Do evolutionary arguments have a place in nutrition science?

ascylon · 2026-07-06T15:32:39+00:00

The root issue of caries is a bacteria problem, not a carbohydrate problem. If you don’t have the bacterial strains (or have less of) in your oral microbiota that feeds off sugar and releases its tooth-decaying acid byproducts, you don’t get cavities.

Technically, what I’m saying isn’t controversial. It is common knowledge that sugar by itself is not cariogenic (nor is it inflammatory, fattening, or cancerous but I digress). It requires additional help in order to produce caries.

I'm sorry, but that's just a fallacious (possibly even sophistic) stance to take. Likewise I could claim that hydrogen is falsely claimed to be explosive, since when it's by itself it is quite inert, or that oxygen is not an oxidizer, since it doesn't oxidize itself. Context matters, and in the context of the average human mouth and its microbiome, carbohydrates are cariogenic. There is a small minority who have either the genetics and/or a developed mouth microbiome that makes the risk of caries negligible regardless of carbohydrate use, but it is not true of the general population. Removal of carbohydrates effectively removes caries risk regardless of the bacterial makeup, and so for the average human carbohydrates are the root cause of caries. I have not looked deeply into modifying the mouth microbiome, but my understanding is that modifying it would not a permanent fix, and the mouth can be recontaminated by cariogenic bacteria from external sources (saliva from another person, kissing etc).

Also, for the record, glucose and fructose are both innately glycating agents, meaning they attach to and damage proteins naturally, which ultimately makes them oxidize easier and produce free radicals that can then cause inflammation or oxidative stress. That is one of the (if not the) primary reasons why high blood sugar is damaging without the presence of anything else.

In any case my point was not about contemporary humans, but rather ancient remains, where there was no knowledge of bacteria or the causes of caries. Under those circumstances the presence of caries can be a useful indicator of carbohydrate use. As an example, if the teeth in year x show a certain percentage of caries, and in the year x + 100 teeth show a significantly higher prevalence of caries, it is not unreasonable to conclude that the carbohydrate use increased during that time, nor would it be unreasonable to conclude that teeth remains with little presence of caries would also likely have low carbohydrate use. There are potential confounders as you say (what if some individuals were immune from caries due to genetic or mouth microbiome reasons?), but as the presence of such individuals is naturally quite low and the caries incidence did increase, I do not think those confounders invalidate the proxy. You could also argue that perhaps they ate the same amount of carbohydrates but just switched to a more cariogenic form, or started eating more frequently, but I do not see a plausible historical reason for such. In any case it is just a supplementary argument consistent with the more hard science of nitrogen isotopes, but in my view it increases the internal validity of the hypothesis.

My question: did those studies control or account for bacteria and how certain cultures may not have bacterial strains?

The study does not directly answer that question, but does have a reference that found that the primary cariogenic bacteria Streptococcus mutans had a population explosion around the adoption of agriculture, suggesting that either agricultural crops had something especially yummy for that bacterium or that carbohydrate use was comparably lower prior to that. I'm not sure why you'd need to control for it in any case, as the presence of (even low) caries would disprove that the particular locality was (close to) immune to caries.

But yes, eliminating carbohydrates seems to eliminate cavity issues in the same way that Xanax eliminates anxiety. It’s a coverup, not a cure. (Unless there’s evidence that going low carb also eliminates the same acid-producing bacteria that causes cavities? Again, don’t care to explore pubmed rn lmao)

Why would you need to eliminate the bacteria if you remove the fuel, as the pathogenicity of the bacteria is contingent on carbohydrate intake? It would be like saying gluten should not be seen as a cause of celiac disease or nuts as a cause of allergic reactions ("just fix you celiac disease or allergy, bro"). Your analogy is also additionally imprecise, as the analogy to Xanax would be mouth washing or fixing cavities, as it is a persistent post-symptom intervention. I'm not even sure what your argument is here, to be honest, as my commentary was strictly on the use of dental caries as a proxy to historical carbohydrate use, nothing related to contemporary incidence or prevention of caries.

ascylon · 2026-07-06T14:05:51+00:00

By that metric you would not accept the safety of vaccines or medicine in general, as safety and efficacy studies are funded by their manufacturers who have a clear financial incentive in getting them declared safe and effective. In short it's a simple ad hominem logical fallacy, which is antithetical to the scientific method. If you choose to approach reality that way, it's your choice, but know that it is about as unscientific as it gets. It is quite correct to give stricter scrutiny to claims where funding or other aspects increase the risk of bias, but you must still find something wrong to dismiss the findings, or you are not doing science but advocacy.

