Physicians and researchers have debated the cause of tuberculosis (TB) for centuries, early observers linking TB with injury, malnutrition or toxins. In Book 1, Of the Epidemics (410–400 BCE), Hippocrates describes the cause of TB as a “weakness of the lung,”1 a view shared in the 1930s by the dentist Weston A. Price.
Price observed that peoples living on their native diets exhibited no cases of TB, in spite of constant exposure to smoke from wood or peat in their dwellings, but that the disease was rampant in those born to parents who consumed the “displacing foods of modern commerce” and had narrow faces with crowded and crooked teeth. He believed that a poor diet in utero and during the period of growth resulted not only in weak facial development, but also a weakness in the lungs, making the offspring especially vulnerable to lung tissue breakdown, a hallmark of the disease.2
Both Hippocrates and Weston Price recognized the role of diet in the treatment of TB. In the era of Hippocrates, treatment took place in temples, where patients received plentiful and good food—especially milk, and particularly asses’ milk—along with fresh air and sea breezes. The Greek physician Galen (129–216 CE) and other physicians of his time recommended fresh air, milk—particularly human breast milk—eating wolf livers and drinking elephant urine. Pedanius Dioscorides, a Greek army surgeon in the service of Nero (54–68 CE), recommended “warming drugs” such as animal fats; and Tertullian (160–225 CE) recommended butter boiled with honey.1
Others fingered toxins as the culprit. In the early 1800s, Thomas Willis speculated that TB was caused by consumption of sugar, resulting in an acidity of the blood.3
Florence Nightingale blamed TB—a huge problem in soldiers during the Crimean War of 1853–1856—as “the monstrous product of breathing foul air.”4
TB became epidemic during the Industrial Revolution of the eighteenth and nineteenth centuries, with observers linking the disease to social conditions of the time—poverty, malnutrition and overcrowding—in the working classes. In 1838 and 1839 in England, between a quarter and a third of those who died of TB were tradesmen and laborers compared to a sixth who were “gentlemen.”5
Enter…The Contagion Theory
The first to propose contagion as the cause of TB was Girolamo Fracastoro, an Italian physician and poet who, in his 1546 work De Contagione, proposed that “phthisis” (the word used for TB in the 16th century), was transmitted by an invisible virus, which he believed was contagious through direct contact with the discharged fluids of the infected.
By the eighteenth century, many Italian physicians had come to share the view that phthisis was infectious, and they avoided doing autopsies on patients who had died from phthisis to protect themselves and their students. But British and American physicians of the time disagreed, with many believing that the disease was hereditary or, like Weston Price, ascribed the illness to constitutional weakness.5
Conventional medicine gives credit to German physician Robert Koch for revealing that “TB is caused by an infectious agent,” with Koch presenting a famous report to the Physiological Society of Berlin on March 24, 1882.6 In his paper, Koch cited the work of researchers who induced tuberculosis in animals by injecting them with tuberculous matter from animals or people that had died of the disease, and especially the experiments of French military surgeon Jean-Antoine Villemin. In 1869, Villemin had seemed to demonstrate that the disease was contagious by injecting tuberculous matter from human cadavers into laboratory rabbits, which then became infected. Villemin observed that soldiers stationed for long periods of time in barracks were more likely to have phthisis than soldiers in the field, and that healthy army recruits from the country often became consumptive within a year or two of taking up their posts.
In his 1882 report, Koch proceeded to describe how he had identified the tuberculosis bacillus by staining tuberculous matter with a blue dye, growing the organism on a preparation of ox blood, and then—using disinfectants at the site of the inoculation—injecting animals with the culture. With few exceptions, the animals developed granulomas containing the bacilli at the site of the injection and in nearby organs, and eventually died.
Also key to Koch’s arguments were the experiments of Austrian scientist Franz Tappeiner, who, Koch reported, “ha[d] been successful with inhalation.” In an 1877 paper, Tappeiner noted “the repeated observation that very healthy girls from a healthy family became phthisic themselves after prolonged care of a phthisic patient and died quickly.” This strengthened Tappeiner’s suspicion that TB was a contagious disease “caused by inhalation of phthisic sputum, which was atomized by coughing in the air,” even though experimental methods available at the time (inoculation, feeding and forced tracheal introduction) had failed to provide conclusive results.
