When Authority Shapes Appetite

By Gary Null PhD

“The body keeps the score.”
— Bessel van der Kolk

When Robert F. Kennedy Jr., now overseeing the major public health agencies of the United States, publicly endorsed the ketogenic diet as an ideal way of eating, his words did not float casually into the air. They landed with weight. In an era of chronic disease, metabolic confusion, and institutional distrust, people listen carefully to those who occupy positions of power. A statement about diet, when made by someone entrusted with national health leadership, does more than describe a personal preference. It signals direction. It shapes conversation. It influences behavior.

And Americans, weary of contradictory nutritional advice and rising health crises, are eager for clarity. We want an answer that feels strong and decisive. High fat. High protein. Low carbohydrates. Simple rules. Clear enemies. Bread becomes the villain. Meat becomes the hero. The message is emotionally satisfying because it restores order to dietary chaos.

But here is where culture begins to blur into biology.

Authority is persuasive. Popularity is contagious. But neither one alters human physiology. Cells do not respond to slogans. Arteries do not adjust to ideology. Hormones do not negotiate with charisma.

Every diet, no matter how fashionable or forcefully promoted, eventually encounters the same reality: the internal chemistry of the human body.

The ketogenic diet promises metabolic efficiency through carbohydrate restriction and insulin suppression. Its advocates speak of fat-burning, mental clarity, metabolic flexibility, and ancestral alignment. It appeals not only to those seeking weight loss, but to those who want to feel disciplined, optimized, and even rebellious against decades of conventional dietary advice.

Yet before we accept any dietary framework as ideal—especially one centered heavily on animal fat and protein—we must ask a deeper question, one that transcends personalities and political movements:

What actually happens inside the body when we eat this way?

Because beneath every dietary philosophy lies a cascade of biochemical events. Nutrients are metabolized. Enzymes activate. Growth pathways accelerate or quiet down. Inflammatory signals rise or fall. Microbial ecosystems shift. Over time, these microscopic responses accumulate into measurable outcomes: vitality or fatigue, resilience or degeneration, longevity or disease.

The ketogenic diet, like many high-protein, high-fat regimens before it, reflects something larger than nutritional science. It reflects a cultural belief—deeply embedded—that strength comes from animal flesh, that abundance of protein builds durability, that carbohydrates weaken us, and that dietary restraint must look muscular to be credible.

We have equated meat with power for generations. We celebrate large portions. We admire appetite as evidence of vigor. We reward excess with applause. In this cultural environment, a diet built around bacon, butter, steak, and organ meats feels not merely nutritional but symbolic. It aligns with a narrative of toughness.

But the body does not respond to symbolism. It responds to chemistry.

And so the question before us is not whether a public figure finds personal success with a given diet. The question is not whether short-term weight loss can be achieved. The question is not whether carbohydrates have been overconsumed in modern processed food culture.

The question is far more precise.

Does a high-protein, high-animal-fat, low-carbohydrate dietary pattern enhance long-term physiological stability—or does it quietly activate pathways that, over years and decades, contribute to inflammation, vascular injury, metabolic strain, and cellular dysregulation?

To answer that honestly, we must step outside dietary tribes and examine what happens beneath the surface.

In the sections that follow, we will move beyond slogans and examine the physiology itself. Not to attack personalities. Not to score ideological points. But to understand the difference between a diet that merely produces rapid results and one that sustains human health across the lifespan.

Because in the end, health is not determined by who promotes a diet. It is determined by what that diet does—cell by cell, organ by organ, year after year. If authority can influence appetite, culture determines what we crave.

The Myth of Protein as Power

If there is one nutrient that has achieved near-mythic status in modern culture, it is protein.

Protein is marketed as strength. Protein is sold as discipline. Protein is framed as the nutrient of athletes, warriors, builders, and survivors. Grocery shelves are lined with protein bars, protein shakes, protein chips, protein-enriched everything. Restaurant menus boast of double patties and extra meat as if abundance itself were evidence of vitality.

But very few people ever stop to ask a basic question:

How much protein does the human body actually need?

For most adults, the requirement is far more modest than cultural messaging suggests. Depending on body size and activity level, many women need roughly forty to fifty grams per day. Many men require somewhere between fifty and seventy grams. Even allowing for variation—pregnancy, recovery from injury, intense athletic training—the numbers rarely approach the levels routinely consumed in a high-protein diet.

Now consider what a single large steak can contain. A generous restaurant portion—sixteen ounces, which many would not consider unusual—delivers several days’ worth of protein in one sitting. And that is often just one component of one meal. Add eggs at breakfast, bacon, cheese, chicken at lunch, yogurt or protein snacks between meals, and the total can easily multiply.

Here is where biology intervenes.

Unlike fat and carbohydrates, which the body can store efficiently, protein has no long-term storage depot. It must be used, converted, or broken down. When intake exceeds physiological need, the body deaminates the excess amino acids. The first byproduct of this process is ammonia—a compound so toxic that the body must rapidly convert it to urea to protect itself. The liver and kidneys shoulder this burden continuously.

Short term, the system adapts. Long term, chronic overload places measurable strain on renal function, increases acid load, and shifts metabolic balance. Excessive protein also stimulates growth pathways such as mTOR and elevates insulin-like growth factor 1 (IGF-1), both of which are associated with accelerated cellular proliferation. Growth is not inherently harmful—but growth signals, chronically activated, are deeply implicated in aging and cancer biology.