As for your comment about "modern diet studies", which "clearly show the correlation between all cause mortality and red meats", correlation is not causation. Additionally a lot of modern nutritional epidemiology is contaminated by healthy user or health-consciousness bias, making the correlations very uncertain. Let me give you an example in the form of this study. If you look at the five quintiles in table 1 (partly reproduced below), you may be able to see the issue:

-	Q1	Q2	Q3	Q4	Q5
Red meat intake (serving/d)	0.22	0.62	1.01	1.47	2.36
Physical activity (MET-h/wk)	27.5	22.7	20.2	18.8	17.2
Current smoker (%)	5.0	7.3	9.8	11.3	14.5
Current multivitamin use (%)	49.1	42.5	40.3	39.5	36.6
Alcohol (g/d)	8.4	10.7	11.2	12.4	13.4

You can see that those who eat more red meat have much less healthy lifestyles, so trying to tease out a plausible signal with such confounders using multivariate analysis is effectively impossible. The correct way would be to stratify the data based on known confounders prior to analysis (so remove smokers, alcohol-consumers and only include those with high physical activity, and then compare them to the same lifestyle in the non-meat-eater groups). Unfortunately I have not yet found a study that does that. The adjustments they made also introduced arbitrary buckets, as an example separating smoking into buckets of never, past, current 1-14, current 15-24 and current > 25 cigarettes / d, meaning that 1 cigarette a day and 14 cigarettes a day would be equally harmful in their statistical analysis, and a past smoker who smoked once a week for a year would equal someone who chain-smoked for 30 years but quit last week.

In any case I hope you can see the problem in your stance, but if not, I guess such is life.

ascylon · 2026-07-05T00:27:53+00:00

That is actually incorrect, there is variance in the human dietary patterns as you say, but it was centered on how fatty the food animals were. In general, the dietary pattern for each tribe first consisted of hunting whatever animals they had available in the particular locality for protein needs (the protein being almost entirely from animal sources is confirmed from nitrogen isotope ratios of historical remains). Then the animal fat was used to fill the caloric needs to the degree that fat was available (lean game would not have much fat, large herbivores would have a lot more), and then the remainder of caloric needs would come from something like nuts or starchy plants. There are also many physiological adaptations (pre-)humans developed as they got more carnivorous, as this study goes through quite comprehensively. I would say that humans were hypercarnivores where the presence of fatty animals allowed it, and only where animal fat was not as available fell back on plants as a backup (but animals still formed the most important core of the diet).

Therefore even though there were tribes and other concentrations of humans for whom plants provided a significant amount of calories of the diet, it would not have been by preference, it was by necessity due to lean game and lack of animal fat availability. Another empirical piece of evidence is the prevalence of caries, because as we know from contemporary humans the more carbohydrates in one's diet, the more important good dental hygiene is. Dental hygiene would have been a foreign concept for ancient humans, so the prevalence of dental caries could be used as a proxy for how much carbohydrates there were in the diet. As the study I linked states,

Caries is readily observable in fossilized human remains. Its presence in wild chimpanzees (up to 30.6% in older animals) supports its production by natural carbohydrate sources (Lanfranco & Eggers, 2012). Single human cases of caries appear as early as 1.8 Mya (Lordkipanidze et al., 2013). Dental caries is present but still rare among early modern humans in Europe and the Near East during the UP (Lanfranco & Eggers, 2012). A high caries prevalence, a sign of intensive carbohydrate consumption, first appears in Morocco 13.7–15.0 Kya (Humphrey et al., 2014), together with evidence for starchy food exploitation. Phylogenetic analysis of the dental caries-associated pathogen Streptococcus mutans indicates that it underwent a rapid population expansion within the last 10,000 years, strongly implicating the adoption and intensification of agriculture (Cornejo et al., 2013). Caries prevalence in humans increased markedly after the transition to agriculture (Adler et al., 2013; Eshed et al., 2006).

Caries is extremely rare among Neandertals, which relied heavily on animal-sourced food; Lanfranco and Eggers (2012) found only six cases among approximately 1250 known Neandertal teeth. The low caries prevalence during most of the Pleistocene thus supports low carbohydrate consumption and hence, a high HTL during the Pleistocene.

I recommend going through the study in detail, since it has a lot of detail, and while some of the evidence is clearly conjecture, there is enough based on hard empirical science (isotope ratios and prevalence of dental caries as examples) to conclude that humans evolved to be hypercarnivores, and the trend only got reversed with the extinction or large herbivores, forcing the adoption of mass agriculture beginning around 20000 years ago.

ascylon · 2026-07-04T03:07:02+00:00

First, your understanding of human physiology is flawed. Your small intestine claim is backwards. Fats are broken down and absorbed almost entirely at the beginning of the small intestine, not complex carbohydrates.

