous runs of the program with disparate starting values. The first 100 000 iterations were discarded and results were reported as posterior medians and intervals on the basis of a further 100 000 iterations. We used various diagnostics available in the package Bayesian Output Analysis to assess convergence.17 In all cases we found no evidence against convergence. We used the same diffuse priors as described elsewhere14 for the odds ratio models and the metaregressions. A diffuse or non-informative prior should not greatly influence the results and reflects little or no prior belief about a particular problem. Mathematically diffuse priors aim to have about equal probability over all plausible values of the variable. For the mean difference model we placed a non-informative normal prior distribution with mean 0 and variance 105 on the overall mean difference. A normal distribution with mean 0 and variance of 13.5 and truncated below 0 was placed on the variable for standard deviation between studies.18 Such a distribution was derived from the notion that the median difference between any two studies was about four days and that a difference of more than 11 days would be extremely unlikely. To determine the influence on the overall results we also undertook a sensitivity analysis in which the priors were made even less informative.

Results
Of the 7093 articles screened on ARDS or sepsis, 439 pertained to steroids in either condition. One investigator reviewed the abstracts of these articles and 62 articles were retrieved for further assessment by three investigators. Fifty five studies were excluded, including two controlled retrospective studies (fig 1⇓),w6 w7 a randomised trial of steroids in severe community acquired pneumonia,19 and five other prospective trials identified by an additional search (see bmj.com).w8-w12 This left nine studies, including two identified by an additional search. Four studies evaluated the preventive use of steroids in critically ill patientsw13-w16 and five assessed the role of steroids after the onset of ARDS.w1-w5 The definitions of ARDS in the studies done before the publication of the American-European consensus definition13 were generally consistent with the consensus definition (table 2⇓). The treatment and control arms had similar baseline characteristics (table 3⇓). Table 4⇓ presents a summary of the study characteristics and quality scores; the lag time from study completion to publication ranged from two to seven years. The reporting of mortality was variable. The steroid dose ranged from methylprednisolone 1 mg/kg/day to 120 mg/kg/day (or equivalent doses of hydrocortisone or dexamethasone) administered from four hours to 30 days (table 5⇓).

[Figure1]
Fig 1 Flow of studies through systematic review
Table 2 
Main outcome measures evaluated and definition of acute respiratory distress syndrome (ARDS) in included studies
Table 3 
Baseline characteristics of steroid treatment and non-steroid treatment arms in study patients
Table 4 
Study characteristics, quality scores, and mortality data of included studies assessing steroids for prevention and treatment of acute respiratory distress syndrome (ARDS)
Table 5 

Steroid dose, type, duration, and total dose used in adults with acute respiratory distress syndrome (ARDS) in included studies

The credible interval for the preventive use of steroids in critically ill patients included 1, indicating that a null effect could not be ruled out. The probability (odds ratio ≥1) was 86.6% suggesting some evidence of an association between steroid therapy and the subsequent development of ARDS: four studies, odds ratio 1.55 (95% credible interval 0.58 to 4.05); SD 0.58 for variability between studies (table 6⇓ and fig 2⇓). Similarly, the probability suggested a weakly increased risk of death associated with steroid therapy in patients who developed ARDS: probability (odds ratio ≥1)=72.8% (table 6⇓ and fig 3⇓), although again the credible interval included 1.

[Figure2]
Fig 2 Effect of preventive steroids on proportion of patients developing acute respiratory distress syndrome (ARDS)
[Figure3]
Fig 3 Subsequent mortality in those who developed acute respiratory distress syndrome
Table 6 
Summary of outcomes in included studies of steroids compared with placebo in prevention and treatment of adults with acute respiratory distress syndrome (ARDS)
In the five therapeutic studies the probability that the odds ratio was one or more was small indicating that giving corticosteroids after the onset of ARDS was associated with a trend (table 6⇑ and fig 4⇓) to reduced mortality (overall odds ratio 0.62, 95% credible interval 0.23 to 1.26, probability (odds ratio ≥1)=6.8%), although the credible interval included 1 so that a null effect could not be ruled out. Some heterogeneity was evident between the studies (standard deviation 0.53). Steroid therapy was associated with substantially more ventilator free days (three studies) compared with controls (mean difference 4.05 days, 95% credible interval 0.22 to 8.71, probability (mean difference ≥0)=97.9%, SD 2.39). When the effect of moderators (time or dose of steroid therapy, year of study completion) on outcomes was explored in the five therapeutic studies, no evidence was found of an association between odds of mortality and time to treatment (fig 4⇓) in (log) hours; β(time)=−0.08 (95% credible interval −1.00 to 0.62), probability (β≥0)=38.7%; total steroid dose; β(dose)=0.06 (95% credible interval −0.94 to 0.97), probability (β≥0)=57.8%; or year of study completion; β(completion year)=−0.01 (95% credible interval −0.17 to 0.14), probability (β≥0)=44.1%.

[Figure4]
Fig 4 Effect of therapeutic steroids on mortality in patients with acute respiratory distress syndrome

As anticipated, definitions for secondary infections varied considerably (table 7⇓). Steroid therapy was not associated with an increase in the number of patients developing new infections. Within the four available therapeutic studies the trend was towards decreased odds of developing pneumonia (probability (odds ratio<1)=76.9%, table 6⇑); although heterogeneity was substantial (SD 1.34, table 6⇑). Metaregression showed a trend towards an increased number of patients developing new infections as steroid dose increased; across seven studies (two preventive trials and five therapeutic trials), β=0.08 (95% credible interval −0.12 to 0.28), probability (β≥0)=81.2%.

Table 7 
Definition of secondary infections in included studies
Sensitivity analysis was undertaken in which the prior for the variability between studies was made increasingly less informative. In all cases the point estimates remained stable, the credible interval became wider, and probabilitychanged slightly. This did not affect any of the interpretations given in the results except for that of ventilator free days, in which the credible interval included zero.

Discussion
This systematic review failed to show a convincing treatment effect of steroids in acute respiratory distress syndrome (ARDS), although trends were found for treatment. Although preventive steroid therapy in critically ill patients may have been associated with detrimental effects on the incidence of ARDS and subsequent mortality, a trend was found to benefit when steroids were given after the onset of ARDS; in particular, a reduction in odds of mortality (probability of reduction 93.2%). The review, however, showed no discernible time or dose effect of steroids on mortality with the therapeutic use of steroids. Although steroids did not increase overall infection risk, a latent dose dependent effect of steroid therapy on infection rates seemed to exist.

The seemingly differential effect of preventive and therapeutic steroid therapy in ARDS, observed in the current meta-analysis, has been previously suggested,20 but the reasons for this are unclear. Key proinflammatory mediators such as tumour necrosis factor α and interleukin 1 have been implicated in the pathophysiology of sepsis with organ dysfunction, the most common cause of ARDS.21 In clinical studies, inhibition of these proinflammatory mediators has not improved outcome22; indeed, antagonism of tumour necrosis factor α23 or interleukin 124 increases mortality in some models of bacterial infection, suggesting a key role for their expression in survival from infection. Preventive steroids may not only impede normal homoeostatic response by inhibiting cytokine production,25 but also contribute to the pathogenesis of ARDS by stimulating the release of macrophage migration inhibiting factor, a proinflammatory cytokine.26 This latter effect remains speculative as release of macrophage migration inhibiting factor by glucocorticoids seems to have a biphasic dose dependency,26 27 28 and protective effects have also been described.29 In addition the high doses of methylprednisolone given to the preventive group may have contributed to an increased risk of infection and poorer outcomes. Steroid therapy after the onset of ARDS may, however, have a different effect by modifying the persistent and protracted inflammation that exacerbates lung injury.

The implications of time to starting therapeutic steroids after onset of ARDS are of some importance and have been highlighted in the recent National Heart, Lung, and Blood Institute ARDS clinical trials network report,w5 where an interaction between time and treatment 14 days after the onset of ARDS was found to be significant. Editorial responses4 30 have also embraced a time-difference of steroid effect; benefits occurring with steroid therapy if started within two weeks of ARDS onset and not subsequently. In the individual trials included in the current meta-analysis, the start of steroid therapy ranged from within 72 hoursw4 to four weeksw5 after ARDS onset. Metaregression with initiation time of treatment as a moderator (fig 5⇓) failed to show any influence on mortality. Although such a differential steroid time effect may have biological plausibility, the interpretation of treatment response rates on the basis of data dependent time cut-off points, albeit defined a priori, is problematic.31 32 Further definition of the optimal time to start steroids is required, possibly by meta-analysis of individual patient data.33
[Figure5]
Fig 5 Association between odds of mortality and time to starting steroids or placebo

Steroids did not seem to have any adverse effect on overall infection rates, including pneumonia, but a trend was found towards increased risk of infection with increasing steroid dose. The enormous variation observed in the steroid dosages20 was primarily because studies in the 1980s used high dose (120 mg/kg/day methylprednisolone) short duration (24-48 hours) steroids as immunomodulatory therapy whereas prolonged (2-4 weeks) low dose (1 mg/kg/day methylprednisolone) anti-inflammatory therapy has been more recently advocated.34 Given the complications of high dose steroids, current use is limited to specific (acute) immunological diseases, with little evidence supporting high dose steroids in ARDS.30

Secondary outcomes such as lung injury score, incidence of hyperglycaemia, and neuromuscular dysfunction could not be systematically evaluated because of publication bias within studies.35 Although the steroid effect on ventilator free days was favourable, and possibly could have an impact on hospital stay and complications, only three studies reported this outcome, and in the sensitivity analysis the credible interval included 0 suggesting the possibility of a null effect. The widening of this interval is not surprising because combination of so few studies results in greater uncertainty in the estimate of the standard deviation between studies and hence wider estimates of the mean difference. Future analysis using a greater number of studies would limit this impact.

Strengths and weaknesses of the review
The number of trials in this meta-analysis and the number of patients randomised to receive steroids (n=561) was relatively small, compounded by stratification into two subgroups; preventive and therapeutic. Although commentators30 34 and a formal review6 have considered a randomised trial on steroids in severe community acquired pneumonia19 in conjunction with other studies of steroids in ARDS, we did not include this study. In this study, which was stopped early, of the 46 enrolled patients only 23 had multilobar involvement and 34 had a partial pressure of oxygen to fractional inspired oxygen ratio of <200. Four patients in the control arm subsequently developed ARDS. Furthermore, it was unclear from the study as to how many patients had bilateral disease. The exclusion of studies on steroid therapy in fat embolism syndrome was justified on the basis that although this is a distinct syndrome that may cause ARDS, the latter is poorly identified in many of these longstanding studies. Fat embolism syndrome is an uncommon cause of ARDS in modern practice and its inclusion may have confounded the interpretation of the effect of steroid treatment on patient cohorts currently considered. Although it would have been preferable to undertake the current meta-analyses adopting the hazard ratio metric10 given the disparate time end points, only one of nine studies reported hazard ratios and in the other studies it was not possible to extract relevant data.

In the metaregression of steroid dose effect, the total dose of steroids (equivalent to the potential maximum use of steroids) was used as a moderator variable, as opposed to the first day dose (table 5⇑), because three of the five therapeutic trialsw3-w5 gave substantial initial bolus steroid doses, thus rendering any regression analysis using the first day dose as problematic. The use of total dose of steroids, however, fails to adjust adequately for the occurrence of early deaths in the treatment arm. One possible solution to these potential biases would be the use of steroid free days, normalised, for example, for intended total dose, similar in intent to ventilator free days.

The meta-analysis of Agarwal et al5 found odds ratios of 0.57 (95% confidence interval 0.25 to 1.32) in “early” ARDS and 0.58 (0.22 to 1.53) in “late” ARDS. The conclusions of this meta-analysis are problematic on several grounds. Firstly, the authors combined both observational and randomised trials in their analysis using the DerSimonian and Laird method of moments (frequentist) estimator. This is not optimal for sparse data that may not be normally distributed36; the method of Warn et al,14 which directly uses binomial likelihoods is apposite for binary outcome data and small samples. Combining observational and randomised trials within a meta-analysis is best undertaken using a hierarchical random effects approach from within the Bayesian paradigm.18 Secondly, problems are inherent in grounding analysis on early to late time data dependent cut-off points. Thirdly, the point estimate of mortality effect quoted by the authors is similar to that of the current meta-analysis. Using a frequentist approach, however, the authors were unable to ascribe a probability to the treatment effect and could only conclude a lack of evidence for a treatment effect on the basis of the 95% confidence interval spanning the null effect.

The “critical appraisal” of Meduri et al6 used fixed effects estimation of the pooled mortality treatment effect with the relative risk metric (relative risk 0.76, 95% confidence interval 0.62 to 0.93) and included the randomised trial19 on steroids in severe community acquired pneumonia (described as early acute lung injury), but did not consider an early trial of steroids in ARDS.w2 The principal concern was that of heterogeneity and its influence on the pooled mortality estimate: “the analysis for mortality was limited by the significant heterogeneity across the five trials . . .”; and its “potential sources” identified by “subgroup analysis based on size of the study . . . timing of initiation of treatment . . . and duration of treatment.”6 Several concerns are raised by this analysis: the identification of heterogeneity (at P=0.09) was confounded by aspects of trial conduct, the use of interim analyses in all five trials considered,w1 w3-w5 19 and stopping the study early in three.w3 w4 19 As previously discussed,37 stopping a trial early biases treatment effects in individual trials and the use of stopping rules may induce artificial heterogeneity into overviews of clinical trials and increase the type I error rate in tests of homogeneity38; the problems associated with repeated subgroup or empirical analyses of cut-off points are also well known—an increase of type I error rates, overestimation of effect at cut-off point levels, and the conceptual problem of sudden noticeable changes in effect at the various levels.39 This is particularly important with respect to the analysis of day 14 time of entry after onset of ARDS in the National Heart, Lung, and Blood Institute ARDS clinical network trials network,w5 which although defined a priori (one of nine “a priori determined covariates . . . examined for a treatment interaction”), had the status of a subgroup effect and was thus hypothesis generating, not a definitive treatment recommendation; showing steroid efficacy by empirical subgroup analyses progressively reduced both total sample size and event number, such that the third subgroup analysis (prolonged methylprednisolone treatment of >1 week’s duration after removing patients randomised after day 14; figure 3 in Meduri et al6) had only 75 events. To ensure more reliable and clinically useful evidence, meta-analyses require appropriately large numbers of events.40

We judge aspects of the analyses in these two reviews as problematic and suggest in the context of the limited number of trials, that a Bayesian perspective is both apposite and, unlike conventional frequentist random effects (DerSimonian-Laird) estimation,41 able to accommodate heterogeneity, and an odds ratio metric is preferred42; a strategy of considering methods based on the random effects model only in the case of heterogeneity6 is “inefficient and can lead to understatement of uncertainty about the underlying effect of interest”43; and in the search for predictors of heterogeneity between studies44 meta-regression involving all available studies, not subgroup-analysis, is optimal.

Conclusions
Some evidence exists for the efficacy of steroid use after the onset of ARDS, without notable side effects such as new infection. We cannot, however, dismiss a null effect. Furthermore, we were unable from the included studies to accurately define the optimal dose, timing, and duration of steroid therapy. Meta-analyses on the basis of a small number of trials with sparse data must be cognisant of limitations in estimation of treatment effects. Thus editorial advocacy to use steroids in ARDS30 34 must be tempered with some circumspection. Definitive treatment recommendations would seem to depend on further randomised trials or meta-analysis of individual patient data.

What is already known on this topic
Corticosteroids as either immunomodulatory or anti-inflammatory agents have potential as therapy in ARDS
A small number of randomised trials and recent systematic reviews have tackled this theory

What this study adds
No convincing treatment effect of steroids in ARDS was evident; the optimal dose, timing, and duration of steroid therapy is not established
Meta-analyses based on a small number of trials with sparse data must be cognisant of limitations in estimation of treatment effects; Bayesian estimation would seem suitable

Footnotes
Contributors: JVP and JLM conceived, designed, and planned the study. JLM is guarantor. PJ, JVP, and IAG were responsible for the electronic search, data collection, abstraction, hand searching of journals, and data entry. JVP, PJ, and IAG quality assessed the trials. JLM and PLG provided statistical expertise. All authors helped draft the manuscript, carried out a literature search of additional articles, and discussed the results.
Funding: None.
Competing interests: None declared.
Ethical approval: Not required.
Provenance and peer review: Not commissioned; externally peer reviewed.

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 Dr. Cameron Kyle-Sidell
Critical Care Doctor from New York City

Blows the Whistle on the dangerous way ventilators \re being used caused up to 70% death rate for people put on ventilators

Please note that after ready the blow information and listing to the above video you will understand why the Prime Minister of the United Kingdom, Borris Johnson who has been diagnosed with some claimed forn of Cororavirus ... is just been given extra oxygen.... probably just using an ozygen mast to improve his low oxygen levels abnd has not been placed on a vertilator which is normally used for the treatment of a viril pheumonia which is what the mainstream medical industry and the governments and the mainstream media around the world .. are all sayiing Corvid-19 is...
There is no doubt that  the Prime Minister of the United Kingdom, Borris Johnsonwould be given the best medical treatment possible in the world and no medical risks would be made with  the Prime Minister of the United Kingdom, Borris Johnson...... so they have just given  the Prime Minister of the United Kingdom, Borris Johnson just extra oxygen ... rather than putting him on a vetilator ..wheh the statistics are clear.... arounf 70% of the people that have been connected to ventilators for the treatement of the  so called "Corvid-19" .. have died.... leaving one think that it is the way the ventilators have been used on patients that has caused them to die .. and not the original disease .. whatever it is.... that caused the, to die...
Please listen carefully to what this man says .... he has NOTHING to gain by sharing this...
I have comments at the end
YT: Dr. Cameron Kyle-Sidell
Critical Care Doctor from New York City
"...Nine days ago I opened an intensive care unit to care for the sick.... Corvid-19 Patients in this city...
In these none days I have seen things that I have never seen seen before .. in treating these patients I have witnessed medical ...  phenomenon   ...that don't make sense in treating a disease that is supposed to be a virus pheumonia ... nine days ago I thought I was opening an intensive care unit to treat patients for a virus causing a  pheumonia ... that was ravaging lungs across the world ... starting out as something mild .... cough a sore throat ... an progressivly increasing the severity until ultimately ending in something called acute respiratory distress syndrome ... of ARDS ... this is the paradime that every hospital in the coutry (USA) is working under ... this is the disease.... ARDS ... that every hospital in preparing to treat .... and this is the disease ... ARDS ... fro which in the next 2 to 6 weeks ...100,000 Americans might be put on a ventilator ... . and yet evrything I have seen in the last nine days....  all the things that just don't make sense .... the patients I've seen in front of me ... the lungs I am trying to improve ... have let me to beleive that Covid-19 is not this disease.... and that we are operating under a medical paradime that is untrue ... in short I believe that we are treating the wrong disease .... and I fear that this misguided treatment will lead to a tremendous amount of harm to great number of people in the United States in a very short time .... as New York City appears to be about 10 days ahead of the country I fell compelled to get this information out.... Covid 19 Lund Disease as far as I can see .... is not a  pheumonia, and should not be treated as one ... rather that it appears that some kind of viril induced disease most resembling high altitude sickness .... it is as if tens or thousands of my fellow New Yorkers are on a plane at 30,000 feet and the cabin pressure is slowly being let out ... these patients are slowly being straved on oxygen .... I've seen patients dependant on ozygen .. take of their oxygen mast and quickly go through a state of anxiety and immotional distress and eventually get blue in the face ....  while they look like patients absolutely on the brink of death ... they do not look like patients dying of  pheumonia .... I have never been a moutain climber and I do not know what the condition are at base camp in the higest peaks in the world .. but i suspect that the patients that I am seeing in front of me look most like as if a person was dropped off the top of mount Everist without time to act on it ....I don't know the final answer of this disease ...  but I am quite sure that a ventilator is not it .... that is not to say that we don't need ventilators ... we absolute;y need them ... they are the olnly way at the time we are able to give a little more oxygen to patients who need it ... but when we treat people with ARDS ... we typically treat ventilators to treat what is called  respiratory failure ... that is that we use the ventilator to do the work that the patients musles that we can no longer do because ... they are too tired to do it ...these patients musles work fine...  I fear that if we are using a false paradime to treat a new disease .. the method that we program the ventilator ... based on a notion of  respiratory failure ... as oposed to oxygen failure ... that this metod.... and there are a great many other number of methods ...we can use with the ventillator ...  but this method being widely adopted at this very momment in every hospital in the USA ... which is based on creating increased pressure on the lungs in order to open them up is actually doing more harm than good . and the presure that we are providing to lungs... we may be providing to lungs that can not stad such high pressure ... that can not take it and that the ARDS that we are seeing that the whole world is seeing maybe nothing more than lung injury that is caused by the ventilator .. I don't know the final answer to the disease ... I do sense that we will have to use ventilators .. we will have to use a great many number of ventilators and we will need a many number of ventilators ... but I sense that we can use them in a much safer way .. in a much safer method ... that safer method challenges long held dogmatic beliefs within the medical comunity and among lung specialists which will not be easy to overcome .. but I really beleive that they must be overcome .. there are hundreds of thousands of lungs at risk ... and the time to overcome them is now ... I am confident that those of us who work bedside with these patients.. those of us that are witnesssing these things that we have never scene before ... dispte the many years we have worked with the many thousands of patients and diseases we have seen ... if we can effectively communicate this to all those that are so important but are bedside .. the resreachers, the administrators ... thos who procure our resources and make our protocols .. the politicians ... our own governments ... if we are able to convince them that this is a disease that is different than anything that we have every seen before .. I am confident that an answer can be found and that effective treatments can be discovered .... and that a plan to diseminate that treatment can be deployed... and the tens of thousands of lives and hundreds of thousands of lungss will be protected ... the time for this is now ... we are stairing into a future where many of our great Americans are going to suffer ... we are all involved in this future ... so i urge you .. for those of us .. who are out there.. those who work bedside I urge you to speak up .. we can change this .. I thank you all for listening... please spread the message and stay safe... "
"... It the light of this important message of this doctor I want to add that he has noting to gain at all by giving you this .. unlike the plethera of people on the news ... like Bill Gates who have a lot to lose by you taking his advice ... this Dr has noting to gain and everything to lose .. but I would like to make a few comments.... and please take my comments like a grain of salt... don't believe anything I say ...  do your own research ... but I would like to poijt put here ...that i smy video on 60 GHz FIEGE I roughly explained how the uptake of ozygen ,,, to homoglobin .. can be potentaially interfered with electro magnetically .. since releasing that video I have had further confirmation from  Molecular Scientists ... specialising in ozygen ... I'll show that later ... it well know that  60GHz is obsorbed by oxygen .. I showed you footage of how the heads of telecome admit under oath that ther have been no industry safety testing of these frequencies that they are saying that they will release in an expedited manner ... 
No safety testing on human
No safely testing on the environment
we need further testing to be done before we continue to unlease these frequencies on the world ... 
That video was subsequently removed  by YouTube... 
Now this doctor admits this.... whatever it is that he has seen coming into hsi ICU is unlike anything that he has ever seen before .... he say that he has witnesses medical   phenomenon in the context of treating a disease that is supposed to be viril pheumonia .. the thing that they are telling you all over the media that is without a doubt... the Dr describes that the paradime that they are told that they would be treating is ARDS ... 
Acute Respiratory Distress Syndrome ARDS.. yet everything I have seen in the laast nine days... all of the things that don't make sense .. patients I'm seeing infront of me... tge lungs I am trying to improve have led me to believe that this Covid -19 is not this disease ... he says it is not behaving as a viril pheumonia.. he says that we are operating in a medical paradime that is untrue.... and he adss that he fears thart this misguided treatment will lend to a tremendous amount of harm to a great number of people in a very short period of time .. are you listening.. he calling this oxygen failure .. and whatever this is can be exasterbated by the use of ventilators .. you heard the dr say it... nome say it.... it is not acting as a viril pheumonia .. and it should not be treated as a viril pheumonia .. again the head doctor in the ICU in New York City is saying this .... not me .. I have no medical advice on this topic .. I'm simply asking? 
Can we confirm that 60  GHzhas actually been unleased in New York City .. are there any whistlebowers out there... who install small cell towers who have seen the fequencies on the side of the cell towers .... come to me and let me know where they have installed this stuff so we can start gather information .. perhaps .. just maybe .. this thing is not what we are being told...

In New York City Skywire uses what’s called lightly licensed 70-80 GHz spectrum for a fixed wireless service

https://www.fiercewireless.com/wireless/special-report-millimeter-wave-spectrum-has-come-a-long-long-way

In New York City, a much smaller company called Skywire uses what’s called lightly licensed 70-80 GHz spectrum for a fixed wireless service, reaching neighborhoods that don’t have adequate broadband from other sources. And it’s not just urban areas. In a paper titled “Millimeter Wave Wireless Communications: New Results for Rural Connectivity,” NYU Wireless researchers described in detail the measurements and models that validate rural millimeter wave path loss models.

o be sure, a lot of spectrum bands are in play at the FCC. Commissioner Jessica Rosenworcel has identified open dockets in the 3.5 GHz, 3.7-4.2 GHz, 6 GHz, 24 GHz, 28 GHz, 32 GHz, 37 GHz, 39 GHz, 42 GHz, 47 GHz, 50 GHz, 70 GHz and 80 GHz, among others.
Meanwhile, the commission is seeking to unleash new spectrum in frequencies above 95 GHz—“way, way up there” spectrum that some see as going overboard. But FCC Chairman Ajit Pai said the point is the U.S. must be open to new technologies that haven’t even been developed. "While we don’t know precisely how far the laws of physics will permit us to go, we do know there’s potential and interest. Engineers and entrepreneurs need to have the ability to push the envelope," he said.

Pai noted that the skeptics have been proven wrong before. So, who knows how far engineers will push the envelope in the next 10 years?
My channel is at great risk of being delited.. For sharing what is being deemed "inappropriate"
Thaks for listening... God Bless You .. I Love You .. I hope to talk to you very soon... 
To ensure we stay connected please go to www.missdanaashlie.com & sign up with your EMAIL for links to uploads in future.
Also, subscribe to "Dana Ashlie too" on YT for a backup channel. 
FCC Modifies Part 15 Rules for Unlicenses Operation in 57-64 GHz Band
Mr. Blumenthal 
Fierce Telecom
Trump's new infrastructure plan allocated $50 Billion to rual area investments, eases small cell deployments 
by Sean Buckly feb 13th 2018  

Figure 1:
Illustrates the atmosperic absorption for millimeter wave frequencies.
At the millimeter wave frequency of 60GHz, the absorption is very high, with 98 percent of the trasnmitted energy absorbed by atmospheric oxygen. While oxygen absorption at 60GHz severely limits range, it also eliminates interferences between same frequency terminals.
Bood In]CO2 Our to Alveoli O2In back into the blood... I'll show that later ... I will show that it is well known that  60 GHz FEGE is obsorbed by oxygen ...
Sub10 Systems: Oxygen absorbtion makes 60 GHz perfect for backhaul  
by 
Fixed Wirelss Communications at 60GHz Unique Oxygen Absorption Properties
News 10th April 2001
Elsevier
Science Direct
Journal of Molecular Spectroscupy 231 (2004) 1-14
Molecular Spectroscupy
60-GHz oxygen band: precise braodening and central fequencies of fine-structure lines, absolute absorption profile at atmosperic pressure, and revision of mixing coefficients 
M.Yu. Tretyakov, M.A. Koshelev. V.V. Dorovskikh, D.S. Makarov, P.W. Rosenkranz
Istutute fo Applied Physics of R.A.S. 46 Uljamora Street, 603950 Nizhmit Norgorad, Russia
Massachuusetts Institute of Technology, Cambridge, M.A. 02139, USA
The demand for bandwidth is gaining at a rapod pace. International Delta Corporation projects that Internet commerce in the United States will grow from $74 billion in 1999 to $708 billion in 2003, with the number of computer users more than doubking from 81 million ti 177 million in the U.S alone. Due tot he tremendous expected growth, reliable fiber optic networls must be installed quickly ...
Mask vs. 60 GHz??
 Altitude sickness, is the mildest form being acute mountain sickness (AMS), is the negative health effect of high altitude, caused by rapid exposure to low amounts of oxygen at high elevation. Symptoms may include headaches, vomiting, tiredness, trouble sleeping, and dizziness.  

Doctors Puzzle Over COVID-19 Lung ProblemsBy Brenda Goodman, MA
https://www.webmd.com/lung/news/20200407/doctors-puzzle-over-covid19-lung-problems 
 April 7, 2020 -- As doctors treat more patients who are severely ill from COVID-19, they’re noticing differences in how their lungs are damaged.

Some patients coming to the hospital have very low oxygen levels in their blood, but you wouldn’t necessarily know it from talking to them. They don’t seem starved of oxygen. They may be a little confused. But they aren’t struggling to breathe.
When doctors take pictures of their lungs -- either with a CT scanner or an X-ray machine -- those also look fairly healthy. The lungs may have a few areas of cloudiness and crazing, indicating spots of damage from their infection, but most of the lung is black, indicating that it is filled with air. 
 One doctor treating COVID-19 patients in New York says it was like altitude sickness. It was “as if tens of thousands of my fellow New Yorkers are stuck on a plane at 30,000 feet and the cabin pressure is slowly being let out. These patients are slowly being starved of oxygen,” said Cameron Kyle-Sidell, MD, an emergency room and critical care doctor at Maimonides Medical Center in Brooklyn who has been posting about his experience on social media.

“A whole bunch of these patients really have low oxygen, but their lungs don’t look all that bad,” says Todd Bull, MD, director for the Center of Lungs and Breathing at the University of Colorado School of Medicine, in Aurora.
Doctors in Italy have noticed the same thing. And in some cases, that might mean patients need to be treated a little differently to ensure the best outcome.
In an editorial in the journal Intensive Care Medicine, Luciano Gattinoni, MD, a guest professor of anesthesia and intensive care at the University of Gottingen in Germany, and one of the world’s experts in mechanical ventilation, says more than half the patients he and his colleagues have treated in Northern Italy have had this unusual symptom. They seem to be able to breathe just fine, but their oxygen is very low.
According to Gattinoni, about 30% of COVID-19 patients who come to the hospital have more classic symptoms of acute respiratory distress syndrome, or ARDS. Their lungs are cloudy on imaging scans, and they’re stiff and inflamed, showing that they aren’t working well. The patients also have low levels of oxygen in their blood, and they are struggling to breathe. They look like patients with severe pneumonia caused by a virus. This is the type of lung trouble doctors are more used to seeing with respiratory diseases like influenza and SARS.

Gattinoni says doctors need to pay attention to how COVID-19 has affected the lungs and breathing of each patient they’re treating before deciding on treatment. Patients with more classic ARDS-type COVID-19 often need mechanical ventilation right away, which forces air into the lungs to increase oxygen.

Patients with respiratory failure who can still breathe OK, but have still have very low oxygen, may improve on oxygen alone, or on oxygen delivered through a lower pressure setting on a ventilator.

Gattinoni thinks the trouble for these patients may not be swelling and stiffening of their lung tissue, which is what happens when an infection causes pneumonia. Instead, he thinks the problem may lie in the intricate web of blood vessels in the lungs.
Normally, when lungs become damaged, the vessels that carry blood through the lungs so it can be re-oxygenated constrict, or close down, so blood can be shunted away from the area that’s damaged to an area that’s still working properly. This protects the body from a drop in oxygen.
Gattinoni thinks some COVID-19 patients can’t do this anymore. So blood is still flowing to damaged parts of the lungs. People still feel like they’re taking good breaths, but their blood oxygen is dropping all the same.
This problem with the blood vessels is similar to what happens in a condition called high-altitude pulmonary edema, or HAPE, says Bull.
HAPE patients recover when you bring them down from a high altitude and give them oxygen. They are sometimes also placed on ventilators and treated with medicines including diuretics to remove fluid that’s flooded their lungs. More research is needed to know if any of those strategies may help COVID-19 patients. Steroids, in particular, have not been shown to help with ARDS and may make it worse.
“Is it possible that there’s a problem with how the blood vessels regulate blood flow? That is, I guess, a possibility, which would be different than what we usually see in ARDS,” Bull says.
“This is just a hypothesis at this point. It has to be proven,” he says.
It’s also important to note that patients with relatively normal-looking lungs can progress to ARDS as the virus attacks their lung tissue, Gattinoni says.
He says these patients with more normal-looking lungs, but low blood oxygen, may also be especially vulnerable to ventilator-associated lung injury, where pressure from the air that’s being forced into the lungs damages the thin air sacs that exchange oxygen with the blood.

In normal breathing, our lungs expand because of negative pressure. A large thin muscle at the bottom of the lungs, called the diaphragm, pulls down and our lungs expand to fill the increased space. But ventilators work by forcing air into the lungs, which is positive pressure, like what happens when you blow up a balloon. These machines can help people whose lungs have become too weak to work, but they can also cause damage because they force the lung to work in a way it wasn’t designed to.
“When those pressures get too high, you can cause trauma to those little air sacs. Those are very fragile,” says Michael Mohning, MD, a pulmonologist and critical care specialist at National Jewish Health in Denver.

