When I began researching the early epidemics of polio, the emerging disease of the 20th century, I quickly found out that the “flu-like” illness of polio was caused by toxic assault from poisons and x-rays. Demographics of the ‘differential diagnoses’ led me even further into correlations of pollution events with disease outbreaks, none more glaring and diffuse perhaps than the Spanish Flu. Understanding the Spanish Flu was a challenge to learn the “hidden” history of World War One.
John Barry’s book “The Great Influenza” states that the Spanish Flu was spread by war conditions and proceeds to make his case based on the movements of men and materiel. Toxic events never get a once-over from Barry but I already knew from patterns of sickness from industrial development that they would be there. Looking for the toxic ‘sensitizer’ for the Spanish Flu, I stumbled into a can of worms about nitrogen poisoning and added it to the perspective of “Spanish Flu on the Comeback” as an overlooked cause of influenza. A serious consequence of too much nitric oxide in your cells is a DOUBLING of the effects of radiation.
There’s alot of veterinary literature on nitrate toxicosis that looks exactly like the horrific version of 1918 flu and is/was a major hazard to livestock, especially cows and pigs. Bacteria in the rumen of these animals converts ‘nitrate’ (concentated in their feed) to nitrite, hence nitric oxide.
Dr. Stefan Lanka has this to say about nitric oxide (http://www.whale.to/a/lanka_h.html) which in very low concentrations controls blood pressure:
“It has to be detoxified by the body immediately because in higher concentrations it acts agressively destroying everything. That’s why the macrophages of the immune system release nitric oxide in high quantities in inflammation reactions; to destroy and digest the bacterial cells. So if you take up nitrites…it means you start the self-destroying process in your own body, especially in the lungs. You’re destroying your lung tissue, and fungal infections are growing on this dead organic matter….
The first cells to suffer oxygen deficiency are the lining of the epithelium, the smallest vessels, where nitrites are transformed into nitric oxide– this is the definition of KS, kaposi sarcoma, when the lining of the smallest vessels develops cancerous form, growing bigger and multiplying….”
The Merck Veterinary Manual
among other resources on the subject offers description of the disease process in animals, basically a conversion by bacteria of nitrates to nitrites which is ten times more toxic than nitrates and supplants oxygen uptake by the cells.
“When unconditioned cattle consume plants containing high levels of nitrates, the the nitrate to nitrite conversion exceeds the ability of the rumen microbes to convert nitrites to ammonia. Blood levels of nitrites increase and alter the hemoglobin in blood cells to produce methemoglobin. Unlike hemoglobin, methemoglobin cannot carry oxygen to the tissues of the body…..
Many species are susceptible to nitrate and nitrite poisoning, but cattle are affected most frequently…young pigs also have gastro-intestinal microflora capable of reducing nitrate to nitrite….
…in acute intoxication [from methemoglobin]…incapable of oxygen transport and resulting anoxia…secondary effects of vasodilation on vascular smooth muscle may occur. [blood ‘pools’ when veins are unable to contract and turns the tissue dark as in cyanosis]. The nitrite ion may also alter metabolic protein enzymes. Ingested nitrates may directly irritate the GI mucosa and produce abdominal pain and diarrhea.
[nitrate toxicosis] although usually acute, the effects…may be subacute or chronic and are reported to include retarded growth, lowered milk production, vitamin A deficiency, goitrogenic effects and increased susceptibility to infection.”
Signs of nitrate/nitrite poisoning:
–usually appear suddenly due to tissue hypoxia and low blood pressure due to vasodilation.
–muscle tremors, weakness and ataxia; early signs when methemoglobin is 30-40%
–brown, cyanotic mucous membranes develop rapidly as methemoglobin exceeds 50%
–dyspnea [irreg. breathing], tachypnea, anxiety, and frequent urination are common
–in some monogastrics, due to non-plant exposures; salivation, vomiting, diarrhea, abdominal pain and gastric hemorrhage
–anoxic convulsions within one hour after a clinical course of 12-24 hours….with a ‘recovery’ [that may] occur but then develop into interstitial pulmonary emphysema with continued respiratory distress; sudden collapse and death can occur
–sudden death without appearance of illness
“Differential diagnoses include poisonings by cyanide, urea, pesticides, toxic gases, chlorides, aniline dyes, aminophenols or pharmaceuticals (i.e. sulfanomides, phenacetin, and acetaminophen) as well as infectious or non-infectious diseases (i.e. grain overload, hypocalcemia, hypomagnesemia, pulmonary adenomatosis, or emphysema)”
An explanation of the nitrogen disease process in humans is best explained by ‘catabolism’, the opposing complement of anabolism and is much of what Dr. Lanka is addressing in his refutation of HIV virus as the cause of AIDS. Catabolism, the breakdown of cell tissue, is essential to release the energy needed for anabolism and is provided for naturally by the minute synthesis of nitric oxide in the body. This is the finely balanced cellular metabolism, subject to disruption by nitrites, compound salts of nitrous acid that recombine under certain conditions.