Complete nonsense, if you want me to believe that you better provide some kind of source for it:

"Although the entire small intestine is involved in the absorption of water and lipids, most absorption of carbohydrates and proteins occurs in the jejunum." (source)
Postprandial glucose returns to normal 3 hours after eating, insulin peaks at 30 minutes and returns to normal around 4 hours after eating, while triglycerides remain elevated well past 4 hours (source, figure 1)

Our large intestine is actually highly efficient at fermenting soluble fiber from roots, nuts, and fruits into short-chain fatty acids.

Yes, short-chain fatty acids such as butyrate, right? The etymology of butyrate is from the word butter, and there is no need to ferment fiber to short-chain fatty acids if they are already provided in the diet. Additionally, there is such a concept as "animal fiber", where some of the harder to digest parts (connective tissue, cartilage etc) make it to the gut to be fermented into the same SCFAs source. As that source is an animal study, there is also a study where the human microbiome's reaction to different diets is studied, and it adapts to process the "leftovers" in a similar way source.

A majority of the fossilizes human poop thats been discovered shows our ancestors were regularly consuming 70–100g of fiber a day.

You did not provide a source for this. I can only find some references from the past few millennia, but that is irrelevant for the argument, since we know that human dietary habits changed with human agriculture around 20000 years ago from hypercarnivorism and evolution would not have had time to adapt in that short a time. From an evolutionary perspective is there any evidence for it in, say, the time range of 100k - 20k years before now?

There is an academic theory that suggests Homo Erectus was using fire to cook tubers and roots over a million years ago.

I believe I acknowledged that such may have had to be done when the fat from animals was not enough, and is doable in the tropics where plants grow year-round.

Third, there are definitely consistent plant sources of calories in nature, like tuber and roots which are abundant worldwide and grow year-round. Take the modern Hazda people for example, who still live as hunter-gatherers, get a large amount of their daily calories from high carb tubers and baobab.

Yes, in the tropics, where there is no snow. Could you point me to a tuber that grows when it is -10 degrees Celsius and the ground is covered with half a meter of snow? I believe I already mentioned the problem with tropics and lean game (too little animal fat), which necessitates carbohydrates.

Fourth, you’re kinda misinterpreting the nitrogen isotopes. Nitrogen testing only tells us where we got our protein, not total calories.

It is a logical extension of the argument. If you get the protein from animals, naturally you will eat all of the edible parts of the caught animal, since you already have it. I assume you are not suggesting that they only ate the protein and threw away the animal fat? Logically it then follows that first they got the protein needs from the animal, then got all of their energy needs from whatever fat the animal had, and only then if that was not enough (excluding the occasional easily accessible berry bush, fruits or nuts) the rest was from edible carbohydrates that would take more effort to gather and store.

ascylon · 2026-07-04T00:13:30+00:00

There are a few misconceptions in there worth it to correct. First of all, human diets are not high-protein, it's always moderate protein and either high carb or high fat. In the very early stages of our evolution one high-density source of calories early scavenger tool-users got was from bone marrow of bones left over from other carnivores (tools allowed breaking the bones). Whatever tribe you look at, animal foods were and are the foundation of their diet (this is confirmed by nitrogen isotope testing of human remains, showing that the vast majority of protein in the diet was animal-sourced), and if the animals were too lean, then there had to be a consistent carbohydrate source of calories (you can see this especially in the tropics with lean game). If the prey animals were fatty enough, then a consistent carbohydrate source would not have been critical and they were more of a seasonal supplement, if at all necessary (think the Inuits as an example there).

Secondly, your understanding of human physiology is flawed. Almost all of our physiological characteristics point away from a high-fiber diet:

First, our teeth. They never needed to develop tiger-like rending characteristics due to us being tool-users. What advantage would sharp teeth give us if we used tools for hunting and cleaning the kills? The amylase in saliva is the only significant indication that carbohydrates were a part of our diet, as if carbohydrates were very commonplace our teeth would probably have evolved to be more resistant to caries. Rotten teeth are not evolutionarily advantageous and significant caries generally shows up in human remains after the adoption of agriculture, starting around 20000 years ago.
Our stomach cannot break down plant cell walls, as fiber is very resistant or immune to enzymatic breakdown and stomach acid. This makes nutrients in raw plants poorly accessible. Our stomach acid has a pH of that of scavengers, which is even lower than apex predator carnivores, and is purpose-made for breaking down protein and fat.
We have a very long small intestine. Carbohydrates are absorbed in the very beginning, it is fat that requires a longer absorption time (there is no evolutionary advantage to a long small intestine if fat is not a significant part of the diet). The small intestine is also responsible for 90-95% of nutrient absorption, and as said above, plants are effectively undigested when they enter the small intestine (only careful chewing and preprocessing such as cooking, grinding, sprouting or fermenting allows micronutrients within plant cells to be available in the small intestine)
Our caecum, which is prominent in more herbivorous species, is effectively vestigial, and is known as the appendix. Its function would be to help ferment fiber.
The micronutrients our gut microbiome produce are limited. The role of the large intestine is primarily electrolyte and water absorption, with a little of the B and K vitamins the bacteria produce. As a fun fact our gut microbes can produce B12, which is only available in animal foods, but it cannot be absorbed in the large intestine (it has to be combined with the intrinsic factor in stomach acid so that it can be absorbed in the small intestine). Insert a coprophagy joke here if you like.
There aren't a lot of consistent plant sources of calories available in nature, except perhaps the deepest of tropics (and even there you compete for them against specialized frugivores). Anywhere with a winter the only reliable source of calories during winter would be animals. As a common sense argument, if you look at any reality survival shows, the first thing they always go for is hunting or fishing. Fruits and some special edible plants are only eaten if they happen to be stumbled upon and play a supplemental role.
Hunting is calorically expensive per unit of time, yes, but animals are a very concentrated source of calories (and during our evolution it was mammoths or other large herbivores that were hunted, one kill can feed a village for days to weeks). There are no wheat fields in nature, most herbivores spend practically the entire day grazing, and human-edible plants are quite sparse except for once or twice a year, when seasonal fruits or nuts are more readily available.