Yet culturally, we rarely frame protein as something to moderate. Instead, we frame it as something to maximize.

Bodybuilders often assume they need extraordinary amounts. Advertisements reinforce the idea that more equals better. Restaurants design challenges around portion size. Entire television programs celebrate competitive overeating. The spectacle of consumption becomes entertainment. Applause follows excess.

But physiology does not applaud.

A high-protein meal rich in saturated animal fat slows digestion. Gastric emptying is delayed. When breakfast is heavy, it may still be processing when lunch arrives. Lunch lingers into dinner. By evening, the digestive system is burdened rather than restored. Add sugar-laden beverages or refined carbohydrates to the mix, and the gut microbiome begins to shift—beneficial bacteria decline while inflammatory species proliferate.

Over time, this pattern becomes normalized. People describe feeling “full” or even entering a “food coma,” mistaking metabolic overload for satisfaction.

The irony is striking. A culture obsessed with protein often overlooks the broader question of metabolic harmony. We measure grams of meat but rarely measure inflammation. We celebrate satiety but rarely consider endothelial function. We count macronutrients but ignore growth signaling pathways quietly accelerating beneath the surface.

Protein is essential. No serious nutritionist disputes that. It is foundational to muscle maintenance, immune function, enzyme production, and tissue repair. But essential does not mean unlimited. More is not inherently superior. Biological systems operate within ranges—thresholds where adequacy becomes excess.

The ketogenic diet elevates protein and fat as primary energy sources. That shift may reduce carbohydrate intake, but it does not eliminate the physiological consequences of protein surplus. Nor does lowering insulin temporarily erase the downstream effects of saturated fat, heme iron, or cooking-derived mutagens.

When we equate protein with power, we adopt a metaphor. When we examine protein metabolically, we encounter a mechanism.

And mechanisms—not metaphors—determine long-term health.

The real question, then, is not whether protein builds muscle in the short term. It clearly can. The deeper question is whether a chronically high intake of animal protein and fat supports the vascular, metabolic, and cellular systems that determine longevity.

To answer that, we must look beyond cultural symbolism and examine patterns of adherence and outcomes in the real world.

The Rise — and Retreat — of Keto

If the ketogenic diet represents metabolic truth, one might expect it to demonstrate staying power. After all, diets that align naturally with human physiology tend to feel sustainable. They do not require constant willpower. They do not produce high dropout rates. They integrate into daily life without extraordinary effort.

But the data tell a more nuanced story.

Federal health agencies do not formally track adherence to ketogenic diets. Instead, we rely on large survey organizations and consumer research groups that monitor dietary patterns year after year. What they reveal is instructive .

At its height—around 2018 to 2020—the ketogenic diet experienced remarkable cultural momentum. Social media amplified testimonials. Influencers promoted dramatic weight-loss stories. Grocery aisles filled with “keto-approved” packaged foods. For a time, it seemed less like a diet and more like a movement.

Yet even at its peak, strict adherence remained relatively modest. Surveys show that roughly 4 percent of Americans report currently following a ketogenic diet. Between 7 and 9 percent describe themselves as following some form of low-carbohydrate regimen, with keto representing a subset of that group. Meanwhile, 15 to 20 percent report having tried keto at some point—but not remaining on it .

Long-term strict adherence consistently falls below 5 percent.

That pattern matters.

When nearly one in five people experiment with a dietary pattern but only a small fraction maintain it over time, we are not observing universal metabolic compatibility. We are observing enthusiasm followed by attrition.

The reasons for attrition are varied. Some individuals report difficulty maintaining such restrictive carbohydrate limits in social settings. Others find the diet monotonous or socially isolating. Still others encounter physiological side effects—constipation, fatigue, elevated cholesterol markers, menstrual irregularities, or digestive discomfort—that dampen early enthusiasm.

But beyond practical inconvenience lies a deeper biological question.

If a diet demands constant vigilance to maintain metabolic equilibrium, is it truly aligned with our long-term needs? If weight loss achieved at three to six months tends to disappear by twelve months—as multiple analyses suggest—then perhaps the mechanism driving early success is not unique metabolic superiority, but caloric restriction and glycogen depletion.

Short-term weight loss often reflects water loss associated with carbohydrate depletion. Glycogen stores bind water; when glycogen drops, water follows. The scale responds quickly. But rapid shifts on the scale do not necessarily translate into durable metabolic repair.

Research also reveals a consistent pattern in clinical trials: dropout rates in ketogenic studies are often significant. Participants begin with motivation but struggle to sustain strict carbohydrate restriction over time . This is not a moral failing. It may reflect the fact that human dietary diversity historically included a broad spectrum of plant foods, fibers, and complex carbohydrates that nourish not only human cells but also the trillions of microbes in the gut.

The ketogenic diet narrows that spectrum dramatically.

This narrowing may produce short-term metabolic shifts. Insulin levels decline. Blood glucose stabilizes. Appetite often decreases, partly because protein and fat increase satiety. But satiety is not synonymous with systemic health. And sustainability is not guaranteed by initial enthusiasm.

Culturally, keto’s popularity illustrates something revealing about modern dietary psychology. We are drawn to bold solutions. We prefer dramatic reversals to gradual refinement. We respond to diets that promise rapid transformation. And we often overlook the quieter question of whether those transformations endure.

