7. Theory 3: DDT Pesticides

Similarly to arsenic, the DDT theory has two variants: direct and indirect. The DDT theory traces back to a 1953 paper by Morton Biskind, Public Health Aspects of the New Insecticides, in which he linked polio to the increased use of DDT.

“In the Philippines and elsewhere in the Far East American troops, who used vast quantities of DDT as insecticides, had a high incidence of poliomyelitis, while it was extremely low in the surrounding native population.”

At first glance, a comparison of DDT usage and polio incidence appears to show a broad correlation. However, the correlation did not persist. DDT use peaked in 1959, while polio cases in the United States began falling sharply from 1952, even before the introduction of the vaccine in 1955. Plausibility, or a temporary correlation, is not proof of causation. Establishing causality requires much greater rigor, and the DDT theory fails to provide convincing evidence.

8. Theory 4: Tonsillectomy

Another proposed explanation is the tonsillectomy theory. In a 1916 paper published during the New York polio epidemic, Dr. Max Talmey suggested that tonsillectomies might increase susceptibility to polio.

“The predisposition to develop [polio] from tonsillectomy … is [due to] the elimination from the system of a valuable protective substance the nature of which is yet unknown.”

This theory has some empirical support. First, a 1953 paper by R.V. Southcott reported:

“Out of 39 patients with bulbar paralysis, 35 had undergone tonsillectomy – a proportion of 90%. … the association between prior tonsillectomy and bulbar poliomyelitis lasted for five to ten years.”

Second, in 1971, Pearay Ogra studied the role of tonsils in the body’s antibody response to the poliovirus. When patients with high levels of poliovirus-specific IgA antibodies had their tonsils removed, antibody levels rapidly declined and, in some cases, disappeared. Another experiment found that patients without tonsils developed significantly fewer antibodies after receiving the poliovirus vaccine than those whose tonsils remained intact.

These findings suggest that tonsils play an important role in strengthening immunity against poliovirus. One speculative argument is that tonsil surgery may expose parts of the lymphatic system, potentially allowing the virus to reach the brainstem more easily and cause fatal bulbar polio.

However, the theory faces a major problem: it does not explain the earliest epidemics. Tonsillectomies were rarely performed on children under five years old, yet 83% of polio deaths in New York in 1916 occurred in that age group. Nor does the theory explain paralysis observed in animals during early outbreaks.

While the tonsillectomy theory may help explain the shift of polio cases toward older age groups, it does not adequately explain the rise of polio itself.

9. Theory 5: Lab Leak Theory

In a 2011 paper, H.V. Wyatt suggested that the 1916 polio epidemic may have resulted from a laboratory leak at the Rockefeller Institute for Medical Research in New York.

Beginning around 1908, researchers worldwide were conducting experiments on monkeys using poliovirus. In a 1910 paper, Simon Flexner of the Rockefeller Institute reported that he had successfully injected the virus into monkeys. The disease proved far deadlier in monkeys than in humans, although it did not spread between monkeys as it did among people.

Flexner reported two virus strains produced through this process: the K-virus and the M.A. virus. By 1914, Harold Amoss had created a virus mixture, later known as the MV (mixed virus), which was distributed internationally for research purposes.

Wyatt proposed that this mixed virus may have crossed from monkeys to humans and then spread through New York, triggering the deadly epidemic. However, he acknowledged the lack of definitive evidence.

“It is not possible to prove that the 1916 epidemic was caused by the escape of MV from the Rockefeller Institute.”

The theory is generally considered weak because these laboratory experiments occurred after lethal epidemics had already begun. Historical records indicate that some earlier outbreaks were nearly as severe as the 1916 epidemic. In addition, the theory does not explain animal epidemics.

10. Theory 6: Virus Mutation and Other Explanations

Several other theories have been proposed. One is that the poliovirus mutated in the late nineteenth century, becoming more virulent. While this idea has some plausibility, there is no direct evidence to support it.

Another theory suggests that medical injections may have provoked polio in some cases, and there is limited empirical evidence supporting this possibility.

A third theory links polio epidemics to calomel, a mercury-containing medicine commonly given to infants in the past.

However, none of these theories adequately explains the full range of evidence, including animal outbreaks. Some researchers have argued that a combination of factors may have contributed to the rise of lethal polio, but this remains speculative rather than scientifically demonstrated.

Conclusion

It is safe to say that no one fully understands why polio became widespread and increasingly lethal from the late nineteenth century onward.

Further research will likely require years of work, including the translation of historical documents written in European languages and the collection and analysis of newspaper archives, journal articles, and books.

Based on the available evidence, the author argues that much of the standard literature on the rise of polio remains speculative and incomplete. Health professionals and historians should therefore exercise caution when making definitive claims about the origins and spread of polio unless those explanations account for all relevant historical and scientific evidence.

END OF ARTICLE