Edward Howell

Aajonus explained that Howell did not want to replicate Pottinger's exact model because cats live too long. Pottinger used 900 cats over a 10-year period, slaughtering animals after they reproduced and examining their organs and vital tissues at each generation. Howell wanted to observe complete lifespans, not just reproductive generations, and he wanted to do it within a shorter window. Rats have a natural healthy lifespan of three years, which made them ideal for Howell's purpose. He could observe a full life from birth to natural death inside a manageable experimental timeframe.

Howell divided his rat populations into two feeding groups. One group ate raw food, consistent with what rats naturally eat, which Aajonus described as primarily meats and animal fats. The other group ate cooked food. The finding was unambiguous in the direction Aajonus expected: every rat in the cooked food group developed diseases, and not minor ailments but the full catalog of diseases that afflict human beings. The rats eating raw food developed no diseases at all. This result mirrored exactly what Pottinger had found with cats decades earlier.

What made Howell's experiment produce a confounding result was the lifespan data. In Pottinger's cats, those fed cooked food lived only two-thirds of their normal lifespan, a clear and measurable reduction. But in Howell's rats, the cooked-food group lived their full three-year lifespan, the same as healthy rats, despite carrying all the diseases of man. This was genuinely puzzling and Howell could not immediately account for it. Aajonus described Howell as scratching his head, spending approximately a full year trying to identify what biological factor in the rat might be compensating for the damage from cooked food and allowing it to live out its normal life even in a diseased state.

During that year, Howell pursued what Aajonus described as a systematic search for chemical or hormonal differences between the cooked-food rats and what might be expected in a healthy population. He tested different chemicals across different areas of the body, looked for hormonal production differences, examined whatever measurable biochemical markers he could identify, and found nothing. No element in the rat's chemistry explained why these diseased animals were nonetheless reaching their natural three-year endpoint when Pottinger's diseased cats had consistently fallen short of their lifespan. The investigators taking notes for Howell were doing so day and night, and all of it pointed nowhere conclusive.

The answer came not from laboratory analysis but from going back to the observational notes themselves. Aajonus described Howell reviewing the written records of everything that had been documented during the experiment, and noticing something that had been recorded but not yet recognized as significant: the rats in the cooked-food groups were eating feces. Not their own feces, but the feces of other rats in the same group. This coprophagic behavior, eating the fecal matter produced by fellow cooked-food rats, was the one variable that distinguished the rat experiment from the cat experiment and that offered a biological explanation for why the rats survived their full lifespan despite being diseased.

Howell's reasoning, as Aajonus relayed it, was that the feces of animals eating even cooked food would still contain bacteria, and those bacteria in the gut, through their own enzymatic and digestive activity, would be producing compounds that partially compensated for what the cooked diet was failing to supply. Aajonus connected this directly to his broader argument that bacteria are not enemies but agents of biological support. The rats were, in effect, gaining something from consuming bacterially active fecal material that partially offset the damage of their cooked diet, which was enough to extend their survival to a normal lifespan even though it was not enough to prevent the diseases themselves.

Once Howell identified coprophagy as the confounding variable, he redesigned the experiment to test the hypothesis. He placed a screen beneath the cooked-food rats so that feces would fall through and be inaccessible for consumption. Aajonus described this as the confirmation that proved Howell's reasoning correct: when the cooked-food rats could no longer eat the feces of other rats, their lifespan dropped significantly, falling short of the natural three-year endpoint. They got the diseases, as before, but they no longer lived their full lives. The screen experiment demonstrated that the coprophagic behavior had been the variable sustaining their lifespan, and that without it, cooked food alone was insufficient to keep them alive for their natural duration.

Aajonus also referenced Howell's findings on reproductive capacity across generations. Animals raised entirely on cooked food through successive generations reached a point of complete sterility. Aajonus described this endpoint as occurring by the third generation in some references and the fourth generation in others, with both figures appearing across his workshop discussions. By that generation, the animals could no longer produce offspring. This paralleled what Pottinger had found with cats, where the progression of disease and dysfunction intensified with each generation raised on cooked food, and the most severely processed foods, such as dehydrated or evaporated milk, produced the worst diseases and the fastest deterioration.

Aajonus praised Howell for doing empirical work rather than theoretical work, which he contrasted with what he saw as the modern nutritionist's tendency to intellectualize everything from a laboratory bench without observing actual animals or humans. However, Aajonus also identified specific areas where Howell's conclusions went wrong because they were based on test-tube chemistry rather than observation of what happens inside living bodies.

The clearest example Aajonus gave was Howell's position on trypsin in raw egg white. Howell, following conventional biochemical reasoning, argued that trypsin in raw egg white acts as an enzyme inhibitor that would bind with and block the absorption of other nutrients. Aajonus flatly rejected this conclusion. His position was that trypsin behaves as an enzyme inhibitor in a test tube, in a laboratory Petri dish, and under controlled artificial conditions, but that this reaction does not occur inside a living animal's body when the substance interacts with the full range of digestive fluids present in the gut. As evidence, Aajonus pointed out that when you examine feces or urine, you do not find trypsin from egg white bound to other amino acids in a way that would prevent their absorption or utilization. The reaction that appears in a laboratory setting simply does not replicate in the body's actual biochemical environment.

Similarly, Aajonus referenced the claim that avidin in raw egg white binds with biotin in raw egg yolk and blocks its absorption. He acknowledged that this binding does occur in laboratory testing, but again argued it does not happen in the body, because the body's interactions with pancreatic secretions and digestive fluids produce reactions that override or prevent the binding seen in isolation. Aajonus used these examples to illustrate a broader methodological criticism: Howell was still susceptible to the error of assuming that what a substance does in a controlled artificial environment predicts what it will do inside a living organism with its full complement of interacting systems.

Aajonus consistently paired Howell with Pottinger as the two major empirical researchers whose work validated the raw food framework through direct animal experimentation. He placed Pottinger's cat studies in the 1930s and Howell's rat studies in the late 1950s through mid-1960s, presenting them as a sequence: Pottinger established the pattern with 900 cats over 10 years, industry tried to suppress and contest those findings, and then Howell came in and replicated the essential result with a different species while adding the additional discovery about bacterial compensation through coprophagy. Aajonus also noted that a major grain and cereal company had privately replicated Pottinger and Howell's general findings as far back as the late 1920s and 1930s, reached the same conclusions, and destroyed all evidence under contractual obligation because the findings showed that cooked commercial food products made animals sick while the raw food they were ostensibly designed to replace kept animals healthy.

Aajonus used Howell's work specifically to introduce his argument about bacteria and high meat, pointing to the rat coprophagy discovery as scientific demonstration that bacterially active material, even in a secondary or fermented form, provides biological support that cooked food cannot supply on its own. The jump from rats eating feces to patients eating aged or fermented raw meat was explicit in his framework: both involve accessing the bacterial and enzymatic activity that is destroyed by cooking and that the body requires for full function.