In my general research and articles, I’ve taken interest in highlighting the scope of nitrogen-based products which exploded into use after the Haber-Bosch process (1910) made atmospheric nitrogen extraction a reality. Though requiring immense inputs of industrial power to do so, Haber-Bosch made nitrogen excessively available and cheap after 1913 by I.G. Farben.
I’m working on a personal theory that nitrate toxicosis is the orginal source of the swine influenza virus as we know it and that the bacterial ‘phage’ work of the 1920s and 30s perfected the “recombinant influenza” viruses we see “evolving” today. The reason that nitrogen poisoning went undiscovered in the 1918 flu, as the Merck vet manual points out, is that nitrate can be ‘lost’ in plasma or postmortem serum and “must be measured promptly”. In live patients methemoglobin can convert back to hemoglobin within 2 hours. This would have eluded most doctors in 1918.
Another question I posed in an article about ‘polio as the flu’ addresses the 1915 and 1916 polio epidemics that erupted and led to the largest quarantines known in US history (to my knowledge). The 1916 epidemic in New York City and the response by health officials is still the only one of its kind.
There’s reason to think that nitrate toxicosis also played a large role in this event. In the profile of this epidemic, it struck hardest at the very young, but included teenagers. NYC would not allow anyone sixteen or under to leave the city. On the record this illness is recorded predominantly as ‘atypical pneumonia’, but the polio component of paralysis is a manifestation of acute toxicity affecting the central nervous system.
At the time, the US was stockpiling munitions for the Allies on the Jersey shore side of the Hudson across from Manhattan until the night of July 30-31 when the cache at Black Tom Island was blown sky-high and incinerated to dust. What had previously been a few dozen cases of ‘polio’ accelerated within 2 weeks to thousands of cases. Child victims of this so-called polio epidemic had their remains turned into ‘filtrate’ by Simon Flexner of the Rockefeller Institute who created a new disease with it –experimental polio. Flexner had an inner conviction that polio was a respiratory tract infection because the victims came down with ‘flu’.
Decades went by before poliovirus was determined to be a disease agent in the 30s (though ‘virus’ was distinctively absent in polio epidemics), and it was designated an intestinal microbe. Poliovirus, they said, enters the bloodstream in the same way that bacteria do, written and published by Simon Flexner, empirical director of the RIMR, in 1896 as microbes [bacteria] that “wander through the intestinal walls with great regularity” from “imperceptible lesions”. This is evidence that an intestinal ‘agent’ in humans manifests as the flu, and it was already known that gut bacteria “cause” pneumonia.
How does this fit the profile of Spanish Flu that broke out 2 years later?
according to this quote from www.medicalecology.org/diseases/influenza/influenza.htm
“Spanish Flu killed more rapidly than any other form of influenza known up to that time. This particular strain of influenza was especially dangerous to young adults….morbidity changed dramatically and was now highest for the very young, and higher yet for persons between the ages of twenty and forty. The elderly appeared to be spared for the most part”. This statement is a KEY feature of polio! The 1916 polio epidemic affected 3 to 6 year olds in greater proportion, but that was rapidly changing to include older and older persons. Originally, “infantile paralysis” in the 1800s was prevalent among even younger children, infants and toddlers. By 1916, young adults were contracting the disease and by the 1950s the 20-40 year-olds were 80% of polio victims. FDR, who had the Spanish Flu as Assistant Sec of the Navy in 1918, got polio 3 years later at the age of 39. The sentence, “and higher yet for persons between the ages of twenty and forty” is deceptively worded and placed, clearly the meaning is that this group saw the largest increase in flu compared to itself as not normally susceptible to flu. A normal flu does, and did, kill the elderly, but the elderly are not a representative group of victims in polio outbreaks.
Spanish Flu appears to be multiple ailments: bacterial pneumonias, nitrate toxicosis, polio and many more. Viral agents were never found! Bacteriophage (virus that infect bacteria) genetics at the Cold Spring Harbor Laboratory encouraged interest in the field in the 1930s. Max Delbrück and Salvador Luria, two “displaced scholars” who were sponsored to leave Europe before WWII, promoted the “Phage Group” in working on the developments of molecular biology which led to experimentation on influenza viruses inserted into common bacteria.