In his presentation, Koch then proceeded to describe experiments in which he inoculated material from scrofulous glands or fungal masses from joints in which no tubercle bacilli could be found. “In these cases, not a single animal became sick, while. . . the animals inoculated with bacilli-containing material. . . always showed an extensive infection with tuberculosis after four weeks.”
He concluded: “All of these facts taken together lead to the conclusion that the bacilli which are present in the tuberculous substances not only accompany the tuberculosis process, but are the cause of it. In the bacillus we have, therefore, the actual tubercle virus [poison].”
Koch’s report was published as a letter in the Times (April 22, 1882), and subsequently in the New York Times, the New York Tribune and other newspapers from around the world, launching the germ theory into public consciousness. Koch won the Nobel Prize in 1905.
A Different Way of Thinking
The case for the infectious nature of TB seems irrefutable. . . yet many are still skeptical, still asking questions. For example, how could “inhalation of phthisic sputum, which was atomized by coughing in the air” cause TB when forced tracheal introduction of tuberculous material had failed to provide conclusive results? If TB is spread by coughing, how is it that any TB caretakers survive? How did Florence Nightingale or any of her nurses survive the Crimean War? If exposure to coughing patients is so deadly, any assignment of medical personnel to a TB ward would be a death sentence.
The skeptic who introduced me to a different way of thinking about TB was the late Mark Purdey, known for his disagreement with government pronouncements about the cause of mad cow disease.7 When some of his dairy cows tested positive for TB, he began to ask questions. Why were so many cows on farms in the area suddenly coming up positive? He noted that for several years, tight finances had prevented farmers from applying lime to their fields, resulting in more acidic soils. He observed, “The relevant issue in respect of TB infection and soil acidity hinges on the fact that acidification of the topsoil leads to an excessive accumulation of available iron—particularly in the regions where soil iron is naturally elevated and rainfall is high.”8
Today, we know a lot more about mycobacteria—the species associated with TB—than nineteenth-century researchers did. Like so many bacteria considered “pathogens,” mycobacteria are iron-loving organisms, which proliferate in environments of excess iron.9 Thus, Koch was able to cultivate the bacillus on iron-rich ox blood, and sometimes on iron-rich meat, but not on other substances. We also know that the TB bacillus is ubiquitous, always there in the soil and most likely in small amounts in animals and humans. Up to nine out of ten people who test positive for the TB bacillus exhibit no signs of the disease—a condition called “latent TB.”
Let us now consider iron oxide—a poison given off by iron that has been heated. Since the beginning of metallurgy, humans have suffered from exposure to iron oxide—men working with iron, of course, but also those exposed to heated iron cookware in enclosed spaces. This can explain the occasional evidence of TB in the remains of preindustrial peoples.
With the Industrial Revolution, however, that exposure increased. Exposure occurred in iron mines, in foundries that worked iron for all the new machinery, in ships with their iron boilers, in railways via the steam from cast iron boilers, in areas of dense pollution where the preferred fuel was certain types of iron-rich coal—iron is the most predominant metal in coal fly ash10—and especially in war. Iron cannons, iron gun barrels, iron hand grenades and iron cookware for feeding the troops all produced iron oxide; in trench warfare, the heavy pollutant would fall into the trenches and linger. Solders living in these trenches suffered massively from TB.
In 1790, a new invention not only increased exposure to iron oxide but also brought it into the drawing room: the cast iron stove.
With its large surface area, the cast iron stove released large amounts of iron oxide, to which not only the cooks and maids in unventilated basements were exposed, but also madame and monsieur enjoying the comfort of a warm room upstairs, as the moist heat rose through iron piping. Or, households may have had a cast iron parlor stove dedicated to heating the living areas. We had just such an arrangement in our farmhouse—a cast iron stove in the entry way with rusty iron piping to take the heat upstairs. Fortunately for the previous owners, the stove remained largely unused after the installation of radiators; though also made of cast iron, radiators are not operated at such hot temperatures as cast iron stoves and are often painted, a practice that would reduce the off-gassing of iron fumes.
During the Industrial Revolution, crowding and poverty in the cities would have greatly increased exposure to iron oxide—whether from pollution, from a cooking pot over a coal fire in crowded quarters or from a cast iron stove in an unventilated room. If a TB patient lay in bed near a cast iron stove for warmth, both the caretaker and the patient would have breathed in iron oxide day and night.