Gattinoni says putting a patient like this on a ventilator under too high a pressure may cause lung damage that ultimately looks like ARDS.
So he cautions that doctors need to be aware of the COVID-19 patients’ symptoms  and need to use the ventilator carefully and sparingly.
In an interview with MDEdge, Gattinoni said one center in central Europe that had begun using different treatments for different types of COVID-19 patients had not seen any deaths among those patients in its intensive care unit. He said a nearby hospital that was treating all COVID-19 patients based on the same set of instructions had a 60% death rate in its ICU.
"This is a kind of disease in which you don't have to follow the protocol -- you have to follow the physiology," Gattinoni said. "Unfortunately, many, many doctors around the world cannot think outside the protocol."
Other experts agree.
“If you over-distend somebody’s lung on mechanical ventilation, you essentially generate more ARDS. You make the lung leaky,” Bull says.
He says pulmonologists have gotten much better at using ventilators to make them safer for patients. Doctors work to keep the pressure on the lung as low as possible, to prevent that damage.
Several recent studies have helped to cut the death rate for patients who need to be on a ventilator. The PROSEVA study, published in The New England Journal of Medicine, showed the death rate among ventilated patients could be as low as 16% under optimal care.
So far, death rates for ventilated patients with COVID-19 have been higher than that. That could be because some COVID-19 patients often need to be on ventilators for a long time, sometimes as long as 2 weeks. They also tend to have other conditions, so it’s possible that they are sicker to begin with. More research is needed to understand why, and doctors will continue to share best practices as they see things that need to be addressed.
WebMD Health News Reviewed by Neha Pathak, MD on April 07, 2020

Doctors Suspect Mystery COVID-19 Lung Problems, Plea for New Approach
https://www.medicinenet.com/script/main/art.asp?articlekey=230110 
  By Peter Schelden on 04/09/2020 
  Some doctors are questioning the way ventilators are being used for people with serious cases of COVID-19. Why? More data shows a high death rate for patients treated under current ventilator practices.
At the same time, these doctors are saying their patients behave more like they have high altitude sickness than a viral infection. They talk about two different types of COVID-19 patients with differing severe lung problems.
While some patients respond to treatment as expected, doctors also describe patients whose lungs seem relatively fine, but who still can't get enough oxygen into their blood. These patients may make up the majority with severe infections.
This is why some are asking other doctors to consider changing how they treat some people in severe condition from COVID-19.
This conflict in treatment approaches shows in real time how doctors are adjusting their tactics against a novel and dangerous infection.
And it shows the persistence and diligence necessary to shift the medical establishment's practices once a treatment protocol has been established, even when evidence begins to show that treatment is less effective than once believed.

NY Doctor Finds Odd Lung Patterns
Assessing the outcomes of COVID-19 patients on ventilators, Brooklyn emergency room physician Dr. Cameron Kyle-Sidell found worse outcomes than expected. He told Medscape that around 70% of COVID-19 patients on ventilators never recover, based on his research.
What's more, the doctor noticed disturbing patterns he had never seen before. COVID-19 patients on ventilators sometimes showed extremely low blood-oxygen concentrations during ventilation, he said. Despite doctors' best efforts, he reported seeing concentrations of oxygen in blood at 10% to 20%, and sometimes even lower – a healthy blood oxygen level is above 95 percent, according to the British Lung Foundation.
Not only that, but some COVID-19 patients seem less obviously impaired by their low blood oxygen levels than he expected.

"In the past, we haven't seen patients who are talking in full sentences and not complaining of overt shortness of breath, with (blood oxygen) saturations in the high 70s," he said. "You get used to seeing certain patterns, and the patterns I was seeing did not make sense."

How Successful Are Ventilators for COVID-19?
Doctors and scientists studying the mortality rate of COVID-19 patients on mechanical ventilators say the available data is tricky to assess. Some studies put the death rate for coronavirus patients put on ventilators as low as 25%. But many report much higher rates, ranging anywhere from about 50% to as high as 98% in one instance.
For example, in a UK study of 98 COVID-19 patients who received "advanced respiratory support," which included invasive ventilation and tracheostomy, 66% died, according to the nation's Intensive Care National Audit and Research Center (ICNARC).

New York City hospitals have reported an even higher COVID-19 ventilator death rate. Roughly 80% or more of patients placed on ventilators there have died, according to AP News. The agency reports that typically only about 40% to 50% of patients on ventilators for non-COVID-19-related lung problems die. The percentage is high compared with the prognosis for some other medical procedures because, in general, doctors hold off on administering invasive ventilation until it is medically necessary, which means the illness is already quite serious before intubation.
Though data continue to emerge, some doctors feel enough already exists to justify new approaches to treating the most serious COVID-19 cases.

Why Ventilators Are Used for COVID-19
Facing COVID-19 for the first time, healthcare workers have largely relied on treatments that have worked in the past.
The primary model for maintaining healthy oxygen levels in patients with severe respiratory symptoms comes from past treatments of patients with acute respiratory distress syndrome (ARDS).
ARDS is not the same as COVID-19, but ARDS may be one of the conditions caused by the coronavirus disease. ARDS, a lung condition that leads to low oxygen levels in the blood, can be caused by various infections and injuries, according to an article edited by MedicineNet medical editor Melissa Conrad Stöppler, MD. She said these causes may include pneumonia, lung injury, and bacterial sepsis.
Some patients with severe COVID-19 appear to improve using ARDS treatment protocols. However, "an overwhelming number of patients" in northern Italy showed characteristics "in sharp contrast to expectations for severe ARDS,"

according to a letter to the editor published in late March by the American Journal of Respiratory and Critical Care Medicine.

The letter's author, anesthesiologist Dr. Luciano Gattinoni, led Brooklyn's Dr. Kyle-Sidell to change his approach at the front lines of treatment. But his efforts to shift the protocol forced the New York doctor to step down from his ICU position to work in the emergency room instead, where he could ethically use his experience and new techniques outside the standard ICU protocol.
Based on Dr. Gattinoni's observations, as well as his own experiences and those of colleagues, Dr. Kyle-Sidell began to look for other conditions as a model—specifically "the bends," or depressurization sickness experienced by SCUBA divers, and high-altitude sickness.

"Clinically (some COVID-19 patients) look a lot more like high-altitude sickness than they do pneumonia," he said.
What Is High Altitude Sickness?
At 8,000 feet above sea level, people may begin to develop high altitude sickness, says MedicineNet medical author William C. Shiel Jr., MD, FACP, FACR.
"As altitude increases, the concentration remains the same but the number of oxygen molecules per breath is reduced," Dr. Shiel said.
This is a danger familiar to mountain climbers, who have to take long breaks from their upwards climb to let their bodies adjust to working with less oxygen, he said.
High altitude sickness often improves with taking breaks when needed, staying hydrated, and eating a proper diet. He also says that two drugs can be taken to help prevent the condition, but also warns of their serious side effects:

DIAMOX (acetazolamide): DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation.
Dexamethasone (a steroid): It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). However steroids have been shown to be unhelpful in treating ARDS, and may worsen symptoms instead.
Dr. Shiel advises that these medications only be taken at the recommendation of a doctor. A study published March 30 specifically warns against treating COVID-19 patients with steroids, as the WHO has reported conflicting evidence with respect to their use in treating viral infections.

Proposing an 'Oxygen First' Strategy
DIAMOX (acetazolamide): DIAMOX (acetazolamide) allows a person to breathe faster and so metabolize more oxygen, thereby minimizing the symptoms caused by poor oxygenation.
Dexamethasone (a steroid): It decreases brain and other swelling reversing the effects of acute mountain sickness (AMS). However steroids have been shown to be unhelpful in treating ARDS, and may worsen symptoms instead.
Dr. Shiel advises that these medications only be taken at the recommendation of a doctor. A study published March 30 specifically warns against treating COVID-19 patients with steroids, as the WHO has reported conflicting evidence with respect to their use in treating viral infections.

Proposing an 'Oxygen First' Strategy
Dr. Kyle-Sidell was influenced to treat his patients differently after reading Dr. Gattinoni's letter.
He described what he found in the letter was a description of two different types of patient with severe lung problems from COVID-19.
"If you think of the lungs as a balloon, typically when people have ARDS or pneumonia, the balloon gets thicker," Dr. Kyle-Sidell told Medscape. "So not only do you lack oxygen, but the pressure and the work to blow up the balloon becomes greater. So one's respiratory muscles become tired as they struggle to breathe. And patients need pressure. What Gattinoni is saying is that there are essentially two different phenotypes, one in which the balloon is thicker. (But) imagine if the balloon is not actually thicker but thinner, so they'd suffer from a lack of oxygen. But it is not that they suffer from too much work to blow up the balloon."
In other words, some COVID-19 patients have little trouble "blowing up the balloon" of their lungs, yet still suffer from low oxygen.
For patients of COVID-19 who show these symptoms, Dr. Kyle-Sidell began to apply an "oxygen first" treatment method.
This means getting patients' blood-oxygen levels as high as possible, and doing so using the lowest air pressure possible, he said.
And for him, that meant stepping down from his role in the intensive care unit.
"These didn't fit the protocol, and the protocol is what the hospital runs on," he told Medscape. "We ran into an impasse where I could not morally, in a patient-doctor relationship, continue the current protocols which, again, are the protocols of the top hospitals in the country. I could not continue those. You can't have one doctor just doing their own protocol. So I had to step down."
The role switch may be good news for the doctor and his 'oxygen first' strategy; in his new emergency room role at Maimonides in Brooklyn, Dr. Kyle-Sidell is setting up to use a new ventilation strategy based on Dr. Gattinoni's latest recommendations.

Doctors Suspect Mystery COVID-19 Lung Problems, Plea for New Approach
THURSDAY, April, 9, 2020 -- Some doctors are questioning the way ventilators are being used for people with serious cases of COVID-19. Why? More data shows a high death rate for patients treated under current ventilator practices.
At the same time, doctors are saying patients are showing mystery COVID-19 lung problems and symptoms. Some behave more like they have high altitude sickness than a viral infection..
[Some doctors are questioning the way ventilators are being used for people with serious cases of COVID-19.]
By Peter Schelden on 04/09/2020 2:00 PM
 
80% of NYC's coronavirus patients who are put on ventilators ultimately die, and some doctors are trying to stop using them

The Downside of Mechanical Vdentilators
being on a ventilator for Covid-19 Long-Term Can be Damaging 
YouTube Statement made by New York Medical peop;e on Yahoo News
Lindsey Theis...
Newsy health and Wellness Reporter T@LINDSEYTHEIS
For realy sick people ventilators could mean the difference between life and death .....however they can come with some harmfull impacts... 
Dr Ben Singer ... Pulmonary and Critical Care Specialist, Northwestern Medicine... 
,... ".. the longer amount of time patients are on a ventilator ..that reflects that their lungs are very slow ...to heal from Covid-19  ..."
Doctors say that patients that seriously ill Covid-19 patients need mecalical ventilation for at least two weeks before they see any recovery .. ventilators use pressure to blow air in and out of the lungs ... bringin oxygen in and taking carbon monoxide out ....  doctors and nurses have to enter a tube into a patients mouth and wind pipe and monitor the patient with a machine  hooked up to the tubes .. they can adjust the pressure of the air ot peep based on a patients oxygen level...
Dr. Brian Boer ... Pulmonary and Critical Care Specialist, University of Nebraska Medical Centre ....
".... the ventilator is doing the work of the normal breathing.. now you are not using your own oxygen muscles .. the machine is actually pushing each breath into you ... ... so your require various amounts of pressure to achieve each breath ... "
One new study found that nearly 1,600 critically ill Covid-19 patients in Italy .... 99% required respiratory support and 88% were intubated ...   and put on a mechanical ventilatior/intubated ... researches guessed the high rate of interbation and ventilation was because these cases had high levels of hipoxia or low blow oxygen levels .... the move sever your  case the higher level of  Positive End-Expiratort Presure (PEEP) Presure Setting on the ventilator ... Dr. Brian Boer heled design the ICU's Covid-19 guidlines at the University of   Nebraska Medical Centre ...  and walked me through some of them ... he says managing the PEEP is a balancing act .... 
".. the more diseased or injured your lung is ... such as Covid-19 or any other for of ARDS .. the lung gets very very stiff .. and so you then reqire much higher pressure or driving pressures with the ventilator to achieve the same sized breath as you would normally breath .. .. so you have to push harder and harder to get he air into the lungs ... and not only that .. to get the air into the lungs.. the efficiency of the oxygen getting into the blood stream and the carbon dioxide getting out of the bl0od stream ... is lower and lower because the lung is so injured ....."
Lindsey Theis...
The problem arises when patients have to stay on a high pressue ventillator setting for a long period of time ...  every hour .... every day on the ventillator increases the risk of permanent lung injury  or infection...
  Dr Ben Singer ... Pulmonary and Critical Care Specialist, Northwestern Medicine...  
".. we are at risk to develop  a new peumonia caused by a bacteria just by virtue of being connected to the ventilator ... 

Lindsey Theis...
For those who survive there are long term mental and physical complications ahead from learning how to eat and speak again and regaining cogitive function  ... Vanderbuilt psychologist  and researcher Dr. James Jackson has spent years researching the pschological impact of former  ICU patients .. 
he says .. besides all the phyical after effects .. as many as 20% struggle with PTSD 
    Dr. James Jackson,  psychologist  and researcher Vanderbuilt  University ...  
".. we think that the trauma of being critically ill .... and it includes being on a ventilator .. but it's not only that .. it's  fear of dying.. it's pain.... they come into hospital .. they experience the insults that critical illness represents .. they expeirience a heady burden of trauma .. and then even though they survive .. which we a all very delighted about ... they have a brad new list of difficulties ... that they didn't have before .. they tend to have problems with their memory ... they have problems with their attention... they have problems with someting we call executive functioning ... they can't balance their check book... they have a hard time driving ...  they can'r read maps... can't program a remote control ... they they are quite disorganised .. then a meaningful percentage of those folks have significant issues with depression ... 
  Lindsey Theis... 
there are less aggresive alternative  to mechanical ventilation ... such as Oxygen Cannulas Pumps .. some dcotors have stocked up with over the head divices such as Helmet Ventilators .. and in a few severe cases ..usually reserved for  cases usually reserved for heart patients  Extracorporeal Membrane Oxygenation ECMO has been efffective .. that is when the blood is rerouted and oxygenate din a machine and giving the lungs a hance to rest ....  givng the lungs a chance to rest ... the FDA have just introduced new rules for  ECMO and bipolminary divices to help expand the availablity of Corvid-19 patients .. but these ventinator devises are expensive .. costing up to $50,000 .... ECMO  is evn more expensive... costing up to $73,000 for one patient ...
For the majority of these Covid-19 patients that are going into the ICU and being put on ventilators ... 
one has to ask.... is it ultimately causing more harm than good.. or .. right now is this still the best line of treatment ... 
  Dr Ben Singer .. 
Ventilators and the standard of car for Covid-19 patients  who devlop lung problems..
  Lindsey Theis... 
But doctors still say that they need ventilators to treat the sever Covid-19 cases ... 
but the more they leard about the Covid-19 Virus the more that the exercose caution ... 
  Lindsey Theis... Newsy 

  Dr. James Jackson,  psychologist  and researcher Vanderbuilt  University ... they are completely disorganised ..
   Dr Ben Singer ... Pulmonary and Critical Care Specialist, Northwestern Medicine...   
The longer time patients are on a ventilator .. that reflects that their lungs are very slow to heal ... 
80% of NYC's coronavirus patients who are put on ventilators ultimately die, and some doctors are trying to stop using them
SINÉAD BAKER
Apr 9th 2020 
https://www.aol.com/article/news/2020/04/09/80-of-nycs-coronavirus-patients-who-are-put-on-ventilators-ultimately-die-and-some-doctors-are-trying-to-stop-using-them/23974089/ 
Some doctors are trying to reduce their reliance on ventilators for some coronavirus patients as the death rate for patients using the machines is abnormally high.
New York officials say 80% of coronavirus patients who used ventilators in the city have died, the Associated Press reported. Unusually high death rates have also been recorded elsewhere in the world.
Ventilators are typically only used for the worst-affected patients and there are no drugs to help treat coronavirus, so this could explain the higher death rate.
But doctors also say that ventilators can be damaging to the lungs, and while it may be an effective way to treat other respiratory illnesses, some are now looking for alternative treatments.
There is still a global ventilator shortage, with doctors and healthcare systems calling for more to be urgently made or bought to treat the worst-affected patients.
Visit Business Insider's homepage for more stories.

Some doctors are trying to use ventilators less frequently as some areas report high death rates amid coronavirus patients who have to use them.
Ventilators are machines used to bring oxygen into peoples' lungs, and are typically only used for patients worst affected by respiratory diseases.

Some 40% to 50% of patients with severe respiratory issues die while on ventilators, the Associated Press (AP) reported, citing experts.
New York City has reported that 80% of its coronavirus patients who were put on ventilators had ultimately died, the AP reported, citing state and city officials. It is the worst-affected state in the US.
There have also been reports of unusually high death rates among patients on ventilators elsewhere in the US, China, and the UK, the AP reported.
Putting a patient on a ventilator is an extreme step saved for the most-affected patients, who typically already have the highest chance of dying from respiratory failure.
The higher death rate could be a direct result of this, as well as the fact that there are so far no drugs that can help fight the coronavirus.

Ventilators could be causing further harm to COVID-19 patients, some doctors warn
Some doctors are also concerned that ventilators could actually be further harming certain coronavirus patients as the treatment is always hard on lungs, the AP reported.

Dr. Tiffany Osborn, a critical care specialist at Washington University School of Medicine, told NPR on April 1 that ventilators can actually damage patients' lungs.
"The ventilator itself can do damage to the lung tissue based on how much pressure is required to help oxygen get processed by the lungs," she said.
Dr. Negin Hajizadeh, a pulmonary critical care doctor at New York's Hofstra/Northwell School of Medicine, also told NPR that while ventilators work well for people suffering from diseases like pneumonia, they don't necessarily for coronavirus patients.
She said that most coronavirus patients in her hospital system have ultimately not recovered despite being given a ventilator.

She added that the coronavirus does a lot more damage to the lungs than illnesses like the flu, as "there is fluid and other toxic chemical cytokines, we call them, raging throughout the lung tissue.
Dr. Eddy Fan, an expert on respiratory treatment at Toronto General Hospital, told the AP: "We know that mechanical ventilation is not benign."
"One of the most important findings in the last few decades is that medical ventilation can worsen lung injury — so we have to be careful how we use it."
Doctors are trying to find other solutions and reduce their reliance on ventilators
The lack of treatment options for coronavirus patients have caused most of the world to turn to ventilators for the worst-affected patients.
But the high death rates among ventilator users have prompted some doctors to find alternatives, and reduce the reliance on ventilators, the AP reported.
Dr. Joseph Habboushe, an emergency medicine doctor in Manhattan, told the AP that it had been routine in the city to place particularly ill coronavirus patients on ventilators until a few weeks ago. Now other treatments are increasingly being tried.
"If we're able to make them better without incubating them, they are more likely to have a better outcome — we think," he said.
According to the AP, doctors are trying things like: putting patients in different positions to try and get oxygen into different parts of their lungs, giving patients oxygen through nose tubes, and adding nitric oxide to oxygen treatments to try and increase blood flow.
New York State Health Commissioner Dr. Howard Zucker said Wednesday that officials are examining other treatments that could be used before ventilation, but said "that's all experimental," the AP reported.

The global ventilator shortage
The global shortage of ventilators has become one of the big stories of the pandemic, as doctors around the world are desperately trying to treat patients.
UK private companies are making them amid a shortage in the health service, but they will likely not be made before the virus peaks in the country.
In Italy, doctors had to decide which patients were more likely to survive in order to decide who they would give a ventilator, and have turned patients away due to the ventilator shortage.

In Spain, police asked people to donate snorkels so that their parts could be used to build makeshift ventilators.

And in the US, New York Gov. Andrew Cuomo has decried a ventilator shortage in the state, while states say they have had to battle the federal government for new ones and enlisted private companies to fix broken ventilators received from the federal stockpile. 
Multiple countries have also accused the US of seizing their orders of medical equipment, including ventilators, though the Trump administration denies this.

Some of the world's biggest manufacturers have also pivoted to starting making ventilators, including Foxconn, the world's biggest iPhone maker, and Ford, GM, and Tesla.

And employees in some US companies, including GE, have protested, calling on their employers to get them to make ventilators.

Read the original article on Business Insider
More from Business Insider:
Obama calls out the lack of a 'robust system of testing' for coronavirus in the U.S.
Officials in at least 6 states are accusing the federal government of quietly diverting their orders for coronavirus medical equipment
Fauci says people should 'just forget about shaking hands' even after the coronavirus threat is over[snorkel masks coronavirus]
Police in Madrid, Spain put out a request on Monday, asking the public to donate full-face snorkel masks that can be used as makeshift ventilators for coronavirus patients.

Madrid Police/Twitter[GE coronavirus]
A GE worker takes part in protest demanding the company to use the workforce to produce ventilators and demanding more safety measures in Massachusetts on April 7, 2020.

REUTERS/Brian Snyder[new york city nyc coronavirus covid 19 body bag hospital temporary morgue nurse gurney AP_20097795630696]
Medical workers wearing personal protective equipment wheel bodies to a refrigerated trailer serving as a makeshift morgue at Wyckoff Heights Medical Center on April 6, 2020, in New York City.
John Minchillo/AP
[ventilator]
Workers make ventilators at the SEAT plant in Barcelona, Spain, on April 7, 2020.
[ventilator]
Workers make ventilators at the SEAT plant in Barcelona, Spain, on April 7, 2020

An emergency field hospital in New York's Central Park has one of the ventilators that are in such high demand during the coronavirus pandemic. - Stephanie Keith/Getty Images

​Past and Present ARDS Mortality Rates: A Systematic ReviewJan Máca, Ondřej Jor, Michal Holub, Peter Sklienka, Filip Burša, Michal Burda, Vladimír Janout and Pavel Ševčík
Respiratory Care January 2017, 62 (1) 113-122; DOI: https://doi.org/10.4187/respcare.04716
http://rc.rcjournal.com/content/62/1/113 

AbstractARDS is severe form of respiratory failure with significant impact on the morbidity and mortality of critical care patients. Epidemiological data are crucial for evaluating the efficacy of therapeutic interventions, designing studies, and optimizing resource distribution. The goal of this review is to present general aspects of mortality data published over the past decades. A systematic search of the MEDLINE/PubMed was performed. The articles were divided according to their methodology, type of reported mortality, and time. The main outcome was mortality. Extracted data included study duration, number of patients, and number of centers. The mortality trends and current mortality were calculated for subgroups consisting of in-hospital, ICU, 28/30-d, and 60-d mortality over 3 time periods (A, before 1995; B, 1995–2000; C, after 2000). The retrospectivity and prospectivity were also taken into account. Moreover, we present the most recent mortality rates since 2010. One hundred seventy-seven articles were included in the final analysis. General mortality rates ranged from 11 to 87% in studies including subjects with ARDS of all etiologies (mixed group). Linear regression revealed that the study design (28/30-d or 60-d) significantly influenced the mortality rate. Reported mortality rates were higher in prospective studies, such as randomized controlled trials and prospective observational studies compared with retrospective observational studies. Mortality rates exhibited a linear decrease in relation to time period (P < .001). The number of centers showed a significant negative correlation with mortality rates. The prospective observational studies did not have consistently higher mortality rates compared with randomized controlled trials. The mortality trends over 3 time periods (before 1995, 1995–2000, and after 2000) yielded variable results in general ARDS populations. However, a mortality decrease was present mostly in prospective studies. Since 2010, the overall rates of in-hospital, ICU, and 28/30-d and 60-d mortality were 45, 38, 30, and 32%, respectively.

Introduction
ARDS is a highly heterogeneous life-threatening severe form of acute respiratory failure. It is characterized by an acute onset of hypoxemia refractory to oxygen treatment and the presence of bilateral pulmonary infiltrates on chest radiograph.1–4 The syndrome is based on alveolar-capillary membrane injury followed by the development of pulmonary edema, which cannot be fully explained by heart failure.1–3 ARDS is usually accompanied by multiple- organ system failure and therefore substantially contributes to high morbidity and mortality in critical care.5,6 It increases the cost of treatment of critical care patients by prolonging ICU and in-hospital stay. Reliable epidemiologic data concerning ARDS are important for all critical care physicians. These data facilitate clinical decision making, with implications for the efficacy of current therapeutic interventions, and suggest ways for their future development.7 Moreover, the data help us to better assess the present clinical and economic impact of the condition and may lead to more appropriate resource distribution.

The history of ARDS should be divided into 3 main periods: (1) before 1995 (before publication of the American-European Consensus Conference [AECC] criteria), (2) from 1995 to 2000 (implementation of the AECC criteria and development of lung-protective mechanical ventilation), and (3) from 2001 to the present (the era of lung-protective mechanical ventilation).

The main goals of this systematic review of the literature are to highlight the complexity of ARDS mortality reporting, to outline the trends over the last 2 decades, and to estimate current mortality rates of ARDS, suggesting benchmarks in various clinical trial designs. Moreover, uncertainties and controversies regarding the topic are assessed, and possible explanations are presented.

Methods
We used the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement as a guide.8 A computerized search through the online web database MEDLINE/PubMed was performed. The search was performed by the MeSH (Medical Subject Headings) system using the key words “acute lung injury” AND “acute respiratory distress syndrome” AND “mortality” AND “outcome” AND ”incidence” AND “clinical trial.” The bibliographies of the retrieved articles were also reviewed. Human studies with >20 subjects published from January 1994 to January 2015 were taken into consideration. Non-English articles were included, provided that they contained all required data. Two independent reviewers (MJ and JO) screened the titles, abstracts, and methodological quality of the articles with a high degree of agreement (93.2%). All eligible articles were retrieved in full text (see online supplement I at http://www.rcjournal.com).

The data collected in a data sheet were as follows: study group characteristics (specific vs mixed ARDS population). We defined a mixed population as a group of subjects with ARDS irrespective of etiology. A group of subjects enrolled into the study primarily due to the presence of a unique diagnosis (ie, multiple trauma, sepsis, burns, military injury) or intervention (ie, extracorporeal oxygenation, high-frequency ventilation) was defined as the specific ARDS population. The specific population was omitted from final analysis to improve generalization of the results. Additional extracted data included number of centers, number of enrolled patients with ARDS, time of enrollment (in months), time period when the study was started and performed, type of mortality, and absolute value of the reported mortality rate. The characteristics of the specific ARDS populations are described in Table 1.

Table 1.
Characteristics of the Specific ARDS Populations
Studies with mixed ARDS populations were divided into 3 groups according to the study's methodology: (1) prospective observational, (2) retrospective observational, and (3) randomized controlled trials (RCTs). In prospective and retrospective observational studies, we considered all enrolled subjects with ARDS; in RCTs, we screened only the mortality rates in the control (non-interventional) group to obtain a set of subjects comparable with the observational ones and to avoid possible influence of the intervention.
The reported mortality rates were also categorized by type: in-hospital, ICU, 28-d, 30-d, 60-d, 90-d, 365-d, etc. Some papers reported more than one type of mortality rate. For further analysis, only the most frequent mortality types were selected, and they were analyzed separately: in-hospital, ICU, 28/30-d mortality (note: 28-d mortality and 30-d mortality were considered together), and 60-d mortality. The rest of the mortality types that were reported rarely in the papers were omitted from further analysis.

To assess the aspect of time, we subdivided the main groups (prospective observational studies, retrospective observational studies, and RCTs) into 3 subgroups in relation to the time of the initiation and performance of the study: (1) before 1995, before the publication of the AECC criteria (subgroup A), (2) from 1995 to 2000, when the highlighted ARDS network study9 was published (subgroup B), and (3) from 2001 to the present (subgroup C). Overall mortality rates (weighted by number of subjects) and their trends over time were calculated for all subgroups. Moreover, we separately calculated the most recent cumulative mortality rates since 2010.

To resolve the bias stemming from different sample sizes among the studies, aggregated mortality rates were computed as a weighted average of the mortality rate reported in each study, with the weight being the number of subjects involved. To assess simultaneous influences of the independent variables on weighted mortality, a binomial family generalized linear model was fitted to the data. Ordered categories A, B, and C, which represent the time periods, were encoded using orthogonal polynomial coding, which allows trends to be captured in a linear or quadratic manner.

The terminology and classification of acute respiratory failure used in this review and during the search of databases respected the usual nomenclature in the respective period of time (eg, the AECC criteria).1,2 The authors are aware of the current recommendations to use only the term ARDS according to the recently published Berlin definition.3
The certified statistician (MB) used R 3.2.0 (R Foundation for Statistical Computing, Vienna, Austria) for statistical analysis and for creating the figures and tables presented in this study.10 The data set obtained underwent statistical assessment for quality. Missing values, outliers, and other suspicious values were noted and double-checked. The analysis of the data set dealt mainly with mortality rates (ie percentage rates of occurrence of some event, which is a random variable with binomial distribution). Therefore, to resolve the bias stemming from different sample sizes among the studies, aggregated mortality rates were obtained by computing arithmetic means of reported mortality rates weighted by numbers of subjects included in the studies. To assess simultaneous influences of multiple variables on weighted mortality, a binomial family generalized linear model was fitted to the data.

Results
Study Selection and Characteristics
The initial search identified 1,265 potentially eligible articles. A total of 1,096 papers were excluded for the following reasons: 843 were considered to be not relevant mainly because of their topic, focus, and methodological quality; 85 involved only pediatric subjects; 20 were preventive; 25 used an inappropriate definition; 6 were missing required data; 94 were reviews/meta-analyses/post hoc analyses; 5 were congress proceedings/reports; 16 were case reports or included fewer than the required number of subjects; and 2 were currently recruiting for trials. The bibliographies of the retrieved articles contained 8 articles that met the inclusion criteria and were additionally considered for this systematic review. In total, the resulting 177 papers reported 189 enrollment intervals (historical cohorts), which we treated as separate studies (see Fig. 1).

Fig. 1.

Flow chart. RCT = randomized controlled trial. Number of studies (*) may be greater than the number of articles because some articles reported results of studies that can be considered separately (eg, 2 or 3 independent historical cohorts).

Mortality Rates in Relation to Study Methodology and Time Period
In general, mortality rates raged from 13 to 80% in the specific group and from 11 to 87% in the mixed group. More studies screened mixed ARDS populations than specific ARDS populations (n = 139 vs n = 50, respectively). Many articles report multiple mortality rates. The list of specific ARDS populations is displayed in Table 1. The total number of subjects in all selected studies was 38,351.

Among the mixed ARDS population, the most frequently reported type of mortality rate was in-hospital (no. = 50), followed by ICU mortality (no. = 34), 28/30-d mortality (no. = 31), and 60-d mortality (no. = 16). Only studies with mixed population were selected for further analysis (no. = 106). The total number of subjects in the mixed group was 25,966. Figure 2 depicts the number of studies and the total number of subjects involved in studies categorized by mortality type and study methodology. Table 2 shows in detail the number of studies, number of subjects, and average mortality rates related to study methodology, mortality type, and time period.


Fig. 2.
Number of studies and participating subjects, grouped by study type and reported type of mortality. RCT = randomized controlled trial.

Table 2.
Number of Studies Related to Study Methodology, Mortality Type, and Time Period

The generalized linear model with the binomial family was used to assess simultaneous influences of various variables (number of centers, number of months, and study design) on mortality rates. A logarithm of odds ratios (logits) was predicted using the linear regression (see online supplement II). The mortality is significantly influenced by the study design. If the type of mortality is 28/30-d or 60-d, the logits (as surrogate for the mortality rate) decrease significantly by 0.44 or 0.45 (both P < .001, respectively). If the study is prospective (ie, prospective observational studies or RCTs), then the reported mortality increases by 0.2 logits (P < .001).

The orthogonal polynomial contrasts allowed us to evaluate the time period linearity and quadraticity, assessing the influence of time period on the reported mortality rates. The mortality rate has a linear decreasing tendency by logit 0.15 in relation to time period (P < .001). Quadratic influences of time period were not identified as statistically significant.

The mortality rates showed significant dependence on the number of centers. With an increasing number of centers included in the studies, the reported mortality rate decreases by 0.003 logits (P < .001). A dependence of mortality rates on the length of the studies (months) was not found (P = .57).

Table 3 shows the detailed mortality rates in defined time periods (A <1995; B 1995–2000; C >2000) grouped by prospectivity or retrospectivity. Lower mortality was reported in retrospective mode in almost all calculable subgroups (9 of 10). A significant difference was found for 28/30-d mortality rates in period A (P < .001), in-hospital mortality in periods B and C (P < .001, and P < .001, respectively), and ICU mortality rates in period B (P = .018) (4 of 10).

Table 3.
Comparison of the Mortality Rates in Studies With Retrospective and Prospective Design in Different Time Periods

The differences between prospective modes of study subgroups (prospective observational studies and RCTs) are described in Table 4. We found higher mortality in prospective observational studies compared with RCTs in 7 of 9 calculable subgroups with significance for in-hospital morality in periods B and C (both P < .001, respectively), in 28/30-d mortality in the same periods (P < .001 and P = .046, respectively), and in 60-d mortality in period C (P < .001) (5 of 9).

Table 4.
Comparison of the Mortality Rates in Studies With Prospective Design in Different Time Periods

Trends and Recent Mortality Rates
A detailed analysis of trends (see Fig. 3) shows that the mortality rate decline is statistically significant for in-hospital mortality in retrospective observational studies, ICU mortality in RCTs, 28/30-d mortality in prospective observational studies and RCTs, and 60-d mortality in RCTs. There was a mild to moderate decrease tendency for ICU mortality in prospective observational studies and for 60-d mortality in RCTs. There was no significant change in mortality for in-hospital RCTs, ICU mortality in retrospective observational studies, and 28/30-d mortality in retrospective observational studies. The significant increase in mortality was observed for in-hospital mortality in prospective observational studies. The data for calculation of the 60-d mortality trend in retrospective observational studies was missing due to a lack of studies reporting the particular type of mortality. Overall, 7 of the 12 subgroups showed a decrease (58%) and 3 showed stagnation (25%) of the mortality rate trend. Moreover, the mortality rate decrease was present in 6 prospective and one retrospective subgroup.


Fig. 3.
Weighted averages of reported mortality rates in retrospective studies (A), prospective studies (B), and randomized controlled trials (C). Reported mortality types are in-hospital, ICU, 28/30-d, and 60-d mortality.
Table 5 summarizes the absolute values of the most recent mortality rates since 2010. Currently, the overall rates of reported in-hospital, ICU, 28/30-d, and 60-d mortality are 45, 38, 30, and 32%, respectively.