A dietary pattern that peaks rapidly and declines suggests excitement, not equilibrium.

This does not mean every individual who adopts keto will experience harm. Biology varies. Some individuals may tolerate higher fat and protein intake for extended periods. But population-level patterns offer insight into compatibility. And at the population level, long-term strict adherence remains uncommon .

The more important question, however, is not how many people follow keto. It is what happens metabolically when they do.

The claims of the ketogenic diet are bold. It promises improved metabolic health, reduced inflammation, cardiovascular protection, mental clarity, and evolutionary alignment. To understand whether these promises hold, we must examine them carefully—not through ideology, but through physiology.

And that is where we turn next.

The Promise — and the Physiology — of Keto

The ketogenic diet is not simply a pattern of eating. It is a set of promises.

Its advocates argue that restricting carbohydrates suppresses insulin, shifting the body into ketosis, where fat becomes the primary fuel source. They suggest that this metabolic state improves weight loss, stabilizes blood sugar, reduces inflammation, enhances mental clarity, and protects against chronic disease.

At first glance, the argument appears coherent. Carbohydrates stimulate insulin. Insulin facilitates glucose uptake and can promote fat storage. Reduce carbohydrates, reduce insulin. Lower insulin, burn fat.

Simple.

But biology rarely unfolds in straight lines.

Ketosis is a metabolic state. It is not, in itself, a health outcome. The body can enter ketosis during prolonged fasting, starvation, uncontrolled diabetes, and certain illnesses. The mere presence of circulating ketones does not automatically indicate improved cardiovascular function, reduced inflammation, or extended lifespan. It indicates a fuel shift.

The distinction is critical.

Another widely repeated claim is that minimizing carbohydrates stabilizes blood sugar and improves insulin sensitivity, particularly in individuals with type 2 diabetes. Short-term studies often show improved glycemic control during initial carbohydrate restriction. But longer-term research complicates the picture .

In animal models, ketogenic diets can induce hepatic insulin resistance within days. Human studies suggest that improvements in blood glucose may be partially attributable to overall calorie reduction and glycogen depletion rather than to the inherent superiority of animal-based macronutrient composition. When caloric intake equalizes, the metabolic advantage often narrows. In some longer-term evaluations, glucose intolerance and impaired insulin sensitivity emerge as concerns .

Weight loss is another pillar of the ketogenic narrative. High fat and protein increase satiety, reducing overall intake. Many individuals report rapid early weight loss. But again, short-term results can mislead.

Weight loss at three to six months frequently attenuates by twelve months. The initial decline often reflects water loss and reduced caloric intake rather than a fundamentally altered metabolic engine . When adherence loosens—as it often does—weight regain can follow.

Perhaps the most contested area involves cardiovascular health.

Keto proponents argue that carbohydrate restriction lowers triglycerides and raises HDL cholesterol. They often dismiss increases in LDL cholesterol as benign, claiming that in the context of low carbohydrate intake, saturated fats lose their harmful effects.

This assertion, however, conflicts with a substantial body of lipid research. Elevated LDL cholesterol and ApoB-containing lipoproteins remain causally linked to atherosclerosis, regardless of carbohydrate intake . Saturated fats from animal products consistently raise LDL levels. The reduction of insulin does not neutralize the impact of increased circulating atherogenic particles.

Meta-analyses do not show sustained long-term cardiovascular advantages for ketogenic diets. In fact, higher intake of saturated fats and red meats is associated with increased cardiovascular risk, even in the context of lower carbohydrate consumption .

Another claim centers on cognitive enhancement. Ketones are described as “clean fuel” for the brain, capable of improving mental clarity and mood. While therapeutic ketogenic diets have legitimate clinical roles in specific neurological conditions, such as refractory epilepsy, extrapolating those findings to the general population is not strongly supported by long-term evidence .

Moreover, diets severely restricting fiber and diverse plant nutrients may impair gut microbiome diversity over time. The gut-brain axis is increasingly recognized as central to cognitive and emotional health. A pattern that narrows microbial diversity may not support optimal neurological resilience.

Then there is the evolutionary argument.

Proponents often assert that humans evolved primarily as meat eaters and that ketogenic or Paleo-style diets align with ancestral biology. Yet emerging research complicates this narrative. Analyses of ancient tooth enamel isotopes from early human ancestors indicate diets heavily based on plant matter—fruits, leaves, tubers, nuts, and other vegetation—rather than sustained mammalian carnivory . The evolutionary story is far more diverse than the modern caricature of perpetual meat consumption.

Taken together, these contradictions reveal a pattern. The ketogenic diet does produce metabolic changes. It can suppress appetite. It can reduce blood glucose in the short term. It can induce measurable ketosis. But metabolic change is not the same as metabolic health.

Suppressing insulin temporarily does not erase the effects of saturated fats on LDL receptors. Elevating ketones does not override inflammatory pathways activated by excessive heme iron or cooking-derived mutagens. Reducing carbohydrates does not eliminate the proliferative signaling stimulated by chronically elevated IGF-1 and mTOR pathways.

In other words, lowering one variable does not cancel out the activation of others.

To understand the long-term implications, we must move beyond surface markers and examine the deeper biological pathways engaged by a chronically high intake of red meat, animal fats, and protein.