Treatment for TB usually involved traveling to the countryside in the summer for fresh air and sunlight—eliminating exposure to iron oxide for a few months. Most protocols also involved consuming raw milk—the lactoferrin in raw milk helps sequester iron and reduces the TB symptoms.11 In addition, the therapy often involved consumption of vitamin A-rich liver or butter—vitamin A is critical to healthy lung function and protection against heavy metals. The patients undergoing these protocols usually improved, but then regressed with renewed exposure to iron oxide when they returned to the cities in the fall.
Such was the plight of poor Violetta, the heroine of Verdi’s opera La Traviata. She develops TB while living a dissolute life in Paris, then recovers during her happy time with Alfredo while living in the countryside and then succumbs again after returning brokenhearted to the ornate parlor stoves of Paris. The stress of grief can rapidly use up protective vitamin A stores.
Iron poisoning is called siderosis, and its symptoms are the same as those of TB—cough and trouble breathing, of course, and sometimes coughing up blood. The characteristic miliary (millet-seed-like) lesions of TB are not exclusive to the disease, but occur in other diseases as well—including siderosis.12 Siderosis can affect other organs besides the lungs—as does TB. One striking similarity is the darkening of the eyes, which occasionally occurs in both siderosis and TB.
Let’s return to Koch’s experiment. He induced lesions and found the TB bacillus in them by injecting the animals with a culture of TB bacillus grown on iron-rich blood. While he could claim that he had “isolated” the organism—in other words, there were no other types of bacteria in the culture—his culture was not “pure,” meaning devoid of other substances. The culture would have been contaminated with iron, of course, and possibly contained toxins produced in the preparation of the ox-serum culture (which was heated several times, a process that can denature the many delicate substances in blood). And finally, the site of the injection was treated with an antiseptic, probably carbolic acid. In other words, there were certainly harmful substances, especially iron, in the injection, and granulomas—interpreted as TB—were the logical result.
When Koch injected animals with material from scrofulous glands or fungal masses, no lesions appeared—but these were not cultured on iron-rich blood that had been heated several times.
The key test is whether TB can be produced in the lungs by exposure to the TB bacillus in the air. For this, Koch relied on the earlier experiment of Tappeiner, so it pays to look at it more closely.13 To prove contagion, Tappeiner purchased three dogs and kept them in a dog stall near a window and a door, “which was closed on all sides and connected to the air only at the front through a lattice-like open door at the top.” Next, Tappeiner obtained sputa from a “phthisical afflicted locksmith.” He ground a tablespoon of this in a porcelain mortar with distilled water and put it in a “steam atomizer from Stiefenhofer.” He placed the atomizer in front of the kennel and allowed the nebulized liquid into the air of the kennel twice a day, for sixty to ninety minutes. The upper lattice opening was hung with oil cloth “to better concentrate the dust.”
At the same time, Tappeiner mixed ground-up sputum into the feed of two other dogs “to try whether absorption from the intestinal tract could also produce tuberculosis.” Tappeiner observed that all five experimental dogs appeared to be quite healthy; they exhibited neither coughing nor diarrhea, ate with the best of appetites and were lively and alert, without any sign of illness save for slight emaciation or lack of growth.
Autopsies on the test animals performed after either three weeks (on one inhalation dog) or six weeks (on the other four dogs) revealed small lesions (called miliary tuberculosis because the lesions resembled millet seeds) in the lungs, kidneys, liver and spleen, and—in the feed dogs—also in the intestinal tract. So, while forced tracheal introduction of tuberculous matter failed to demonstrate contagion, a tiny amount of aerosolized sputum on a jet of steam did the trick.
I have been unable to locate a picture of a “steam atomizer from Stiefenhofer” but all the atomizing devices of the era were made with iron and brass.
Heated brass can also give off iron fumes, as well as arsenic fumes, a double whammy.14 So, did a tiny amount of bacillus from the lungs of TB patients induce lesions in the animals, or was it iron (and possibly arsenic) fumes in the steam?
The key question, not answered in Tappeiner’s report, concerns the two feed dogs—were they in a different stall but in the same room as the three inhalation dogs? If so, they would also have been subject to the steam and thus would not represent a real control.
Looking in All the Wrong Places
Germ theory dictates the current treatment for TB—antibiotics and vaccinations—which health officials claim has successfully reduced the death rate from this terrible disease.