Table 5.
Absolute Values of the Most Recent Mortality Rates, Since 2010

Discussion
Reporting of ARDS epidemiology is extremely heterogeneous. Its variability is based not only on differences between causal factors (type and intensity) and route of lung injury (pulmonary vs extrapulmonary ARDS) but also on genetic background, the presence of various complications (ie, secondary infections), and either acute or chronic comorbidities. The cause of death in patients with ARDS is usually not lung pathology per se but mostly concurrent extrapulmonary organ dysfunction. Early mortality is often related to the causal factor of the lung injury, and late mortality is more associated with complications (eg, sepsis and multiple-organ system failure).11,12

From the first clinically relevant description of acute lung injury/ARDS in 196713 to the early 1990s, the epidemiological data often yielded ambiguous and biased results due to the lack of generally accepted diagnostic criteria. The studies also included subjects with infantile respiratory distress syndrome, acute kidney injury, fluid overload, drug intoxication, disseminated intravascular coagulation, and burns.14 AECC criteria established in 1994 enhanced the diagnostic accuracy of the syndrome and facilitated research in the field. However, many articles published in this period reported mortality rates in a surprisingly wide range from 15 to 72%.6,15–25 Our findings confirmed the wide span of mortality rates during the time period (ie, from 13 to 80% in the specific group and from 11 to 87% in the mixed group). The third period (since 2001) is characterized by the implementation of lung-protective mechanical ventilation positively affecting the mortality of ARDS.9

The mentioned mortality differences could be explained by a type of the causal pathologic condition (eg, sepsis and hospital-acquired/ventilator-associated pneumonia are associated with higher mortality, whereas trauma-related injury or aspiration is associated with a lower mortality).26,27 The incidence of nosocomial infections varies among regions,28 with the type of pathogen (viruses vs bacteria, antibiotic-sensitive vs multidrug-resistant bacteria) also playing a significant role.29,30 The other explanations are as follows: population-based features (eg, composition of genetic factors, age, and sex); environmental features (eg, level of economic development, prevailing type of industry, local environment, cultural habits); health-care system differences (eg, health-care policy and area coverage, type of health insurance, and financial resources); research-related factors (eg, variability in the process of diagnosis; time factors [length of the enrollment, years vs months]; number of centers and ICUs involved; number of ICU beds; and type of data collection, processing, and storage). More reasons for the mortality-related differences could be (1) the data acquisition in various regions during specific time periods (ie, the changes in etiological patterns during year [incidence of viral infections in late winter, incidence of multiple traumas during warm seasons]; (2) the incomplete application of favorable interventions for patients with ARDS in routine practice; (3) the absence of discrimination between the terms acute lung injury and ARDS in diagnostic process or using the inappropriate term “acute respiratory failure”; (4) changes in the frequency of specific forms of ARDS (eg, due to outbreaks of various infectious diseases [severe acute respiratory syndrome or influenza A H1N1 2009]); (5) gradual increases in mean age and the number of serious comorbidities of subjects; and (6) differences in the general hospital management of subjects after discharge from ICU, which might contribute up to 3–15% of the overall mortality.31,32 These mentioned factors might also limit our analysis and findings. Moreover, we observed that the types of mortality rates reported by studies often vary (eg, overall, 28-d, 30-d, 60-d, 90-d, in-hospital, ICU, 8-week), which significantly contributed to the inconsistency among clinical studies. The 28/30-d mortality and 60-d mortality are qualitatively different from ICU and in-hospital mortality. We suggest that due to the extended hospital stay of patients with ARDS, the ICU and especially in-hospital mortality are close to or may even be longer than 28/30 d. The 60-d mortality is described in a limited number of studies mostly reporting just one type of mortality. One can see in Figure 3 that in the corresponding time periods, in almost all cases, overall 28/30-d mortality is lower than 60-d mortality, as could be expected. The same applies also for ICU and in-hospital mortality. The particular study methodology could have a significant influence on reported mortality values and might be a source of bias.

Given the known problems of static mortality data, an analysis of the kinetics (trends) of mortality rates over time33–38 seems more valuable. In the period before 1994, several studies reported steady mortality rates (51 ± 19%) from 1967 to 1994.39 However, Milberg et al40 reported different results, describing a steady state of mortality from 1983 to 1987 and a subsequent decline until 1993. In another single-center study, the cohorts of subjects in specific years (1982, 1990, 1994, and 1998) presented a decrease in overall mortality, from 68% in 1982 to 29% in 1996, with a plateau in the mid-1990s.41 In 2008, Zambon and Vincent15 analyzed 72 studies, including a total number of 11,426 subjects, and described a tendency for mortality to decrease from 1994 to 2006. They reported a wide range of mortality rates, from 15 to 72%, with an overall pooled mortality of 43%. They observed reductions in mortality in both interventional and non-interventional studies (trials with and without inclusion/exclusion criteria, respectively). The authors suggested that the improvement in survival may not have only been due to better respiratory management, but several other non-pulmonary factors could also have played a role (eg, better timing and rationalization of therapeutic interventions [antibiotic administration, fluid therapy, blood transfusions], glucose control, hygienic measures, improved infection source control and overall sepsis management).15 The second study challenged the decrease in mortality trends. It analyzed data from 89 studies conducted between 1984 and 2006, including 53 observational and 36 randomized trials with a total of 18,900 subjects. The reported overall pooled mortality rate was 44%. The observational studies showed a decrease in mortality until 1993, but the overall mortality did not decrease from 1994 to 2006. The mortality value was lower in RCTs (36%) than it was in observational studies (44%).16 We subdivided the studies in greater detail according to time, study methodology, and reported type of mortality rate. In contrast to Phua et al,16 we found a significant decreasing tendency for in-hospital mortality in retrospective observational studies, ICU mortality in RCTs, and 28/30-d mortality in prospective observational studies and RCTs over all 3 followed time periods. Furthermore, Phua et al16 found a significant difference between observational and randomized trials (including prospective studies and both interventional and non-interventional arms of RCTs). We did not conclusively confirm their results, because only 5 of 9 of calculable subgroups (56%) were significantly different. The reason for the difference might be that we analyzed a different number of studies (139 vs 89, respectively) including more subjects (25,996 vs 18,900). Moreover, we subdivided the studies according to mortality type and deliberately did not include interventional arms of RCTs due to possible influence of particular intervention on mortality results.

Moreover, we performed a comparison based on prospectivity versus retrospectivity. We found that prospective studies (prospective observational studies and non-interventional arms of RCTs considered together) report significantly higher mortality rates only in 4 of 10 calculable subgroups (40%) compared with retrospective observational studies. Thus, we did not confirm the presumed disadvantage of retrospective data collection: the inability to enroll all eligible patients and missing opportunity to collect all required data.

In the regression model, we found that the number of centers negatively correlated with reported mortality. The reason might be that the studies including more centers enrolled fewer patients per center with more focused management considered as a modified Hawthorne effect within medical staff. The length of the time interval of subjects' enrollment has no significant influence on reported mortality. We suggest that the high variability of the length of studies prevents the demonstration of significance. The linear tendency of mortality to decrease over time might be considered as the most important finding.

Finally, to present the most recent mortality data, we additionally calculated the overall rates for in-hospital, ICU and 28/30-d and 60-d mortality (45, 38, 30, and 32%, respectively) since 2010. We suggest these values as possible benchmarks for further clinical trials reporting the particular types of mortality.

Due to our experience with adult patients only, we omitted results from pediatric studies, and age <18 y of the subjects was one of the exclusion criteria. However, we are aware of the fact that children of adolescent age are somatically almost identical to adults and could have been included. It might be considered as a limitation of this review. However, we were afraid of problems that might have been caused by including the data of school-age and younger children with different physiology and ARDS risk factors compared with adults.

Conclusions

The reported mortality rates are highly heterogeneous and often biased, and their interpretation has many limitations. We advise against the unqualified adoption of reported mortality data from different studies performed in different time periods. Comparing these data with routine practice could be misleading, and using them in designing new clinical trials could diminish the value of the research results. We suggest carefully taking into account the study methodology (observational vs randomized and retrospective vs prospective, specific vs mixed ARDS population), with preference given to prospective modes of data collection and critical consideration of the age and length of the study. The mortality trends suggest a decreasing tendency in prospectively designed studies over time; however, mortality remains high.

Acknowledgments
We thank Dr E David G McIntosh (Imperial College, London, United Kingdom) for the final correction of the manuscript.
Footnotes
Correspondence: Jan Máca MD, Department of Anesthesiology and Intensive Care Medicine, University Hospital, Ostrava, 17. listopadu 1790, 708 52 Ostrava-Poruba, Czech Republic. E-mail: jan.maca@fno.cz.
This study was supported by Grants SVV 260 026 and MO 1012, Charles University Prague. The authors have disclosed no conflicts of interest.

Supplementary material related to this paper is available at http://www.rcjournal.com.


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ARDS (Acute Respiratory Distress Syndrome) Symptoms, Causes, and Life Expectancy

Survival rates for ARDS vary depending on age, the underlying cause of ARDS, associated illnesses, and other factors. Some studies estimate that the mortality rate for ARDS is 36% to 52% per 100,000 people, depending upon their current health condition. Some people who survive recover completely.Jan 12, 2012  

​https://www.medicinenet.com/ards/article.htm

​

​ARDS (acute respiratory syndrome) definition and facts*

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*ARDS facts Medically Edited by: Melissa Conrad Stöppler, MD

ARDS, or acute respiratory distress syndrome, is a lung condition that leads to low oxygen levels in the blood. ARDS can be life threatening. This is because your body's organs, such as the kidneys and brain, need oxygen-rich blood to work properly.
Most people who develop ARDS are in the hospital for other serious health problems. Rarely, people who aren't hospitalized have health problems that lead to ARDS, such as severe pneumonia. If you have trouble breathing, call your doctor right away. If you have severe shortness of breath, call an ambulance or emergency medical services like 911 immediately.
Causes of ARDS includes infections, injuries, or other conditions that cause the lung's tiny blood vessels to leak more fluid than normal into the lungs' air sacs. This prevents the lungs from filling with air and moving enough oxygen into the bloodstream.
Some common conditions and factors that cause to ARDS are sepsis, pneumonia, severe bleeding caused by an injury, an injury to the chest or head, breathing in harmful fumes or smoke, and inhaling vomited stomach contents from the mouth.
Risk factors for ARDS include any condition or illness that can directly or indirectly injure the lungs.
The first signs and symptoms of ARDS are feeling like you can't get enough air into your lungs, rapid breathing, and low oxygen levels in the blood. Other signs and symptoms depend on the cause of the condition. They may occur before ARDS develops.
Your doctor will diagnose ARDS based on your medical history, a physical exam, and the results from tests.
Treatment of ARDS iinvolves with oxygen therapy, fluids, and medicines. Treatments are done in a hospital's intensive care unit. Patients who have ARDS may develop other medical problems while in the hospital. The most common problems are infections, pneumothorax (collapsed lung), lung scarring, and blood clots. The survival rate for people with ARDS is dependent upon the underlying disease as well as the overall health status of the patient.
Some people fully recover from ARDS. Others continue to have health problems. These problems may include shortness of breath, tiredness and muscle weakness, depression, and problems with memory and thinking clearly.
You can take steps to recover from ARDS and improve your quality of life. Ask your family and friends to help with everyday activities. Don't smoke and avoid secondhand smoke and other lung irritants, such as harmful fumes. Go to pulmonary rehabilitation if you doctor recommends it. Join a support group for ARDS. Seek help from your health care team if you feel depressed.
ARDS treatment has improved in recent years. As a result, the survival rate for ARDS is improving. Researchers are studying new treatments for the condition.

What is ARDS?

ARDS, or acute respiratory distress syndrome, is a lung condition that leads to low oxygen levels in the blood. ARDS can be life threatening because your body's organs need oxygen-rich blood to work well.

People who develop ARDS often are very ill with another disease or have major injuries. They might already be in the hospital when they develop ARDS.

To understand ARDS, it helps to understand how the lungs work. When you breathe, air passes through your nose and mouth into your windpipe. The air then travels to your lungs' air sacs. These sacs are called alveoli (al-VEE-uhl-eye).

Small blood vessels called capillaries run through the walls of the air sacs. Oxygen passes from the air sacs into the capillaries and then into the bloodstream. Blood carries the oxygen to all parts of the body, including the body's organs.

In ARDS, infections, injuries, or other conditions cause the lung's capillaries to leak more fluid than normal into the air sacs. This prevents the lungs from filling with air and moving enough oxygen into the bloodstream.

As a result, the body's organs (such as the kidneys and brain) don't get the oxygen they need. Without oxygen, the organs may not work well or at all.

People who develop ARDS often are in the hospital for other serious health problems. Rarely, people who aren't hospitalized have health problems that lead to ARDS, such as severe pneumonia.

If you have trouble breathing, call your doctor right away. If you have severe shortness of breath, call 9-1-1.

ARDS symptoms and signs

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The first signs and symptoms of ARDS are feeling like you can't get enough air into your lungs, rapid breathing, and a low blood oxygen level.

Other signs and symptoms depend on the cause of the ARDS. They may occur before ARDS develops. For example, if pneumonia is causing ARDS, you may have a cough and fever before you feel short of breath.

Sometimes, people who have ARDS develop signs and symptoms such as low blood pressure, confusion, and extreme tiredness. This may mean that the body's organs, such as the kidneys and heart, aren't getting enough oxygen-rich blood.

Most people who develop ARDS are in the hospital for other serious health problems. Rarely, people who aren't hospitalized have health problems that lead to ARDS, such as severe pneumonia.

If you have trouble breathing, call your doctor right away. If you have severe shortness of breath, call 9-1-1.

What causes ARDS?

Many conditions or factors can directly or indirectly injure the lungs and lead to ARDS. Some common ones are:

Sepsis. This is a condition in which bacteria infect the bloodstream.
Pneumonia. This is an infection in the lungs.
Severe bleeding caused by an injury to the body.
An injury to the chest or head, like a severe blow.
Breathing in harmful fumes or smoke.
Inhaling vomited stomach contents from the mouth.

It's not clear why some very sick or seriously injured people develop ARDS and others don't. Researchers are trying to find out why ARDS develops and how to prevent it.

Who is at risk?

People at risk for ARDS have a condition or illness that can directly or indirectly injure their lungs.

Direct Lung Injury

Conditions that can directly injure the lungs include:

Pneumonia. This is an infection in the lungs.
Breathing in harmful fumes or smoke.
Inhaling vomited stomach contents from the mouth.
Using a ventilator. This is a machine that helps people breathe; rarely, it can injure the lungs.
Nearly drowning.

Indirect Lung Injury

Conditions that can indirectly injure the lungs include:

Sepsis. This is a condition in which bacteria infect the bloodstream.
Severe bleeding caused by an injury to the body or having many blood transfusions.
An injury to the chest or head, such as a severe blow.
Pancreatitis (PAN-kre-a-TI-tis). This is a condition in which the pancreas becomes irritated or infected. The pancreas is a gland that releases enzymes and hormones.
Fat embolism (EM-bo-lizm). This is a condition in which fat blocks an artery. A physical injury, like a broken bone, can lead to a fat embolism.
Drug reaction.

How do doctors diagnose the condition?

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Your doctor will diagnose ARDS based on your medical history, a physical exam, and test results.

Medical History

Your doctor will ask whether you have or have recently had conditions that could lead to ARDS.

Your doctor also will ask whether you have heart problems, such as heart failure. Heart failure can cause fluid to build up in your lungs.

Physical Exam

ARDS may cause abnormal breathing sounds, such as crackling. Your doctor will listen to your lungs with a stethoscope to hear these sounds.

He or she also will listen to your heart and look for signs of extra fluid in other parts of your body. Extra fluid may mean you have heart or kidney problems.

Your doctor will look for a bluish color on your skin and lips. A bluish color means your blood has a low level of oxygen. This is a possible sign of ARDS.

Diagnostic Tests
You may have ARDS or another condition that causes similar symptoms. To find out, your doctor may recommend one or more of the following tests.

Initial Tests
The first tests done are:
An arterial blood gas test. This blood test shows the oxygen level in your blood. A low level of oxygen in the blood may be a sign of ARDS.
Chest X-ray. This test is used to take pictures of the structures in your chest, such as your heart, lungs, and blood vessels. It can show whether you have extra fluid in your lungs.
Blood tests, such as a complete blood count, blood chemistries, and blood cultures. These tests help find the cause of ARDS, such as an infection.
A sputum culture. This test is used to study the spit you've coughed up from your lungs. A sputum culture can help find the cause of an infection.

Other Tests
Other tests used to diagnose ARDS include:
Chest computed tomography (to-MOG-rah-fee) scan, or chest CT scan. This test uses a computer to create detailed pictures of your lungs. A chest CT scan may show lung problems, such as fluid in the lungs, signs of pneumonia, or a tumor.
Heart tests that look for signs of heart failure. Heart failure is a condition in which the heart can't pump enough blood to meet the body's needs. This condition can cause fluid to build up in your lung

How is ARDS treated?
ARDS is treated in a hospital's intensive care unit. Current treatment approaches focus on improving blood oxygen levels and providing supportive care. Doctors also will try to pinpoint and treat the underlying cause of the condition.

Oxygen Therapy
One of the main goals of treating ARDS is to provide oxygen to your lungs and other organs (such as your brain and kidneys). Your organs need oxygen to work properly.
Oxygen usually is given through nasal prongs or a mask that fits over your mouth and nose. However, if your oxygen level doesn't rise or it's still hard for you to breathe, your doctor will give you oxygen through a breathing tube. He or she will insert the flexible tube through your mouth or nose and into your windpipe.

Before inserting the tube, your doctor will squirt or spray a liquid medicine into your throat (and possibly your nose) to make it numb. Your doctor also will give you medicine through an intravenous (IV) line in your bloodstream to make you sleepy and relaxed.
The breathing tube will be connected to a machine that supports breathing (a ventilator). The ventilator will fill your lungs with oxygen-rich air.
Your doctor will adjust the ventilator as needed to help your lungs get the right amount of oxygen. This also will help prevent injury to your lungs from the pressure of the ventilator.
You'll use the breathing tube and ventilator until you can breathe on your own. If you need a ventilator for more than a few days, your doctor may do a tracheotomy (tra-ke-OT-o-me).
This procedure involves making a small cut in your neck to create an opening to the windpipe. The opening is called a tracheostomy (TRA-ke-OS-to-me). Your doctor will place the breathing tube directly into the windpipe. The tube is then connected to the ventilator.

Supportive Care
Supportive care refers to treatments that help relieve symptoms, prevent complications, or improve quality of life. Supportive approaches used to treat ARDS include:
Medicines to help you relax, relieve discomfort, and treat pain.
Ongoing monitoring of heart and lung function (including blood pressure and gas exchange).
Nutritional support. People who have ARDS often suffer from malnutrition. Thus, extra nutrition may be given through a feeding tube.
Treatment for infections. People who have ARDS are at higher risk for infections, such as pneumonia. Being on a ventilator also increases the risk of infections. Doctors use antibiotics to treat pneumonia and other infections.
Prevention of blood clots. Lying down for long periods can cause blood clots to form in the deep veins of your body. These clots can travel to your lungs and block blood flow (a condition called pulmonary embolism). Blood-thinning medicines and other treatments, such as compression stocking (stockings that create gentle pressure up the leg), are used to prevent blood clots.
Prevention of intestinal bleeding. People who receive long-term support from a ventilator are at increased risk of bleeding in the intestines. Medicines can reduce this risk.
Fluids. You may be given fluids to improve blood flow through your body and to provide nutrition. Your doctor will make sure you get the right amount of fluids. Fluids usually are given through an IV line inserted into one of your blood vessels.

What are the complications from ARDS?
If you have ARDS, you can develop other medical problems while in the hospital. The most common problems are:
Infections. Being in the hospital and lying down for a long time can put you at risk for infections, such as pneumonia. Being on a ventilator also puts you at higher risk for infections.
Pneumothorax (collapsed lung). This is a condition in which air or gas collects in the space around the lungs. This can cause one or both lungs to collapse. The air pressure from a ventilator can cause this condition.
Lung scarring. ARDS causes the lungs to become stiff (scarred) and makes it hard for them to expand and fill with air. Being on a ventilator also can cause lung scarring.
Blood clots. Lying down for long periods can cause blood clots to form in your body. A blood clot that forms in a vein deep in your body is called a deep vein thrombosis. This type of blood clot can break off, travel through the bloodstream to the lungs, and block blood flow. This condition is called pulmonary embolism.

Living with ARDS
Some people fully recover from ARDS. Others continue to have health problems. After you go home from the hospital, you may have one or more of the following problems:
Shortness of breath. After treatment, many people who have ARDS recover close-to-normal lung function within 6 months. For others, it may take longer. Some people have breathing problems for the rest of their lives.
Tiredness and muscle weakness. Being in the hospital and on a ventilator (a machine that supports breathing) can cause your muscles to weaken. You also may feel very tired following treatment.
Depression. Many people who've had ARDS feel depressed for a while after treatment.
Problems with memory and thinking clearly. Certain medicines and a low blood oxygen level can cause these problems.
These health problems may go away within a few weeks, or they may last longer. Talk with your doctor about how to deal with these issues. Also, see the suggestions below.

Getting Help
You can take steps to recover from ARDS and improve your quality of life. For example, ask your family and friends for help with everyday activities.
If you smoke, quit. Smoking can worsen lung problems. Talk to your doctor about programs and products that can help you quit. Also, try to avoid secondhand smoke and other lung irritants, such as harmful fumes.

If you have trouble quitting smoking on your own, consider joining a support group. Many hospitals, workplaces, and community groups offer classes to help people quit smoking.
Go to pulmonary rehabilitation (rehab) if your doctor recommends it. Rehab might include exercise training, education, and counseling. Rehab can teach you how to return to normal activities and stay active.
Your rehab team might include doctors, nurses, and other specialists. They will work with you to create a program that meets your needs.

Emotional Issues and Support
Living with ARDS may cause fear, anxiety, depression, and stress. Talk about how you feel with your health care team. Talking with a professional counselor also can help. If you're very depressed, your doctor may recommend medicines or other treatments that can improve your quality of life.
Joining a patient support group may help you adjust to living with ARDS. You can see how other people who have the same symptoms have coped with them. Talk to your doctor about local support groups or check with an area medical center.
Support from family and friends also can help relieve stress and anxiety. Let your loved ones know how you feel and what they can do to help you.

What is the prognosis and survival rate for ARDS?
More people are surviving ARDS now than in the past. One likely reason for this is that treatment and care for the condition have improved. Survival rates for ARDS vary depending on age, the underlying cause of ARDS, associated illnesses, and other factors. Some studies estimate that the mortality rate for ARDS is 36% to 52% per 100,000 people, depending upon their current health condition.

Some people who survive recover completely. Others may have lasting damage to their lungs and other health problems.
Researchers continue to look for new and better ways to treat ARDS.
What are other names for ARDS?
Acute lung injury
Adult respiratory distress syndrome
Increased-permeability pulmonary edema
Noncardiac pulmonary edema
ARDS used to be called stiff lung, shock lung, and wet lung.​​

A remote Amazonian tribe has recorded its first coronavirus case.

Rosie Perper 10th April 2020

https://www.insider.com/yanomami-tribe-amazon-records-coronavirus-case-2020-4 

Brazilian health officials confirmed the first case of COVID-19, the disease caused by the new coronavirus, among the remote Yanomami tribe in the Amazon. 
The Yanomami tribe is made up of approximately 38,000 people and is considered to be the largest relatively isolated tribe in South America.
Brazilian Health Minister Luiz Henrique Mandetta said at a press conference on Wednesday that a 15-year-old boy from the indigenous tribe has tested positive for the disease. 
Brazilian health officials confirmed the first case of COVID-19, the disease caused by the new coronavirus, among the remote Yanomami tribe in the Amazon. 

Health Minister Luiz Henrique Mandetta said at a press conference on Wednesday that a 15-year-old boy from the indigenous tribe has tested positive for the disease. 

Mandetta said that the case was "worrying," particularly because of the remote community's separation from the outside world. 
According to Brazilian newspaper Globo, the boy was admitted to the intensive care unit at a hospital in Roraima, Brazil's northernmost state located in the Amazon region, on April 3. He reported shortness of breath, fever, chest pain, and sore throat. 

According to Globo, the boy first tested negative for the disease but later tested positive. He remains in the ICU. 

Brazilian health officials confirmed the first case of COVID-19, the disease caused by the new coronavirus, among the remote Yanomami tribe in the Amazon. 
The Yanomami tribe is made up of approximately 38,000 people and is considered to be the largest relatively isolated tribe in South America.
Brazilian Health Minister Luiz Henrique Mandetta said at a press conference on Wednesday that a 15-year-old boy from the indigenous tribe has tested positive for the disease. 
Visit Insider's homepage for more stories.

The Yanomami tribe is made up of approximately 38,000 people and is considered to be the largest relatively isolated tribe in South America, with over 9.6 million hectares (2.3 million acres) of land along the Venezuelan border.

The tribe has dealt with deadly outbreaks of infectious disease, including measles and flu, in the past when military agencies, miners, and religious missionary groups exposed the tribe to diseases they had no immunity to. 

Brazi has confirmed at least seven coronavirus cases among its indigenous populations, according to Globo. Indigenous people across several states have closed off villages from outside communities to protect themselves against the coronavirus. 

According to Globo, respiratory disease is already the leading cause of death among native populations in Brazil. The country's health ministry has created a national crisis committee in order to monitor the impacts of COVID-19 on indigenous people and prevent further spread.

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80% of NYC's coronavirus patients who are put on ventilators ultimately die, and some doctors are trying to stop using them
https://www.businessinsider.com/coronavirus-ventilators-some-doctors-try-reduce-use-new-york-death-rate-2020-4?r=US&IR=T

A patient with COVID-19, the illness caused by the coronavirus, wears a snorkeling mask converted into a ventilator in Paris on April 1. REUTERS/Benoit Tessier/File Photo

Sinéad Bake
Some doctors are trying to reduce their reliance on ventilators for coronavirus patients because of reports of abnormally high death rates for patients using the machines, The Associated Press reported on Wednesday.
New York City officials have said at least 80% of coronavirus patients who were on ventilators in the city died, the AP reported. Unusually high death rates have also been recorded elsewhere in the US and the world.

Ventilators are typically used only for the worst-affected patients, and there are no drugs approved to treat COVID-19, so this could help explain the higher death rate.
But doctors have also said ventilators can damage the lungs — and while the machines may be an effective way to treat other respiratory illnesses, some are looking for alternative treatments.
Because there is a global ventilator shortage, doctors and healthcare systems have called for more to be made or bought quickly to treat the worst-affected patients.

Visit Business Insider's homepage for more stories.

How Ventilators Are Used to Keep Covid-19 Patients Alive
Bloomberg Markets and Finance
Mar.27 -- Hospitals are “preparing for war,” says Emory University School of Medicine Carlos Del Rio. He explains how ventilators help patients suffering from the coronavirus and looks at the timeframe for finding a vaccine. He speaks on "Bloomberg Surveillance."
CategoryNews & Politics

Bill Gates warns tens of millions could be killed by bio-terrorism  

This article is more than 3 years old Microsoft founder and philanthropist tells Munich security conference genetic engineering could be terrorist weapon
Microsoft founder and philanthropist tells Munich security conference genetic engineering could be terrorist weapon

Ewen MacAskill Defence correspondent in Munich  
Wed 14 Feb 2018
https://www.theguardian.com/technology/2017/feb/18/bill-gates-warns-tens-of-millions-could-be-killed-by-bio-terrorism 

Bio-terrorism could kill 30 million people in a year, says Bill Gates  
A chilling warning that tens of millions of people could be killed by bio-terrorism was delivered at the Munich security conference by the world’s richest man, Bill Gates
Gates, who has spent much of the last 20 years funding a global health campaign, said: “We ignore the link between health security and international security at our peril.”

The Yanomami tribe is made up of approximately 38,000 people and is considered to be the largest relatively isolated tribe in South America, with over 9.6 million hectares (2.3 million acres) of land along the Venezuelan border.

A bridge between life and death: Most COVID-19 patients put on ventilators will not survive
John Bacon USA TODAY - Apr 8, 2020
https://eu.usatoday.com/story/news/health/2020/04/08/coronavirus-cases-ventilators-covid-19/2950167001/  

While governors, mayors and hospital officials conduct much-publicized life-and-death struggles to acquire ventilators, for most COVID-19 patients the oxygen-providing apparatus will merely serve as a bridge from life to death.

New York Gov. Andrew Cuomo recently estimated that only 20% of coronavirus patients placed on ventilators "will ever come off." Dennis Carroll, who led the U.S. Agency for International Development's infectious disease unit for more than a decade, told USA TODAY perhaps one-third of COVID-19 patients on ventilators survive. 

But for many, ventilators represent their last chance.
"If you were one of the one-third, I suspect you’d be very appreciative that that capability was available," Carroll said.
Ventilators won't fix the ailments that put patients on them, but they can provide support until other treatments work or the patient's body overcomes the disease. And physicians are determined to use the tool in the last-ditch effort to keep patients alive.
At Lenox Hill Hospital on Manhattan's Upper East Side, "hope huddles" allow emergency room staffers to take a moment amid the suffering to discuss small victories – such as successful "extubations" when patients are weaned from the machines.
"Our goal is to save the most number of lives possible, while also being realistic when evaluating a person’s chances of survival," said Robert Glatter, an emergency physician at Lenox Hill.

'Buying time' for coronavirus patients
A ventilator uses "positive pressure" to blow air into the lungs through a tube inserted in the patient’s nose or mouth and moved down into the airway. Longer-term ventilation can involve the tube being introduced through the windpipe. Patients generally exhale on their own, but sometimes the ventilator helps with that as well. 

"Ventilators aren’t really making any therapeutic contributions," said Ogbonnaya Omenka, an assistant professor and public health specialist at Butler University's College of Pharmacy and Health Sciences. "What they do in essence, is provide life support – and buy time for the patient."

An emergency field hospital in New York's Central Park has one of the ventilators that are in such high demand during the coronavirus pandemic.
Stephanie Keith/Getty Images
Some patients may be on a ventilator for only a few hours or days, but experts say COVID-19 patients often remain on the ventilators for 10 days or more. 

Longer duration of intubation is often related to worsening acute respiratory distress syndrome, ARDS. And patients who have issues with kidneys or other organs in addition to lungs stay intubated for longer periods of time.

Melissa Nolan, an infectious disease expert and professor at the University of South Carolina, said people on ventilators tend to be the most critically ill patients and often are receiving renal or cardiovascular mechanical support that can further complicate their chance of recovery.
There are risks associated with ventilators. The artificial breathing tube sometimes can allow germs to enter the lungs, causing infection. But for these patients there are no alternatives.
"Ventilation and intubation are currently our best tools for treating the pulmonary manifestations of COVID-19 – and often clinicians' only choice" given the lack of effective drug therapies, Nolan said
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Glatter said it's impossible to accurately predict how many days each person who is intubated will require use of the ventilator. It ultimately depends on a patient's degree of lung involvement, he said.

"The reality is that the longer a person remains intubated, the chance for survival decreases," Glatter said. "Simply put, they are unable to be weaned off the ventilator."
Early COVID-19 symptoms can include fever, a dry cough and shortness of breath. Most patients essentially heal themselves in a couple weeks. For some, however, the challenge to the lungs becomes critical.
Dr. Marjorie Jenkins, dean of the University of South Carolina School of Medicine, said that without ventilators, COVID-19 induced ARDS is "uniformly fatal."

"Doctors are on the front lines to save lives, not to allow patients to suffer a horrible death," she said. "A death that comes via slow painful suffocation for minutes, hours, perhaps days.”

Physicians lack the "granular details" of the disease's presentation, course and outcomes, Jenkins said. But how a patient deals with the virus appears to be a function of their immune system response, genetics and environmental and lifestyle factors such as smoking, along with other conditions, she said.

Patients with underlying ailments – such as hypertension, diabetes, obesity, chronic lung disease asthma, sleep apnea and cardiovascular disease – are at higher risk for "adverse outcomes" and thus more likely to require mechanical ventilation as their disease progresses, Glatter said.

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The outcome for these patients is based on how they respond to specific treatments and measures, not just the ventilator itself, Glatter said. The ventilator, he said, is just one aspect of the overall resuscitation of the patient.  

"Ventilators are saving lives all over world during this global pandemic," Jenkins said. "Medical personnel are trained to do everything possible to save a life. This is no different."

The effort to secure more ventilators
Some hospitals are desperate for more ventilators. The University of Mississippi Medical Center is building its own, using garden hoses, lamp timers and other gadgets found at local hardware stores. Physicians at New York's Mount Sinai Health System have repurposed machines used to treat sleep apnea.

General Motors this week announced a $500 million deal to make 30,000 ventilators for the national stockpile, and Ford has pledged to make 50,000 ventilators in 100 days. California was among states providing ventilators to the national stockpile, sending 500 – on the condition that they will get them back if needed later.
Jenkins also works for Prisma Health, a not-for-profit health organization in South Carolina that partnered with others to develop a device that allows a ventilator to be split between two patients. The device was approved by the FDA in just two weeks. The goal: double ventilatory capacity "to prevent our front line personnel from having to make the call of who lives or dies.”
Most ventilator patients are monitored in an ICU, hooked up to monitors that measure vital signs including blood pressure, heart rate, respiratory rate, oxygen saturation as well as tracking and measuring the effects of the ventilator itself on the person’s heart and lungs. Ventilators, especially for cases of COVID-19, involve highly trained intensive care professionals – anesthesiologists, nurses and respiratory therapists.

Florida travelers with coronavirus visited 46 U.S. states before diagnosis
Providing sufficient staff is becoming a problem as COVID-19 patients overwhelm hospitals, Omenka said. And more of those health care professionals, dealing with the highly contagious disease every day, are becoming patients.

"The health care system is getting increasingly burdened," Omenka said. "With the exponential rise in cases and depletion of front-line health care workers, the level of care for intensive care may become compromised."