Because the body does not evaluate diets in slogans. It evaluates them through signaling cascades, inflammatory mediators, lipid transport particles, and cellular repair mechanisms.

And those mechanisms, once activated repeatedly over years, tell a clearer story than any short-term testimonial ever could.

What Happens Inside the Body: The Quiet Pathways of Strain

When we step away from dietary slogans and examine physiology directly, a striking pattern emerges. The human body does not respond to high intakes of red meat, saturated fat, and animal protein in a single isolated way. It responds through multiple parallel pathways — cardiovascular, metabolic, inflammatory, and cellular growth mechanisms that interact over time.

No single steak causes disease. No single meal produces catastrophe. The concern lies in repetition. In chronic activation. In pathways stimulated daily, year after year.

One of the most studied mechanisms involves the cardiovascular system.

Red meat is rich in saturated fats, heme iron, L-carnitine, and choline. When L-carnitine and choline are metabolized by certain gut bacteria, they produce trimethylamine (TMA), which the liver converts into trimethylamine N-oxide, or TMAO. Elevated TMAO levels are associated with endothelial dysfunction, increased platelet aggregation, and accelerated atherosclerosis . TMAO impairs reverse cholesterol transport and promotes plaque formation inside arteries.

At the same time, saturated fats reduce hepatic LDL receptor activity and increase circulating LDL particles — particularly ApoB-containing lipoproteins that directly contribute to plaque development . When LDL particles infiltrate the arterial wall and become oxidized, immune cells engulf them, forming foam cells and fatty streaks. Over time, these lesions progress into unstable plaques.

Systemic inflammation compounds the process. High saturated fat intake activates inflammatory transcription factors such as NF-κB, elevating markers like C-reactive protein. The vascular lining becomes less resilient. Nitric oxide production declines. The arteries stiffen.

The cumulative effect is measurable. Higher red meat intake is associated with elevated cardiovascular risk, with some analyses suggesting up to an 18 percent increase in fatal cardiovascular events per 50 grams per day . These are population-level patterns, not isolated anecdotes.

But the vascular system is only one arena.

High animal protein intake stimulates insulin-like growth factor 1 (IGF-1) and activates mTOR — a central cellular growth regulator. These pathways are essential for growth and repair. Yet chronically elevated signaling through IGF-1 and mTOR is strongly implicated in accelerated aging and tumor proliferation .

When this growth signaling occurs alongside cooking-derived mutagens — such as heterocyclic amines (HCAs) and N-nitroso compounds formed during high-heat preparation — the environment becomes more permissive to DNA damage. Heme iron further catalyzes oxidative reactions within the gut, promoting lipid peroxidation and cytotoxic aldehyde formation . Over time, these processes contribute to higher risks of colorectal, pancreatic, breast, and prostate cancers.

In breast tissue, elevated IGF-1 combined with estrogenic stimulation — whether endogenous or influenced by dietary patterns — can promote cellular proliferation. In pancreatic tissue, high fat intake chronically stimulates digestive hormone release, increasing cellular turnover. In the colon, heme iron and endogenous nitrosation create a microenvironment of chronic irritation and mutation .

Again, none of this is immediate. It is cumulative.

Metabolic pathways reveal a similar story.

Heme iron, abundant in red meat, increases iron stores in tissues. Excess iron acts as a pro-oxidant, generating reactive oxygen species that impair insulin signaling. Saturated fats accumulate in muscle and liver cells, forming lipid intermediates such as ceramides and diacylglycerols that interfere with insulin receptor function . The result is progressive insulin resistance — a precursor to type 2 diabetes.

In the liver, chronic exposure to excess saturated fat overwhelms mitochondrial oxidation capacity. Lipid accumulation leads to steatosis, then inflammation, and potentially non-alcoholic fatty liver disease. mTOR overactivation further drives lipogenesis and metabolic dysfunction .

Kidneys and bones are not exempt. High animal protein intake increases dietary acid load, raising urinary calcium excretion and lowering urinary citrate — a natural inhibitor of kidney stone formation. Over time, this acid burden contributes to stone risk and mineral imbalance .

The immune system also adapts to dietary signals. High saturated fat intake activates innate immune receptors such as TLR4, promoting chronic low-grade inflammation. Gut microbiome diversity declines when fiber intake falls, reducing short-chain fatty acid production that normally supports immune regulation. Increased intestinal permeability allows bacterial endotoxins to enter circulation, amplifying systemic inflammatory tone .

Chronic inflammation is subtle. It does not feel dramatic. It is not always accompanied by obvious symptoms. But over decades, low-grade inflammation is one of the strongest predictors of cardiovascular disease, metabolic syndrome, neurodegenerative disorders, and overall mortality.

When these pathways are viewed together, a coherent pattern appears.

A diet centered heavily on red meat, saturated fats, and high animal protein activates:

• Lipid pathways that elevate atherogenic particles
• Growth pathways that stimulate cellular proliferation
• Oxidative pathways that increase DNA damage
• Inflammatory pathways that impair vascular and immune balance
• Metabolic pathways that promote insulin resistance

The body adapts for a time. But adaptation is not immunity.

The most sobering data reflect cumulative risk. Higher red meat consumption has been associated with approximately 9 to 13 percent higher all-cause mortality per half-serving daily increase . That increase is not explained by one single mechanism, but by the convergence of many.

