Spanish Flu, Part 2: Causes

Since the germ theory was meant to explain contagion, and since the Spanish Flu clearly wasn’t contagious, the rational thing to do would be to abandon the germ theory as an explanation for influenza and to look at the question from the perspective of terrain theory: What were young and middle-aged adults being exposed to that other people weren’t? A terrain perspective teaches us that we should probably be looking for either a deficiency or an intoxication that could be capable of explaining the events of 1918.

Recall that the symptoms of Spanish Flu included kidney swelling and fatty liver. Those are typical of poisonings, but weren’t known to result from attacks by microbes¹. It makes more sense to look for something that the victims were given rather than to look for something that the victims were deprived of. If we’re looking for an explanation of the Spanish Flu in terms of terrain theory, then we should therefore be looking for an intoxication that can result in these specific symptoms. What was poisoning these organs and others?

Another hint lies in the ages of those who were most affected. Respiratory diseases are generally thought to be most dangerous for very small children and for the elderly, but this disease had a habit of attacking people in the prime of their life. As Dawn Lester and David Parker said, the disease mainly affected adults between the ages of 20 and 40. Moreover, Rosenau said that his volunteers who were mostly between 18 and 30 were from “the most susceptible age.”

As the modern terrain theorist Daniel Roytas has pointed out, the Spanish Flu took place during World War I, and, perhaps not coincidentally, there was quite a lot of chemical warfare employed in killing soldiers. In particular, there were the various different kinds of battle gas, most notably a gas known as phosgene. Roytas relates that,

During the Great War, over 150,000 tonnes of chemical warfare agents were produced worldwide, with approximately 125,000 tonnes being deployed on the battlefields. These gasses could persist in the environment for weeks, possibly months, after being deployed because they were heavier than the air and not readily soluble in water. These gasses were so poisonous, doctors were forced to evacuate entire wards if a man was brought in still wearing contaminated clothing. The gas residue on the affected individuals’ clothing readily dispersed into the air and would irritate the eyes of medical workers, making it impossible to see.

Roytas went on to explain how the gases would usually kill quickly, but in those cases where a person didn’t get a dose large enough to cause a swift death, a person would have some pretty interesting symptoms:

Symptoms of severe gas poisoning were initially mild, presenting as a flu-like illness, before progressing rapidly over several hours to bronchitis, pneumonia, and pulmonary oedema (an acute-respiratory-distress-like syndrome). Eventually, those severely poisoned with gas would die. Dyspnoea and cyanosis were hallmarks of gas poisoning. Men clutched their chests as they gasped for air. They coughed up blood and frothy yellow sputum as their bodies turned a deep blue-purple colour—a serious condition known as ‘heliotrope cyanosis’. The cyanosis was so pronounced, that many medical practitioners feared the black death had returned. Depsite the wide range of serious side effects, the lethal effects of poison gas were primarily due to respiratory failure and right-sided heart failure.

It’s remarkable how much the symptoms of battle gas poisoning align with the symptoms of the Spanish Flu. This would also explain why the disease attacked military men so hard—they were the primary victims of battle gas. It would also explain why the disease simply wasn’t contagious. Roytas therefore contends that the primary cause of the Spanish Flu was phosgene battle gas—no germ needed.

Dawn Lester and David Parker actually supplied an alternative to the battle gas hypothesis, and it too aligns the Spanish Flu with terrain theory. But in order for the reader to see more clearly, we’ll need to give some historical background.

Bayer was originally a dye manufacturer in Germany in the mid-1800s, but with the rise of allopathic drug-based medicine, many dye manufacturers began manufacturing drugs for physicians to prescribe. Bayer entered the market for pharmaceuticals in 1881. One of Bayer’s products was diacetylmorphine, more commonly known as heroin, which was supposed to be a non-addictive substitute for morphine. The word “heroin” was actually originally Bayer’s brand name for the substance. But in the early 1900s, at the same time that Bayer was selling heroin to unsuspecting victims, there was another chemical that Bayer was producing for prescription: acetylsalicylic acid.

