Iatrogenic Tragedy circa 1918-1919

Dr. Weeks Comment: Doctors know that inflammation drives all chronic degenerative illnesses making the disease progress more rapidly while worsening symptoms and often proving fatal.  To repeat: All diseases!  For example: Cancer metastasizes using inflammatory pathways.  We know that anti-inflammatory agents therefore reduce the risk of cancer spreading.  Inflammation causes more heart attacks and cardiac deaths than does the outdated and nearly abandoned “high cholesterol” risk factor. Upon autopsy, most people who die of a sudden unexpected heart attack have no blockages; it was inflammation which killed them. (So, the next time your doctor recommends testing your cholesterol levels – look him or her in the eye and ask “Don’t you want to know my hs-CRP and homocysteine and fibrinogen levels instead?”) Diabetes and gout also are made worse by inflammation. Acne is inflammatory.  So is eczema and psoriasis. Even the top psychiatric journals agree that inflammation makes all psychiatric illnesses worse.  Schizophrenia.  Depression.  PTSD   Again… “ALL”.   So why hasn’t your doctor urged you to take adequate anti-inflammatory agents and why hasn’t she or he followed-up and tested you anti-inflammatory markers (hs-CRP and ESR) to make certain you are in the safe zone?
The reason is simple:  doctors are afraid of anti-inflammatory agents because of the narrow therapeutic window: too little doesn’t work, too much kills… it is hard to kit the right dose. This class of drugs is too powerful and if the patient takes too many, the doctor fears that the patient will die of kidney or liver failure or by bleeding to death from an ulcer. Ringing in the ears is the least of your worries. (When I trained in medicine in the early 1980’s doctors told patients “take aspirin until your ears start to ring then cut back.”) The problem is with the patients:  if one is good, more is better so patients in pain are sore tempted to keep popping pills.  TAKE HOME message: since a hepatotoxic dose of acetaminophen is 5 grams,  the difference between a safe dose and a dose that can start to kill you could be just two tablets of Extra Strength Tylenol.

“…Acetaminophen overdose sends as many as 78,000 Americans to the emergency room annually and results in 33,000 hospitalizations a year, federal data shows. Acetaminophen is also the nation’s leading cause of acute liver failure, according to data from an ongoing study funded by the National Institutes for Health…”  (source  HERE)

Of course, Big Pharma and it pawn the FDA are complicit  in 1977, an expert panel of scientists and doctors convened by the FDA advised that putting put a “severe liver damage” warning on the drug was “obligatory”. We now know, as noted in an August report,  that it only took the FDA 32 years to add the warning.
The drugs are too dangerous and the FDA and Big Pharma could not care less.
We need safer anti-inflamatory agents and here they are  SOUL and CORE  and study this before eating the anti-inflammatory diet.
But…. It could be worse. For example, you could have sought expert medical care during the 1918-1919 outbreak of the Spanish influenza.  It turns out that the flu virus itself was not so lethal; it was the doctors who were killing everyone: iatrogenesis 101.
Edward’s fever kept getting higher and higher…aspirin…was given to him by the 1/2-handful over and over…
This cautionary tale is well worth reading below….

Salicylates and Pandemic Influenza Mortality, 1918-1919 Pharmacology, Pathology, and Historic Evidence

The high case-fatality rate””especially among young adults””during the 1918-1919 influenza pandemic is incompletely understood. Although late deaths showed bacterial pneumonia, early deaths exhibited extremely “wet,” sometimes hemorrhagic lungs. The hypothesis presented herein is that aspirin contributed to the incidence and severity of viral pathology, bacterial infection, and death, because physicians of the day were unaware that the regimens (8.0-31.2 g per day) produce levels associated with hyperventilation and pulmonary edema in 33% and 3% of recipients, respectively. Recently, pulmonary edema was found at autopsy in 46% of 26 salicylate-intoxicated adults. Experimentally, salicylates increase lung fluid and protein levels and impair mucociliary clearance. In 1918, the US Surgeon General, the US Navy, and the Journal of the American Medical Association recommended use of aspirin just before the October death spike. If these recommendations were followed, and if pulmonary edema occurred in 3% of persons, a significant proportion of the deaths may be attributable to aspirin.

In February 1919…Edward’s fever kept getting higher and higher…aspirin…was given to him by the 1/2-handful over and over…Edward sweated through his mattress…Dr.…could not save his patient.

””Clella B. Gregory, Pandemic Influenza Storybook, US Department of Health and Human Services [1]

The unprecedented overall mortality and the mortality rate among young adults during the 1918-1919 influenza pandemic are incompletely understood. Deaths in the United States peaked with a sudden spike in October 1918. Later, Wade Hampton Frost [2] studied surveys of 8 US cities and found that, for every 1000 persons aged 25-29 years, ∼30% were infected with influenza virus, and 1% died of pneumonia or influenza. This 3% case-fatality rate has been called, “perhaps the most important unsolved mystery of the pandemic” [3, p 1022].