This does not mean that every individual consuming meat will develop disease. Human biology is resilient and influenced by countless variables — genetics, physical activity, total caloric intake, micronutrient status, stress levels, and environmental exposures.

But patterns matter.

When a dietary pattern repeatedly stimulates pathways known to contribute to atherosclerosis, tumor proliferation, metabolic dysfunction, and chronic inflammation, it becomes difficult to argue that such a pattern represents an optimal long-term foundation for public health. And yet, culturally, these mechanisms are rarely discussed.

Instead, we debate carbohydrates. We celebrate ketosis. We argue over insulin. Meanwhile, the deeper biological story unfolds quietly — cell by cell, vessel by vessel, year after year.

To understand why many continue to champion animal-heavy diets despite this evidence, we must examine not only biochemistry but ideology.

When science grows complex, culture often seeks simpler stories.

And that brings us to one of the most influential voices in the modern ancestral nutrition movement.

The Weston A. Price Narrative: Romance, Tradition, and the Limits of Observation

Long before keto became fashionable, long before Paleo rebranded ancestral eating for the digital age, a dentist named Weston A. Price traveled the world.

In the 1920s and 1930s, Price visited isolated communities in Switzerland, the Scottish Highlands, Africa, Polynesia, Australia, and the Americas. He documented dental structure, facial development, and general physical health among populations largely untouched by industrialized Western diets. His 1939 book, Nutrition and Physical Degeneration, argued that these traditional cultures exhibited robust health because of diets rich in animal fats, organ meats, fermented foods, and unprocessed products .

Price described what he called “timeless principles.” He observed strong dental arches, minimal tooth decay, and what he interpreted as superior physical vitality. He concluded that nutrient-dense animal foods—rich in fat-soluble vitamins A, D, and what he termed “Activator X” (later associated with vitamin K2)—were central to this health.

His work became foundational for the modern Weston A. Price Foundation, established in 1999. The Foundation promotes grass-fed meats, organ meats, raw and full-fat dairy, bone broths, animal fats such as butter and tallow, and fermented foods. It rejects industrial seed oils, criticizes vegetarian and vegan diets, and challenges what it calls the “lipid hypothesis”—the idea that saturated fat and cholesterol contribute to cardiovascular disease .

At first glance, the appeal is understandable.

There is something deeply comforting about the idea that traditional peoples possessed nutritional wisdom lost to modern society. There is also legitimacy in criticizing ultra-processed foods, hydrogenated fats, refined carbohydrates, and industrial food systems. In that respect, many of Price’s broader critiques of modern food culture resonate even today.

But the leap from observational anthropology to universal prescription is where caution becomes necessary.

Price’s work was largely descriptive. He photographed. He recorded impressions. He compared dental health between isolated communities and those exposed to Westernized diets. What he did not conduct were controlled clinical trials, randomized interventions, or modern epidemiological analyses .

The Weston A. Price Foundation itself does not conduct randomized controlled trials, nor does it fund large-scale medical research in the modern scientific sense . Much of its literature relies on historical data, older studies, and internal publications. Some of the citations commonly referenced are decades old. Critics note that the Foundation does not consistently apply contemporary epidemiological methods or control for confounding variables .

This distinction matters.

Observation can inspire hypotheses. It cannot confirm causation.

For example, traditional Swiss villagers consuming raw dairy and animal fats in the 1930s were not simultaneously exposed to industrial air pollution, sedentary office work, ultra-processed foods, artificial lighting cycles, or chronic psychosocial stress at modern levels. Indigenous communities eating wild game also consumed diverse plant foods, fibrous tubers, and naturally fermented products. Their meat was not factory-farmed, nor was it typically consumed in the quantities normalized by modern industrial abundance.

Context cannot be stripped away.

The Foundation often argues that rising heart disease in the twentieth century coincided with declining animal fat consumption and increasing industrial seed oils . It challenges the diet-heart hypothesis and cites analyses suggesting that saturated fat may not be directly associated with cardiovascular disease. Yet many of these analyses are criticized for failing to account adequately for substitution effects—what replaces saturated fat in the diet—and for other confounders.

Meanwhile, contemporary large-scale epidemiological studies consistently associate higher red meat consumption with increased total and cardiovascular mortality . The International Agency for Research on Cancer classifies processed meat as a Group 1 carcinogen and red meat as a probable carcinogen. These classifications arise not from ideology, but from cumulative risk assessments.

This does not mean that every element of traditional dietary practice was harmful. Fermentation, for example, can enhance nutrient availability and microbial diversity. Avoidance of ultra-processed industrial fats is widely supported. But elevating animal fat and saturated fat as inherently protective requires a stronger evidentiary foundation than historical observation alone can provide.

There is also a philosophical dimension.

When modern society becomes anxious about technological change, institutional failure, or chronic disease, there is a tendency to romanticize the past. The ancestral diet becomes a symbol of purity. Simplicity is equated with authenticity. Complexity is viewed as corruption.

But history is rarely so tidy.

Indigenous diets varied enormously. Some populations consumed more plant-based patterns. Others relied more heavily on animal foods depending on geography and climate. No single “ancestral” template exists.

The danger arises when selective examples are universalized.

The modern ancestral narrative often emphasizes organ meats, grass-fed beef, raw dairy, and saturated fats while minimizing contemporary epidemiological evidence linking high red meat intake to cardiovascular disease, certain cancers, and metabolic dysfunction. It positions itself as corrective to mainstream nutrition while relying heavily on observational data from nearly a century ago.