Acetylsalicylic acid is a modified form of a chemical that’s alleged to be naturally found in willow bark, a chemical which had previously been used in some traditional remedies. Just like diacetylmorphine being referred to by the brand name “heroin,” acetylsalicylic acid has become more commonly referred to by Bayer’s brand name for the substance: aspirin. Because of World War I though, Bayer lost its assets and trademarks in the US. After February of 1917, Bayer no longer held the patent on aspirin in the United States. As Karen Starko put it,

After Bayer executives were charged with violating the Trading with the Enemies Act in August 1918, advertisements encouraged confidence in aspirin.

Those advertisements would have been coming from Sterling Drug. After the US government was in possession of the patent for aspirin, it sold the patent to Sterling Drug for $5.3 million².

Now since the allopaths were in control of medical education via the Flexner report, and since Sterling Drug was in possession of government-granted monopoly privileges via “intellectual property” over aspirin, it’s not hard to see what Sterling Drug would want to do: Produce large quantities of aspirin and encourage physicians to prescribe it in large doses³. The unfortunate result was that people were being prescribed potentially lethal doses of aspirin.

For reference, it’s now understood that a person shouldn’t take more than 4 grams of aspirin in a single day, and that if a person is taking aspirin on consecutive days, then toxicity can result from doses as little as 2 or 3 grams per day. Contrast this with the doses of aspirin that were widely being prescribed in 1918: Anywhere from 8 to 31 grams per day. Moreover, it was common to prescribe aspirin for: influenza.

Therefore, at least with the benefit of hindsight, it should only be expected that many people were dying of aspirin overdoses in 1918. It’s probably therefore the case that many cases of Spanish Flu were the result of people trusting their physicians. Moreover it’s probably not a coincidence that that physician from Camp Devens reported, “These men start with what appears to be an attack of la grippe or influenza, and when brought to the hospital they very rapidly develop the most viscous type of pneumonia that has ever been seen.” The problem was that going to the hospital was the way to get a lethal dose of aspirin.

But Starko continued connecting the dots:

Official recommendations for aspirin were issued on 13 September 1918 by the US Surgeon General, who stated aspirin had been used in foreign countries “apparently with much success in the relief of symptoms,” on 26 September 1918 by the US Navy, and on 5 October 1918 by The Journal of the American Medical Association. Recommendations often suggested dose regimens that predispose to toxicity as noted above. At the US Army camp with the highest mortality rate, doctors followed Osler’s treatment recommendations, which included aspirin, ordering 100,000 tablets⁴. Aspirin sales more than doubled between 1918 and 1920.

The number of deaths in the United States increased steeply, peaking first in the Navy in late September, then in the Army in early October, and finally in the general population in late October. Homeopaths, who thought aspirin was a poison, claimed few deaths. Others may have suspected that aspirin was responsible. On 23 November, 1918, Horder wrote in The Lancet that, for “intensely toxic cases…aspirin and all so-called febrifuge drugs must be rigidly excluded from the treatment.”

The final piece of evidence that ties everything together is the symptomology of an aspirin overdose, which was also uncovered by Karen Starko. At excessively high doses of aspirin, the drug can cause pulmonary edema, coughing up blood, brain swelling, abnormal states of consciousness, “cloudy” kidney swelling, fatty liver, and cyanosis. These happen to be the exact symptoms of the Spanish Flu.

Further, Starko gave a hypothesis as to why the disease typically avoided children and the elderly but hit working-age people so hard, and it has to do with generational attitudes: The elderly who had been having the occasional flu their whole lives would have been more skeptical about the necessity of using some new drug to cope with the disease. Parents might have been cautious about giving brand new drugs to their children, while young adults may have been willing to use new drugs if they were recommended by a physician. Working-age people, and particularly young adults, would have therefore been the most likely to use the drug.