Shortages in ICU beds for ventilator patients is also a problem but not an insurmountable one, Glatter said. Demand for ventilators, ICU nurses and doctors to care for these critically ill patients is more pressing, he said. 
"We can be creative, create space for makeshift ICUs to help accommodate ventilated patients," Glatter said.
Makeshift ICU beds, homemade ventilators – all are part of the unrelenting battle between the world of medicine and a pandemic that has brought the world to its knees.
“Health professionals and hospitals are doing their very best to save lives during this pandemic," Jenkins said. "Every opportunity to leverage our resources is being explored and engaged.”
Published  Apr 8, 2020

A patient with COVID-19, the illness caused by the coronavirus, wears a snorkeling mask converted into a ventilator in Paris on April 1. REUTERS/Benoit Tessier/File Photo

American Journal of Respiratory and Critical Care Medicine
https://www.atsjournals.org/doi/full/10.1164/ajrccm.158.1.9708031 

Acute Respiratory Distress Syndrome Caused by Pulmonary and Extrapulmonary Disease

Different Syndromes?LUCIANO GATTINONI , PAOLO PELOSI , PETER M. SUTER , ALESSIA PEDOTO , PAOLA VERCESI , and ALFREDO LISSONI
https://doi.org/10.1164/ajrccm.158.1.9708031       PubMed: 9655699
Received: August 07, 1997
 

To assess the possible differences in respiratory mechanics between the acute respiratory distress syndrome (ARDS) originating from pulmonary disease (ARDSp) and that originating from extrapulmonary disease (ARDSexp) we measured the total respiratory system (Est,rs), chest wall (Est,w) and lung (Est,L) elastance, the intra-abdominal pressure (IAP), and the end-expiratory lung volume (EELV) at 0, 5, 10, and 15 cm H2O positive end-expiratory pressure (PEEP) in 12 patients with ARDSp and nine with ARDSexp. At zero end-expiratory pressure (ZEEP), Est,rs and EELV were similar in both groups of patients. The Est,L, however, was markedly higher in the ARDSp group than in the ARDSexp group (20.2 ± 5.4 versus 13.8 ± 5.0 cm H2O/L, p < 0.05), whereas Est,w was abnormally increased in the ARDSexp group (12.1 ± 3.8 versus 5.2 ± 1.9 cm H2O/L, p < 0.05). The IAP was higher in ARDSexp than in ARDSp (22.2 ± 6.0 versus 8.5 ± 2.9 cm H2O, p < 0.01), and it significantly correlated with Est,w (p < 0.01). Increasing PEEP to 15 cm H2O caused an increase of Est,rs in ARDSp (from 25.4 ± 6.2 to 31.2 ± 11.3 cm H2O/L, p < 0.01) and a decrease in ARDSexp (from 25.9 ± 5.4 to 21.4 ± 55.5 cm H2O/L, p < 0.01). The estimated recruitment at 15 cm H2O PEEP was − 0.031 ± 0.092 versus 0.293 ± 0.241 L in ARDSp and ARDSexp, respectively (p < 0.01). The different respiratory mechanics and response to PEEP observed are consistent with a prevalence of consolidation in ARDSp as opposed to prevalent edema and alveolar collapse in ARDSexp.

The acute respiratory distress syndrome (ARDS) is thought to be a uniform expression of a diffuse and overwhelming inflammatory reaction of the pulmonary parenchyma to a variety of serious underlying diseases. The most frequent causes include sepsis, severe pneumonia, peritonitis, and multiple trauma (1, 2).

However, the possible differences in lung dysfunction between ARDS resulting from pulmonary disease and that resulting from extrapulmonary disease have not been examined systematically. Mechanical properties of the respiratory system may be related to underlying pathology, at least in the early phases of ARDS (3). For instance, when the prevalent pathology is lung tissue consolidation such as in pneumonia, application of positive end-expiratory pressure (PEEP) should induce only a moderate lung recruitment, increased elastance of the respiratory system (i.e., reduction of respiratory compliance), and possible alveolar overdistension. On the other hand, when the prevalent pathology is interstitial edema and alveolar collapse, PEEP should induce remarkable lung recruitment, with a decrease of the elastance of the respiratory system (i.e., increase in respiratory compliance).

We hypothesized that ARDS caused by pulmonary disease is associated with predominant consolidation, whereas ARDS caused by extrapulmonary disease is associated with prevalent interstitial edema and alveolar collapse. To test this hypothesis, we studied patients with ARDS of different origins and divided them into two groups. The first group included patients with ARDS caused by a “direct” insult to the lung, i.e., pulmonary ARDS (ARDSp), and the second group included patients with ARDS developing after an “indirect” insult, i.e., extrapulmonary ARDS (ARDSexp). We report here the respiratory mechanics observed in the two types of the syndrome and discuss possible physiopathologic and clinical implications.METHODS
Section:

Study Population and Classification of Patients
Approval for this investigation was granted by the Ethical Committee of our Institution, and informed consent was obtained from the next of kin of the patients before inclusion in the study. Between December 1994 and June 1996, 21 unselected consecutive mechanically ventilated patients with ARDS were examined. Nineteen of them were in-hospital patients and two were patients transferred from other hospitals. ARDS was defined according to the criteria established by the American-European Consensus Conference on ARDS (4), i.e., acute onset, PaO2 /Fi O2 < 200 mm Hg (regardless of PEEP level), bilateral infiltrates seen on frontal chest radiograph, and pulmonary artery occlusion pressure below 18 mm Hg. We excluded patients in whom air leaks prevented a correct measurement of respiratory mechanics.

These 21 patients made up the total population and their data were compared for similarities to and differences from previous studies on ARDS. Twelve patients were assigned to the ARDSp group, and nine were assigned to the ARDSexp group by three independent physicians, blinded as to the results of the measurements, and the clinical course. Assignment was based on history, clinical presentation, and microbiological results (Table 1). As shown in the table all of the patients were studied during the early phase of ARDS. Eleven of the 12 patients with ARDSp had diffuse pneumonia with positive airway cultures, and none had positive blood cultures. In the nine patients with ARDSexp airway cultures were positive in three; these three also had positive blood cultures. Of the nine patients with ARDSexp, seven had undergone surgery 10 ± 7 d before the study.

Table 1. MICROBIOLOGIC FINDINGS
Patient No. Diagnosis Airway Cultures Blood Cultures Abdominal Cultures Days from Intubation/ ARDS Onset* Survived/Died
ARDSp
1 Pneumonia Legionella † — — 3/0 D
2 Pneumonia‡ — — — 1/0 S
3 Pneumonia Candida — — 1/0 S
4 Hemorrhagic alveolitis — — — 3/2 S
5 Pneumonia Klebsiella — — 0/0 D
6 Pneumonia Klebsiella — — 3/1 S
Enterobacter
7 Pneumonia Cytomegalovirus — — 8/2 D
8 Pneumonia Pneumocystis — — 0/0 D
Aspergillus
Staph. aureus
9 Pneumonia Legionella † — — 1/0 S
10 Pneumonia Candida — — 1/1 D
11 Pneumonia Pseudomonas — — 5/4 S
12 Pneumonia Pneumocystis — — 2/1 S
ARDSexp
1 Polytrauma — — — 3/0 D
2 Polytrauma Staph. aureus Staph. aureus Staph. aureus 0/0 D
Enterobacter Enterobacter
Bacteroides
3 Intestinal — — — 1/0 S
Infarction
4 Polytrauma Pseudomonas Candida — 0/0 S
5 Peritonitis — — — 3/0 D
6 Peritonitis Pseudomonas Staph. aureus Staph. aureus 1/0 S
7 Hemorrhagic shock — — — 3/2 S
8 Peritonitis — — Enterobacter 1/0 S
Bacteroides
9 Intestinal — — — 12/3 D
infarction

*Time elapsed between intubation and the day of the study; ARDS onset = time elapsed between the ARDS onset, i.e., the day on which the AECC-ARDS criteria were fulfilled and the day of the study.
†Serology.
‡Interstitial pneumonia of unknown origin.

Every patient had an arterial cannula, a Swan-Ganz pulmonary- artery catheter and a urinary catheter inserted for clinical monitoring. The Simplified Acute Physiology Score (SAPS) (5) and the number of organ dysfunctions (6) were recorded on the day of the study. The characteristics of the patients population are summarized in Table 2.

Table 2. PATIENT CHARACTERISTICS*
Both Groups (n = 21) Group 1 ARDSp(n = 12) Group 2 ARDSexp(n = 9) p Value
Sex, M/F 14/7 8/4 6/3 NS
Age, yr 46.0 ± 18.9 38.6 ± 13.5 55.9 ± 21.3 < 0.05
Height, cm 172.9 ± 10.0 172.3 ± 8.2 173.7 ± 12.6 NS
Weight, kg 69.7 ± 15.7 70.4 ± 13.7 68.8 ± 18.7 NS
SAPS 11.8 ± 4.3 10.8 ± 4.5 13.2 ± 3.9 NS
MOF, n 2.9 ± 1.3 2.8 ± 1.2 3.3 ± 1.4 NS
Days before the study 2.5 ± 2.9 2.3 ± 2.3 2.7 ± 2.7 NS
Mortality, S/D 11/10 6/6 5/4 NS
ICU Stay, d 21.7 ± 14.9 18.2 ± 9.7 26.4 ± 19.5 NS

Definition of abbreviations: Group 1 = ARDS caused by pulmonary disease; Group 2 = ARDS caused by extrapulmonary disease; SAPS = Simplified Acute Physiology Score; MOF = multiple organ failure; S = survived; D = died; ICU = Intensive Care Unit; NS = not significant between groups.
*Data are expressed as mean ± SD.

Procedure
In all patients while in the supine position, we measured the elastic properties of the lung and chest wall (in triplicate), the end-expiratory lung volume (EELV), and the intra-abdominal pressure at four different PEEP levels (0, 5, 10, and 15 cm H2O) applied in random order. The other ventilator settings were kept constant throughout the entire protocol, which lasted between 25 and 30 min.

All the patients were ventilated with a Siemens Servo 900 C ventilator in the volume control mode with constant inspiratory flow (Table 3). The patients of both groups were ventilated following the guidelines recommended by the American College of Chest Physicians (7). Before the investigation, the patients were sedated with fentanyl (2 to 3 μg/kg) and diazepam (0.1 to 0.2 mg/kg), and paralyzed with pancuronium bromide (0.1 to 0.2 mg/kg).

Table 3. VENTILATORY SETTING, GAS EXCHANGE, AND HEMODYNAMIC VARIABLES*
Both Groups (n = 21) Group 1 ARDSp(n = 12) Group 2 ARDSexp(n = 9) p Value
Vt, L 0.688 ± 0.142 0.686 ± 0.129 0.692 ± 0.166 NS
V˙, L/s 0.493 ± 0.082 0.507 ± 0.092 0.475 ± 0.068 NS
V˙ e, L/min 9.88 ± 2.05 9.39 ± 1.89 10.60 ± 2.20 NS
RR, breaths/min 14.5 ± 2.7 14.0 ± 2.5 15.3 ± 3.1 NS
PEEP, cm H2O 10.4 ± 4.0 10.9 ± 3.2 9.7 ± 4.9 NS
Fi O2 , % 77 ± 20 80 ± 21 74 ± 19 NS
PaO2 , mm Hg 97.8 ± 20.6 91.7 ± 20.4 105.9 ± 18.9 NS
PaCO2 , mm Hg 46.3 ± 8.7 48.3 ± 9.6 43.6 ± 6.9 NS
pH 7.34 ± 0.09 7.32 ± 0.09 7.37 ± 0.08 NS
PaO2 /Fi O2 134.8 ± 42.0 123.8 ± 45.3 149.4 ± 34.4 NS
HR, beats/min 21.7 ± 14.9 116.6 ± 17.5 110.8 ± 22.4 NS
Pa, mm Hg 83.0 ± 15.1 84.5 ± 14.9 82.3 ± 26.7 NS
Ppa, mm Hg 28.6 ± 5.6 28.2 ± 6.3 29.3 ± 4.6 NS
Ppao, mm Hg 13.7 ± 4.7 13.9 ± 4.8 13.3 ± 4.8 NS
Pcv, mm Hg 9.0 ± 4.3 8.1 ± 4.2 10.0 ± 4.5 NS
CI, L/min/m2 4.1 ± 1.8 4.6 ± 1.4 3.8 ± 1.7 NS
WB, L/d −0.385 ± 1.836 −0.220 ± 0.905 −0.590 ± 2.701 NS

Definition of abbreviations: Group 1 = ARDS caused by pulmonary disease; Group 2 = ARDS caused by extrapulmonary disease; Vt = tidal volume; V˙ = inspiratory flow; V˙ e = minute ventilation; RR = respiratory rate; PEEP = positive end-expiratory pressure; Fi O2 = inspired oxygen concentration; HR = heart rate; Pa = mean arterial pres- sure; Ppa = mean pulmonary artery pressure; Ppao = pulmonary artery occlusion pressure; Pcv = central venous pressure; CI = cardiac index; WB = water balance; NS = not significant between groups.

*Data are expressed as mean ± SD.

Respiratory Mechanics
Respiratory mechanics were assessed as previously reported (8). Airway pressure (Pao) and gas flow were measured and recorded by a computerized system (CP-100 Pulmonary Monitor; Bicore Monitoring System, Irvine, CA) at the endotracheal tube opening. Esophageal pressure (Pes) was determined from an esophageal balloon inflated with 0.5-1 ml of air, positioned at the lower third of the esophagus, as confirmed by the chest roentgenograph. The validity of Pes was verified by the “occlusion test” according to the principle of Baydur and colleagues (9). Volume was obtained by digital integration of the flow signal.

Static Elastance of Total Respiratory System, Lung, and Chest Wall
We recorded Pao and Pes during a 3 to 4 s airway occlusion at end- expiration and at end-inspiration. Static elastance of the total respiratory system (Est,rs) was computed as Est,rs = DPao/Vt, where DPao is the difference between end-inspiratory and end-expiratory airway pressure and Vt is the tidal volume. Static elastance of the chest wall (Est,w) was computed as DPes/Vt, where DPes is the difference between end-inspiratory and end-expiratory esophageal pressure. Static lung elastance (Est,L) was calculated as (Est,L = Est,rs − Est,w). End-expiratory volume corresponded to the elastic equilibrium volume in each patient, as evidenced by zero flow during an expiratory pause and absence of changes in Pao after airway occlusion.

Resistance of the Total Respiratory System, Lung, and Chest Wall
Maximal (Rmax,rs) and minimal (Rmin,rs) resistances of the respiratory system were computed from Pao as (Pmax′ − P2)/V˙ and (Pmax′ − P1)/V˙, where Pmax′ is the maximal pressure value after occlusion corrected for the tube resistance, P1 is the pressure recorded after the immediate drop from Pmax, P2 is the plateau pressure and V˙ is the flow immediately preceding the occlusion. Rmin,rs represents the “ohmic” resistive component of the respiratory system, and Rmax,rs includes Rmin,rs plus the “additional” respiratory resistance (DR,rs) caused by stress relaxation and/or time-constant inequalities within the respiratory system tissues. Because there was no appreciable drop in Pes immediately after the occlusion (i.e., P1 in the esophageal tracings was not identifiable), Rmin,rs reflects essentially airway resistance (Rmin,L), and minimal chest wall resistance (Rmin,w) can be considered negligible. As a consequence, maximal chest wall resistance (Rmax,w) is entirely due to the viscoelastic properties of the chest wall tissues (i.e., Rmax,w = DR,w). “Additional” resistance of the lung (DR,L) was obtained as DR,rs-DR,w whereas the sum of Rmin,L + DR,L gives the maximal lung resistance (Rmax,L).

End-expiratory Lung Volume (EELV)
EELV was measured at zero end-expiratory pressure (ZEEP) using a closed-circuit helium dilution method (10). To compute EELV at each level of PEEP, we measured the total exhaled volume after PEEP removal during an expiratory period long enough to reach zero flow. This total exhaled volume represented the volume of the lung above the EELV at ZEEP, at the end of tidal inspiration. Therefore, EELV was computed as: EELV at ZEEP + (total exhaled volume − tidal volume).

Estimated Lung Recruitment
To estimate the lung recruitment by PEEP, we had to differentiate, in the measured lung volume, the component caused by the inflation of pulmonary units already open and the component caused by the recruitment of previously collapsed pulmonary units. To do so we assumed that pulmonary units open at ZEEP inflate with tidal volume or PEEP according to the elastance present at ZEEP (predicted volume). This was calculated by adding to EELV the amount expected to be gained with PEEP according to the elastance (DPao/Vt) determined at ZEEP. Lung volume recruitment was then computed as measured minus predicted volume, i.e., EELV at PEEP − (EELV at ZEEP + PEEP/Est,rs at ZEEP).

The basic assumption for this estimate of alveolar recruitment relies on the finding that specific elastance of pulmonary units in ARDS is near to normal (3, 11), indicating that the elastance decrease with PEEP is likely due to the recruitment of the new pulmonary units. This assumption has been adopted by other investigators also (12).

Intra-abdominal Pressure
Intra-abdominal pressure was measured using a transurethral bladder catheter (13). One hundred milliliters of normal saline were infused through the urinary catheter into the bladder. The catheter was then clamped and the intra-abdominal pressure was recorded by a pressure transducer as mean pressure at end-expiration. Zero was set at the level of the pubis.

Statistical Methods
Data are expressed as mean ± standard deviation (SD), unless otherwise specified. In each group, statistical comparisons between PEEP levels were done using analysis of variance (ANOVA). Individual comparisons (ZEEP versus PEEP) were obtained using Student's paired t test. Individual comparisons between the two groups, at each level of PEEP, were performed using Student's unpaired t test. Bonferroni's correction for multiple comparisons was applied.

The anthropometric characteristics, number of organ dysfunctions, acute physiology score, and outcome for all patients are summarized in Table 2. We found no differences in any variable between the ARDSp or ARDSexp groups, except for age, which was significantly lower in the patients with ARDSp. Similarly, as shown in Table 3, no differences were noted for the ventilatory setting, gas exchange, and hemodynamic variables measured before the PEEP trial. The average daily water balance from the onset of ARDS to the day of the study was also similar between the ARDSp and the ARDSexp groups.

Elastance of the Total Respiratory System, Lung, and Chest Wall
The total population. The high values of Est,rs and Est,L, the moderate increase in Est,w, and low EELV are typical of ARDS (Table 4). When PEEP was increased from 0 to 15 cm H2O, Est,rs and Est,L did not change significantly, Est,w decreased slightly, and intra-abdominal pressure increased by an average of 1.8 ± 1.7 cm H2O. As expected, EELV increased significantly with PEEP.

Table 4. ELASTANCE, LUNG VOLUME, AND INTRA-ABDOMINAL PRESSURE FOR THE WHOLE ARDS POPULATION AT DIFFERENT PEEP LEVELS*
PEEP (cm H2O)
0 5 10 15
Est,rs, cm H2O/L 25.7 ± 5.7 24.9 ± 6.9 24.4 ± 7.2 27.0 ± 10.3
Est,L, cm H2O/L 17.5 ± 6.0 17.7 ± 7.3 17.6 ± 8.2 20.0 ± 11.7
Est,w, cm H2O/L 8.2 ± 4.5† 7.2 ± 4.4‡ 6.8 ± 4.1‡ 7.0 ± 3.7‡
EELV, L 0.576 ± 0.264† 0.798 ± 0.321‡ 1.049 ± 0.377† 1.297 ± 0.383‡
IAP, cm H2O 14.4 ± 8.2† 14.8 ± 7.9 14.8 ± 8.1 16.1 ± 8.6‡

Definition of abbreviations: Est,rs = elastance of the total respiratory system; Est,L = elastance of the lung; Est,w = elastance of the chest wall; EELV = end-expiratory lung volume; IAP = Intra-abdominal pressure.

*Data are expressed as mean ± SD.
†p < 0.01 between PEEP and ANOVA.
‡p < 0.01 compared with PEEP 0 cm H2O.

ARDS of pulmonary versus extrapulmonary origin at ZEEP. As shown in Figure 1, Est,rs was similar for both types of ARDS at ZEEP (25.4 ± 6.2 versus 26 ± 5.4 cm H2O/L, p = NS), but Est,L was higher in ARDSp (20.2 ± 5.4 versus 13.8 ± 5.0 cm H2O/L in ARDSexp, p < 0.01) indicating a stiffer lung. Est,w was more than twofold higher in ARDSexp than in ARDSp (12.1 ± 3.8 versus 5.2 ± 1.9 cm H2O/L, p < 0.01), indicating a stiffer chest wall. This latter finding was possibly due to higher intra-abdominal pressure, which amounted to 22.2 ± 6.0 and 8.5 ± 2.9 cm H2O in ARDSexp and ARDSp, respectively (p < 0.01). The close correctional between Est,w and intra-abdominal pressure is shown in Figure 2.

[figure]

Fig. 1.Changes of static elastances of the respiratory system (Est,rs), lung (Est,L), and chest wall (Est,w) as a function of PEEP in patients with ARDS caused by pulmonary disease (Group 1, top panel ) with in ARDS caused by extrapulmonary disease (Group 2, bottom panel ). Comparison within each group: *p < 0.05 versus PEEP 0 cm H2O; **p < 0.01 versus PEEP 0 cm H2O. Comparison between the two groups; ▴p < 0.05 versus Group 1; ▴▴p < 0.01 versus Group 1.Download figure | Download Powerpoint
[figure]
Fig. 2.Chest wall static elastance (Est,w) as a function of intra-abdominal pressure (IAP), Solid circles refer to patients of Group 1 (ARDS caused by pulmonary disease); open circles refer to patients of Group 2 (ARDS from extrapulmonary disease). Regression equation: Est,w = 1.65 ± 0.46* AP; r = 0.84, p < 0.01.

Because the fluid management in the individual patients might account for the differences we found in respiratory system mechanics, we looked for a possible relationship between mechanics of the total respiratory system, lung, and chest wall and IAP versus the daily fluid balance of the day of the study, the cumulative fluid balance of the 48 h before the study, and the cumulative fluid balance from the day of intubation and the day of ARDS onset to the day of the study. None of these relationships reached statistical significance.

PEEP response in ARDS of pulmonary or extrapulmonary origin. Increasing PEEP from 0 to 15 cm H2O led to opposite effects on elastance in the two types of ARDS, as shown in Figure 1. In ARDSp (upper panel), increasing PEEP caused an increase of Est,rs mainly caused by an increase in Est,L whereas in ARDSexp (lower panel) PEEP resulted in a significant decrease in Est,rs caused by the reduction in both Est,L and Est,w. Increasing PEEP from 0 to 15 cm H2O led to a slight increase in intra-abdominal pressure (p < 0.01) in both groups and amounted, at 15 cm H2O PEEP, to 10.0 ± 3.4 and 24.3 ± 6.1 cm H2O in ARDSp and ARDSexp, respectively. These results indicate a stiffer lung in ARDSp, which does not improve with PEEP, while in ARDSexp there is a stiffer thoracoabdominal cage and a more compliant lung, which both improve with increasing PEEP. As shown in Figure 3 (left panel), the pressure-volume relationship of the total respiratory system of patients with ARDSp was essentially the same at each PEEP level. This suggests that, at end-expiration, PEEP keeps already open pulmonary units more inflated, but no recruitment occurs. This pattern is substantially different in ARDSexp (right panel) where an upwards shift of the pressure-volume curve of the total respiratory system was observed, indicating significant recruitment of pulmonary units by PEEP. The difference in response between ARDSp and ARDSexp with regard to end-expiratory lung volume and recruitment is shown in Table 5.

[figure]
Fig. 3.Pressure-volume (P-V) relationship in patients with ARDS caused by pulmonary disease, (Group 1, left panel ) and with ARDS caused by extrapulmonary disease (Group 2, right panel ) as a function of PEEP. As shown, in Group 1, the P-V relationships follow systematically the same line, with a slope decreasing at 15 cm H2O (i.e., decreased compliance), whereas the P-V relationships of Group 2 patients are shifted upwards as a function of PEEP (i.e., at the same pressure of volume is greater at higher PEEP, suggesting recruitment). The slope of P-V relationship increases with PEEP, indicating the compliance improvement. Data are presented as mean ± standard error.

Table 5. END-EXPIRATORY LUNG VOLUME AND ESTIMATED RECRUITMENT FOR ARDS CAUSED BY PULMONARY OR EXTRAPULMONARY DISEASE AT DIFFERENT PEEP LEVELS*

PEEP (cm H 2 O)
0 5 10 15
EELV, L
ARDSp 0.556 ± 0.254† 0.762 ± 0.319‡ 0.970 ± 0.381‡ 1.150 ± 0.356‡,§
ARDSexp 0.602 ± 0.291† 0.847 ± 0.338‡ 1.155 ± 0.367‡ 1.494 ± 0.340‡
Estimated recruitment, L
ARDSp −0.002 ± 0.088 −0.003 ± 0.098§ −0.031 ± 0.092‖
ARDSexp 0.043 ± 0.120† 0.153 ± 0.200** 0.293 ± 0.241†,†
Definition of abbreviation: EELV = end-expiratory lung volume.
*Data are expressed as mean ± SD.
†p < 0.01 between PEEP and ANOVA.
‡p < 0.01 compared with PEEP 0 cm H2O.
§p < 0.05 compared with ARDSexp.
‖p < 0.01 compared with ARDSexp.
**p < 0.05 compared with PEEP 5 cm H2O.
F5-164p < 0.01 compared with PEEP 5 cm H2O.

Resistance of the total respiratory system, lung, and chest wall. In Table 6 are summarized, for the whole population, the resistances (“ohmic” and additional) of the total respiratory system, lung, and chest wall as a function of PEEP. As shown, we observed a significant decrease with PEEP of the “ohmic” resistance, whereas DR,rs significantly increased mainly because of the lung component.

Table 6. RESISTANCES IN THE WHOLE ARDS POPULATION AT DIFFERENT LEVELS OF PEEP*
PEEP (cm H2O)
0 5 10 15
Rmax,rs, cm H2O/L/s 10.4 ± 2.6 10.7 ± 3.0 10.8 ± 4.1 13.2 ± 6.4
Rint,rs, cm H2O/L/s 4.7 ± 2.0† 4.6 ± 2.2 3.2 ± 2.0§ 2.9 ± 2.1§
Rmax,L, cm H2O/L/s 7.8 ± 2.8 8.1 ± 2.8 8.2 ± 3.8 10.3 ± 6.8
DR,rs, cm H2O/L/s 5.7 ± 2.0† 6.1 ± 2.2 7.6 ± 3.3‡ 10.3 ± 5.7§
DR,L, cm H2O/L/s 3.1 ± 1.5† 3.5 ± 1.9 4.9 ± 3.1‡ 7.4 ± 6.0§
DR,w, cm H2O/L/s 2.6 ± 1.6 2.6 ± 1.7 2.6 ± 1.8 2.9 ± 1.8

Definition of abbreviations: Rmax,rs = total resistance of the respiratory system; Rint,rs = airway resistance; Rmax,L = total resistance of the lung; DR,rs = “additional” resistance of the respiratory system; DR,L = “additional” resistance of the lung; DR,w = chest wall resistance.

*Data are expressed as mean ± SD.

Bill Gates warns that a coronavirus-like outbreak will probably happen 'every 20 years or so'Rosie Perper

https://www.businessinsider.com/bill-gates-warns-coronavirus-outbreak-likely-every-20-years-2020-4?r=US&IR=T

​Microsoft co-founder Bill Gates said that people are now realizing that a viral outbreak similar to COVID-19 will likely happen "every 20 years or so." 
Speaking to the Financial Times earlier this month, Gates said that COVID-19 was the "biggest event that people will experience in their entire lives" and said world leaders and global policymakers have "paid many trillions of dollars more than we might have had to if we'd been properly ready."
The 67-year-old billionaire has been warning about the risk of a pandemic disease for years, stating that a global health crisis like coronavirus could wipe out 30 million people in less than a year. 
Visit Business Insider's homepage for more stories.

Microsoft co-founder Bill Gates said that this coronavirus pandemic was the "biggest event that people will experience in their entire lives," and warned that a viral outbreak will likely happen "every 20 years or so." 
Gates discussed the global fight against the novel coronavirus with the Financial Times via Skype on April 2. FT posted the interview and transcript online on April 8.
He said world leaders and global policymakers have "paid many trillions of dollars more than we might have had to if we'd been properly ready."
"This is the biggest event that people will experience in their entire lives," Gates told FT. 

He said that in response to this outbreak, future governments will have "standby diagnostics, deep antiviral libraries, and early warning systems."

"The cost of doing all those things well is very small compared to what we're going through here," he said. "And so now people realize, 'OK, there really is a meaningful probability every 20 years or so with lots of world travel that one of these [viruses] will come along.' And so the citizens expect the government to make it a priority." 
He said he was confident that lessons learned from this outbreak will encourage people to better prepare for next time, but lamented that the cost this time around was too high. 
"It shouldn't have required a many trillions of dollars loss to get there," he said. "The science is there. Countries will step forward."
The 67-year-old billionaire has been warning about the risk of a pandemic disease for years, stating that a global health crisis like coronavirus could wipe out 30 million people in less than a year. 

In 2015, Gates gave a Ted Talk warning that the world was "not ready" for an impending pandemic. 

​In February, the Bill and Melinda Gates Foundation pledged $100 million last month to fight the coronavirus outbreak, designating money towards vaccine research, frontline responders, prevention measures, and treatment efforts around the world.

​

​

A Yanomami woman with traditional ornaments. DeAgostini/Getty Images 

Cameron Kyle-Sidell

Patients need OXYGEN NOT PRESSURE!!! The ventilators may be causing lung damage because of PRESSURE. Needs to be immediately investigated. 100,000 - 250,000 Americans at risk of lung injury. Change can happen. The time is NOW!! #oxygennotpressure #thetimeisnow
CategoryPeople & Blogs

Debate in England on health related effects of electromagnetic fields and 5G.
A very powerful speech on the risks of 5G by MP Tonia Antoniazzi at Westminster Hall.
“We can no longer hide and pretend it is not happening and this cannot be swept under the carpet”
U.S. senator Blumenthal raises concerns on 5G wireless technology’s potential health risks 


​​EU 5G Appeal – Scientists warn of potential serious health effects of 5G
https://www.jrseco.com/european-union-5g-appeal-scientists-warn-of-potential-serious-health-effects-of-5g/

In an appeal to the European Union, more than 180 scientists and doctors from 36 countries warn about the danger of 5G, which will lead to a massive increase in involuntary exposure to electromagnetic radiation. The scientists urge the EU to follow Resolution 1815 of the Council of Europe, asking for an independent task force to reassess the health effects.
“We, the undersigned scientists, recommend a moratorium on the roll-out of the fifth generation, 5G, for telecommunication until potential hazards for human health and the environment have been fully investigated by scientists independent from industry. 5G will substantially increase exposure to radiofrequency electromagnetic fields (RF-EMF) on top of the 2G, 3G, 4G, WiFi etc. for telecommunications already in place. RF-EMF has been proven to be harmful for humans and the environment.”

Initiatiators
One of the initiators is Dr. L. Hardell, Professor of Oncology at Örebro University in Sweden. He states: “The telecom industry is trying to roll out technology that may have very real, unintended harmful consequences. Scientific studies, both recently and over many years, have identified harmful effects on health when testing wireless products under realistic conditions. We are very concerned that the increase in radiation exposure by 5G leads to damage that cannot be reversed”.

Hardell: “The fifth generation (5G) of radio frequency radiation is now being developed. This is done without dosimetric determination or study of the possible health effects. The media praise in particular all the possibilities that this technology promises to offer, such as the self-propelled car and Internet of Things (IoT). The consequences for the health of humans, plants and animals are not discussed at all. Politicians, governments and the media are responsible for unbalanced information. Ordinary people are not informed of conflicting opinions about this technological development. Health effects from radio frequency radiation are a non issue in the media, at least in Sweden, but also in most other countries”.

PDF document by Martin L. Pall, PhD, one of the initiators: 5G: Great risk for EU, US and international health – Compelling evidence for eight distinct types of great harm caused by EMF exposures and the mechanism that causes them

EU Reflex study shows DNA damage caused by radiation from wireless devices and mobile phones

5G Network
The expansion of the 5G network, intended to enable faster wireless transmission of larger amounts of data, requires the installation of many more antennas in urban areas. In this way, the scientists argue, there is no longer anyone escaping the potentially harmful effects of radiation. After all, we are already exposed to 2G, 3G, 4G and Wi-Fi radiation.

Industry’s influence on studies and safety limits
It has been shown that studies on the health impact of electromagnetic radiation in the past have often been influenced by industry. The scientists insist that independent studies on the effects of 5G radiation “to ensure the safety of the population” should now be carried out. They therefore ask the European Commission to postpone the expansion of the 5G network “until the potential risks to human health and the environment have been thoroughly investigated by scientists independent of industry”.

Problems with official ICNIRP exposure limits for electromagnetic radiation
“In conclusion, this article demonstrates that the EU has given mandate to a 13member, nongovernmental private group, the ICNIRP, to decide upon the RF radiation guidelines. The ICNIRP, as well as SCENIHR, are well shown not to use the sound evaluation of science on the detrimental effects of RF radiation, which is documented in the research … These two small organizations are producing reports which seem to deny the existence of scientific published reports on the related risks.” – Appeals that matter or not on a moratorium on the deployment of the fifth generation, 5G, for microwave radiation, L. Hardell & R. Nyberg, MOLECULAR AND CLINICAL ONCOLOGY, 3 Jan 2020.

How much is safe? Radiation authorities rely on controversial group for safety advice – Investigate Europe

FCC: Captured Agency
Response of the European Commission
In question E-003975/2018, Nicola Caputo (S&D) asked the European Commission whether it intends to set up a European task force of independent and impartial scientists on electromagnetic fields to examine the health risks. In her reply the European Commission states that ‘under Article 168 of the Treaty on the Functioning of the European Union, the primary responsibility for protecting the public from potential harmful effects of electromagnetic fields remains with the Member States, including the choice of measures to be adopted based on age and health status.’

In question P-001526-19 Michèle Rivasi (Verts/ALE) asked for an assessment of biological and health impact of 5G: “The 5G Infrastructure Public Private Partnership project (5G PPP) is the world’s largest project of its kind, with EUR 700 million in EU funding. The rollout of 5G will expose people to increased microwave and radiofrequency electromagnetic radiation. … Will the 5G PPP fund any study on the biological impact of 5G radiation? Will the Commission conduct any prior impact assessment on the launching of 5G in the EU, in particular as regards human health? Could it explain how an impact assessment would be conducted, or if one has already taken place, could it provide details on how it was done?”

Insurance companies
Insurer Swiss Re: electromagnetic radiation highest risk category
Major Austrian insurer AUVA finds effects of cell phones on DNA, EEG and human proteins
Lloyd’s insurance company does not cover health damage caused by electromagnetic radiation
Slovenia halts 5G to Investigate Health and Safety

“Slovenia stops the introduction of 5G technology:

We do not know if it is dangerous to humans”. 

In Slovenia 5G had been halted, officials take more time to investigate health effects of the new technology. A letter from Minister Rudi Medved states they will reopen the debate on potential health risks.

Netherlands: Parliament asks for independent investigation on 5G health risks
In the Netherlands, the Parliament is concerned about the health risks of radiation from the new 5G network. Political parties urgently want to know what the state of affairs is regarding possible dangers before masts are installed on a large scale. GroenLinks urged the Health Council of the Netherlands to carry out an independent investigation into 5G radiation. Member of parliament Laura Bromet: We still do not know about the dangers to public health. Little research has been undertaken into the effects of 5G. We have to take people’s concerns seriously and investigate this.

