Also called the “Spanish” flu, it is (falsely) claimed to have killed up to 50-100 million people worldwide, including 675,000 Americans (claiming the lives of more soldiers than the trenches of WWI). Millions more got sick but survived. According to research uncovered by F. William Engdahl: The deaths “…were NOT due to ‘flu’ or a virus, but to pneumonia caused by massive bacterial infection.” While the medical men and medical hospitals were losing 33% of their flu cases, the non-medical hospitals such as BATTLE CREEK, KELLOGG and MACFADDEN’S HEALTH-RESTORIUM were getting almost 100% healings with their water cure, baths, enemas, etc. NIAID has said there is no evidence of a flu and that common respiratory bacteria was responsible. Starko’s work supports that and offers a scientific perspective on how aspirin was the likely cause of the two types of deaths seen during 1918, one slow and one incredibly rapid. A nationwide vaccination drive to profit off of the spoiled vaccines left over from WWI which mandated vaccines for everyone in the military.
When the United States entered WWI in April 1917, the fledgling pharmaceutical industry had something they had never had before: a large supply of human test subjects. During the war years of 1918 to 1919, the U.S. Army ballooned to 6 million men, of which 2 million were sent overseas. The Rockefeller Institute for Medical Research took advantage of this new pool of human guinea pigs to conduct vaccine experiments.
In January 1918, vaccines were administered to soldiers at Ft. Riley, Kansas. Shortly afterward, the vaccine was offered by the Division Surgeon to the camp at large. The vaccine used was made in the laboratory of The Rockefeller Institute. Between Jan. 21 and June 4 of 1918, Dr. Frederick L. Gates reported an experiment in which soldiers were given three doses of a bacterial meningitis vaccine. The vaccines were spitball dosages of a vaccine serum derived from horses.
The details are available in a report by Dr. Gates: “Antimeningitis Vaccination and Observation on Agglutinins in the Blood of Chronic Meningococcus Carriers.”
Gates wrote that men in the experiment showed flu-like symptoms, including cough, 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.
Then, shortly before breakfast on Monday, March 11, came the commencement of the first wave of the 1918 so-called influenza. By noon, camp surgeon Edward R. Schreiner had over 100 sick men on his hands, all apparently “suffering from the same malady.”
From Dr. Gates’ report:
Reactions … Several cases of looseness of the bowels or transient diarrhea were noted. This symptom had not been encountered 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, etc., at the time of injection.
Sometimes 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 pains” in the joints and muscles, which in 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.
According to Gates, they injected random dosages of an experimental bacterial meningitis vaccine into soldiers. Afterward, some of the soldiers had symptoms that were characterized as “simulated” meningitis, but Dr. Gates advances the fantastical claim that it wasn’t actual meningitis.
In 1918, “influenza” or flu was a catchall term for a disease of unknown origin. The misdirection term “Spanish Flu” has never been corrected. Whodathunk? It helped disguise the origin of the pandemic. If there were any real justice in this world, it would be called the “Rockefeller pandemic.”
By some strange coinkydink, even modern technology has not been able to pinpoint the killer influenza strain from this pandemic. The “Spanish flu” attacked healthy people in their prime. Bacterial pneumonia attacks people in their prime. Flu attacks the young, old and immuno-compromised.
In actuality bacterial pneumonia was the real killer — and thousands of autopsies confirm this fact.
Researchers looked at more than 9,000 autopsies, and “there were no negative (bacterial) lung culture results.”
So an experimental anti-meningoccic serum that was derived from horses was injected into soldiers who would be entering the cramped and unsanitary living conditions of war. What could possibly go wrong?
The Institute said it distributed the bacterial serum to England, France, Belgium, Italy and other countries during WWI. Ultimately, these Rockefeller Institute quacks killed millions of people via bacterial lung infections from 1918 to 1919.
An article from 2008 on the U.S. Centers for Disease Control’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. influenzae, and S. aureus.
Fourteen of the largest training camps had reported influenza outbreaks in March, April, or May, and recovered infected troops carried the virus with them aboard ships to France. As soldiers in the trenches became sick, the military evacuated them from the front lines and replaced them with healthy men. This process continuously brought the virus into contact with new hosts—young, healthy soldiers in which it could adapt, reproduce, and become extremely virulent without danger of burning out.