We know that physicians were handing out lethal doses of aspirin, and we know that the symptoms of Spanish Flu exactly matched the symptoms of aspirin poisoning. Once Starko has brilliantly juxtaposed these insights for us, it doesn’t take a genius to draw a line from aspirin to the Spanish Flu, and it obviously doesn’t take a germ to explain what happened. Then the fact that the disease wasn’t contagious ceases to be an unexplainable anomaly, and instead just makes sense: Overdoses aren’t contagious. These points are the nail in the coffin for the germ theory of Spanish Flu. So it appears that the germ has been shoehorned in because of assumptions about the nature of disease rather than actual evidence. This was a noncontagious disease because it was a mass poisoning event, not a germ pandemic.

Many of these pieces of evidence were taken from Karen Starko’s 2009 paper titled Salicylates and Pandemic Influenza Mortality, 1918-1919 Pharmacology, Pathology and Historic Evidence, which almost tells the story of the Spanish Flu in full. She said,

Therefore, it is likely that severe salicylate intoxication, including pulmonary edema, developed in some persons who followed the recommended 1918 dosing regimens.

But the one piece of evidence that she appears to be missing is that the Spanish Flu was simply not a contagious disease, as Rosenau and others demonstrated. Because she appears not to be aware that the Spanish Flu wasn’t at all contagious, she tried to explain the disease in terms of aspirin toxicity and some kind of infection (i.e. a terrain-germ hybrid theory, even if she didn’t use that terminology), but there’s simply no evidence that infection was causing disease to any degree at all. There is no evidence that the Spanish Flu was connected to any germ, and the simpler explanation is certainly that it was a mass poisoning event without any germ involved.

As far as I’m aware, Dawn Lester and David Parker appear to have been the first to revive the knowledge that the homeopaths had a century ago by combining the insights from the Rosenau experiments with the insights from Karen Starko’s historical investigations. The Spanish Flu is thus explained in their book What Really Makes You Ill as aspirin poisoning. In the book Can You Catch A Cold? by Daniel Roytas, his chapter dedicated to the Spanish Flu also mentions the aspirin theory in passing, although he prefers the battle gas theory. The reader would be wise to pick up both books, but, whether we say that it was aspirin or battle gas, the Spanish Flu was definitely a mass poisoning event.

Before summarizing some of the lessons from the Spanish Flu, we ought to recognize and address the position that the Spanish Flu was caused by a bacterial infection. This is important because it appears that there are even some voices that are generally skeptical of medical orthodoxy who nevertheless take it for granted that the Spanish Flu was caused by a bacterial infection, even though this is at odds with the evidence presented so far.

There is research claiming that bacterial pneumonia was the cause of death during the Spanish Flu pandemic. One 2008 paper titled Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness claimed that the majority of deaths likely resulted from “secondary bacterial pneumonia caused by common upper respiratory-tract bacteria.” But how is it that the researchers came to this conclusion? As always, we need to check to see if the methodology used by the researchers is sufficient to justify their claims.

What the researchers did was examine lung tissue obtained during autopsy from 58 influenza fatalities from the Spanish Flu pandemic. These samples had been stored at the National Tissue Repository of the Armed Forces Institute of Pathology. They also examined more than 1,500 bacteriological records contemporary to the flu pandemic. Altogether, records for over 8,000 people from 15 different countries were examined. The results: “for all age groups death was predominantly associated with pneumonia and related pulmonary complications.”

So what they really found was an association in some historical data, and from that they jumped to causal conclusions. But we already know that epidemiological data can’t be used to draw positive causal conclusions, so this kind of methodology is simply incapable of what the authors attempted to use it for. Sure, most people might have had bacteria in their lungs, but where is the evidence that the bacteria caused the disease rather than the other way around? No attempt was made to demonstrate Koch’s postulates for any bacterium alleged to cause the symptoms of Spanish Flu, so the researchers couldn’t have possibly shown that bacteria were the cause of anything. Moreover, because we know that the disease wasn’t contagious, we can therefore conclude that the disease couldn’t have been caused by a bacterial invasion. If it really were the case that germs had been the cause of death in a majority of cases, then Rosenau should have been able to see contagion in his experiments, but he didn’t. Note also that there’s nothing contradictory about their epidemiological data and the identification of aspirin as the cause of disease.