Resolution opposing 5G by the municipality of Rome
The Rome resolution asks “the mayor to stop the 5G trial and not to raise the limit values ​​in the threshold of electromagnetic radiation avoiding the positioning of millimeter microwave antennas on homes, schools, day centers, recreation centers, street lamps and more.” Rome Councilor Massimiliano Quaresima stated, “I am in favor of technological progress but not on the experimentation of 5G technology in the absence of scientific data on the repercussions for health.”

Germans petition Parliament to stop 5G auction on health grounds
A petition asking the German Parliament to stop the award of 5G frequencies has reached 54,643 signatures, surpassing the quorum, reports ‘Diagnose: Funk’. The petioners request the German Parliament to suspend the procedure to award 5G frequencies based on scientifically justified doubts about the safety of this technology.

Debate in England on health related effects of electromagnetic fields and 5G.
A very powerful speech on the risks of 5G by MP Tonia Antoniazzi at Westminster Hall.
“We can no longer hide and pretend it is not happening and this cannot be swept under the carpet”
U.S. senator Blumenthal raises concerns on 5G wireless technology’s potential health risks 
 https://youtu.be/bzUv1F2ZhlM

EU 5G Appeal – Scientists warn of potential serious health effects of 5G
https://www.jrseco.com/european-union-5g-appeal-scientists-warn-of-potential-serious-health-effects-of-5g/

In an appeal to the European Union, more than 180 scientists and doctors from 36 countries warn about the danger of 5G, which will lead to a massive increase in involuntary exposure to electromagnetic radiation. The scientists urge the EU to follow Resolution 1815 of the Council of Europe, asking for an independent task force to reassess the health effects.
“We, the undersigned scientists, recommend a moratorium on the roll-out of the fifth generation, 5G, for telecommunication until potential hazards for human health and the environment have been fully investigated by scientists independent from industry. 5G will substantially increase exposure to radiofrequency electromagnetic fields (RF-EMF) on top of the 2G, 3G, 4G, WiFi etc. for telecommunications already in place. RF-EMF has been proven to be harmful for humans and the environment.”

Initiatiators
One of the initiators is Dr. L. Hardell, Professor of Oncology at Örebro University in Sweden. He states: “The telecom industry is trying to roll out technology that may have very real, unintended harmful consequences. Scientific studies, both recently and over many years, have identified harmful effects on health when testing wireless products under realistic conditions. We are very concerned that the increase in radiation exposure by 5G leads to damage that cannot be reversed”.

Hardell: “The fifth generation (5G) of radio frequency radiation is now being developed. This is done without dosimetric determination or study of the possible health effects. The media praise in particular all the possibilities that this technology promises to offer, such as the self-propelled car and Internet of Things (IoT). The consequences for the health of humans, plants and animals are not discussed at all. Politicians, governments and the media are responsible for unbalanced information. Ordinary people are not informed of conflicting opinions about this technological development. Health effects from radio frequency radiation are a non issue in the media, at least in Sweden, but also in most other countries”.

PDF document by Martin L. Pall, PhD, one of the initiators: 5G: Great risk for EU, US and international health – Compelling evidence for eight distinct types of great harm caused by EMF exposures and the mechanism that causes them

EU Reflex study shows DNA damage caused by radiation from wireless devices and mobile phones

5G Network
The expansion of the 5G network, intended to enable faster wireless transmission of larger amounts of data, requires the installation of many more antennas in urban areas. In this way, the scientists argue, there is no longer anyone escaping the potentially harmful effects of radiation. After all, we are already exposed to 2G, 3G, 4G and Wi-Fi radiation.

Industry’s influence on studies and safety limits
It has been shown that studies on the health impact of electromagnetic radiation in the past have often been influenced by industry. The scientists insist that independent studies on the effects of 5G radiation “to ensure the safety of the population” should now be carried out. They therefore ask the European Commission to postpone the expansion of the 5G network “until the potential risks to human health and the environment have been thoroughly investigated by scientists independent of industry”.

In an appeal to the European Union, more than 180 scientists and doctors from 36 countries warn about the danger of 5G, which will lead to a massive increase in involuntary exposure to electromagnetic radiation. The scientists urge the EU to follow Resolution 1815 of the Council of Europe, asking for an independent task force to reassess the health effects.
“We, the undersigned scientists, recommend a moratorium on the roll-out of the fifth generation, 5G, for telecommunication until potential hazards for human health and the environment have been fully investigated by scientists independent from industry. 5G will substantially increase exposure to radiofrequency electromagnetic fields (RF-EMF) on top of the 2G, 3G, 4G, WiFi etc. for telecommunications already in place. RF-EMF has been proven to be harmful for humans and the environment.”

Initiatiators
One of the initiators is Dr. L. Hardell, Professor of Oncology at Örebro University in Sweden. He states: “The telecom industry is trying to roll out technology that may have very real, unintended harmful consequences. Scientific studies, both recently and over many years, have identified harmful effects on health when testing wireless products under realistic conditions. We are very concerned that the increase in radiation exposure by 5G leads to damage that cannot be reversed”.


Hardell: “The fifth generation (5G) of radio frequency radiation is now being developed. This is done without dosimetric determination or study of the possible health effects. The media praise in particular all the possibilities that this technology promises to offer, such as the self-propelled car and Internet of Things (IoT). The consequences for the health of humans, plants and animals are not discussed at all. Politicians, governments and the media are responsible for unbalanced information. Ordinary people are not informed of conflicting opinions about this technological development. Health effects from radio frequency radiation are a non issue in the media, at least in Sweden, but also in most other countries”.

PDF document by Martin L. Pall, PhD, one of the initiators: 5G: Great risk for EU, US and international health – Compelling evidence for eight distinct types of great harm caused by EMF exposures and the mechanism that causes them

EU Reflex study shows DNA damage caused by radiation from wireless devices and mobile phones

5G Network
The expansion of the 5G network, intended to enable faster wireless transmission of larger amounts of data, requires the installation of many more antennas in urban areas. In this way, the scientists argue, there is no longer anyone escaping the potentially harmful effects of radiation. After all, we are already exposed to 2G, 3G, 4G and Wi-Fi radiation.

Industry’s influence on studies and safety limits
It has been shown that studies on the health impact of electromagnetic radiation in the past have often been influenced by industry. The scientists insist that independent studies on the effects of 5G radiation “to ensure the safety of the population” should now be carried out. They therefore ask the European Commission to postpone the expansion of the 5G network “until the potential risks to human health and the environment have been thoroughly investigated by scientists independent of industry”.

Problems with official ICNIRP exposure limits for electromagnetic radiation
“In conclusion, this article demonstrates that the EU has given mandate to a 13member, nongovernmental private group, the ICNIRP, to decide upon the RF radiation guidelines. The ICNIRP, as well as SCENIHR, are well shown not to use the sound evaluation of science on the detrimental effects of RF radiation, which is documented in the research … These two small organizations are producing reports which seem to deny the existence of scientific published reports on the related risks.” – Appeals that matter or not on a moratorium on the deployment of the fifth generation, 5G, for microwave radiation, L. Hardell & R. Nyberg, MOLECULAR AND CLINICAL ONCOLOGY, 3 Jan 2020.

How much is safe? Radiation authorities rely on controversial group for safety advice – Investigate Europe

FCC: Captured Agency
Response of the European Commission
In question E-003975/2018, Nicola Caputo (S&D) asked the European Commission whether it intends to set up a European task force of independent and impartial scientists on electromagnetic fields to examine the health risks. In her reply the European Commission states that ‘under Article 168 of the Treaty on the Functioning of the European Union, the primary responsibility for protecting the public from potential harmful effects of electromagnetic fields remains with the Member States, including the choice of measures to be adopted based on age and health status.’

In question P-001526-19 Michèle Rivasi (Verts/ALE) asked for an assessment of biological and health impact of 5G: “The 5G Infrastructure Public Private Partnership project (5G PPP) is the world’s largest project of its kind, with EUR 700 million in EU funding. The rollout of 5G will expose people to increased microwave and radiofrequency electromagnetic radiation. … Will the 5G PPP fund any study on the biological impact of 5G radiation? Will the Commission conduct any prior impact assessment on the launching of 5G in the EU, in particular as regards human health? Could it explain how an impact assessment would be conducted, or if one has already taken place, could it provide details on how it was done?”

Insurance companies
Insurer Swiss Re: electromagnetic radiation highest risk category
Major Austrian insurer AUVA finds effects of cell phones on DNA, EEG and human proteins
Lloyd’s insurance company does not cover health damage caused by electromagnetic radiation
Slovenia halts 5G to Investigate Health and Safety

“Slovenia stops the introduction of 5G technology: We do not know if it is dangerous to humans”. In Slovenia 5G had been halted, officials take more time to investigate health effects of the new technology. A letter from Minister Rudi Medved states they will reopen the debate on potential health risks.

Netherlands: Parliament asks for independent investigation on 5G health risks
In the Netherlands, the Parliament is concerned about the health risks of radiation from the new 5G network. Political parties urgently want to know what the state of affairs is regarding possible dangers before masts are installed on a large scale. GroenLinks urged the Health Council of the Netherlands to carry out an independent investigation into 5G radiation. Member of parliament Laura Bromet: We still do not know about the dangers to public health. Little research has been undertaken into the effects of 5G. We have to take people’s concerns seriously and investigate this.

Resolution opposing 5G by the municipality of Rome
The Rome resolution asks “the mayor to stop the 5G trial and not to raise the limit values ​​in the threshold of electromagnetic radiation avoiding the positioning of millimeter microwave antennas on homes, schools, day centers, recreation centers, street lamps and more.” Rome Councilor Massimiliano Quaresima stated, “I am in favor of technological progress but not on the experimentation of 5G technology in the absence of scientific data on the repercussions for health.”

Germans petition Parliament to stop 5G auction on health grounds
A petition asking the German Parliament to stop the award of 5G frequencies has reached 54,643 signatures, surpassing the quorum, reports ‘Diagnose: Funk’. The petioners request the German Parliament to suspend the procedure to award 5G frequencies based on scientifically justified doubts about the safety of this technology.

Debate in England on health related effects of electromagnetic fields and 5G.
A very powerful speech on the risks of 5G by MP Tonia Antoniazzi at Westminster Hall.
“We can no longer hide and pretend it is not happening and this cannot be swept under the carpet”
U.S. senator Blumenthal raises concerns on 5G wireless technology’s potential health risks 
 https://youtu.be/bzUv1F2ZhlM

Problems with official ICNIRP exposure limits for electromagnetic radiation
“In conclusion, this article demonstrates that the EU has given mandate to a 13member, nongovernmental private group, the ICNIRP, to decide upon the RF radiation guidelines. The ICNIRP, as well as SCENIHR, are well shown not to use the sound evaluation of science on the detrimental effects of RF radiation, which is documented in the research … These two small organizations are producing reports which seem to deny the existence of scientific published reports on the related risks.” – Appeals that matter or not on a moratorium on the deployment of the fifth generation, 5G, for microwave radiation, L. Hardell & R. Nyberg, MOLECULAR AND CLINICAL ONCOLOGY, 3 Jan 2020.

How much is safe? Radiation authorities rely on controversial group for safety advice – Investigate Europe

FCC: Captured Agency
Response of the European Commission
In question E-003975/2018, Nicola Caputo (S&D) asked the European Commission whether it intends to set up a European task force of independent and impartial scientists on electromagnetic fields to examine the health risks. In her reply the European Commission states that ‘under Article 168 of the Treaty on the Functioning of the European Union, the primary responsibility for protecting the public from potential harmful effects of electromagnetic fields remains with the Member States, including the choice of measures to be adopted based on age and health status.’

In question P-001526-19 Michèle Rivasi (Verts/ALE) asked for an assessment of biological and health impact of 5G: “The 5G Infrastructure Public Private Partnership project (5G PPP) is the world’s largest project of its kind, with EUR 700 million in EU funding. The rollout of 5G will expose people to increased microwave and radiofrequency electromagnetic radiation. … Will the 5G PPP fund any study on the biological impact of 5G radiation? Will the Commission conduct any prior impact assessment on the launching of 5G in the EU, in particular as regards human health? Could it explain how an impact assessment would be conducted, or if one has already taken place, could it provide details on how it was done?”

Insurance companies
Insurer Swiss Re: electromagnetic radiation highest risk category
Major Austrian insurer AUVA finds effects of cell phones on DNA, EEG and human proteins
Lloyd’s insurance company does not cover health damage caused by electromagnetic radiation
Slovenia halts 5G to Investigate Health and Safety


“Slovenia stops the introduction of 5G technology: We do not know if it is dangerous to humans”. In Slovenia 5G had been halted, officials take more time to investigate health effects of the new technology. A letter from Minister Rudi Medved states they will reopen the debate on potential health risks.

Netherlands: Parliament asks for independent investigation on 5G health risks
In the Netherlands, the Parliament is concerned about the health risks of radiation from the new 5G network. Political parties urgently want to know what the state of affairs is regarding possible dangers before masts are installed on a large scale. GroenLinks urged the Health Council of the Netherlands to carry out an independent investigation into 5G radiation. Member of parliament Laura Bromet: We still do not know about the dangers to public health. Little research has been undertaken into the effects of 5G. We have to take people’s concerns seriously and investigate this.

Resolution opposing 5G by the municipality of Rome
The Rome resolution asks “the mayor to stop the 5G trial and not to raise the limit values ​​in the threshold of electromagnetic radiation avoiding the positioning of millimeter microwave antennas on homes, schools, day centers, recreation centers, street lamps and more.” Rome Councilor Massimiliano Quaresima stated, “I am in favor of technological progress but not on the experimentation of 5G technology in the absence of scientific data on the repercussions for health.”

Germans petition Parliament to stop 5G auction on health grounds
A petition asking the German Parliament to stop the award of 5G frequencies has reached 54,643 signatures, surpassing the quorum, reports ‘Diagnose: Funk’. The petioners request the German Parliament to suspend the procedure to award 5G frequencies based on scientifically justified doubts about the safety of this technology.

Debate in England on health related effects of electromagnetic fields and 5G.
A very powerful speech on the risks of 5G by MP Tonia Antoniazzi at Westminster Hall.
“We can no longer hide and pretend it is not happening and this cannot be swept under the carpet”
U.S. senator Blumenthal raises concerns on 5G wireless technology’s potential health risks 
 https://youtu.be/bzUv1F2ZhlM

 

​20 Vitamins and Supplements To Boost Immune Health for COVID-19
https://www.medicinenet.com/covid_19_supplements/article.htm 

What supplements should I take for Coronavirus (COVID-19)?
Picture of vitamin C, a supplement that can help protect against COVID-19.

The recent COVID-19 coronavirus outbreak causes a variety of telltale signs and symptoms, ranging from fever and dry cough, to more extreme symptoms requiring immediate medical help such as difficulty breathing and confusion. 
We do not currently have any vaccines or antiviral medications that specifically prevent, cure, or treat COVID-19, so treatment will usually involve managing symptoms with supportive treatments. 
If you have relatively mild COVID-19 symptoms and don’t have any other medical conditions that would put you at high risk for developing complications of COVID-19 (over the age of 65, diabetes, COPD, heart disease, kidney disease, HIV, asthma, undergoing cancer treatment), these vitamins and supplements might help strengthen your immune system to fight coronavirus.
It is important to note that no vitamin or supplement can cure COVID-19, nor is there solid evidence any non-FDA-approved vitamin or supplement has any effect on COVID-19. Immune supporting effects of supplements and vitamins in the context of the coronavirus is theoretical.
Vitamins and supplements may interact with one another in your system and with prescription or over-the-counter medications. Notify your doctor about all the drugs and supplements you are taking, and do not start a vitamin regimen without consulting your physician.

What vitamins can help prevent COVID-19 and other illnesses?

Because COVID-19 comes with cold and flu-like symptoms, Vitamins B, C and D, as well as zinc may be helpful in boosting your immune system and fighting the illness in the same way they can help you get over a cold or flu.

Vitamin C
Generally, vitamin C can help you fight a cold faster or ease your cold symptoms if you were taking it prior to getting sick. As an antioxidant, vitamin C can help reduce inflammation—and lung inflammation is a severe symptom of COVID-19, which can lead to respiratory distress or even death. So if you’re still healthy, it doesn’t hurt to start taking vitamin C now. 

Vitamin D
The primary function of vitamin D is to help your body maintain optimal blood levels of calcium and phosphorous, which you can get through exposure to the sun’s ultraviolet rays, or through supplements and the foods you eat. 

Getting enough vitamin D can also protect you from respiratory infection. Vitamin D supplementation significantly decreases the chance of respiratory tract infections, based on clinical studies published in the Journal of Pharmacology and Pharmacotherapeutics.

B Complex vitamins
Vitamin B6 is essential to keeping your immune system in top condition. Be sure to get enough vitamin B as a supplement, as part of your daily diet (you can easily get your daily intake from fortified cereals) or in a multivitamin. 

Zinc
Popping a zinc throat lozenge, or taking an over-the-counter cold remedy with zinc in it (as a syrup or tablet) helps shorten the length of rhinovirus colds. Zinc also helps symptoms—nasal congestion, nasal drainage, sore throat, and cough—resolve sooner.
Zinc has also been found to help produce and activate T-cells (t-lymphocytes), which trigger the body to respond to infections, according to the NIH.
For a faster recovery, start taking zinc to treat your illness within the first 24 hours of symptoms. A proper dose of zinc is 75 mg, but beware: Taking more than 150mg per day of zinc could cause zinc toxicity and also have a negative impact on your immune system.
If you’re taking more than one zinc medication, check with your doctor first to prevent adverse reactions.

What are the best supplements to take during COVID-19 crisis?
Whether eaten as a whole food or in the form of a pill, the following supplements may help keep you healthy and your immune system in top shape to combat coronavirus. Once again, benefits are theoretical.

Elderberry
Full of antiviral and anti-inflammatory properties, elderberry syrup is used as a remedy for colds, flus, and bacterial sinus infections. Elderberry works by reducing swelling in the mucus membranes. 
Some studies suggest elderberry extract reduces the duration of the flu, which is why some believe it may also help your immune system against coronavirus (COVID-19) infection.

Mushrooms
Mushrooms are high in selenium and B vitamins like riboflavin and niacin, which are needed to keep the immune system running optimally. Mushrooms are also high in polysaccharides, sugar-like molecules that boost immune function.

Astragalus
Astragalus is an herb, and its root is used in medicine. Typically used to strengthen the immune system and treat the common cold, upper respiratory infections, seasonal allergies, swine flu, astragalus is also used to fight bacteria and viruses. 

Its effectiveness against illness doesn’t have a lot of research behind it, although in treating seasonal allergies, 160 mg of astragalus root extract (Lectranal by Milsing d.o.o.) by mouth daily for 3-6 weeks was found to improve symptoms such as running nose, itching, and sneezing.

Selenium
Selenium is a mineral with a variety of uses, including preventing bird flu and swine flu. A potent antioxidant, selenium can boost immune function, except in those with autoimmune disorders, who could experience a negative impact on their immune system.

Garlic 
Garlic’s antiviral properties may be helpful in reducing the severity of symptoms in colds, flu or COVID-19 infections. 
In one study, people who took garlic supplements during cold season caught fewer colds than those who took placebo pills. Garlic may also shorten the duration of a cold. While you can eat garlic fresh, you can also take it in the form of a supplement.

Andrographis
A plant used in medicine for a variety of ailments, andrographis is frequently used as a painkiller and fever reducer, and to treat the common cold and flu.
Taking andrographis extract in combination with Siberian ginseng (Kan Jang, Swedish Herbal Institute) may improve symptoms of the common cold when started within 72 hours of feeling sick. 
According to another study, patients with flu who took a specific Andrographis extract in combination with Siberian ginseng (Kan Jang, Swedish Herbal Institute) felt better more quickly than patients taking amantadine, a drug approved by the federal Food and Drug Administration (FDA) to prevent Asian flu and treat Influenza A. They also experienced fewer complications after the flu: sinus pain, breathing problems and coughing (bronchitis).

Licorice root
Licorice root, when used as a gargle, may be used to soothe the pain of a sore throat, a common symptom of coronavirus, according to a 2009 study in the journal Anesthesia & Analgesia. Additionally, licorice root can loosen congestion and reduce inflammation. You can also chew a piece of licorice root or drink it as a tea.

Pelargonium sidoides
Also known as Umckaloabo among other names, pelargonium sidoides is commonly taken by mouth for upper respiratory infections including bronchitis, sinusitis, sore throat, tonsillitis, and the common cold. 
Taking a specific extract of pelargonium sidoides seems to help reduce symptoms and clear up the common cold after 10 days of treatment. It also lessens symptoms of bronchitis in adults within 48 hours of feeling sick. 

Curcumin
Curcumin is derived from the Curcuma longa plant, commonly known as turmeric. Curcumin is used in Ayurvedic and Chinese medicine for its analgesic, anti-inflammatory, and antiseptic activity. Curcumin can help fight inflammation and aid the body’s immune response, as found by a study published in Molecules.

Echinacea
Echinacea has been used to treat colds symptoms upon first signs of illness, but the research on its efffectiveness varies. Some research shows that taking echinacea can reduce the risk of catching a cold by 45% to 58%. But other research shows that taking echinacea does not prevent the common cold when you are exposed to cold viruses.
Early research shows that taking a specific echinacea product (Monoselect Echinacea, PharmExtracta, Pontenure, Italy) daily for 15 days might improve the response to the flu vaccine in people with breathing problems such as bronchitis or asthma, and these are high-risk types who could suffer complications of COVID-19.

When combined with antibacterial and antiseptic sage as a throat spray, echinacea and sage were found by a 2009 study to ease the pain of a sore throat.

Propolis
Propolis, a resin-like material from the buds of poplar and cone-bearing trees, is used for boosting the immune system, and as an antioxidant and anti-inflammatory agent. Some evidence suggests that propolis might help prevent or reduce the duration of common colds and other upper respiratory tract infections.
Acai berryAcai berry is such a potent antioxidant and stimulator of the immune system, researchers are studying it as a potential treatment for all kinds of conditions, and it's often touted as a supporting of general health and immune function. 


What alternative medicine supplements can I take to stay healthy from COVID-19?
The Chinese government and state-linked news agencies touted traditional Chinese medicine for symptom relief during the original December 2019 coronavirus outbreak in Wuhan, China.

There is little good evidence that TCM is effective, but it has been correlated with some reduction in symptom duration in some studies. 

Based on studies of traditional Chinese medicine (TCM) focused on the prevention of severe acute respiratory syndrome (SARS) and H1N1 influenza, researchers found:

None of the participants who took TCM contracted SARS in the 3 SARS studies. 
The infection rate of H1N1 influenza in the CM group was significantly lower than the non-CM group in the H1N1 studies.

The following supplements, as noted in the Chinese Journal of Integrative Medicine, are suggested for treating and/or preventing coronavirus symptoms:

Radix astragali (Huangqi, or astragalus)—boosts the immune system and may prevent colds and upper respiratory infections.
Radix glycyrrhizae (Gancao, or licorice root)—relieves sore throat and cough, and may ease symptoms of COVID-19.
Radix saposhnikoviae (Fangfeng, or siler root)—in traditional Chinese medicine, it’s commonly used to treat general aches, headaches, fever, cold, and allergic rhinitis.
Rhizoma Atractylodis Macrocephalae (Baizhu, or Atractylodes)—in traditional Chinese medicine, it’s used to support lung health.
Lonicerae Japonicae Flos (Jinyinhua, or honeysuckle)—decreases inflammation in upper respiratory tract infections including colds, influenza, swine flu, and pneumonia; other viral and bacterial infections.
Fructus forsythia (Lianqiao, or forsythia)—decreases inflammation of small air passages in the lung (bronchiolitis), tonsillitis, sore throat, fever, and more.
Both studies, however, warn against using TCM as the standard treatment or prevention protocol for any of these infections.
Before taking any herbal supplements, check with your doctor first if there may be any interactions with other medications you are currently taking.

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Dan Patrick- Lieutenant Texas Governor  said he was willing to give up his life to preserve the US economy from the effect of efforts to tackle the coronavirus

A Deep Look into the Biology and Evolution of COVID-19
 University of California Television (UCTV)
(00:11 - Introduction - Suresh Subramani, 04:25 - Big Picture Questions About COVID-19 - Emily Troemel, 14:58 - The SARS-CoV-2 Virus - Matt Daugherty, 29:22 - Predicting the Next Pandemic - Justin Meyer, 41:45 - Group Discussion) UC San Diego infectious disease researchers provide an overview of the biology and evolution of the SARS-CoV-2 virus, cause of COVID-19 disease which is sweeping the globe in a pandemic. They share their expertise in the dynamics of host-pathogen interactions and viral life-cycles and how they relate to this global challenge. [Show ID: 35811]
UCTV is the broadcast and online media platform of the University of California, featuring programming from its ten campuses, three national labs and affiliated research institutions. UCTV explores a broad spectrum of subjects for a general audience, including science, health and medicine, public affairs, humanities, arts and music, business, education, and agriculture. Launched in January 2000, UCTV embraces the core missions of the University of California -- teaching, research, and public service – by providing quality, in-depth television far beyond the campus borders to inquisitive viewers around the world. (https://www.uctv.tv)
CategoryEducation

Revisionist History: Vaccines and the "Spanish Flu" of 1918-19
DID A VANCCINE EXPERIMENT ON U.SOLDIERS CAUSE THE "SPANISH FLUE"?
The 1918-19 bacterial vaccine experiment may have killed 50-100 million people
by Keven Barry, 
President
First Freedoms, Inc.

November 7, 2018
Part 1 of a 5 part series
The  "Spanish Flu" kills an estimated 50-100 million people during a pandemic in 1918-19. 

What is the story we have told about this pandemic isn't true? What if, the killer infection was neither the flu not Spanish in origin?
Newly analyzed  documents reveal that the "Spanish Flu" may have been a military vaccine experiment gone awry. In looking back on the 100th anniversary of the end of World War 1, we need to delve deeper to solve this mystery.

Summary
The reason modern technology has not been able to pinpoint the killer influenza strain from this pandemic is because influenza was not the killer.
More soldiers died during WWI from disease than from bullets.
The pandemic wa snot flue. An estimated 95%9 or higher) of the deaths were caused by bacterial pneumonia, not influenza/a virus.
The pandemic was not Spanish. The first cases of bacterial pneumonia in 1918 trace back to military base in Fort Riley, Kansas.
From January 21-June 4, 1918, an experimental bacterial meningitis vaccine cultured in horses by Rockefella Institute got Medical Research in New York was injected into soldiers at Fort Riley.
During the remainder of 1918 as those soldiers - often living and traveling under poor sanitary conditions- were sent to Europe to fight they spread bacterial at every stop between Kansas and the front line trenches  in France.
One study describes soldiers "with active infections (who) were aerosolizing the bacteria that colonized outposts their noses and throats, while others -often, in the same "breathing spaces" - were profoundly susceptible to invasion and rapid spread through their lungs by their own or others' colonizing bacteria." (1)

The  "Spanish Flu" attacked healthy people in their prime. Bacterial pneumonia attacks people in their prime. Flu attacks the young, old and immune compromised.

During WWI, the Rockefeller Institute also sent the antimeningococcic serum to England, France, Belgium, Italy and other countries, helping spread the pandemic worldwide.
During the pandemic  of 1918-19, the so-called  "Spanish Flu" killed 50-100 million people, including many soldiers. many people do not realize that disease killed far more soldiers on all sides than macine guns or mustard gas or anything else typically associated with WWI.
I ave personal connection to the  "Spanish Flu". Among those killed by disease in 1918-19 are members of my parents' families. In my father's side, his grandmother Sadie Hoyt died from  pneumonia in 1918. Sadie's sister Marian also joined the Navy. She dies from "the influenza" in 1919. On my mother's side, two of her father's sisters died in childhood. All of the family members who died lived in new York City. I suspect many American families, and many families worldwide, were impacted in similar ways by the mysterious  "Spanish Flu"..
In 1918, "influenza" or flu was a catchall term for disease of unknown origin. It didn't carry the specific meaning it does today. It meant some mystery disease which dropped out of the sky. In fact,  influenza is from the Medieval Latin "influential" in an astrological sense, meaning a visitation under the influence of the stars.

Why Is What Happened 100 Years Ago Important Now?
Between 1900-1920, there were enormous efforts underway in the industrial world to build a better society. I will use New York as an example to discuss three major changes to society which occurred in NY during that time and their impact on mortality from infectious diseases.

Comment:
This is completely debatable if we take a larger view of what society is and what society should be...and what there cities are designed to do which is... herding people into an unnatural environment which is unnatural and disconnecting people from their natural design ,,,"
One has to question whether the creation of city was really creating a better society ... 
" by herding people into an unnatural environment of unnatural design".

1. Clean Water and Sanitation
In the late 19th century through the early 20th Century, New York built an extraordinary system to bring clean water to the city from the Catskills, a system still in use today. New York City also built over 6000 miles of sewer to take away and treat waster, which protects the drinking water. The World Health Organization acknowledges the importance of clean water and sanitation in combating infectious diseases. (2)

2. Electricity
In the late 19th century through the early 20th century, New York built a power grid and wired the city so  power was available in every home. Electricity allows for refrigeration. Refrigeration is an unsung hero as a public health benefit. When food is refrigerated from farm to table, the public is protected from potential infectious diseases. Cheap renewable energy is important for many reasons, including combating infectious diseases.

3. Pharmaceutical
In the late 19th century through the early 20th century, New York became the home of the Rockefeller Institute for medical Research (now Rockefeller University). the Institute is where the modern pharmaceutical industry was born, The Institute pioneered many of the approaches the pharmaceutical industry used today. including the preparation of vaccine serum, for better or worse. the vaccine used in the Fort Rile experiment on soldiers was made in horses.
US Mortality Rates data from the turn on the 20th Century to 1965 clearly indicates that clean water, flushing toilets, effective sewer systems and refrigerated foods all combined to effectively deduce mortality from infectious diseases BEFORE vaccines for those diseases became available.
Have doctors and the pharmaceutical manufacturers taken credit for reducing mortality from infectious diseases which rightfully belongs to sandhogs, plumbers, electricians and engineers?
If hubris at the Rockefeller Institute in 1918 led to a pandemic disease which killed millions of people, what lessons can we learn and apply to 2018?


 The Disease Was Not Spanish
While watching an episode of American Experience on PBS a few months ago, I was surprised to hear that the first cases of 
" "Spanish Flu" occurred at Fort Riley, Kansas in 1918. I thought, how is it possible this historically important event could be so badly misnamed 100 years ago and never corrected?

Why "Spanish?".
Spain was one of a few countries not involved in World War 1. Most of the countries involved in the was censored their press. Fee from censorship concerns, the earliest press reports of people dying from disease in large numbers came from Spain. the waring countries did not want to additionally frighten the troops, so they were content to scapegoat Spain. Soldiers on all sides would be asked to cross no man's land into machine gun fire, which was frightening enough without knowing that the trenches were a disease breeding ground.

One hundred years later, it's long past time to drop "Spanish" from all discussion of this pandemic. If the flue started at a United States military base in Kansas, then the disease could and should be more aptly named. In order to present future disasters, the US (and the rest of the world) must take a hard look at what really caused the pandemic.

It is possible that one of the reasons the Spanish Flu never corrected is that it helps disguise the origon of the pandemic. If the origin of the pandemic involved a vaccine experiment on US may prefer calling it Spanish Flue instead of The Fort Riley Bacteria of 1918, or something similar. The Spanish Flu instead of The Fort Riley Bacteria of 1918, or something similar. The Spanish Flu started at the location this experiment bacterial vaccine was given making it the prime suspect as the source of the bacterial infections which killed so many.

It would be much more difficult to maintain the marketing mantra of “vaccines saves lived” if a vaccine experiment originating in the United States during the years of primitive manufacturing caused the deaths of 50-100 million people.
“Vaccines save lives …. except we may have killed 50-100 million people in 1918-19” is a far less effective sales slogan than the overly simplistic “vaccines saves lives”.

The Disease Which Killed So Many Was Not Flue Or A Virus. It Was Bacterial
During the mid-2000’s there was much talk about “pandemic preparedness”. Influenza vaccine manufacturers in the United State received billions of taxpayer dollars to develop vaccines to make sure we don’t have another lethal pandemic “flue”, like the one in 1918-19.
Capitalizing on the “flue” part of “Spanish” flu helped vaccine manufacturers procure billion dollar checks from governments, even though scientists knew at the time that bacterial pneumonia was the the real killer. It was not my opinion that bacterial pneumonia was the killer - thousands of autopsies confirm this fact. According to a 2008 National Institute paper, bacterial pneumonia was the killer in a minimum of 93/7% of the 1918-19 autopsies reviewed. It is likely higher than 92.7%. The researchers looked at more than 9000 autopsies, and “there were no negative (bacterial) lung culture results.”

“... In the 68 higher-quality autopsy series, in which the possibility of unreported negative cultures could be excluded, 92.7% of autopsy lung cultures were positive for 1 Bacterum …. in one study of approximately 9000 subjects who were followed from clinical presentation with influenza to resolution or autopsy, researches obtained, with sterile technique, cultures of either pneumococci or streptococci from 164 of 167 lung tissue samples. There were 89 pure cultures of pneumococci, 19 cultures from which only streptococci were recovered;

34 that yielded mixtures of pneumococci and/or streptococci; 22 that yielded a mixture of pneumococci, streptococci and other organisms (prominently pneumococci, and nonhemolytic streptococci), and 3 that yielded  nonhemolytic streptococci alone. There were no negative lung culture results.” (3)

Pneumococci or streptococci were found in “164 of (the) 167 lung tissue samples” autopsied. That is 98.2% bacteria was the killer.
Where Did The Spanish Flue Bacterial Pneumonia of 1918-19 Originate?
When the United States declared war in April 1917, the fledgling Pharmaceutical industry had something they have never had before - a large supply of human subjects in the form of the US military’s first draft. Pre-war in 1917, the US Army was 286,000 men. Post-war in 1920, the US army disbanded, and had 296,000 men. During the war years 1918-19, the US Army ballooned to 6,000,000 men with 2,000,000 men being sent overseas. The Rockefeller Institute for Medical Research took advantage of this new pool of human guinea pigs to conduct vaccine experiments.