This is not to dismiss Price entirely. It is to contextualize him.

Observation begins a conversation. Controlled science continues it.

And when controlled human data, mechanistic research, and large population studies converge in a direction that contradicts romantic narratives, intellectual honesty requires that we weigh that convergence carefully.

The deeper question is not whether traditional cultures consumed animal products. Many did.

The question is whether high consumption of red meat and saturated fats, in the context of modern life, supports vascular integrity, metabolic resilience, and longevity.

Nostalgia is not data.

To explore this contrast more fully, we turn next to one of the most misunderstood plant foods in the modern debate — a food often portrayed as hormonally disruptive or dangerous yet supported by a substantial body of evidence.

Soy.

Soy: Fear, Hormones, and What the Evidence Actually Shows

If red meat has been culturally associated with strength, soy has often been burdened with suspicion.

In popular discourse, soy is frequently described as hormonally disruptive, feminizing, or even carcinogenic. It is accused of altering testosterone levels in men, stimulating estrogen-sensitive cancers in women, impairing thyroid function, and interfering with nutrient absorption. Entire movements have emerged warning against its inclusion in modern diets.

Yet when one steps back from rhetoric and examines the literature, a different picture emerges.

Soybeans and soy-derived foods are nutritionally dense. They provide complete plant protein, meaning they contain all essential amino acids required by the human body. They are rich in polyunsaturated fats — including omega-3 alpha-linolenic acid — and contain fiber, folate, magnesium, potassium, iron, and a wide range of bioactive compounds.

Among those compounds are isoflavones such as genistein and daidzein — plant-derived molecules sometimes labeled “phytoestrogens.” The term itself has contributed to misunderstanding. Isoflavones bind weakly to estrogen receptors, but their activity differs significantly from endogenous human estrogen. In some tissues they exert mild estrogen-like effects; in others they act as modulators or even antagonists.

Laboratory and animal studies using high-dose isolated compounds have occasionally raised concerns. But human data tells a more reassuring story.

Meta-analyses and reviews suggest that higher soy intake is associated with modest reductions in LDL cholesterol and triglycerides, contributing to an estimated 13 percent lower risk of cardiovascular disease in some analyses. Higher soy protein and isoflavone intake has been associated with approximately 23 percent lower risk of type 2 diabetes, particularly in women.

Breast cancer data are especially instructive. In several population studies, moderate soy intake is associated with up to 32 percent lower breast cancer risk, and post-diagnosis consumption is linked to reduced recurrence and overall mortality. Prostate cancer risk reductions in the range of 20 to 30 percent have also been observed in certain analyses. Overall cancer mortality in some meta-analyses appears modestly lower — approximately 12 percent — among individuals with moderate soy intake.

These associations do not prove causation in isolation. But they contradict the narrative that soy consumption inherently promotes hormone-sensitive cancers.

Much of the confusion arises from conflating whole soy foods with isolated isoflavone supplements. Whole foods such as tofu, tempeh, edamame, natto, and miso contain fiber, peptides, antioxidants, and a complex matrix of nutrients that influence absorption and metabolism. Fermented soy products, in particular, reduce anti-nutrient content and increase bioavailability of beneficial compounds such as vitamin K2.

There are legitimate nuances. Slight elevations in thyroid-stimulating hormone (TSH) have been observed in some trials, but without significant changes in active thyroid hormone levels in iodine-sufficient individuals. In rare cases of iodine deficiency or untreated hypothyroidism, caution may be warranted. Extremely high doses of isolated genistein supplements are not equivalent to moderate intake of whole soy foods.

Context matters.

What is striking philosophically is the asymmetry of fear.

Plant-derived phytoestrogens that bind weakly to receptors provoke widespread alarm. Yet diets rich in animal products containing growth factors, cholesterol-derived hormones, and saturated fats that stimulate IGF-1 and mTOR pathways rarely evoke comparable cultural anxiety.

Why do we fear mild plant compounds while dismissing strong proliferative signals from animal proteins?

Part of the answer lies in narrative simplicity. Soy is foreign to some Western traditions. It is associated with vegetarian and vegan communities, which are sometimes perceived as ideologically driven. Red meat, by contrast, is embedded in cultural rituals, national identity, and concepts of masculinity.

But biology is indifferent to symbolism.

Soy is not mandatory for health. One can construct a nutritious plant-forward diet without it. But the claim that soy is inherently harmful is not strongly supported by modern human data. When consumed in moderate amounts as whole or fermented foods, soy appears compatible with cardiovascular health, metabolic function, and possibly cancer risk reduction.

That does not make soy a miracle food. It makes it an example.

An example of how dietary narratives can become detached from evidence. An example of how plant-based foods can be caricatured while animal-heavy diets are romanticized. An example of how fear can overshadow nuance. Which brings us to a broader cultural puzzle.

If the evidence supporting plant-forward eating patterns continues to accumulate, why do so few people adopt them?

Evidence alone rarely changes behavior. Identity does.

If Plant-Based Eating Is So Strong, Why Do So Few Adopt It?

If dietary debates were settled purely by data, the conversation might look very different.