But note that mortality from TB was already falling, long before these interventions (see Figure 1). As stainless steel and aluminum gradually replaced cast iron in stoves, furnaces and industrial equipment, household exposure to iron oxide gradually declined.
That does not mean we have solved the problem of TB, which is still the world’s number one killer, with over three thousand deaths per day attributed to the disease (see Figure 2).
These TB deaths occur mainly in the developing world, where cast iron stoves and cookware (pots and griddles) are still widely used, often in unventilated hovels. Iron mining and iron works are also common, typically with little concern for safety; coal is still used in power plants and domestic settings in these areas.
Even in the U.S., TB remains a problem (see Figure 3).
Maybe we have failed to solve the mystery of TB because we are looking in the wrong place. Could it be that the bacillus associated with the disease is not the cause but actually the therapy? Could it be that excess iron in the tissues calls on these ubiquitous critters to serve as a clean-up crew? Could it be that Florence Nightingale—a mere nurse!—was the one who got it right in fingering poisonous gases, and that the effects of this poison are exacerbated by poor nutrition and prenatal injury?
Likewise, we will not solve the Covid problem if we are looking in the wrong place, and if we blame continuing outbreaks—even in the vaccinated—on new virus variants until we run out of Greek letters. My colleague Tom Cowan and I are not alone in proposing microwave radiation poisoning from Wi-Fi and 5G as a major cause of this mysterious illness. The epidemiology fits; the biology fits. The solution is not vaccines and antivirals, but the hard, unglamorous work of cleaning up our houses, workplaces, hospitals and towns—and eating protective foods—so that we can live safely with this new technology.
UPDATE: Guess what! In homeopathy, iron and arsenic (Ferrum Phosphoricum and Arsenicum Album) in potentized form (very diluted and succussed) are indicated for tuberculosis. The idea in homeopathy is that something that in large quantities would make someone sick can, in potentized form, make one well. Just another indication that exposure to fumes of iron, and possibly to arsenic, is the cause of TB.
Many thanks to Tamara Romaine for her translation of the Tappeiner article from German into English.
- Frith J. History of tuberculosis. Part 1 – Phthisis, consumption and the White Plague. Journal of Military and Veterans’ Health. 2014;22(2):29-35.
- Price WA. Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects. New York: Paul B. Hoeber, Inc; 1939. Available at: https://healthwyze.org/archive/nutrition_and_physical_degeneration_doctor_weston_a_price.pdf
- Macinnis P. Bittersweet: The Story of Sugar. St Leonards, New South Wales, Australia: Allen & Unwin; 2003.
- Frith J. History of tuberculosis. Part 2 – the sanatoria and the discoveries of the tubercle bacillus. Journal of Military and Veterans’ Health. 2014;22(2):36-41.
- Barberis I, Bragazzi NL, Galluzzo L, Martini M. The history of tuberculosis: from the first historical records to the isolation of Koch’s bacillus. J Prev Med Hyg. 2017;58(1):E9-E12.
- Koch R. Die Ätiologie der Tuberkulose [The etiology of tuberculosis]. Berliner Klinischen Wochenschrift, No. 15, April 10, 1882, pages 221–230. First presented at a meeting of the Physiological Society of Berlin, March 24, 1882. https://asm.org/ASM/media/docs/1882p109.pdf
- Purdey M. Educating RIDA: An underground scientific journey into the origins of spongiform disease. Wise Traditions, 2002;3(1):11-18.
- The iron has it – Mark Purdey on bTb. Bovine TB Blog, May 8, 2006. https://bovinetb.blogspot.com/2006/05/iron-has-it-mark-purdey-on-btb.html
- Aust AE, Ball JC, Hu AA, et al. Particle characteristics responsible for effects on human lung epithelial cells. Res Rep Health Eff Inst. 2002 Dec;(110):1-65; discussion 67-76.
- Actor JK. Lactoferrin: a modulator for immunity against tuberculosis related granulomatous pathology. Mediators Inflamm. 2015;2015:409596.
- Furqan M, Butler J. Miliary pattern on chest radiography: TB or not TB? Mayo Clin Proc. 2010;85(2):108.
- “Selective leaching.” https://en.wikipedia.org/wiki/Selective_leaching
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Spring 2022🖨️ Print post