Rather than attempting to fulfill Koch’s postulates with a suspect microbe, proving that it causes symptoms of Spanish Flu, they resort to distractions like epidemiology. The reader might also be interested to know that one of the authors of this 2008 paper was none other than Anthony Fauci. Apparently a person can make extremely basic mistakes with respect to establishing causality and nevertheless become the director of the National Institute of Allergy and Infectious Diseases.

Another lesson that we need to keep in mind moving forward is that even medical researchers can apparently confuse pulmonary edema and bacterial pneumonia. This makes sense though, because there isn’t really a hard line where one becomes the other. Both involve the lung filling with fluid. It just depends on the amount of bacteria present whether the condition will be diagnosed as pulmonary edema or as bacterial pneumonia. All lungs contain bacteria, so even in the case of a patient with pulmonary edema, there will be bacteria. At some point though, there are enough bacteria that the condition suddenly becomes known as “bacterial pneumonia.” These really shouldn’t be thought of as distinct conditions, but rather as different degrees or even stages of the same condition. This lesson means that it’s plausible for a drug to induce pulmonary edema in a patient, who ends up dying because of the drug, with his death then being misattributed to a bacterial pneumonia instead of to a drug overdose. In other words: A person can be murdered with a drug, with the death then being blamed on a microbe as cover. This will be important later on.

Barring the battle gas hypothesis, the only explanation for the Spanish Flu that’s consistent with the epidemiological record of bacterial pneumonia and with what we know about the toxicity of aspirin is thus: People who were sick for other reasons checked into hospitals, whereupon they were given lethal doses of aspirin, which resulted in pulmonary edema. In the distant future, researchers looked back on this pulmonary edema and called it bacterial pneumonia—a loaded term to the extent that people take it to mean that the bacteria are the cause rather than an effect—and then attempted to infer causality from that epidemiological data, with the result that many people now mistakenly believe that the 1918 Flu pandemic was caused by bacterial pneumonia rather than drug toxicity. This has led many people to believe that the Spanish Flu pandemic would have gone differently had antibiotics been in use at the time. They imagine that things would have gone differently if only there were antibiotics, but there’s no way of accessing this counterfactual. And, since there’s no evidence that antibiotics alleviate aspirin toxicity (or battle gas toxicity), it’s very dubious that antibiotics could have been of any help at all against the Spanish Flu. The bacteria weren’t the cause of disease, but were rather a downstream consequence of drug-induced lung damage. Something else damaged the victim’s lungs, causing them to fill with fluid, and it was in this water-logged, decaying lung tissue that bacteria found a place they could easily proliferate. Cyanosis probably had to do with circulatory issues downstream from the lung damage. The same poison that damaged the lungs also caused brain swelling, kidney swelling, and fatty liver. For millions of victims, aspirin was the source, not the cure, of their Spanish Flu.

Very importantly, the Spanish Flu can be added to the growing list of diseases that were previously thought to be contagious, such as scurvy, but which are actually better explained by terrain theory. The Spanish Flu serves as a solemn reminder that we must always be careful not to just assume contagion where it has not yet been very firmly established to happen. It only makes sense to put faith in contagion after a disease has been unambiguously shown to pass from one person to another.

And it shouldn’t be surprising that the Spanish Flu was a physician-induced disease when we remember that, in those days, mercury and heroin were still being prescribed. But surely it couldn’t have been long after the Spanish Flu that medical men began to actually perform rigorous science in order to establish causation, right? Surely it was by rigorous science that medical heroes identified a polio germ and then developed a vaccine in the 1950s, and that’s why none of us are suffering from polio today, right?