Large bodies of epidemiological research consistently associate higher consumption of whole plant foods — vegetables, fruits, legumes, whole grains, nuts, seeds — with lower rates of cardiovascular disease, certain cancers, type 2 diabetes, and overall mortality. Clinical programs led by physicians such as Dean Ornish and John McDougall have demonstrated reversal or stabilization of cardiovascular disease using plant-centered approaches.

Yet despite decades of evidence, strict vegetarian and vegan diets remain uncommon in the United States.

Long-running survey data tell a consistent story. Gallup, which has tracked vegetarianism for decades, reports that approximately 4 percent of Americans identify as vegetarian and about 1 percent identify as vegan. Other large survey organizations place vegetarian adherence between 4 and 6 percent and vegan adherence between 1 and 3 percent. A broader category — “plant-based,” which may include flexible or partial adopters — reaches roughly 10 to 15 percent.

These numbers have remained relatively stable for years.

Why?

If plant-forward eating is associated with lower inflammation, improved endothelial function, reduced LDL cholesterol, enhanced insulin sensitivity, and lower chronic disease risk, why is adoption so limited?

The answer is not ignorance alone.

Diet is not merely a nutritional decision. It is a social identity. It is family tradition. It is comfort, memory, ritual, belonging. It is tied to masculinity, to celebration, to holiday gatherings, to regional pride. Food signals affiliation. To change it is to shift identity.

Plant-based eating, particularly in its strictest forms, is often perceived as restrictive or ideological. Some advocates have unintentionally reinforced this perception by presenting dietary change in moral absolutes. When food becomes a moral battleground, resistance hardens.

There is also the psychology of taste conditioning. Modern food systems are engineered for hyper-palatability. Salt, sugar, and fat combinations stimulate dopamine pathways that reinforce habitual consumption. Ultra-processed foods hijack reward circuits. Even when individuals intellectually understand health risks, behavior is shaped by neural reinforcement patterns built over decades.

Industry influence plays a role as well. Animal agriculture is deeply integrated into economic systems, advertising networks, and political structures. Cultural messaging around meat is persistent and well-funded. Plant foods are rarely marketed with comparable intensity.

And then there is the illusion of invulnerability.

Chronic diseases unfold slowly. Atherosclerosis develops over decades. Insulin resistance builds gradually. Cancer progression often spans years before detection. Because consequences are delayed, dietary patterns can appear benign for long periods. Immediate pleasure outweighs distant risk in the human decision-making hierarchy.

This is not a failure of intelligence. It is a feature of human psychology.

Even within plant-based communities, nuance is required. One can adopt a vegetarian diet and still consume refined carbohydrates, excess sodium, and ultra-processed foods. Simply removing meat does not automatically confer metabolic health. Whole-food quality matters.

But the broader pattern remains: diets rich in fiber, phytonutrients, unsaturated fats, and diverse plant compounds consistently align with lower inflammatory markers and improved cardiometabolic profiles.

The paradox, then, is cultural rather than scientific.

We live in an era of abundant nutritional data, yet behavior changes slowly. We celebrate bold dietary experiments like keto, even when long-term adherence remains low. We hesitate to adopt plant-forward patterns, even when supported by decades of research.

Perhaps this reveals something deeper about human nature.

We are drawn to dramatic shifts, not gradual refinement. We prefer narratives of rebellion over narratives of moderation. We admire diets that feel countercultural or muscular. We overlook those that appear ordinary.

But health rarely emerges from dramatic gestures.

It emerges from sustained alignment between physiology and habit.

Which brings us to the central distinction that underlies this entire discussion.

The difference is not between keto and vegan. It is not between meat eaters and plant eaters. It is not between ancestral and modern.

The real distinction is between dietary patterns that activate inflammatory, proliferative, and atherogenic pathways — and those that quiet them.

And that distinction is biological, not ideological.

The Real Distinction: Healthy vs. Dangerous Diets

At this point, it should be clear that the central question is not whether one can lose weight on keto. Many can.

It is not whether traditional cultures consumed animal foods. Many did.

It is not whether soy is flawless or meat is poison. Nutrition is rarely absolute. The real distinction lies elsewhere.

It lies in whether a dietary pattern, sustained over years, activates biological pathways that promote resilience — or whether it chronically stimulates mechanisms that increase cumulative risk.

Healthy diets are not defined by trends, celebrity endorsement, or ideological fervor. They are defined by what they do inside the body.

A healthy dietary pattern tends to:

Lower circulating ApoB and LDL particles
Improve endothelial function and nitric oxide availability
Reduce systemic inflammation
Support insulin sensitivity
Promote microbial diversity in the gut
Moderate growth signaling pathways such as mTOR and IGF-1
Provide fiber, phytonutrients, antioxidants, and micronutrients in abundance

Dangerous dietary patterns — especially when practiced long term — tend to do the opposite.

They elevate atherogenic lipoproteins.
They increase inflammatory markers such as CRP.
They stimulate chronic growth signaling.
They impair insulin receptor sensitivity.
They narrow microbial diversity.
They increase oxidative stress and lipid peroxidation.

These effects do not announce themselves loudly. There is no immediate siren when endothelial dysfunction begins. There is no dramatic symptom when ApoB creeps upward. There is no early pain signal when chronic inflammation quietly simmers.

The body adapts.

But adaptation is not the same as protection.