Mortality was driven by 2 overlapping clinical-pathologic syndromes: an early, severe acute respiratory distress (ARDS)-like condition, which was estimated to have caused 10%-15% of deaths (sequential autopsy series are lacking) [3)]; and a subsequent, aggressive bacterial pneumonia “superinfection,” which was pres-ent in the majority of deaths [45].

Factors that contributed to the severity of illness and death (eg, viral pathogenicity, bacterial colonization, immune response, smoking, preexisting conditions, and treatment) remain to be elucidated. Of most interest are those amenable to intervention, because fear of another 1918-like influenza pandemic drives pandemic planning today.

Recent studies suggest enhanced pathogenicity of certain influenza viruses as well as abnormal immune host responses. The 1918 influenza H1N1 virus, in contrast to a conventional human H1N1 influenza virus (A/Kawasaki/173/01), infected the lower respiratory tract, produced acute respiratory distress, and was associated with a dysregulated antiviral response in a cynomologous macaque model [6]. Also, the 1918 viral polymerase complex (PA, PB1, and PB2) promoted growth of the 1918 virus in the lower respiratory tract of ferrets [7]. Similarly, 2003 human H5N1 isolates, like 1997 human H5N1 isolates, induced overproduction of proinflammatory cytokines in human macrophages in vitro [8].

However, it is unlikely that the virus and immune responses alone were responsible for the 1918 deaths. As recently reviewed by Brundage and Shanks [4], most persons had self-limited disease with case-fatality rates of <2%, and mortality and case-fatality rates differed widely among populations. During the fall of 1918, death and influenza case-fatality rates ranged from 0.58% to 3.3% and 2.1% to 10%, respectively, in the 12 US Army camps with >10,000 cases of influenza or pneumonia each [910]. Frost [2] noted that the wide variation in mortality rates between cities, some of which were close together, was not explained by climate, population density, preventive measures, or other environmental characteristics. These observations suggest the importance of factors related to location rather than the virus itself. Likewise, the unusual mortality rate among young adults remains unexplained. Salicylate has been suggested [31112], and increased mortality rates have been found in ferrets exposed to influenza, aspirin, and an arginine-deficient diet, compared with each alone or in 2 combinations [13], yet mechanistic and epidemiologic evidence has not been fully explored.

The hypothesis presented herein is that salicylate therapy for influenza during the 1918-1919 pandemic resulted in toxicity and pulmonary edema, which contributed to the incidence and severity of early ARDS-like lungs, subsequent bacterial infection, and overall mortality. Pharmacokinetic data, which were unavailable in 1918, indicate that the aspirin regimens recommended for the “Spanish influenza” predispose to severe pulmonary toxicity.

A confluence of events created a “perfect storm” for widespread salicylate toxicity. The loss of Bayer’s patent on aspirin in February 1917 allowed many manufacturers into the lucrative aspirin market. Official recommendations for aspirin therapy at toxic doses were preceded by ignorance of the unusual nonlinear kinetics of salicylate (unknown until the 1960s), which predispose to accumulation and toxicity; tins and bottles that contained no warnings and few instructions; and fear of “Spanish” influenza, an illness that had been spreading like wildfire.

More recently, influenza deaths have been attributed to salicylate. From the 1950s to the 1980s, thousands of deaths among children following influenza and other infections (eg, Reye syndrome) were unexplained until studies identified aspirin as the major contributor [1416], and aspirin label warnings were followed by a disappearance of the condition [17]. Reye syndrome toxicity (vomiting, hyperventilation, delirium, and coma, with brain swelling and fat in the liver and proximal renal tubules) develops after ∼4 days of salicylate therapy [14] with reported mean daily doses of 25 mg/kg [18]. (Adults with salicylate toxicity present mainly with abnormal consciousness and respiratory distress [19].) Also, a recent avian influenza A-associated fatality involved Reye syndrome and aspirin use [20], and several autopsies of persons who had avian influenza revealed hemorrhagic lungs, fatty liver changes, and swollen kidneys [21] consistent with salicylate intoxication.

Four lines of evidence support the role of salicylate intoxication in 1918 influenza mortality: pharmacokinetics, mechanism of action, pathology, and the spate of official recommendations for toxic regimens of aspirin immediately before the October 1918 death spike. (Grains of aspirin used in older texts are converted to milligrams as follows: 1 grain equals 65 mg).

Aspirin Regimens (Dose and Schedule) Recommended in 1918 Are Now Known to Regularly Produce Toxicity

In 1977, a US Food and Drug Administration panel [22] recommended that the maximum safe daily dose of aspirin for the general population was 4000 mg, with a mean hourly rate of 167 mg/h, and that “dosing regimens exceeding either this total daily dosage or mean hourly rate provide a significantly greater risk without a compensating therapeutic benefit” (p 35360). As an example of the unusual nonlinear kinetics of salicylate, the panel noted that simulations show that, after increasing the dose from 2 to 4 g daily (given every 6 h), “the total amount of drug in the body at steady state will increase from 1.3 grams to 5.3 grams, a 400% increase.”

for the excellent COMPLETE article,   CLICK HERE

Stop your NSAIDs and anti-inflammatory agents and EAT THE SEED – the anti-inflammatory seed 


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