A Report On Antimeningitis Vaccination and Observations On Agglutinnins In The Blood of Chronic Meningococcus Carriers
Frederic L. Gates
From the Base Hospital, Fort Riley, Kansas, and The Rockerfeller Institute for Medical Research, New York.
Received July 200th, 1919.
Author’s note: Please read the Fort Riley paper in its entirety so you can appreciate the carelessness of the experiments conducted on these troops.
 

Between January 21st and June 4th, 1918. Dr Gates reports on an experiment where soldiers were given 3 does of a bacterial meningitis vaccine. Those conducting the experiments on the soldiers were just spitballing dosages of a vaccine serum made in horses.
The vaccination regime was designed to be 3 doses. 4792 men received the first done, but only 4,257 got the 2nd dose (down 11%), and only 3,702 received all three doses (down 22.7%). A total of 1,090 men were not there for the 3rd dose.

What happened to these soldiers?
Where they shipped Est by train from Kansas to board a ship to Europe?

Were they in the Fort Riley hospital?

Dr Gates’s report doesn’t tell us.
An article accompanying the American Experience broadcast I watched sheds some light on where these 1,090 men might be. Gates began his experiments in January 1918. By March of that year. “ 100 men a day” were entering the infirmary at Fort Riley. Are some of these the men missing from Dr. Gates’ report - the ones who did not get the 2nd or 3rd dose?
Shortly before breakfast on Monday, March 11, the first domino would fall signaling the commencement  of the first wave of the 1918 influenza. Company cook Albert Gitchell reported to the camp infirmary with complaints of a “bad cold”. Right behind him came Corporal W. Drake voicing similar complaints. By noon, camp surgeon Edward R. Schreiner had over 100 sick men on his hands all apparently suffering from the same malady …” (5)
Gates does report that several of the men in the experiment had flu like symptoms: coughs, vomiting and diarrhea after receiving the vaccine. These symptoms are a disaster for men living in barracks, travelling on trains to the Atlantic Coast, sailing to Europe, and living and fighting in trenches. The unsanitary conditions at each step of the journey are an ideal environment for a contagious disease like bacterial pneumonia to spread.

From Dr. Gates’s report
“ …. Reactions …. Several cases of looseness of the bowels or transient diarrhea were noted. This symptom had not been encounteres before. Careful inquiry in individual cases often elicited the information that men who complained of the effects of vaccination were suffering from mild coryza, bronchitis at the time of injection …”
 “Sometime the reaction was initiated by a chill or chilly sensation, and a number of men complained of fever  or feverish sensations during the following night. Next in frequency came nausea (occasionally vomiting), dizziness, and general “aches and lains” in the joints and musles, which is a few instances were especially localized in the neck or lumbar region, causing stiff neck or stiff back. A few injections were followed by diarrhea. The reactions, therefore, occasionally simulated the onset of epidemic meningitis and several vaccinated men were sent as suspects to the Base Hospital for diagnosis.” (4)
According to Gates they injected random dosages of an experimental bacterial meningitis vaccine into soldiers. Afterwards, some of the soldiers had symptoms which “simulated” meningitis, but Dr. Gates advances the fantastical claim that it wasn’t actual meningitis.

The soldiers developed flu-like symptoms. Bacterial meningitis, then and now, is known to mimic flue-like symptoms. (6) Perhaps the similarity of early symptoms of bacterial meningitis and bacterial pneumonia to symptoms of flu is why the vaccine experiments at Fort Riley have been able to escape scrutiny as a potential cause of the Spanish Flu for 100 years and counting.

How Did The “Spanish Flu”Spread So Widely So Quickly?
There is an element of a perfect storm in how Gates bateria spread. WWI ended only 10 months after the first injections. Unfortunately for the 50-100 million who dies, those soldiers injected with horse-infused bacterial moved quickly during those 10 months. An article from 2008 on the CDC’s website describes how sick WWI soldiers could pass along the bacteria to others by becoming “cloud adults.”

“Finally, for brief periods and to varying degrees, affected hosts became “cloud adults” who increased the aerosolization of colonizing strains of bacteria, particularly pneumococci, hemolytic streptococci, H, influence, and S. aurens. For several days during local epidemics - particularly in crowed settings such as hospital wards, military camps, troop ships, and mines (and trenches) - some persons were immunogically susceptible to, infected with, or recovering from infections with influenza virus. Persons with active infections were aerosolizing the bacteria that colonized their noses and throats, while others often in the same “breathing spaces” - were profoundly susceptible to invasion of and rapid spread through their lungs by their own or other’s colonizing bacteria. (1)
 
Three times in his report on the Fort Riley vaccine experiment, Dr. Gates states that some soldiers had a “severe reaction” indicating “an unusual individual susceptibility to the vaccine.” While the vaccine made many sick, it only killed those who were susceptible to it. Those who became sick and survived became “cloud adults” who spread the bacteria to others, which created into cloud adults, spreading to others where it killed the susceptible, repeating the cycle until there were no longer wartime unsanitary conditions, and there were no longer millions of soldiers to experiment on.
The toll on US troops was enormous and it is well documented. Dr. Carol Byerly describes how the “influenza” travelled like wildfire through the US military (substitute “bacteria” for Dr. Byerly’s “influenza” or “virus”):

…. Before any travel ban could be imposed, a contingent of replacement troops departed camp Devens (outside of Boston) for Camp Upton, Long Island, the Army’s debarkation point for France, and took influenza with them. Medical officers at Upton said it arrived “ abruptly on September 13, 1918 with 38 hospital admissions, followed by 86 the next day, and 193 the next. Hospital admissions peaked on October 4th with 483 and 40 days, camp Upton sent 6,131 men to the hospital for influenza. Some developed pneumonia so quickly that physicians diagnosed it simply by observing the patient rather than listening to the lungs …..(7)

The United States was not the only country in possession of the Rockefeller Institute’s experimental bacterial vaccine. A 1919 report from the Institute states: “References should be made that before the United States entered the war (in April 1917) the Institute had resumed the preparation of antimenigococcic serum, in order to meet the requests of Englanf, France, Belgium, Italy and other countries.” The same report states: “In order to meet the suddenly increased demand for the curative serums worked out at the Institute a special stable for horses was quickly erected “ (8)

An experiment antimeningoccic serum made in horses and injected into soldiers who would be entering the cramped and unsanitary living conditions of wat …what could possibly go wrong?

Is the bacterial serum made in horses at the Rockefeller Institute which was injected into the US soldiers and distributed to numerous other countries responsible for the 50-10 million people killed by bacterial lung infections in 1918-19?

The Institute says it distributed the bacterial serum to England, France, Belgium, Italy and other countries during WWI. Not enough is known about how these countries experimented on their soldiers. I hop independent researches will take an honest look at these questions.
 
The Road To Hell Is Paved With Good Intentions
I do not believe that anyone involved in these vaccine experiments was trying to harm anyone. Some will see the name Rockefeller and yell, “Illuminati” or “culling the herd” .
I do not believe that’s what happened. I believe standard medical hubris is responsible -doctor “playing God” …thinking they can tame nature without creating unanticipated problems. With medical hubris, I do not think the situation has changed materially over the past 100 years.

What Now?
Article 3- Human Dignity and Human Rights
In Part 1, I asked if medical products made in horses may have played a role in the new disease which killed millions worldwide in the panemic of 1918-1919.

The December 1917 issue of Popular Mechanics Magazine (3) sheds light on the vaccine manufacturing process of 100 years ago. The feature article. “How New York City’s Health Department Makes Serums and Vaccines for the United States Army” describes processes in place in 1917.
“ After the horse has been inoculated with the disease poison in gradually increasing does he is bled and his serum is found to be antitoxin. This is administered to human beings and renders them immune to the disease …. Some horses give more antitoxin serum than others. The same horse may be used at several different times for the preparation of distinctly different antitoxins … Horses are used in the preparation of diphtheria, tetanus antitoxin and antimeningococcus serum.”
It is difficult to believe that they the same horses to make mutiple disease serums, but they did. If safely had been a concern, perhaps certain horses would have been dedicated to procuring serum for one disease (or “poisen” as contaminated serums were then given to soldiers (an to the public).

Species Jump?
Were pathogens transferred from horses to humans in mass quantities in ways they had never transferred before?
Humans and horses had interacted closely for centuries, but horse serum had no been injected into humans in that way before, by passing the human immune system.
Is it possible that this new method of exposure caused the bacterial pneumonias which ripped human lungs apart in ways never seen before?
Could pathogens relatively harmless to horse lungs make a species-jump and destroy human lungs?
In 1919, a Dutch military veterinarian named Captain Emile Bemelmans “ developed an extensive theory on the relation betweem human and animal influenza … In 1919, he argued that ‘the human ‘flu’ and the so called ‘infectious disease of the breast’ of horror are exactly identical in aetiological, bacterriological and epidemiological senses’.

IN her 2014 paper   “Spanish flue and army horses: what historians and biologists can learn from a history of animals with flue during the 1918-1919 influenza pandemic”. Dr. Floor Haalboom describes Bemelman’s work:

“In 1919, Bemelman’s argument on the identical nature of human and horse influenza in the Nederlandsch Tijdschrift voor Geneeskundae (the Dutch medical journal) was reviewed in the veterinary journal,

…in 1914 he extended his theory on horse flue to several human and animal infectious diseases in an article in the Dutch medical journal. Bemelmans listed human influenza as an example amoung many other animal and human diseases which he thought were accompanied by(deadly) infections of streptococci. Although he did not yet argue that human and horse flue were exactly equal, he did explicitly note their similarities: ‘Also between the human influenza and the so called breast disease in horses peculiar similarities exist’…

…in these papers, Bemelmans addressed the nature of influenza) although he still preferred the name ‘flu’) of both humans and horses. He opposed the ideas that Pfeiffer’s bacterium or a filterable virus caused the disease, but thought toxins made by the bacterial streptococci were responsible for its deadly secondary complications.” (4)


Dr, Bemelmans’s contemporaneous observations have largely been lost to history, in part because of the self important attitude of the medical community. The hubris of the medical community prevented them from listening to a lowly veterinarian. However, Dr. Bemelman’s observations and persistence in getting them published are extraordinarily valuable. His awareness at the time that bateria was the killer of both humans and horses in the pandemic of 1918-19 put him decades ahead if his contemporaries. The NIN paper describinh bacteria as the predominant killer was published in 2008. (5)

If Dr, Bemelmans was correct that horses and humans were suffering from an identical disease, are there diseases identical (or very similar) in both horses and humans?

Do any of those diseases target the lungs?
“Animal Models - A Neglected Medical Resource”.
Cornelious, CE, DVM, Ph.D,
N. Engl J Med 1969; 282:934-944(6)

In a 1969 paper Kansas State University veterinarian Dr Charles Cornelius compiled a list of diseases which were very similar or identical in humans and various other species. Among the diseases identical/very similar humans and horses is pulmonary emphysema, which targets the lungs.
Did a pathogen which causes pulmonary emphysems “species-jump” from horses to humans in these serums and vaccines?
The vaccines were obviously manufactured in primative, unavoidably unsafe conditions and then given to WWI soldiers as an experiment.
What exactly was in the serums and vaccines made in the horses at the Rockefeller Institute - espcially considering that the same individual horses were used for variety of serums for multiple diseases?

Recall from Part 1 that Streptococci bateria were commonly found in the tissue samples from the autopsies of those who dies in 1918-19 (5).
Cornelius said human and horse pu;monary emphysema are identical. Bemelmans reported that humans and horses were suffering from the same disease.
Did doctors treating soldiers suffering from “Spanish Flu” report on encountering a new killer type of pulmonary emphysema, causing lung damage that they had never seen before?

Pulmonary Emphysema At Camp Hancock Georgia
Acute Pulmonary Emphysema Observed During the Epidemic if Influenzal Pneumonia at Camp Hancock, Georgia” …Robert G.Torrey
American Journal of the Medical Sciences 1919. p. 170-181 (7)
 Captain Dr. Torrey served at Camp Hancock, just outside of Augusta, GA, The soldiers who came through Camp Hancock were likely on their way to Charleson, SC to board ships to France, but many of them would not survive to get to the front. Thousands died at Camp Hancock. Some who survived the illness likely made it to the ships, potentially passing the infections bacteria to other soldiers in the unsanitary conditions which were rampant during WWI.

From Dr, Torrey’s Report:
….Certain conditions were invariably present, including an intense bronchitis and peribronchitis similar to that found in a previous epidemic of pure hemolytic streptococcus infection (Scarlet Fever). There was also present from the first a destructive softening of the lung parenchyma. In addition to this there was always an early and persisting generalized pulmonary emphysema which frequently was the main factor in causing death by interference with the mass movement of venous blood. These conditions were found in every case examined at autopsy. Except for frequent otitis media ( ear infection) there were almost no complications or sequelae outside of the chest.

The pulmonary emphysema, with consequent venous statis, accounted for the cyanosis (turning blue/purple color), epistaxis (nosebleeds) and fixation of the chest in the phase of extreme inspiration (inhaling), with low stand of the diaphram, which characterized these cases, and also accounted for the paradoxical physical signs ( paradoxical breathing) in which fluid developed in the chest.”

Torry describes what happened to these soldiers as they died. They were coughing, becoming “cloud adults” (8)(as described in Part 1) it looked like a bacterial infection to him. Autopsies showed tissue had been damaged, which restricted blood flow, turning the dying a bluish/purple color, due to lack of oxygen. When the patients tried to inhale, their diaphrams constricted instead of explanded, the opposite of what diagragms are supposed to do. (9)

Fluids then filled their lungs, and many di dnot survive, literally the fluid in their lungs strangling the soldiers to death.
Fluid In The Lungs Strangled The Human Victims of Spanish Flue - Strangles?

There is a highly contagious horse respiratory infection called Strangles (or Distemper). If these disease can kill horse, what would it do to human lungs if introduced into humans, via injection and therefore bypassing the immune system, on a mass scale?

“Strangles is a highly contagious upper respiratory infection of horses cause by the bacteria Streptococcus equi subspecies equi (S. equi). It is transmitted by inhilation or direct contact with contaminated surfaces ( for example horses sharing water buckets).” (10)

Did streptococcus equi contaminate the serums and vaccines made in horses produced at the Rockefeller Institute and injected into soldiers in a vaccine experiment?
Was streptococcus equi in the medical serums given to the soldiers as treatments?

Was it some other pathogen which species jumped?
Did medical hubris lead to a mistake which caused a species jump which killed 50-100 million people years ago?
What Now?
The vaccine industry is always looking for human test subjects. They have the most success when they are able to find populations who are not in a position to refuse. Soldiers  (9), infants, the disables, prisoners, those in developing nations - anyone not in a position to refuse.

Vaccine experimentation on vulnerable populations is not an issue of the past. Watch this video clip of Dr. Stanley Plotkin where he describes using experimental vaccines on orphans, the mentally retarded, prisoners, and those under colonial rule. The deposition was in January 2018. The hubris of the medical community is the same or worse now than it was 100 years ago. Watch as Dr Plotkin admits to writing. “The question is whether we are to have experiments performed on fully functioning adults and on children who are potentially contributors to society or to perform initial studies in children and adults who are human in form but not in social potential.” Please watch the horrifying video clip. (10)

 In part because the global community is well aware of medical hubris and well aware of the poor record of medical ethics, the Universal Declaration on Bioethics and Human Rights developed international standards regarding the right to informed consent to preventative medical procedures like vacinaton. The international community is well aware that the pharmaceutical industry makes mistakes and is always on the lookout for human test subjects. The Declaration states that individuals have the human right to consent to any preventative medical intervention like vaccination.

 Comment:
This all happened right through WWI so that all these soldiers that were vaccinated with this bacterial horse which included a highly contagious horse respiratory infection called Strangles (or Distemper), would go on to cause the infection and death of 50 to 100 million people on planet earth… which was way more than actually died during WWI of gun fire…
….………….
Vaccine experimentation on vulnerable populations is not an issue of the past.
During the mid-2000’s there was much talk about “pandemic preparedness”. Influenza vaccine manufacturers procure billion dollar checks from

The first documentary movie on CCP virus, Tracking Down the Origin of the Wuhan Coronavirus - 2,158,502 views - NTD
As the world is gripped by the ongoing pandemic, many questions remain about the origin of the Chinese Communist Party (CCP) virus—commonly known as the novel coronavirus. Join Epoch Times senior investigative reporter Joshua Philipp as he explores the known facts surrounding the CCP virus and the global pandemic it caused.

COVID-19 Umbrella Term to Operate a Fake Pandemic: Not 1 Disease, Not 1 Cause
 April 8, 2020
By Makia Freeman
https://thefreedomarticles.com/covid-19-umbrella-term-fake-pandemic-not-1-disease-cause/ 
AT A GLANCE... - THE STORY:
People are dying around the world – that's real. But how many are genuine COVID-19 cases?
THE IMPLICATIONS:
The main trick of the pandemic propaganda is to fool you into thinking that for COVID-19 there has to be 1 virus, 1 cause and 1 disease.
The COVID-19 umbrella term
has been used in an absolutely unscientific, manipulative and deceptive way to justify this manufactured coronavirus crisis, which the evidence shows is a fake pandemic. The international lockdown which covers around 100 nations and at least 20% of the world right now is based upon the idea that there is a new distinct virus SARS-CoV2 which is spreading, infecting and causing the disease COVID-19. However, there are many key foundational questions which cannot be adequately answered. The most important of these is that the virus itself has never been isolated nor thoroughly proven to be causing the disease (or more accurately diseases) that people have! This is in addition to the obvious manipulation of the figures with false positives and other sleights of hand such as inflating the numbers by counting anyone who merely had the virus as “dead from” the virus. The coronavirus fails Koch’s postulates. The Emperor has no clothes – and all the power grabs and emergency decrees are based on lies. We are not looking at 1 virus, 1 cause and 1 disease; we are looking a cluster of diseases and a variety of causes, hidden by the COVID-19 umbrella term to fuel the fake pandemic narrative.

COVID-19 Coronavirus Fails Koch’s Postulates
German scientist Robert Koch (Heinrich Hermann Robert Koch, 1843-1910) made great contributions to the field of microbiology. He is considered to be one of the founders of the field of modern bacteriology. He identified the specific causative agents of TB (tuberculosis), cholera and anthrax. For his work on TB, he was awarded the Nobel Prize in 1905 in Physiology or Medicine. Koch established 4 criteria to identify the causative agent of a particular disease. These criteria have become a gold standard for determining the existence of an infectious agent and for isolating and verifiying what is causing a disease. The criteria are a set of conditions known as Koch’s postulates. They are:
The microorganism must be identified in all individuals affected by the disease, but not in healthy individuals.
The microorganism can be isolated from the diseased individual and grown in culture.
When introduced into a healthy individual, the cultured microorganism must cause disease.
The microorganism must then be re-isolated from the experimental host, and found to be identical to the original microorganism.
Firstly, the coronavirus SARS-CoV2 (allegedly causing the disease COVID-19) has not been shown to be present only in sick people and not in healthy ones. There are countless cases of people having this virus with mild, minor or zero symptoms. Recently Iceland tested a relatively large percentage of its population (around 5,000 people out of 364,000) and found that 0.86% (close to 1%) of Icelanders had the coronavirus. The symptoms? Little or none:
“Importantly, approximately half of the people who tested positive for COVID-19 are non-symptomatic, according to Gudnason as reported by BuzzFeed. The other half is mostly showing “very moderate cold-like symptoms.””
Secondly, the virus has never been isolated – which must be done with proper equipment such as electron microscopes and which cannot be achieved through CT scans (as the Chinese were using) and the flawed PCR test (more on this below). The January 24th 2020 study published in the New England Journal of Medicine entitled A Novel Coronavirus from Patients with Pneumonia in China, 2019 describes how the scientists arrived at the idea of COVID-19: they took lung fluid samples and extracted RNA from them using the PCR test. It admits that the coronavirus failed Koch’s postulates:
“Further development of accurate and rapid methods to identify unknown respiratory pathogens is still needed … our study does not fulfill Koch’s postulates.”
Are RNA Samples and a Genetic Sequence Proof of a New Coronavirus?
David Crowe doesn’t believe there is even sufficient evidence to justify calling this a new virus, let alone a pandemic. In his paper Flaws in Coronavirus Pandemic Theory, he writes:
“The world is suffering from a massive delusion based on the belief that a test for RNA is a test for a deadly new virus …

If the virus exists, then it should be possible to purify viral particles. From these particles RNA can be extracted and should match the RNA used in this test. Until this is done it is possible that the RNA comes from another source, which could be the cells of the patient, bacteria, fungi, etc. There might be an association with elevated levels of this RNA and illness, but that is not proof that the RNA is from a virus. Without purification and characterization of virus particles, it cannot be accepted that an RNA test is proof that a virus is present.
Definitions of important diseases are surprisingly loose, perhaps embarrassingly so.

A couple of symptoms, maybe contact with a previous patient, and a test of unknown accuracy, is all you often need. While the definition of SARS, an earlier coronavirus panic, was self-limiting, the definition of the new coronavirus disease is open-ended, allowing the imaginary epidemic to grow. Putting aside the existence of the virus, if the coronavirus test has a problem with false positives (as all biological tests do) then testing an uninfected population will produce only false-positive tests, and the definition of the disease will allow the epidemic to go on forever.
This strange new disease, officially named COVID-19, has none of its own symptoms.

Fever and cough, previously blamed on uncountable viruses and bacteria, as well as environmental contaminants, are most common, as well as abnormal lung images, despite those being found in healthy people.”
He concludes:
“The coronavirus panic is just that, an irrational panic, based on an unproven RNA test, that has never been connected to a virus.

And which won’t be connected to a virus unless the virus is purified. Furthermore, even if the test can detect a novel virus the presence of a virus is not proof that it is the cause of the severe symptoms that some people who test positive experience (but not all who test positive). Finally, even if the test can detect a virus, and it is dangerous, we do not know what the rate of false positives is. And even a 1% false positive rate could produce 100,000 false positive results just in a city the size of Wuhan and could mean that a significant fraction of the positive test results being found are false positives.
The use of powerful drugs because doctors are convinced that they have a particularly potent virus on their hands, especially in older people, with pre-existing health conditions, is likely to lead to many deaths. As with SARS.
There is very little science happening. There is a rush to explain everything that is happening in a way that does not question the viral paradigm, does not question the meaningfulness of test results, and that promotes the use of untested antiviral drugs.”
Yes, anti-viral drugs (which do a lot of damage to your body), and, more to the point, mandatory vaccinations.
We All Have Viruses, All The Time, as Part of our Virome and Immune System
Speaking of the “viral paradigm”, if you haven’t already seen it, please check out my earlier article Deep Down the Virus Rabbit Hole – Question Everything which introduces the idea that viruses are not what you think. The humble virus is deeply misunderstood. The human body is composed of 6 trillion cells, 60 trillion bacteria and 380 trillion viruses. Just as we have a microbiome of friendly bacteria which forms the basis of our immune system and 2nd brain in our gut, so too do we have a virome (a collection and community of viruses) which play a role in our healing. Through the ascendency of germ theory over host theory/terrain theory, the mainstream paradigm now teaches that viruses are “bad guys”, infectious agents “out there”, who can invade the body – thus reinforcing the need for Big Pharma drugs and vaccines. Viruses come from exosomes or tiny particles our bodies produce. They are not infectious agents. The exosome theory states that if cells are poisoned, they produce viruses (secretions) to clean up the toxins. This is what the plant kingdom does; when a tree has a beetle infestation, it makes a hormonal secretion to tell other trees to defend themselves.
Thus, Operation Coronavirus is not only a fake pandemic, but also a colossal and unprecedented worldwide psy op, based on exploiting our ignorance over the true nature of viruses. What a scam!!
Fake Tests for a Fake Pandemic
Insiders and whistleblowers such as the one in the article Insider Exposes COVID-19 Coronavirus Scam have revealed how there are coronavirus test kits being distributed which don’t even test for the specific SARS-CoV2 strain! They just test for generic coronavirus (coronavirus is defined as the “common cold” in medical encyclopedias) which of course will produce more false positive (as the NWO agenda dictates). Meanwhile, the Medical Industry relies on the PCR test which I have exposed in other articles as wholly inadequate. The PCR Test is a surrogate test since it doesn’t actually isolate the virus. The founder of the PCR test Kary Mullins has admitted that you can’t use PCR “to prove infectious etiology or to diagnose an infectious disease.” Besides, you can manipulate the results PCR will yield by choosing how many cycles (amplifications) to run. For some diseases, if you lower the number of cycles to 35, it can make everyone appear negative, while if you increase them to above 35, it can make everyone appear positive.
COVID-19 Umbrella Term: Remember There is Not 1 Cause and Not 1 Disease
Many people are grasping the importance of all the above information, and are now rightly asking: what is actually happening, if viruses cannot spread? What are people getting sick from? What is causing all the disease?
Before addressing that, it’s crucial to understand this one point:

there is not 1 virus, there is not 1 cause and there is not 1 disease.
The NWO (New World Order) propagandists have created the appearance of an international pandemic by exploiting many common assumptions people have, including the idea of 1 disease caused by 1 infectious agent. Remember, the COVID-19 umbrella term can cover numerous symptoms (coughing, shortness of breath, increased mucus, fatigue, etc.) which may be caused by any number of things. Jon Rappaport wrote this piece on April 1st, very appropriately since it was April Fools Day:
“I keep pounding on this, because it’s the main illusion, and it’s the hardest illusion to dispel. People hang on to it like a life raft. The stage magicians present the “pandemic” as one disease with one cause, and people buy in immediately. Some people who reject the coronavirus as the cause present ANOTHER single cause—they’re falling for the basic con job. There are people in Wuhan who have pneumonia because of the horrendous air quality in the city. There are people in New York who have ordinary flu-like illness. There are people in Italy who have histories of multiple, long-term, serious health conditions—pneumonia, flu, cardiac problems, kidney problems—made far worse through treatment with toxic drugs. There are people in hospitals around the world who, after being diagnosed with COVID, are dosed with powerful toxic antiviral drugs. There are people on breathing ventilators who are being given too much oxygen and too much pressure—and their lungs collapse. There are perfectly healthy people who are testing positive for the virus because the test is irreparably flawed… All these people are called “COVID cases.”
The stage magic trick is easy to see, once you grasp the tactics: Claim to have discovered a new virus. Say it is spreading and needs to be contained. Invent an umbrella label for the epidemic: COVID-19. Start pulling all sorts of people with all sorts of different conditions under the umbrella and say they’re all “cases.” Use a diagnostic test that will automatically turn out many verdicts of “infected.” And you have the illusion of a pandemic.
Or you might get this: “No, it’s not the coronavirus, it’s really 5G technology that’s making people sick and killing them.” STILL falling for the magic trick. In certain places, 5G might be harming people. Indeed. And some of those people might be labeled as COVID. Yes. But “the whole thing” isn’t 5G, because THERE ISN’T ONE WHOLE THING.
There is no “it.””
This is the illusion we need to dispel: there is not 1 cause and there is not 1 disease.
COVID-19 Umbrella Term Fakery:

If All Different Kinds of Disease are Being Falsely Ascribed to COVID-19, What is Happening?
This frontline NYC doctor Cameron Kyle-Sidell states here and here from firsthand experience that he is seeing a lot of patients been brought in and suffering from what seems like altitude sickness, a severe shortness of breath and lack of oxygen. He thinks they should be treated for hypoxemia (a condition where the oxygen content in the arterial blood is below normal, like altitude sickness) and not for ARDS (Acute Respiratory Distress Syndrome, by definition a respiratory disease). This means less use of ventilators and breathing tubes, because as he says, it is highly likely the pressure from the ventilators may be damaging patients’ lungs. They need oxygen not pressure. He states that apparent COVID-19 patients do not appear to be suffering from anything resembling viral pneumonia.
When many people break out with a disease in the same region, it is easy to assume they are “catching” it from one another. Bill Gates-Netflix propaganda films like Contagion reinforce this programming. However this is an assumption. It is just as possible the people in a certain geographical area are all being subjected to the same poison and thus reacting in the same way. In other words, it could be because of a local contaminant rather than an infectious agent. What appears like contagion may actually be the consequence of mass long-term poisoning, but governments and corporations are never going to confess to that when they have a scapegoat killer virus they can blame instead.
So what are the causes? There are too many to list. For starters, many COVID-19 are false positive cases or died with the virus but not from the virus. Many other COVID-19 patients are elderly, have compromised immune systems or have co-morbidities. On top of that, consider the following:

1. Air pollution: the air in Wuhun China and Milan Italy is notoriously bad. Many of the symptoms people experienced there are perfectly explainable due to the atrocious air quality;
2. GMOs: GM crops, and thus glyphosate, have long contaminated the global food supply;
3. Biofuel made with GM corn: as Dr. Thomas Cowan speculates in this video, GM corn biofuel is now used in place of regular fuel. What happens when it is burned, used up and dispersed into the air for everyone to breathe in all the GMOs and glyphosate?;
4. Vaccines: the residents of Wuhan were reportedly mass vaccinated before the outbreak; and
5. EMF (e.g. Wi-Fi and 5G): the word has got out that the 5G 60GHz frequency interferes with oxygen absorption. Is it just a coincidence that the NHY doc above is revealing that people now have symptoms of hypoxemia or hypoxia?
There are many more. This is not an exhaustive list. The point is that there are many causes and many diseases occurring right now which are being lumped under the term COVID-19 to bolster the illusion of a raging pandemic.
Final Thoughts: Is this a Pandemic or a Scamdemic?
If you didn’t know the history of fake pandemics, you might think that the WHO (World Health Organization), the USG (United States Government) and other world governments would have solid evidence for declaring a health emergency. They don’t. Asking key fundamental questions about how the nature of the COVID-19 disease, and how the virus is being isolated and tested, reveal a house of cards. There are serious fundamental flaws in the pandemic propaganda. This is unadulterated COVID-19 umbrella term fakery. What is happening here is not some wild killer virus, but a carefully crafted script to engineer a worldwide crisis and to blame mass long-term poisoning on a tiny invisible particle whose existence has yet to be conclusively proven as an infectious agent.

Is this a pandemic or a scamdemic?
Makia Freeman is the editor of alternative media / independent news site The Freedom Articles and senior researcher at ToolsForFreedom.com. Makia is on Steemit and FB.y Makia Freeman
https://thefreedomarticles.com/covid-19-umbrella-term-fake-pandemic-not-1-disease-cause/ 
AT A GLANCE... - THE STORY:
People are dying around the world – that's real. But how many are genuine COVID-19 cases?

THE IMPLICATIONS:
The main trick of the pandemic propaganda is to fool you into thinking that for COVID-19 there has to be 1 virus, 1 cause and 1 disease.
The COVID-19 umbrella term
has been used in an absolutely unscientific, manipulative and deceptive way to justify this manufactured coronavirus crisis, which the evidence shows is a fake pandemic. The international lockdown which covers around 100 nations and at least 20% of the world right now is based upon the idea that there is a new distinct virus SARS-CoV2 which is spreading, infecting and causing the disease COVID-19. However, there are many key foundational questions which cannot be adequately answered. The most important of these is that the virus itself has never been isolated nor thoroughly proven to be causing the disease (or more accurately diseases) that people have! This is in addition to the obvious manipulation of the figures with false positives and other sleights of hand such as inflating the numbers by counting anyone who merely had the virus as “dead from” the virus. The coronavirus fails Koch’s postulates. The Emperor has no clothes – and all the power grabs and emergency decrees are based on lies. We are not looking at 1 virus, 1 cause and 1 disease; we are looking a cluster of diseases and a variety of causes, hidden by the COVID-19 umbrella term to fuel the fake pandemic narrative.

COVID-19 Coronavirus Fails Koch’s Postulates
German scientist Robert Koch (Heinrich Hermann Robert Koch, 1843-1910) made great contributions to the field of microbiology. He is considered to be one of the founders of the field of modern bacteriology. He identified the specific causative agents of TB (tuberculosis), cholera and anthrax. For his work on TB, he was awarded the Nobel Prize in 1905 in Physiology or Medicine. Koch established 4 criteria to identify the causative agent of a particular disease. These criteria have become a gold standard for determining the existence of an infectious agent and for isolating and verifiying what is causing a disease. The criteria are a set of conditions known as Koch’s postulates. They are:
The microorganism must be identified in all individuals affected by the disease, but not in healthy individuals.
The microorganism can be isolated from the diseased individual and grown in culture.
When introduced into a healthy individual, the cultured microorganism must cause disease.
The microorganism must then be re-isolated from the experimental host, and found to be identical to the original microorganism.

Firstly, the coronavirus SARS-CoV2 (allegedly causing the disease COVID-19) has not been shown to be present only in sick people and not in healthy ones. There are countless cases of people having this virus with mild, minor or zero symptoms. Recently Iceland tested a relatively large percentage of its population (around 5,000 people out of 364,000) and found that 0.86% (close to 1%) of Icelanders had the coronavirus. The symptoms? Little or none:
“Importantly, approximately half of the people who tested positive for COVID-19 are non-symptomatic, according to Gudnason as reported by BuzzFeed. The other half is mostly showing “very moderate cold-like symptoms.””
Secondly, the virus has never been isolated – which must be done with proper equipment such as electron microscopes and which cannot be achieved through CT scans (as the Chinese were using) and the flawed PCR test (more on this below). The January 24th 2020 study published in the New England Journal of Medicine entitled A Novel Coronavirus from Patients with Pneumonia in China, 2019 describes how the scientists arrived at the idea of COVID-19: they took lung fluid samples and extracted RNA from them using the PCR test. It admits that the coronavirus failed Koch’s postulates:

“Further develpment of accurate and rapid methods to identify unknown respiratory pathogens is still needed … our study does not fulfill Koch’s postulates.”
Are RNA Samples and a Genetic Sequence Proof of a New Coronavirus?
David Crowe doesn’t believe there is even sufficient evidence to justify calling this a new virus, let alone a pandemic. In his paper Flaws in Coronavirus Pandemic Theory, he writes:

“The world is suffering from a massive delusion based on the belief that a test for RNA is a test for a deadly new virus … If the virus exists, then it should be possible to purify viral particles. From these particles RNA can be extracted and should match the RNA used in this test. Until this is done it is possible that the RNA comes from another source, which could be the cells of the patient, bacteria, fungi, etc. There might be an association with elevated levels of this RNA and illness, but that is not proof that the RNA is from a virus. Without purification and characterization of virus particles, it cannot be accepted that an RNA test is proof that a virus is present.
Definitions of important diseases are surprisingly loose, perhaps embarrassingly so. A couple of symptoms, maybe contact with a previous patient, and a test of unknown accuracy, is all you often need. While the definition of SARS, an earlier coronavirus panic, was self-limiting, the definition of the new coronavirus disease is open-ended, allowing the imaginary epidemic to grow. Putting aside the existence of the virus, if the coronavirus test has a problem with false positives (as all biological tests do) then testing an uninfected population will produce only false-positive tests, and the definition of the disease will allow the epidemic to go on forever.