Also contributing to the high mortality of this pneumonia outbreak was the overuse of aspirin.
Salicylates are weak acids that cross cell membranes relatively easily; thus, they are more toxic when blood pH is low. Dehydration, hyperthermia and chronic ingestion increase salicylate toxicity because of greater distribution of salicylate to tissues. Excretion of salicylates increases when urine pH increases. Drugs that increase urinary HCO3 should be avoided because they worsen metabolic acidosis and decrease blood pH.
The most common salicylate is aspirin, but the group also includes bismuth subsalicylate (such as in Pepto-Bismol). Drugs that decrease respiratory drive should be avoided if possible, because they may impair hyperventilation and respiratory alkalosis, decreasing blood pH [source].
From the 1950s to the 1980s, thousands of deaths among children following influenza and other infections (e.g., Reye Syndrome) were unexplained until studies identified aspirin as the major contributor. Reye Syndrome toxicity (vomiting, hyperventilation, delirium and coma, with brain swelling and fat in the liver and proximal renal tubules) develops after approximately four days of salicylate therapy with reported mean daily doses of 25 mg/kg. Adults with salicylate toxicity present mainly with abnormal consciousness and respiratory distress.
Autopsy reports from 1918 are consistent with what we know today about the dangers of aspirin toxicity, as well as the expected viral causes of death. In 1918, physicians did not fully understand either the dosing or pharmacology of aspirin, yet they were willing to recommend it. Its use was promoted by the drug industry, endorsed by doctors wanting to “do something” and accepted by families and institutions desperate for hope.
An abstract from the aforementioned study states that 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. In 1918, the U.S. Surgeon General, the U.S. Navy, and the Journal of the American Medical Association recommended use of aspirin just before the October death spike. The hypothesis presented 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.
Not Just 1918
Citing articles from various medical journals in his landmark report from 2002, “Toxic and Deadly NSAIDs, an Investigative Report,” Roman Bystrianyk summarizes. AID- (anti-inflammatory drugs) :
“Over 100,000 people are hospitalized for GI bleeding and of those 16,500 die every year. And these values are considered ‘conservative.’
“Also the figures only include prescription NSAIDs used to treat only arthritis and only in the United States. If prescription and over the counter NSAID-related hospitalizations and death rates were counted for not only arthritis, but for all conditions, and throughout the world, the figures would no doubt be enormous. Taking those figures and applying them over the many years that this class of drug that has been available since the early 1970s and the numbers would be horrific. And yet, no study to date has attempted to quantify these figures.”
Bystrianyk then reposts a graph from The New England Journal of Medicine article by M. Wolfe, et al., “Gastrointestinal Toxicity of Nonsteroidal Anti-inflammatory Drugs” (June 17, 1999, Vol. 340, No. 24, pp. 1888-1889) that shows this alarming statistic relative to other causes of deaths:
“Another important observation is that most people have no warning signs that these drugs are causing them internal damage before ending up in the hospital with a serious medical condition. And as we have seen from the statistics, approximately 10% of these hospitalizations end in death. …
“Even aspirin, the first NSAID that was synthesized over 100 years ago by Felix Hoffman at Bayer industries is not free of risk. And considering that aspirin is being highly recommended to reduce the incidence of heart disease we must consider the gastrointestinal damage being caused as well.”
Bystrianyk then quotes J. Weil, et al., from their 2005 British Medical Journal article entitled “Prophylactic aspirin and risk of peptic ulcer bleeding”:
“We found that no particular dose of aspirin between 75 mg and 300 mg daily currently used in cardiovascular prophylaxis is free of risk of causing bleeding from gastric or duodenal ulcers. Even very low (75 mg) doses of aspirin reportedly caused gastric bleeding in volunteers. … Some 10,000 episodes of ulcer bleeding occur in people aged 60 and over each year in England and Wales. … It [sic] may be deduced that 900 of the 10,000 episodes could be associated with and ascribed to prophylactic aspirin use. A general change to low doses (75 mg) of aspirin would not eliminate the risk. …” [Emphasis added]
Winter Watch Takeaway: Also be especially on guard about Ibuprofen and sleep aids. I was using (too much) Ibuprofen for Achilles tendonitis and ran into an old college friend who is a leading pain specialist. Ibuprofin is hard on the liver as well. He recommended circummin instead. The dose shown here would be much lower in children and smaller individuals.