One of the most misunderstood aspects of modern diet culture is the confusion between short-term metabolic shifts and long-term biological outcomes. Ketosis can be achieved within days. Weight loss can occur within weeks. But atherosclerosis develops over decades. Insulin resistance accumulates gradually. Cancer progression involves years of cellular mutation and proliferation.

The metric we choose determines the conclusion we reach.

If we measure success by how rapidly the scale changes, certain diets appear victorious.
If we measure success by inflammatory load, endothelial function, lipid transport particles, and cellular signaling pathways, the picture becomes more complex.

High intake of red meat and saturated animal fat has been repeatedly associated with increased cardiovascular risk, certain cancers, insulin resistance, and overall mortality. These associations are supported by mechanistic pathways that explain how lipid metabolism, heme iron, TMAO production, and growth signaling converge over time.

By contrast, dietary patterns emphasizing whole plant foods consistently correlate with lower inflammatory markers, improved lipid profiles, reduced diabetes risk, and lower cardiovascular events in large populations.

This does not require dietary extremism. It does not require ideological purity. It requires pattern recognition.

When we step back from dietary tribes and examine convergence across epidemiology, mechanistic biology, and clinical observation, a consistent theme emerges: diets rich in fiber, unsaturated fats, diverse plant compounds, and moderate protein intake tend to align with longevity markers. Diets centered heavily on red meat, saturated fats, and high animal protein tend to activate pathways associated with chronic disease risk.

The distinction is not moral. It is mechanistic.

This reframing matters culturally.

Because once we remove dietary identity from the equation, we can ask more grounded questions:

Does this pattern improve endothelial function?
Does it reduce ApoB?
Does it quiet inflammatory cascades?
Does it enhance insulin sensitivity?
Does it support microbial diversity?

If the answer is consistently no — or if the answer is mixed but risk signals accumulate — then enthusiasm should be tempered with caution.

Public figures will continue to promote dietary approaches. Movements will rise and fall. Cultural momentum will shift.

But biology does not follow fashion cycles.

The human vascular system has not changed in fifty years. The inflammatory cascade has not been redefined by social media. mTOR signaling does not adjust to political preference.

In the end, the body responds to chemistry — not charisma.

Which leaves us with a practical question:

If the goal is long-term vitality rather than short-term transformation, what does that look like in daily life?

Choosing Biology Over Identity

In a culture saturated with dietary claims, the most radical act may be restraint.

Not restraint in calories alone, but restraint in allegiance.

Diets become identities. Keto, Paleo, carnivore, vegan, plant-based. Each offers belonging. Each offers a narrative of certainty. Each promises clarity in a world of nutritional noise.

But health does not require identity. It requires alignment.

When we strip away trend, ideology, and personality, a few consistent principles remain.

First, moderation matters. The human body does not require extraordinary quantities of protein to function optimally. Meeting physiological needs is sufficient. Chronic excess does not confer added advantage and may activate growth and inflammatory pathways that accumulate risk over time.

Second, fiber is not optional. A diverse and resilient gut microbiome depends on fermentable plant fibers. Short-chain fatty acids produced by microbial fermentation help regulate inflammation, insulin sensitivity, and immune balance. Diets that dramatically restrict fiber narrow microbial diversity and alter metabolic signaling.

Third, fat quality matters. Unsaturated fats from nuts, seeds, olives, and certain plant oils consistently demonstrate favorable effects on lipid profiles and endothelial function. Saturated fats from animal sources elevate atherogenic lipoproteins in most individuals, regardless of carbohydrate intake.

Fourth, pattern outweighs perfection. Occasional deviations do not define a dietary life. What matters is the cumulative pattern across years. A diet centered primarily on whole plant foods, moderate in total protein, low in processed meats, and mindful of total saturated fat intake aligns more closely with the biological markers associated with longevity.

None of this requires absolutism.

It does not require moral condemnation of those who eat differently. It does not require confrontation at family gatherings. It does not require evangelism.

It requires discernment.

The goal is not to win a dietary argument. It is to reduce inflammatory load, support vascular integrity, stabilize glucose metabolism, and preserve cellular resilience over decades.

If someone chooses to consume animal products, portion size and frequency matter. Emphasizing quality, minimizing processed meats, and maintaining diversity of plant intake can mitigate some risk. But elevating animal fat and protein to the center of the dietary pattern, particularly under the belief that carbohydrates are inherently dangerous, ignores the cumulative biological pathways we have examined.

The deeper lesson is cultural.

We are drawn to bold solutions. We admire extremes. We respond to dramatic narratives. Yet health, in practice, is usually incremental and steady. It reflects daily alignment between physiology and habit.

Public figures will continue to endorse diets. Trends will surge and recede. Social media will amplify testimonials. But the underlying biology remains constant.

Inflammation still damages endothelium.
Excess ApoB still drives plaque formation.
Chronic mTOR activation still accelerates growth signaling.
Insulin resistance still impairs metabolic balance.

These processes are indifferent to politics.

In the end, the distinction between healthy and dangerous diets is not ideological. It is cumulative. It is measured not by enthusiasm but by outcome.

And the most reliable guide is neither celebrity endorsement nor nostalgic romanticism, but the quiet, consistent evidence of how the body responds over time.

Choose biology over identity.

Choose sustainability over spectacle.

Choose long-term vitality over short-term applause.

Because the body keeps its own records — and it never forgets.

Leaders will continue to speak. Movements will continue to rise.
But the final authority is neither political nor cultural.
It is biological.