This strange new disease, officially named COVID-19, has none of its own symptoms. Fever and cough, previously blamed on uncountable viruses and bacteria, as well as environmental contaminants, are most common, as well as abnormal lung images, despite those being found in healthy people.”

He concludes:
“The coronavirus panic is just that, an irrational panic, based on an unproven RNA test, that has never been connected to a virus. And which won’t be connected to a virus unless the virus is purified. Furthermore, even if the test can detect a novel virus the presence of a virus is not proof that it is the cause of the severe symptoms that some people who test positive experience (but not all who test positive). Finally, even if the test can detect a virus, and it is dangerous, we do not know what the rate of false positives is. And even a 1% false positive rate could produce 100,000 false positive results just in a city the size of Wuhan and could mean that a significant fraction of the positive test results being found are false positives.
The use of powerful drugs because doctors are convinced that they have a particularly potent virus on their hands, especially in older people, with pre-existing health conditions, is likely to lead to many deaths. As with SARS.
There is very little science happening. There is a rush to explain everything that is happening in a way that does not question the viral paradigm, does not question the meaningfulness of test results, and that promotes the use of untested antiviral drugs.”
Yes, anti-viral drugs (which do a lot of damage to your body), and, more to the point, mandatory vaccinations.

We All Have Viruses, All The Time, as Part of our Virome and Immune System
Speaking of the “viral paradigm”, if you haven’t already seen it, please check out my earlier article Deep Down the Virus Rabbit Hole – Question Everything which introduces the idea that viruses are not what you think. The humble virus is deeply misunderstood. The human body is composed of 6 trillion cells, 60 trillion bacteria and 380 trillion viruses. Just as we have a microbiome of friendly bacteria which forms the basis of our immune system and 2nd brain in our gut, so too do we have a virome (a collection and community of viruses) which play a role in our healing. Through the ascendency of germ theory over host theory/terrain theory, the mainstream paradigm now teaches that viruses are “bad guys”, infectious agents “out there”, who can invade the body – thus reinforcing the need for Big Pharma drugs and vaccines. Viruses come from exosomes or tiny particles our bodies produce. They are not infectious agents. The exosome theory states that if cells are poisoned, they produce viruses (secretions) to clean up the toxins. This is what the plant kingdom does; when a tree has a beetle infestation, it makes a hormonal secretion to tell other trees to defend themselves.

Thus, Operation Coronavirus is not only a fake pandemic, but also a colossal and unprecedented worldwide psy op, based on exploiting our ignorance over the true nature of viruses. What a scam!!

Fake Tests for a Fake Pandemic
Insiders and whistleblowers such as the one in the article Insider Exposes COVID-19 Coronavirus Scam have revealed how there are coronavirus test kits being distributed which don’t even test for the specific SARS-CoV2 strain! They just test for generic coronavirus (coronavirus is defined as the “common cold” in medical encyclopedias) which of course will produce more false positive (as the NWO agenda dictates). Meanwhile, the Medical Industry relies on the PCR test which I have exposed in other articles as wholly inadequate. The PCR Test is a surrogate test since it doesn’t actually isolate the virus. The founder of the PCR test Kary Mullins has admitted that you can’t use PCR “to prove infectious etiology or to diagnose an infectious disease.” Besides, you can manipulate the results PCR will yield by choosing how many cycles (amplifications) to run. For some diseases, if you lower the number of cycles to 35, it can make everyone appear negative, while if you increase them to above 35, it can make everyone appear positive.

COVID-19 Umbrella Term: Remember There is Not 1 Cause and Not 1 Disease
Many people are grasping the importance of all the above information, and are now rightly asking: what is actually happening, if viruses cannot spread? What are people getting sick from? What is causing all the disease?

Before addressing that, it’s crucial to understand this one point: there is not 1 virus, there is not 1 cause and there is not 1 disease.
The NWO (New World Order) propagandists have created the appearance of an international pandemic by exploiting many common assumptions people have, including the idea of 1 disease caused by 1 infectious agent. Remember, the COVID-19 umbrella term can cover numerous symptoms (coughing, shortness of breath, increased mucus, fatigue, etc.) which may be caused by any number of things. Jon Rappaport wrote this piece on April 1st, very appropriately since it was April Fools Day:

“I keep pounding on this, because it’s the main illusion, and it’s the hardest illusion to dispel. People hang on to it like a life raft. The stage magicians present the “pandemic” as one disease with one cause, and people buy in immediately. Some people who reject the coronavirus as the cause present ANOTHER single cause—they’re falling for the basic con job. There are people in Wuhan who have pneumonia because of the horrendous air quality in the city. There are people in New York who have ordinary flu-like illness. There are people in Italy who have histories of multiple, long-term, serious health conditions—pneumonia, flu, cardiac problems, kidney problems—made far worse through treatment with toxic drugs. There are people in hospitals around the world who, after being diagnosed with COVID, are dosed with powerful toxic antiviral drugs. There are people on breathing ventilators who are being given too much oxygen and too much pressure—and their lungs collapse. There are perfectly healthy people who are testing positive for the virus because the test is irreparably flawed… All these people are called “COVID cases.”

The stage magic trick is easy to see, once you grasp the tactics: Claim to have discovered a new virus. Say it is spreading and needs to be contained. Invent an umbrella label for the epidemic: COVID-19. Start pulling all sorts of people with all sorts of different conditions under the umbrella and say they’re all “cases.” Use a diagnostic test that will automatically turn out many verdicts of “infected.” And you have the illusion of a pandemic.

Or you might get this: “No, it’s not the coronavirus, it’s really 5G technology that’s making people sick and killing them.” STILL falling for the magic trick. In certain places, 5G might be harming people. Indeed. And some of those people might be labeled as COVID. Yes. But “the whole thing” isn’t 5G, because THERE ISN’T ONE WHOLE THING.

There is no “it.””
This is the illusion we need to dispel: there is not 1 cause and there is not 1 disease.

COVID-19 Umbrella Term Fakery: If All Different Kinds of Disease are Being Falsely Ascribed to COVID-19, What is Happening?
This frontline NYC doctor Cameron Kyle-Sidell states here and here from firsthand experience that he is seeing a lot of patients been brought in and suffering from what seems like altitude sickness, a severe shortness of breath and lack of oxygen. He thinks they should be treated for hypoxemia (a condition where the oxygen content in the arterial blood is below normal, like altitude sickness) and not for ARDS (Acute Respiratory Distress Syndrome, by definition a respiratory disease). This means less use of ventilators and breathing tubes, because as he says, it is highly likely the pressure from the ventilators may be damaging patients’ lungs. They need oxygen not pressure. He states that apparent COVID-19 patients do not appear to be suffering from anything resembling viral pneumonia.

When many people break out with a disease in the same region, it is easy to assume they are “catching” it from one another. Bill Gates-Netflix propaganda films like Contagion reinforce this programming. However this is an assumption. It is just as possible the people in a certain geographical area are all being subjected to the same poison and thus reacting in the same way. In other words, it could be because of a local contaminant rather than an infectious agent. What appears like contagion may actually be the consequence of mass long-term poisoning, but governments and corporations are never going to confess to that when they have a scapegoat killer virus they can blame instead.
So what are the causes? There are too many to list. For starters, many COVID-19 are false positive cases or died with the virus but not from the virus. Many other COVID-19 patients are elderly, have compromised immune systems or have co-morbidities. On top of that, consider the following:
1. Air pollution: the air in Wuhun China and Milan Italy is notoriously bad. Many of the symptoms people experienced there are perfectly explainable due to the atrocious air quality;
2. GMOs: GM crops, and thus glyphosate, have long contaminated the global food supply;
3. Biofuel made with GM corn: as Dr. Thomas Cowan speculates in this video, GM corn biofuel is now used in place of regular fuel. What happens when it is burned, used up and dispersed into the air for everyone to breathe in all the GMOs and glyphosate?;
4. Vaccines: the residents of Wuhan were reportedly mass vaccinated before the outbreak; and
5. EMF (e.g. Wi-Fi and 5G): the word has got out that the 5G 60GHz frequency interferes with oxygen absorption. Is it just a coincidence that the NHY doc above is revealing that people now have symptoms of hypoxemia or hypoxia?

There are many more. This is not an exhaustive list. The point is that there are many causes and many diseases occurring right now which are being lumped under the term COVID-19 to bolster the illusion of a raging pandemic.

Final Thoughts: Is this a Pandemic or a Scamdemic?
If you didn’t know the history of fake pandemics, you might think that the WHO (World Health Organization), the USG (United States Government) and other world governments would have solid evidence for declaring a health emergency. They don’t. Asking key fundamental questions about how the nature of the COVID-19 disease, and how the virus is being isolated and tested, reveal a house of cards. There are serious fundamental flaws in the pandemic propaganda. This is unadulterated COVID-19 umbrella term fakery. What is happening here is not some wild killer virus, but a carefully crafted script to engineer a worldwide crisis and to blame mass long-term poisoning on a tiny invisible particle whose existence has yet to be conclusively proven as an infectious agent.

Is this a pandemic or a scamdemic?
Makia Freeman is the editor of alternative media / independent news site The Freedom Articles and senior researcher at ToolsForFreedom.com. Makia is on Steemit and FB.

Dr. Cameron Kyle-Sidell
Critical Care Doctor from New York City

ΝYC-ΙCU DR unknowingly describes the EFFECTS of 60GHz on patients.
https://www.youtube.com/watch?v=1EWQPgF6-UQ
Dana Ashlie
My commentary at the end. Here is my video that was REMOVED from YT: https://www.brighteon.com/42d3cd7d-ac... Keep a link to my brighteon channel in case I'm taken down... Here is a link to this doctors full video: https://www.youtube.com/watch?v=k9GYT...
Category: People & Blogs

ΝYC-ΙCU DR unknowingly describes the EFFECTS of 60GHz on patients.
https://www.youtube.com/watch?v=1EWQPgF6-UQ
Dana Ashlie
My commentary at the end. Here is my video that was REMOVED from YT: https://www.brighteon.com/42d3cd7d-ac... Keep a link to my brighteon channel in case I'm taken down... Here is a link to this doctors full video: https://www.youtube.com/watch?v=k9GYT...
Category: People & Blogs

COVID-19 Umbrella Term to Operate a Fake Pandemic: Not 1 Disease, Not 1 Cause
 April 8, 2020
By Makia Freeman
https://thefreedomarticles.com/covid-19-umbrella-term-fake-pandemic-not-1-disease-cause/ 
AT A GLANCE...
THE STORY:
People are dying around the world – that's real. But how many are genuine COVID-19 cases?
THE IMPLICATIONS:
The main trick of the pandemic propaganda is to fool you into thinking that for COVID-19 there has to be 1 virus, 1 cause and 1 disease.
The COVID-19 umbrella term
has been used in an absolutely unscientific, manipulative and deceptive way to justify this manufactured coronavirus crisis, which the evidence shows is a fake pandemic. The international lockdown which covers around 100 nations and at least 20% of the world right now is based upon the idea that there is a new distinct virus SARS-CoV2 which is spreading, infecting and causing the disease COVID-19. However, there are many key foundational questions which cannot be adequately answered. The most important of these is that the virus itself has never been isolated nor thoroughly proven to be causing the disease (or more accurately diseases) that people have! This is in addition to the obvious manipulation of the figures with false positives and other sleights of hand such as inflating the numbers by counting anyone who merely had the virus as “dead from” the virus. The coronavirus fails Koch’s postulates. The Emperor has no clothes – and all the power grabs and emergency decrees are based on lies. We are not looking at 1 virus, 1 cause and 1 disease; we are looking a cluster of diseases and a variety of causes, hidden by the COVID-19 umbrella term to fuel the fake pandemic narrative.

​The next outbreak? We’re not ready | Bill Gates
TED
Visit http://TED.com to get our entire library of TED Talks, transcripts, translations, personalized talk recommendations and more. In 2014, the world avoided a horrific global outbreak of Ebola, thanks to thousands of selfless health workers -- plus, frankly, thanks to some very good luck. In hindsight, we know what we should have done better. So, now's the time, Bill Gates suggests, to put all our good ideas into practice, from scenario planning to vaccine research to health worker training. As he says, "There's no need to panic ... but we need to get going." The TED Talks channel features the best talks and performances from the TED Conference, where the world's leading thinkers and doers give the talk of their lives in 18 minutes (or less). Look for talks on Technology, Entertainment and Design -- plus science, business, global issues, the arts and more. You're welcome to link to or embed these videos, forward them to others and share these ideas with people you know. For more information on using TED for commercial purposes (e.g. employee learning, in a film or online course), submit a Media Request here: http://media-requests.TED.com Follow TED on Twitter: http://twitter.com/TEDTalks Like TED on Facebook: http://facebook.com/TED Subscribe to our channel: http://youtube.com/TED

Doctors say outlook for COVID-19 patients on ventilators grim
CBC News: The National
Doctors say that ventilators are reserved for COVID-19 patients who are critically ill and that once they’re on them, many don’t survive.  »»» Subscribe to The National to watch more videos here: https://www.youtube.com/user/CBCTheNa... Voice Your Opinion & Connect With Us Online: The National Updates on Facebook: https://www.facebook.com/thenational The National Updates on Twitter: https://twitter.com/CBCTheNational »»» »»» »»» »»» »»» The National is CBC Television's flagship news program. Airing six days a week, the show delivers news, feature documentaries and analysis from some of Canada's leading journalists.
Category: News & Politics 

ANONYMOUS' ADDRESS TO THE CITIZENS OF AUSTRALIA -Gather Truths

​Technology-enabled disinformation is corrosive to democratic processes and institutions. There is no way to put the genie back in the bottle – increasingly we may be unable to have shared understandings of the world – or trust that videos, photos, audio recordings, ‘scientific’ studies or legal documents are authentic. Civility in civic discourse and integrity are increasingly quaint notions. Authoritarians will weaken checks and balances, turn courts into extensions of those in power and thus undermine representative democracy – enabled by the manipulation of digital media to stoke fear and mask inconvenient truths. We’re already at a point when even educated citizens in first-world societies are unable to distinguish fact from fiction. And we’re already seeing fear of the ‘other’ stoked to the point where inhumane treatment of children is accepted in this country. Extreme partisanship is putting all of our democratic institutions at risk to the point that shared power and orderly transitions may not exist in 10 years. Civil unrest seems inevitable. We have institutional actors denying and actively disabling climate science and hiding public information about the consequences of climate change, for example. We can look forward to less cooperation among nations, more mass migrations, drought, food shortages, economic disruption and more manipulation of public sentiment. Drones, for example, may soon deliver packages but may find even more utility as delivery systems for bombs and as means to invade personal and political boundaries. Democracy only works if there is an informed citizenry. And right now, we have a booming misinformation infestation eating away at citizenship and democratic institutions.”

COVID-19- what occurs during endotracheal intubation and mechanical ventilation
Nucleus Medical MediaBE

https://www.youtube.com/watch?v=V8VIw0fk4X0  
Hospitals and health systems can license this video for marketing or patient use. Learn more: http://www.nucleushealth.com/ This video, created by Nucleus Medical Media, shows what occurs during endotracheal intubation and mechanical ventilation if you are in an emergency situation involving severe respiratory problems, or if you are having general anesthesia during a surgical procedure. If you have severe respiratory problems, the oxygen levels in your blood may drop too low, or the carbon dioxide levels may rise too high. Either of these conditions can result in damage to your vital organs, including your heart and brain. Under these circumstances, you may need additional oxygen or breathing support through mechanical ventilation. ANH00024

Dr. Thomas Cowan Covid19 fails koch's postulates
Rick Friedrich
This video was going to be added to the video ("Statistical Fallacies, Crisis Management and another New World Order" https://youtu.be/uBVqGeyxbuU ) but it would have made for a 4 hour video so I divided into two videos. I share this video in the context of my video about statistical fallacies as an example.

The Out Of The Shadows documentary lifts the mask on how the mainstream media & Hollywood manipulate & control the masses by spreading propaganda  - CIA Involved in Hollywood deciding what film content people see
outofshadows.org The Out Of The Shadows documentary lifts the mask on how the mainstream media & Hollywood manipulate & control the masses by spreading propaganda throughout their content. Our goal is to wake up the general public by shedding light on how we all have been lied to & brainwashed by a hidden enemy with a sinister agenda. This project is the result of two years of blood, sweat, and tears by a team of woke professionals. making a donation at outofshadows.org Category: People & Blogs

Bill Gates spoke to the Financial Times via a video chat on April 2. 
Screenshot/Financial Times

Live: Trump, White House Coronavirus Task Force Hold Briefing | NBC News

Deep Down the Virus Rabbit Hole – Question Everything April 1, 2020 By Makia Freeman
Watch out! The killer virus is coming!
https://thefreedomarticles.com/deep-down-virus-rabbit-hole-question-everything/
Watch out! The killer virus is coming!
Well … maybe not. Behind any pandemic, there are always a long set of assumptions that underpin the medical reports and subsequent political and legal decisions. These assumptions are barely recognizable since they are routinely reported as facts. However, to truly justify everything that’s happening all over the world right now – social distancing, surveillance, censorship, lockdowns, quarantine, medical martial law, economic crashes, new digital currencies, governmental emergency powers – with mandatory vaccinations and human microchipping slated to come – those in charge at the Department of Propaganda have to convince you that those assumptions are facts. So, we’re going to take a journey down the rabbit hole to ask some fundamental questions not only about the coronavirus but also the mysterious entity of the virus itself. What is a virus? Can a virus cross from animal to human? Can it cross from human to human? Did you know the CDC admitted that their beloved PCR test is essentially useless, as it doesn’t tell you whether a virus is causing disease? Is it 100% proven that viruses cause disease in humans anyway? How do the competing theories of germ theory and host theory/terrain theory play into this? So, buckle up, open your mind and get prepared for a ride.
What Is a Virus? 
Mainstream Western Medicine (allopathy) developed due to the influence of the Rockefellers who created it to help sell their petroleum drugs which became the basis for today’s Big Pharma medicines. The Rockefellers and other NWO (New World Order) central banking bloodline families overtook the schools and curricula for Medicine, and shut down competition like homeopathy, via the Flexner Report.
The Rockefellers made sure that allopathy would be purely focused on pharmaceuticals and blocked proper nutritional knowledge from doctors.
This is the same mainstream medical system that sets the definitions for things like viruses, so let’s begin with a healthy dose of skepticism. This is also the same Rockefeller family that funded the UN (and donated land for its HQ in New York), whose Rockefeller Foundation has co-opted education and whose Rockefeller Foundation released a 2010 paper analyzing how governments could/should react to a pandemic scenario..
 Rockefeller Foundation released a 2010 paper analyzing how governments could/should react to a pandemic scenario..
​According to this mainstream scientific mindset, viruses are entities composed of DNA or RNA fragments (genetic material) and encased in a protein cover and/or lipid (fat) envelope. They are not technically alive, requiring a cell host to replicate. They are tiny – far tinier than a bacterium – and unlike a bacterium they are not a cell, so they don’t have a respiratory, circulatory or nervous system. The virus is said to be right on the border of the living and the non-living.
However, there is an important alternative view of the virus.
The late primal diet/raw meat advocate Aajonus Vonderplanitz (who died in 2013) gave this fascinating interview during the swine flu hoax of 2009, when everyone was freaking out (not as much as with the coronavirus, but in a similar vein to the hyped ebola and zika outbreaks). He claimed the following:
– viruses are created by the body to clean itself when friendly bacteria can no longer break down all the waste;
– all viruses are good viruses, being necessary cellular responses;
– viruses are like a solvent or soap, made by cells to help dissolve and eliminate toxins (a solvent is something that will make the solute [the thing to be dissolved] turn into a solution [liquid]);
– viruses are specific to the cell that created them;
– viruses cannot cross species;
– viruses don’t exist outside of bodies; and
– that the only way that a virus can cross species is if it’s made in a factory and injected, i.e. extracted, kept in a lab, genetically altered and modified, weaponized, then made into vaccines and bioweapons.
Dormant viruses and latent viruses can exist in our bodies all the time without causing disease. The mere presence of a virus in an organism doesn’t tell you anything about the health of that organism. It is quite possible that due to all the toxicity in our world (junk food, GMO crops, chlorinated and fluoridated water, poisoned skies), our body has to make a solvent to help us get rid of the toxins.
Interestingly, the main points in the interview with Aajonus are also explained in this recent video by Australian Tom Barnett.
​What if the body is producing viruses in response to toxicity?
What if their apparent spreading and replication is due to the body making many of them to clean up a mess
​French scientist Antoine Bechamp (more on him below) did experiments that led him to discover tiny particles which he called microzymas and which others have called protids, somatids or exosomes. These tiny particles are pleomorphic (taking on many shapes) and may well go through a life cycle where they begin as ‘buds’ (which is what the word ‘germ’ means etymologically) or offshoots, and later develop into viruses or bacteria. The fact that microbes can be pleomorphic is a very important concept to understand. This idea is also relevant when it comes to understanding what cancer is and how to heal it naturally. In an earlier article Inner Terrain vs. Outer Terrain: Which Do You Emphasize for Good Health?, I explained:
“Bechamp theorized that germs were actually the chemical byproducts, dead tissue and degenerative aspects of a body’s unbalanced state. He stated living entities called microzymas (tiny enzymes) created bacteria in response to host and environmental factors.
“Claiming discovery that the “molecular granulations” in biological fluids were actually the elementary units of life, Béchamp named them microzymas—that is, “tiny enzymes”—and credited them with producing enzymes and were the builders of cells while “evolving” amid favorable conditions into bacteria. Denying that bacteria could invade a healthy animal and cause disease, Béchamp claimed instead that unfavorable host and environmental conditions destabilize the host’s native microzymas, whereupon they decompose host tissue by producing pathogenic bacteria.””
James Hildreth MD from Johns Hopkins University declared:
“The virus is fully an exosome in every sense of the word.”
Piezoelectrical Repair Crews
This video which highlights aspects of the fake coronavirus pandemic also talks of viruses as entities created by the body that do not do any harm and are designed to carry waste. The video creator refers to viruses as a “piezoelectrical repair crew”, with a polysaccharide coating on their heads, who can travel to a damaged cell and facilitate glycolysis (the conversion of sugar into energy). In other words, they go to a cell needing a repair and give it energy (sugar) and electricity (a kind of jump start). According to this viewpoint, blaming a virus for damage is like blaming an innocent helper at the scene of the crime; just because someone saw a crime and came to help does not mean they caused the crime. The situation is similar to the demonization of cholesterol which I have discussed elsewhere; it turns out that cholesterol is an essential nutrient and at the scene of bodily damage to repair it, not because it caused it. By the way, around 8 years ago Berkeley scientists turned harmless viruses into piezoelectric generators.

The Flawed PCR Test; You Might Have the Virus – But So What? That Doesn’t Mean You’re Sick
Even if you strongly believe in germ theory (more on this below), there are some serious problems with the generally accepted method of testing for a virus. It’s called the PCR (Polymerase Chain Reaction) test. The PCR test amplifies a specific region of a DNA strand (the DNA target). It is qualitative not quantitative; in other words, it can tell you if a virus is present or not, but it can’t tell you in what quantities, and it can’t make any accurate assessment about whether the presence of that virus or not is enough to cause disease. As I pointed out in my article 6 Solid, Scientific Reasons to Assuage Your Coronavirus Panic, the CDC (US Center for Disease Control) itself admits that a positive coronavirus COVID-19 test (using the PCR method) doesn’t mean the virus is causing the disease/symptoms you may have! These are the actual words of the CDC:
“Positive [test] results are indicative of active infection with 2019-nCoV but do not rule out bacterial infection or co-infection with other viruses. The agent detected may not be the definite cause of disease.”

Is it 100% Proven That Viruses Cause Disease in Humans?
Amazingly, no – it is not. Germ theory is just that: a theory. For those wanting a more technical explanation of this alternative understanding of viruses, check out Dr. Thomas Cowan, Dr. Andrew Kaufman and especially Dr. Stefan Lanka. Kaufman has given some recent interviews with Crrow777 and Richie from Boston where he elaborates upon the idea that viruses have never been proven to cause disease. Both Cowan and Kaufman discuss the tests that were done after the 1918 Spanish Flu (an outbreak which it turns out was caused by EMFs/electrification and/or vaccines) where they had sick people breathe into healthy people’s mouths. The healthy people didn’t get sick. Likewise, they had sick horses sneeze and cough mucus, fluids, droplets, etc. into a bag, put food in that bag, then gave that food to healthy horses. They were unable to make the healthy horses sick.
Dr. Stefan Lanka is the king in this area. He is a German biologist and virologist who came to understand we have been lied to on a grand scale regarding the nature of the virus. He offered a reward of €100,000 for anyone who could scientifically prove that measles was a virus. That case that went all the way to the German Supreme Court where he won. Paul Fassa reports:
“At first it appeared he had lost. But Dr. Lanka took his loss to a higher court with more experts and the backing of two independent laboratories. He wound up not having to pay. It turned out that the “proof” provided was a composite of several different electron microscope images. And the composite involved different components of damaged cells. The composite could not be duplicated. The German Federal Supreme Court confirmed that there was not enough evidence to prove the existence of the measles virus.”

Dave Mihalovic reports in the article Biologist Proves Measles Isn’t A Virus, Wins Supreme Court Case Against Doctor:
“In a recent ruling, judges at the German Federal Supreme Court (BGH) confirmed that the measles virus does not exist. Furthermore, there is not a single scientific study in the world which could prove the existence of the virus in any scientific literature. This raises the question of what was actually injected into millions over the past few decades. Not a single scientist, immunologist, infectious disease specialist or medical doctor has ever been able to establish a scientific foundation, not only for the vaccination of measles but any vaccination for infants, pregnant women, the elderly and even many adult subgroups.”
Lanka has spoken out against similar viral epidemics or pandemics, such as the H5N1 bird flu scare (which was being hyped in 2005). Finally, there are even other prominent virologists like professor Peter Duesberg who have stated with solid evidence that HIV does not cause AIDS. Here are some more quotes from Lanka (who speaks German, so translated into English):
“What viruses are there at all, then, and what are they doing?
Structures which you can characterize as viruses there are in many species of bacteria and in simple life forms, similar to the bacteria. They are elements of together-living of different cells in a common cell type which have remained independent
This is called a symbiosis, an endosymbiosis, which has arisen in the course of the process of different cell types’ and structures’ combining, an endosymbiosis which has brought forth the present cell type, that type of cells of which humans, animals and plants consist … Very important: Viruses are component parts of very simple organisms, for instance of the confervacea type of algae, a particular species of a one-celled chlorella alga and of very many bacteria. As existing there, these viral component parts are called phages. In complex organisms however, in particular in humans, or in animals or plants, such structures which you might call viruses have never been seen.
In contrast to the bacteria in our cells, the mitochondria, or the bacteria in every plant, the chloroplasts, which cannot leave the common cell, since they are dependent on the metabolism of the common cell, viruses can leave the cell, since they are not carrying out any survival-vital tasks within the cell.
Viruses, thus, are component parts of the cell which have turned their entire metabolism over to the common cell and therefore can leave the cell. Outside the common cell, they are helping other cells, in that they are transferring construction and energy substances. Any other function of theirs has never been observed.

Those actual viruses which have been scientifically demonstrated to exist are performing, in the very complex processes of interactions of different cells, a helping, a supporting and in no case a destructive function.

Also in the case of diseases, actually neither in the diseased organism nor in a bodily fluid has any structure which you could characterize as a virus ever been seen or isolated. The proposition that there is any sick-making virus whatsoever is a transparent swindle, a fatal lie with dramatic consequences.”

Lanka also drops this bombshell:
“Why then are disease-causing viruses still being maintained to exist?
The school medicine protagonists/practitioners need the paralysing, stupid-making and destructive fear of disease causing phantom viruses as a central basis for their existence:
Firstly, in order to harm many people with vaccinations, in order to build up for themselves a clientele of chronically ill and ailing objects who will put up with anything being done to them.
Secondly, in order not to have to admit that they are failing totally in their treatment of chronical illnesses and have killed and are killing more people than all wars so far have made possible. Every school medicine practitioner is conscious of this, but only very few dare to speak about it. Therefore it’s no wonder either that among professional groups, it is that of the school medicine practitioners that has the highest suicide rate, far surpassing other professional groups.
Thirdly, the school medicine practitioners need the paralysing and stupid-making fear of diabolical viruses, in order to conceal their historical origin as an oppression and killing instrument of the Vatican’s when it was struggling to rise in the world, having developed out of the usurping West Roman army.”
To understand all this, we have to revisit germ theory and terrain theory.
Germ Theory vs. Terrain Theory
In the aforementioned article Inner Terrain vs. Outer Terrain: Which Do You Emphasize for Good Health?, there have been 2 competing theories which have influenced thought in many fields (medicine, biology and many more): germ theory and terrain theory/host theory. This started in the 1800s in France when Louis Pasteur championed the germ theory (the world is full of pathogenic germs, microbes, bacteria, etc. which can infect you if you are unlucky enough) and Antoine Bechamp and Claude Bernard championed the terrain theory (microbes can change from one type to another according to the blood or tissue where they reside). The quote attributed to 1 or more of these 3 men is “the germ is nothing, the inner terrain is everything.”
Pasteur (the same man after which pasteurization is named) won out and germ theory became the more dominant philosophy of the two. This has had the unfortunate effect of making people more scared of their environment and more susceptible to propaganda by Big Pharma (we’re here to protect you; just take your drugs and vaccines and everything will be OK). It has also led people to take less responsibility for their inner terrain, via poor dietary and lifestyle choices, meaning a weakened host and lowered immune system – thus becoming more susceptible to disease. But what if we had it wrong? What if it is far more important to emphasize your own strength, health and terrain than to worry about possible germs floating around everywhere that could kill you? What if this whole coronavirus crisis is making everyone OCD, scared of every surface, scared of basic and natural human contact, forgetful of their internal strength and forgetful of the power of their gut microbiome and immune system?

Can a Virus Cross from Animal to Human, or Human to Human?
According to the people quoted above, the answer is no.
A virus is made specifically by your body for the purpose of healing via excretion and clean-up of toxins.
According to this new way of understanding, a virus is made specifically for a cell, group of cells or organ, so viruses don’t even cross organs, let alone from one human body to another.
Where is a Real Picture of the Virus Causing COVID-19?
In a world where everything – literally everything – is photographed and video-recorded, why are there no actual pictures of the virus, the actual coronavirus supposedly causing all this mayhem? It shouldn’t be that hard to get an electron microscope and take a picture. Why are we only given CGIs (computer generated images)?

The Importance of Iodine and Oxygen Amidst the Coronavirus Crisis
On another note, given all the panic and fear surrounding COVID-19, it is important to revisit some health fundamentals right now – specifically iodine and oxygen.
Iodine is a very important mineral, the only halogen that the body needs. However, if you don’t have enough, the body grabs chemically similar elements (the other halogens: fluorine, chlorine and bromine), all of which are toxic. If you have too much of these, you will get sick. Have you noticed how some nations are spraying chloride bleach on everything in reaction to the supposed killer virus, thus exposing you to more chloride? Also, the 6 GHz frequency (used in many wireless phones, routers and other devices) affects your iodine absorption. One symptom of iodine deficiency is respiratory distress (also a symptom of COVID-19). Iodine deficiency is also implicated in cancer.

5G is undeniably connected to the coronavirus, but we still don’t exactly understand how. 5G was first rolled out in Wuhan, China, the epicenter of the outbreak.
. However, not everyone around 5G is getting sick. One possible cause is the new frequency band it will be using (60 GHz or WiGig which is the new name for 60GHz Wi-Fi). Just as the 6 GHz frequency affects iodine absorption, the 60 GHz frequency affects oxygen absorption. In fact, the 60 GHz frequency attenuates or weakens the oxygen molecule. This can lead to O2 molecules not binding so easily to hemoglobin – meaning you don’t take in as much oxygen. This leads to under-oxygenation or hypoxia, the forerunner to disease. Again, just as with iodine, a symptom of oxygen deficiency is respiratory distress (also a symptom of COVID-19).
Hmm … it’s almost as if this virus is providing the perfect excuse and acting as a scapegoat for the toxic chemicals and EMF which are damaging us long-term all the time …

If Viruses Can’t Cross Species, Bodies or Be ‘Caught’,
Then What Happens When One Person Appears to ‘Catch’ the Flu from Someone Else?
This is the key question.
If viruses really are completely different than what almost all of us have been taught to believe, how can we explain apparent viral contagions or viral infections?
Are they real?
Well, certainly many people have experienced getting sick right after being around other people who were sick

The real issue is how?
One possible answer is that the terrain of the recipient was lowered at the point of infection, whether because they were worried or anxious they would get sick (fear lowers the immune system), had the thought they would get sick (and unconsciously gave that thought power) or developed some kind of emotional entrainment or frequency match with the sick person. It’s all about creating a frequency lock. In life, we all have strong and weak moments; in those weaker moments we become more susceptible to disease. The great genius Nikola Tesla said that
 “The day that science begins to study non-physical phenomena, it will make more progress in one decade than in all the previous centuries of its existence.” He also said that “If you want to find the secrets of the universe, think in terms of energy, frequency and vibration.”

Is catching disease not about “evil germs out to infect us” but rather about our mental and emotional state, our immune system, our microbiome and our susceptibility?
Conclusion: Use This Crisis as an Opportunity to Look at Viruses in a Different Way
It would be wise amidst all the fear over the coronavirus COVID-19 if were to all remember that germ theory is just that – a theory – and that we have the power to take charge of our own health. We can strengthen our immune system with healthy food choices, enough sunshine (vitamin D), sufficient exercise and adequate sleep. We can choose to reduce or eliminate exposure to toxins like fluoride, chlorine, aluminum, mercury and EMF wireless radiation. We can supplement with things that boost our immunity – like vitamin C, antioxidants, iodine and oxygen – and natural anti-viral medicine like olive leaf extract, medicinal mushrooms and oregano oil.
It is a maxim of life that knowledge decreases fear. What if the real conspiracy here is the exploitation of the mass ignorance regarding the true nature of the virus? What if there is no such thing as a killer virus? What if the real virus here is fear itself – fear of the virus, fear of the unknown and fear of death? It hardly bares stating that the NWO controllers are master manipulators who intimately understand how to exploit human psychology. Now is the time for people to dive in and question everything they thought they knew. It is an opportunity to gain new levels of comprehension, understanding and knowledge – so that we may remain free.
After all, we cannot be free if we continue to remain ignorant, else our ignorance will continue to be exploited.
*****
Makia Freeman is the editor of alternative media / independent news site The Freedom Articles and senior researcher at ToolsForFreedom.com. Makia is on Steemit and FB.
Sources:
https://thefreedomarticles.com/digital-dollar-us-bills-mention-central-bank-digital-currency/
https://thefreedomarticles.com/emergency-powers-worldwide-gov-power-grabs-scripted-agenda/
https://thefreedomarticles.com/western-medicine-rockefeller-medicine/
https://thefreedomarticles.com/flexner-report-rockefeller-ama-takeover/
https://thefreedomarticles.com/tax-exempt-foundations-rockefeller-fronts/
https://thefreedomarticles.com/2010-rockefeller-foundation-paper-plan-exploit-pandemic/
https://www.youtube.com/watch?v=ctvt0ansKkw
https://thefreedomarticles.com/ebola-hoaxing-it-up/
https://thefreedomarticles.com/zika-or-insecticide-pyriproxyfen-behind-microcephaly-cases/
https://m.facebook.com/story.php?story_fbid=638176716728974&id=100016099539778
https://www.youtube.com/watch?v=3aUhWt8Aj-Y
https://thefreedomarticles.com/cancer-busting-myths-cancer-microbe-p1/
https://thefreedomarticles.com/plastic-oils-vs-saturated-fats/
https://www.extremetech.com/extreme/129389-berkeley-scientists-turn-harmless-virus-into-piezoelectric-generator
https://thefreedomarticles.com/6-solid-scientific-reasons-to-assuage-your-coronavirus-panic/
https://www.fda.gov/media/134922/download
https://www.youtube.com/watch?v=KUw1Rzbde5U
https://www.youtube.com/watch?v=HQQtOQUkUoI
https://www.youtube.com/watch?v=NcS60a9cdg4
https://www.youtube.com/watch?v=MLD2NTe9pfM
https://vaccineimpact.com/2017/german-supreme-court-upholds-biologists-claim-that-measles-virus-does-not-exist/
https://vaccinationdanger.blogspot.com/2017/02/measles-is-not-virus.html
https://www.youtube.com/watch?v=pB8g0b-FkW0
http://whale.to/b/lanka.html
https://thefreedomarticles.com/inner-terrain-vs-outer-key-good-health/
https://rupress.org/jcb/article/162/6/960/33690/When-is-a-virus-an-exosome
https://thefreedomarticles.com/coronavirus-5g-connection-coverup-vaccines-transhumanism/

19aztecone74 - This interview with Dr. Vonderplanitz is from a 2009 interview on Super Human Radio. He died under mysterious circumstances in 2013.
​Dormant viruses and latent viruses can exist in our bodies all the time without causing disease. The mere presence of a virus in an organism doesn’t tell you anything about the health of that organism. It is quite possible that due to all the toxicity in our world (junk food, GMO crops, chlorinated and fluoridated water, poisoned skies), our body has to make a solvent to help us get rid of the toxins.​  If you feel sick and get a PCR test any random virus DNA might be identified even if they aren’t at all involved in your sickness which leads to false diagnosis. And coronavirus are incredibly common. A large percentage of the world human population will have covi DNA in them in small quantities even if they are perfectly well or sick with some other pathogen. Do you see where this is going yet?  If you want to create a totally false panic about a totally false pandemic – pick a coronavirus.

Improved Survival of Patients With Acute Respiratory Distress Syndrome (ARDS): 1983-1993January 25, 1995  
John A. Milberg, MPH; Donna R. Davis, RN; Kenneth P. Steinberg, MD; et alLeonard D. Hudson, MD
Author Affiliations
JAMA. 1995;273(4):306-309. doi:10.1001/jama.1995.03520280052039
https://jamanetwork.com/journals/jama/article-abstract/386597 

Objective.  —To analyze temporal trends in acute respiratory distress syndrome (ARDS) fatality rates since 1983 at one institution.
Design.  —Cohort.
Setting.  —Intensive care units of a large county hospital.

Patients.  —Consecutive adult patients (≥18 years of age) meeting ARDS criteria were identified through daily surveillance of intensive care units (N=918 from 1983 through 1993). The major causes were sepsis syndrome in 37% and major trauma in 25%; 37% had other risks. Sixty-five percent were male. The median age was 45 years (range, 18 to 92 years); 70% were younger than 60 years.

Main Outcome Measure.  —Hospital mortality.
Results.  —Overall fatality rates showed no trend from 1983 to 1987, declined slightly in 1988 and 1989, and decreased to a low of 36% in 1993 (95% confidence interval, 25% to 46%). The crude rates were largely unchanged after adjustment for age, ARDS risk, and gender distribution. While patients both younger than 60 years and 60 years or older experienced declines in fatality rate, the larger decrease occurred in the younger cohort. In sepsis patients, ARDS fatality rates declined steadily, from 67% in 1990 to 40% in 1993 (95% confidence interval, 23% to 57%). The decline in sepsis-related ARDS fatality was confined largely to patients less than 60 years of age. Trauma patients and all other patients also experienced declines in fatality rates after 1987, although these trends were not as strong and consistent as in the sepsis population.

Conclusions.  —In this large series, we observed a significant decrease in fatality rates occurring largely in patients younger than 60 years and in those with sepsis syndrome as their risk for ARDS. We are unable to determine the extent to which experimental therapies or other changes in treatment have contributed to the observed decline in the ARDS fatality rate. Institution-specific rates and temporal trends in ARDS fatality rates should be considered in clinical trials designed to prevent ARDS and the high mortality associated with this syndrome.(JAMA. 1995;273:306-309)

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Acute Respiratory Distress SyndromeThe Berlin Definition
The ARDS Definition Task Force*
Author Affiliations
JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669
https://jamanetwork.com/journals/jama/article-abstract/1160659  

The acute respiratory distress syndrome (ARDS) was defined in 1994 by the American-European Consensus Conference (AECC); since then, issues regarding the reliability and validity of this definition have emerged. Using a consensus process, a panel of experts convened in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) developed the Berlin Definition, focusing on feasibility, reliability, validity, and objective evaluation of its performance. A draft definition proposed 3 mutually exclusive categories of ARDS based on degree of hypoxemia: mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg), moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) and 4 ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (≤40 mL/cm H2O), positive end-expiratory pressure (≥10 cm H2O), and corrected expired volume per minute (≥10 L/min). The draft Berlin Definition was empirically evaluated using patient-level meta-analysis of 4188 patients with ARDS from 4 multicenter clinical data sets and 269 patients with ARDS from 3 single-center data sets containing physiologic information. The 4 ancillary variables did not contribute to the predictive validity of severe ARDS for mortality and were removed from the definition. Using the Berlin Definition, stages of mild, moderate, and severe ARDS were associated with increased mortality (27%; 95% CI, 24%-30%; 32%; 95% CI, 29%-34%; and 45%; 95% CI, 42%-48%, respectively; P < .001) and increased median duration of mechanical ventilation in survivors (5 days; interquartile [IQR], 2-11; 7 days; IQR, 4-14; and 9 days; IQR, 5-17, respectively; P < .001). Compared with the AECC definition, the final Berlin Definition had better predictive validity for mortality, with an area under the receiver operating curve of 0.577 (95% CI, 0.561-0.593) vs 0.536 (95% CI, 0.520-0.553; P < .001). This updated and revised Berlin Definition for ARDS addresses a number of the limitations of the AECC definition. The approach of combining consensus discussions with empirical evaluation may serve as a model to create more accurate, evidence-based, critical illness syndrome definitions and to better inform clinical care, research, and health services planning.  


Lung Neutrophils in the Adult Respiratory Distress Syndrome
Clinical and Pathophysiologic Significance1,2, 

Jeffrey E. Weiland , W. Bruce Davis , John F. Holter , 
Jeannette R. Mohammed , Paul M. Dorinsky , and James E. Gadek
 https://www.atsjournals.org/doi/abs/10.1164/arrd.1986.133.2.218


Although neutrophils are of pathogenetic importance in various animal models of acute lung injury, their role in the adult respiratory distress syndrome (ARDS) is unclear. To study the significance of lung neutrophils in this disorder, patients with ARDS (n=11) were evaluated by bronchoalveolar lavage within 24 h of admission to the intensive care unit. Patients with non-ARDS respiratory failure requiring mechanical ventilation (n=4) and normal volunteers (n=12) were also studied. Neutrophils constituted 67.6 ± 9.8% of recovered lavage cells in patients with ARDS compared with only 4.0 ± 2.4% of cells in mechanically ventilated control patients and 0.8 ± 0.2% in normal volunteers (p < 0.005, both comparisons). Furthermore, in patients with ARDS (n=6) evaluated serially by bronchoalveolar lavage at 72−h intervals, neutrophil percentages decreased from 91 ± 3.2% (initial lavage) to 42.8 ± 12% (final lavage) (p < 0.005). Lung neutrophils also predicted the severity of abnormalities in gas exchange and lung protein permeability. That is, the percentage of neutrophils correlated directly with the alveolar-arterial Po2 difference (r = 0.69, p < 0.01) and lavage fluid total protein concentrations (r = 0.62, p < 0.01). Because large numbers of lung neutrophils were present in these patients, ARDS lavage fluid was assayed for neutrophil mediators relevant to the pathogenesis of acute lung injury. Neutrophil elastase activity was not detected in any ARDS lavages, although elastase was antigenically present in most samples and appeared to be com-plexed to alpha−1−antitrypsin. In contrast to elastase, neutrophil collagenase was readily detectable in ARDS fluid. ARDS lavage fluid also contained high levels of myeloperoxidase (MPO) activity that appeared to be of neutrophil origin. This MPO was cytotoxic for normal lung parenchymal cells when incubated in the presence of the MPO system cofactors H2O2 and halide anion. Thus, lung neutrophils in ARDS correlate with abnormalities of gas exchange and lung protein permeability, and neutrophil products capable of mediating lung injury can be recovered from the lungs of these patients. These findings suggest a central role for neutrophils in the pathogenesis of ARDS.  

Improved Survival of Patients With Acute Respiratory Distress Syndrome (ARDS): 1983-1993January 25, 1995  
John A. Milberg, MPH; Donna R. Davis, RN; Kenneth P. Steinberg, MD; et alLeonard D. Hudson, MD
Author Affiliations
JAMA. 1995;273(4):306-309. doi:10.1001/jama.1995.03520280052039
https://jamanetwork.com/journals/jama/article-abstract/386597 

Objective.  —To analyze temporal trends in acute respiratory distress syndrome (ARDS) fatality rates since 1983 at one institution.
Design.  —Cohort.
Setting.  —Intensive care units of a large county hospital.

Patients.  —Consecutive adult patients (≥18 years of age) meeting ARDS criteria were identified through daily surveillance of intensive care units (N=918 from 1983 through 1993).

The major causes were sepsis syndrome in 37% and major trauma in 25%; 37% had other risks. Sixty-five percent were male.

The median age was 45 years (range, 18 to 92 years); 70% were younger than 60 years.

Main Outcome Measure.  —Hospital mortality.

Results.  —Overall fatality rates showed no trend from 1983 to 1987, declined slightly in 1988 and 1989, and decreased to a low of 36% in 1993 (95% confidence interval, 25% to 46%). The crude rates were largely unchanged after adjustment for age, ARDS risk, and gender distribution. While patients both younger than 60 years and 60 years or older experienced declines in fatality rate, the larger decrease occurred in the younger cohort. In sepsis patients, ARDS fatality rates declined steadily, from 67% in 1990 to 40% in 1993 (95% confidence interval, 23% to 57%). The decline in sepsis-related ARDS fatality was confined largely to patients less than 60 years of age. Trauma patients and all other patients also experienced declines in fatality rates after 1987, although these trends were not as strong and consistent as in the sepsis population.

Conclusions.  —In this large series, we observed a significant decrease in fatality rates occurring largely in patients younger than 60 years and in those with sepsis syndrome as their risk for ARDS. We are unable to determine the extent to which experimental therapies or other changes in treatment have contributed to the observed decline in the ARDS fatality rate. Institution-specific rates and temporal trends in ARDS fatality rates should be considered in clinical trials designed to prevent ARDS and the high mortality associated with this syndrome.(JAMA. 1995;273:306-309)

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Acute Respiratory Distress SyndromeThe Berlin Definition

The ARDS Definition Task Force*
Author Affiliations
JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669
https://jamanetwork.com/journals/jama/article-abstract/1160659  
The acute respiratory distress syndrome (ARDS) was defined in 1994 by the American-European Consensus Conference (AECC); since then, issues regarding the reliability and validity of this definition have emerged. Using a consensus process, a panel of experts convened in 2011 (an initiative of the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine) developed the Berlin Definition, focusing on feasibility, reliability, validity, and objective evaluation of its performance. A draft definition proposed 3 mutually exclusive categories of ARDS based on degree of hypoxemia: mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg), moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) and 4 ancillary variables for severe ARDS: radiographic severity, respiratory system compliance (≤40 mL/cm H2O), positive end-expiratory pressure (≥10 cm H2O), and corrected expired volume per minute (≥10 L/min). The draft Berlin Definition was empirically evaluated using patient-level meta-analysis of 4188 patients with ARDS from 4 multicenter clinical data sets and 269 patients with ARDS from 3 single-center data sets containing physiologic information. The 4 ancillary variables did not contribute to the predictive validity of severe ARDS for mortality and were removed from the definition. Using the Berlin Definition, stages of mild, moderate, and severe ARDS were associated with increased mortality (27%; 95% CI, 24%-30%; 32%; 95% CI, 29%-34%; and 45%; 95% CI, 42%-48%, respectively; P < .001) and increased median duration of mechanical ventilation in survivors (5 days; interquartile [IQR], 2-11; 7 days; IQR, 4-14; and 9 days; IQR, 5-17, respectively; P < .001). Compared with the AECC definition, the final Berlin Definition had better predictive validity for mortality, with an area under the receiver operating curve of 0.577 (95% CI, 0.561-0.593) vs 0.536 (95% CI, 0.520-0.553; P < .001). This updated and revised Berlin Definition for ARDS addresses a number of the limitations of the AECC definition. The approach of combining consensus discussions with empirical evaluation may serve as a model to create more accurate, evidence-based, critical illness syndrome definitions and to better inform clinical care, research, and health services planning.  

​The EMF 5G Fix

www.emf5gfix.com  
Dr Don Paris talks about  The EMF 5G Fix 
  There is one quillian times more radio electromagnetic in a atmosphere over the last 50 years..
which is killing insects, plant amd humans..
The book 
"Regaining Wholeness Through the Suble Dimensons.. where Science Meets Magic.".. by  Dr Don Paris PHh.D.

https://www.chiorganizer.com/5gfix-disc
".... Putting in tens of millions of 5G antennas without a singe biological test of safety 
has to be the stupidest idea nyone has had in the history of the world....." 
Martin L, Pal, PhD
Professor Ementus of Biochemistry and medical Sciences at Washington State University.

60 Ghz Electro magnetic waves that are produced by 5G Towers and Satellites circling plant earth is the GHZ level
that absorbs oxygen .... and the has the effect of absorbing Oxygen tha the body needs .. 
leaving humans short of oxygen ... that si the issue causing the sickness and causing people to have trouble breathing..
the  60 Ghz Electro magnetic waves that are produced by 5G Towers and Satellites circling plant earth aree robbing oxygen from humans ..... the medical issue is simply a lack of oxygen which needs a oxygen mast connectd to an oxygen cylinder.
.... and is not a viril pheumonia ....with a ventilator hooked up to a erson after the person is sedated.
The ventilators are ripping healthy lungs apart...
which is like putting a high pressure hose down a person;s throat ... 
when they only needed a glass of water
https://www.chiorganizer.com/5gfix-disc
Dr Don Paris talks about  The EMF 5G Fix 
  There is one quillian times more radio electromagnetic in a atmosphere over the last 50 years..
which is killing insects, plant amd humans..
The book 
"Regaining Wholeness Through the Suble Dimensons.. where Science Meets Magic.".. by  Dr Don Paris PHh.D.​
Did you know that your mobile phone uses the same mrcriwave frequencies that microwave ovens use?
More 5G info plus how you can protect yourslef from EMF's
Have you every wondered how you can protect yourself from these microwave freqencies 
that are being speard around the cities by 5G towers?
There is pelnty of evidence ,, there are thousands of studies that have show that microwave frequencies coming from cell phones and other microwave radiating devices are harmfull to your health ...
The World health Organisation has actually issued a warning saying that ...
"Cell phone radiation is a Class B Carcinogen.." and is the same as Asbestos..

In the early 1990's I was talking to Dr. Bon Beck and Eldenberg worked in the government and the CIA developing Scalar Technologies.. Weaonry and Scalar Communications... we were  talking about what was coming in the future... Bob was gravely concerned about what was coming for the children because of the total surveylance ... and weaponisation of electromagnetic freqencies... that they were already developing back then ... 
They have both  has passed has passed away now .. but their predictions have come true with the advent of 5G Electronic magnetic Technology...Have you ever felt tried after working on your computer or talking on your cell phone for a lomg time?
That used to happejn to bme as well untill I realised that the frequencies that were coming out of my cell phone were actually effecting me... these freqencies .... are omitting microwave radiations... 

Because … Coronavirushttps://thefreedomarticles.com/because-coronavirus-anything-goes/  
April 6, 2020
By Makia Freeman

AT A GLANCE...
THE STORY:
Anything and everything under the sun is being justified due to a mysterious killer virus.
THE IMPLICATIONS:
Are people so programmed, so psychologically dependent on authority and so afraid that they will allow the desecration and destruction of hard-earned rights and freedoms – as is happening right now worldwide?

[because coronavirus]
Authorities worldwide continue to offer up the lame excuse of “because coronavirus” to justify new vague, broad, unending and very dangerous powers to a scared and shellshocked public that, for the most part, has given up its faculty of critical thinking.

Because Coronavirus.
That’s what we being told. Everything has to change, cherished rights must be eliminated and new emergency powers have to be given to authorities … because of a virus that still has not been isolated, purified and proven beyond all doubt to be the cause of the alleged pandemic. It is clear the COVID-19 numbers in and of themselves are being grossly manipulated, due to many reasons such as false positives and counting everyone who died with the virus in their body as a coronavirus death or fatality (even if it had nothing to do with their death). Sadly, everyone is in such a panic that they can’t think clearly. Governments around the world are passing dangerous laws which are deliberately vague, broad and often without an expiration date. Is liberty dying to thunderous applause and the scared cries of people for an authority figure to save them?

Because Coronavirus: Hungary Gets a Dictator
Hungarian Prime Minister Viktor Orban effectively oversaw the transition of his country from a democracy to a dictatorship. On March 30th 2020, the Hungarian Parliament bestowed upon Orban the right to rule by decree (i.e. the power to bypass the national assembly) and to suspend existing laws. Not only that, but Hungary (which is an EU member) suspended future elections! This makes Orban the world’s newest dictator. This is an incredible development in a continent that prides itself upon democracy and a frightening abdication of power and responsibility by the Hungarian Parliament – all over a tiny, invisible virus that still has not killed more people than a seasonal flu, even taking into consideration the manipulated numbers.

Because Coronavirus: Philippines’ President Duterte Orders Cops and Soldiers to Shoot Quarantine Violators if Need Be

Philipppines’ President Rodrigo Duterte, known for his ‘tough-guy’ attitude and his threats to shoot and kill drug users and dealers, was granted emergency powers and $5.4 billion to deal with the coronavirus crisis. This was after an earlier draft law (that got changed and didn’t pass) that would have allowed him as president to take over private businesses! The New York Times wrote that ““This limitless grant of emergency powers is tantamount to autocracy,” a Philippine rights group, the Concerned Lawyers for Civil Liberties, said in a statement. The lawyers noted that Mr. Duterte had once compared the country’s Constitution to a “scrap of toilet paper.”” Duterte said the following in a televised address:

“It is getting worse. So once again I’m telling you the seriousness of the problem and that you must listen.

My orders to the police and military…if there is trouble and there’s an occasion that they fight back and your lives are in danger, shoot them dead. Is that understood?

Dead.”

Because Coronavirus: Eastern European Governments Grab Power and Target Dissidents
The Govenment of Slovenia has set up the Krizni stab Republike Slovenije (the Crisis Headquarters of the Republic of Slovenia) led by the rather corrupt Slovenian PM Janez Jansa. The Australian ABC reports:

Within hours, Mr Jansa’s Crisis Headquarters dismissed the heads of the defence force, the military intelligence agency and the national police … [independent reporter] Zgaga said the new Slovenian administration was using the coronavirus emergency as a means by which to entrench its power. “I believe it is a systematic campaign to threaten any critical voices, to make them silent, so as to stifle journalists, any critical intellectuals, and citizens,” Zgaga said.”

The same thing is happening in other Eastern European nations, notably Poland, Bulgaria and Kosovo:

“In Warsaw, the ruling Law and Justice Party is planning to press ahead with a presidential election in early May. While President Andrzej Duda holds court on television, thanks to Poland’s pliant state broadcaster, the Opposition is banned on health grounds from holding rallies. In Bulgaria, the Parliament granted new powers to the Government to use mobile phone data to track the populace — ostensibly to police the quarantine of those infected or exposed to COVID-19. It has also set up checkpoints around Roma communities — an ethnic minority often pilloried in Bulgarian society. Last Wednesday, Kosovo’s Government collapsed and its prime minister was deposed after President Hashim Thaci, a former militiaman once accused of war crimes,  attempted to shift all executive power to an emergency security council which he heads.”


Because Coronavirus: Thailand’s Government Censors News and Intimidates Journalists

After declaring a state of emergency of March 24th 2020, Thai Prime Minister Prayuth Chan-ocha assumed the authority to impose curfews and censor the news media. Journalists there have been sued and intimidated for criticizing the government’s response to the outbreak. On March 25th, Chan-ocha issued a list of prohibitions (original in Thai here), including vague and broad restrictions on freedom of speech and freedom of the press:

“Within hours, Mr Jansa’s Crisis Headquarters dismissed the heads of the defence force, the military intelligence agency and the national police … [independent reporter] Zgaga said the new Slovenian administration was using the coronavirus emergency as a means by which to entrench its power. “I believe it is a systematic campaign to threaten any critical voices, to make them silent, so as to stifle journalists, any critical intellectuals, and citizens,” Zgaga said.” 

 The same thing is happening in other Eastern European nations, notably Poland, Bulgaria and Kosovo:


“In Warsaw, the ruling Law and Justice Party is planning to press ahead with a presidential election in early May. While President Andrzej Duda holds court on television, thanks to Poland’s pliant state broadcaster, the Opposition is banned on health grounds from holding rallies. In Bulgaria, the Parliament granted new powers to the Government to use mobile phone data to track the populace — ostensibly to police the quarantine of those infected or exposed to COVID-19. It has also set up checkpoints around Roma communities — an ethnic minority often pilloried in Bulgarian society. Last Wednesday, Kosovo’s Government collapsed and its prime minister was deposed after President Hashim Thaci, a former militiaman once accused of war crimes, attempted to shift all executive power to an emergency security council which he heads.”

Because Coronavirus: Thailand’s Government Censors News and Intimidates Journalists
After declaring a state of emergency of March 24th 2020, Thai Prime Minister Prayuth Chan-ocha assumed the authority to impose curfews and censor the news media. Journalists there have been sued and intimidated for criticizing the government’s response to the outbreak. On March 25th, Chan-ocha issued a list of prohibitions (original in Thai here), including vague and broad restrictions on freedom of speech and freedom of the press:

Final Thoughts: Anything Goes Because Coronavirus
When people submit to fear and shut off their faculty of critical thinking, manipulators pounce upon the chance to push forward their schemes of control. It is well known that governments have a set of desired powers on the shelf, waiting for the perfect chance to enact and execute them. They draft laws in advance and wait for the right timing. For those at the very peak of the NWO pyramid, they don’t wait for the right timing; they create the right timing by generating a problem or the perception of a problem. Remember, it doesn’t even have to be a real problem, as long as people believe there is a problem and are sufficiently afraid. Perception is everything.

NWO insider Henry Kissinger is quoted as saying:
“Today Americans would be outraged if UN troops entered Los Angeles to restore order; tomorrow they will be grateful! This is especially true if they were told there was an outside threat from beyond whether real or promulgated, that threatened our very existence. It is then that all peoples of the world will pledge with world leaders to deliver them from this evil. The one thing every man fears is the unknown. When presented with this scenario, individual rights will be willingly relinquished for the guarantee of their well being granted to them by their world government.” 

 Operation Coronavirus is changing every corner of all the earth and seemingly leaving no nation untouched. This is a scripted agenda for worldwide transformation if there ever was one.

*****
Makia Freeman is the editor of alternative media / independent news site The Freedom Articles and senior researcher at ToolsForFreedom.com. Makia is on Steemit and FB.
Sources:
*https://thefreedomarticles.com/emergency-powers-worldwide-gov-power-grabs-scripted-agenda/
*https://thefreedomarticles.com/6-solid-scientific-reasons-to-assuage-your-coronavirus-panic/
*https://www.businessinsider.com/hungary-prime-minister-viktor-orban-seizes-full-control-during-outbreak-2020-3
*https://www.nytimes.com/2020/03/30/world/europe/coronavirus-governments-power.html
*https://www.reuters.com/article/us-health-coronavirus-philippines-dutert/shoot-them-dead-philippine-leader-says-wont-tolerate-lockdown-violators-idUSKBN21K0AY
*https://www.abc.net.au/news/2020-04-02/eastern-european-regimes-exploit-coronavirus/12109720
*http://www.ratchakitcha.soc.go.th/DATA/PDF/2563/E/069/T_0010.PDF
*https://www.tlhr2014.com/?p=16625
*https://www.wsws.org/en/articles/2020/03/25/norw-m26.html
*https://thefreedomarticles.com/creating-exploiting-coronavirus-crisis-problem-reaction-solution/
*https://www.activistpost.com/2020/04/tunisia-deploys-robo-cop-to-enforce-coronavirus-lockdown.html

 Dr. Cameron Kyle-Sidell
Critical Care Doctor from New York City
Blows the Whistle on the dangerous way ventilators \re being used caused up to 70% death rate for people put on ventilators

Wikipedia Exposed Media - WEM www.wikipediaexposed.org

FREEDOM TO PROVIDE FACTS, INFORMATION, OPINION AND DEBATE WIKIPEDIA EXPOSED MEDIA - TRUTHFUL NEWS MEDIA, ENCOURAGE OPEN DEBATE

Gattinoni says putting a patient like this on a ventilator under too high a pressure may cause lung damage that ultimately looks like ARDS.
So he cautions that doctors need to be aware of the COVID-19 patients’ symptoms  and need to use the ventilator carefully and sparingly.
In an interview with MDEdge, Gattinoni said one center in central Europe that had begun using different treatments for different types of COVID-19 patients had not seen any deaths among those patients in its intensive care unit. He said a nearby hospital that was treating all COVID-19 patients based on the same set of instructions had a 60% death rate in its ICU.
"This is a kind of disease in which you don't have to follow the protocol -- you have to follow the physiology," Gattinoni said. "Unfortunately, many, many doctors around the world cannot think outside the protocol."
Other experts agree.
“If you over-distend somebody’s lung on mechanical ventilation, you essentially generate more ARDS. You make the lung leaky,” Bull says.
He says pulmonologists have gotten much better at using ventilators to make them safer for patients. Doctors work to keep the pressure on the lung as low as possible, to prevent that damage.
Several recent studies have helped to cut the death rate for patients who need to be on a ventilator. The PROSEVA study, published in The New England Journal of Medicine, showed the death rate among ventilated patients could be as low as 16% under optimal care.
So far, death rates for ventilated patients with COVID-19 have been higher than that. That could be because some COVID-19 patients often need to be on ventilators for a long time, sometimes as long as 2 weeks. They also tend to have other conditions, so it’s possible that they are sicker to begin with. More research is needed to understand why, and doctors will continue to share best practices as they see things that need to be addressed.

How to Avoid Coronavirus - Covid 19 Protecting Your Family
Brian Boxer Wachler
Reassuring Video - Learn the Facts from a Lung Specialist Doctor - How to Avoid Coronavirus - He Treats These Patients All Day in a New York Hospital. Our Office Remains Open to Help People with Vision/Eye Problems. Contact Us at 310-860-1900 or info@boxerwachler.com.
CategoryHowto & Style

Bill Gates: 'We're in big trouble' until the U.S. has better coronavirus testing 

Aarthi Swaminathan Reporter Yahoo Finance
April 9, 2020

https://www.biography.com/business-figure/bill-gates

Microsoft (MSFT) founder and billionaire Bill Gates warns that America needs to get its coronavirus testing sorted quickly — until then, “we’re in big trouble.”

Coronavirus in the U.S. is “still completely mis-prioritized,” Gates told CNBC on Thursday. 
“The natural thing would be to do like South Korea did, and create a unified system — that we haven't gotten any interest from the federal level,” Gates said. “The thinking is to create a website that you go in and enter your situation and it would give you a priority number, and then hopefully all the people who control the capacity limit the priority level that they accept, so they're giving these very quick results and to the right people.”

And “until we have that, we're in big trouble,” he stressed, “because as a percentage of 330 million [Americans], we're not going to be able to test many people … [and] we need to know that number because that deeply affects rebounds when opening up. And there is some data that suggests it's not a gigantic number but very, very important to pin that down.”

Gates previously said that the Gates Foundation is spending “billions” — which has not been independently verified — on a vaccine for the coronavirus. He also called for an “extreme shutdown” and widespread testing before social distancing guidelines could relaxed and the economy restarts.
Once “we get our act together countrywide and if the compliance is very high and that testing including some innovations like a self-swab that our foundation has driven and those get into place by early June, we'll be looking at some type of opening up.”

PCR v. serological tests
Gates noted that “the access to the backend capacity of what's called a PCR [or polymerase chain reaction] machine is completely unmanaged. You can have somebody without symptoms who gets tested every day in some wealthy community… and you can have a healthcare worker… waiting three or four days.”
The PCR test is essentially what we know today as swab testing. The way it works is that the PCR method is a “fast and inexpensive technique” to “amplify” small segments of DNA which can then be used by labs to examine bacteria or viruses. In other words, if someone has the coronavirus, the PCR test amplifies their DNA such that scientists can study it and in just a few hours compute a result.
“The PCR test ... that is the key to tracing contacts and really getting people to go into serious quarantine,” Gates said, adding that a serological test “only goes positive after you've infected most everyone you're going to infect.”
He continued: “Any time the queue [for testing] is over 24 hours, that's complete mismanagement. Because the value of the result is far less worthwhile when you're not getting it very, very quickly. The best case is the PCR test goes positive before you're symptomatic or infectious and then you can act in such a way that you never infect anyone else.” 

Microsoft principle founder Bill Gates participates in a discussion during a luncheon of the Economic Club of Washington June 24, 2019 in Washington, DC. (Photo: Alex Wong/Getty Images)

Older people would rather die than let Covid-19 harm US economy – Texas official

Coronavirus outbreak

Lois Beckett in San Francisco
 @loisbeckett - Tue 24 Mar 2020 
https://www.theguardian.com/world/2020/mar/24/older-people-would-rather-die-than-let-covid-19-lockdown-harm-us-economy-texas-official-dan-patrick  

Lieutenant governor Dan Patrick tells Fox News: ‘Do we have to shut down the entire country for this? I think we can get back to work’  

As Donald Trump pushed to re-open the US economy in weeks, rather than months, the lieutenant governor of Texas went on Fox News to argue that he would rather die than see public health measures damage the US economy, and that he believed “lots of grandparents” across the country would agree with him.
“My message: let’s get back to work, let’s get back to living, let’s be smart about it, and those of us who are 70-plus, we’ll take care of ourselves,” Lt Gov Dan Patrick, a 69-year-old Republican, told Fox News host Tucker Carlson on Monday night.
“Don’t sacrifice the country,” Patrick said. “Don’t do that.”

Patrick said he feared that public health restrictions to prevent coronavirus could end American life as he knows it, and that he is willing to risk death to protect the economy for his grandchildren.
“You know, Tucker, no one reached out to me and said, ‘As a senior citizen, are you willing to take a chance on your survival in exchange for keeping the America that all America loves for your children and grandchildren?’” Patrick said. “And if that’s the exchange, I’m all in.”
“That doesn’t make me noble or brave or anything like that,” he added. “I just think there are lots of grandparents out there in this country like me.”

At the White House’s coronavirus briefing Monday night, the administration’s coronavirus response coordinator, Dr Deborah Birx, said that emerging data from Europe suggested that 99% of the coronavirus deaths were people over age 50, and that many had pre-existing conditions. That “doesn’t change the need to protect the elderly”, Birx said.

Trump, who has raised concerns about the damage that coronavirus prevention measures are doing to the US economy, said he was eager to return for the country to return to normal as soon as possible, and suggested that an economic crisis might result in more deaths, through suicide, than a global pandemic. 

He did not answer questions from journalists about whether he would abide by the advice of public health experts if they told him next week that the government needed to keep restrictive measures in place over the longer term to prevent the spread of the virus. 

Patrick, a Texas Republican, praised the president’s focus on the economy on Monday and said that it had “lifted” his heart.
“I don’t want the whole country to be sacrificed,” Patrick said. “I’ve talked to hundreds of people … and everyone says pretty much the same thing: We can’t lose our whole country. We’re having an economic collapse.”
“We’re going to be in a total collapse, recession, depression, collapse in our society if this goes on for another several months,” Patrick said. “As the president said, the mortality rate is so low. Do we have to shut down the entire country for this? I think we can get back to work.”
Patrick said that, as someone who turns 70 next week, he was in the high-risk group, but that he was willing to give up his life for his six grandchildren.

“Look, I’m going to do everything I can do to live,” Patrick said. “But if you said, are you willing to take a chance … If I get sick, I’ll go and try to get better, but if I don’t, I don’t.”