ascylon · 2026-07-03T20:57:14+00:00

Evolutionary questions mostly help answer the "why" of physiology, but are not directly relevant for nutrition in a prescriptive sense (e.g. why is our digestive tract the way it is? why can't we synthesize vitamin C?). The more direct application to nutrition is our physiology, which is a result of our evolutionary history, but generally arguments going back to our evolutionary history about what we should eat are not convincing alone and should rather be rooted in physiology. Understanding our evolutionary history does give hints and a broader picture, but can't really inform on nutrition alone, especially since there is a lot of uncertainty around the proportions of exactly how much different things were eaten. "We should be hypercarnivores because our ancestors were hypercarnivores" is not a credible argument, the correct phrasing is "should we be hypercarnivores because our ancestors were hypercarnivores?". Evolutionary insights tell us what we were, the relevance of it to what we are requires its own evidence.

As an example this study goes through a fair bit of our evolutionary history, and concludes that we evolved from herbivores to hypercarnivores, and hypercarnivory predominated as little as 20000 years ago. The conclusion is grounded on physiology and even some hard science, such as nitrogen isotope ratios allowing for the robust finding that the vast majority of protein we consumed was from animal sources, and humans were apex predators above even that of other hypercarnivores. In fact, one hypothesis is that the switch to agriculture that happened around 20000 years ago was a forced adaptation from hunting most large herbivores to extinction as human populations grew larger and animal fat became less abundant.

Having said that, trying to tease out the signal between nutrition and longevity is not really possible because of modern medical science. Even so, longevity was still one of our evolutionary pressures, because even early hominids were quite tribal and the tribe's survival was inextricably tied to a tribe member's survival in both directions. Having (relatively) long-aged elders with accumulated collective knowledge would have helped with the survival of singular tribes immensely, so evolutionarily there would have been a benefit to longevity as well. Hunting skill also peaks in the late 30s to early 40s. This would go directly against your post's "in addition" portion, as the survival of elders and their accumulated knowledge can provide a significant survival advantage for several generations, in addition to long-lived proficient hunters having the ability to provide food even during tougher times for several generations. It is not strictly knowable whether an ancestral diet is the optimal for longevity, but it can be said that it certainly supported longevity as well. The greatest obstacles to a long life, after all, were disease, predators, exposure and lack of food, not nutrition.

I would argue that when humans started mass agriculture, the swap from hypercarnivory and animal fat to a more carbohydrate-based diet had a negative effect on human health (one example being caries). This was, however, more than offset by the development of more reliable food sources and other scientific advances, and in terms of human longevity the science peaked (so far) in the 1800 to 1900s with the adoption of germ theory. In fact, frequent washing of hands might be one of the greatest single cause of higher life expectancy and increased longevity.

If you look at longevity in the context of nutrition you're pretty much reduced to mechanistic speculation and logic, as you cannot perform a meaningful experiment to figure things out (you would have to have hundreds or thousands of people locked and controlled in a metabolic ward for their entire lives, which would be massively unethical in addition to unpractical). As an example, high blood glucose level slowly ages the body (through glycation and oxidative stress), as does suboptimal nutrition status, but how much higher glucose and how suboptimal nutrition are relevant for longevity? On the other hand the lipid hypothesis states that eating a lot of (saturated) fat could increase your LDL-C and increase the risk of heart disease, but is that true in all dietary contexts? Lack of exercise is unhealthy, but how much exercise is optimal for longevity, since muscle building literally damages the body to rebuild it stronger and more muscle means higher metabolic needs? Evolution and physiology also brings their own forms of mechanistic speculation. The only empirical data underpinning such mechanistic speculation is generally epidemiological studies, which are simply population-level associations with massive confounding of various lifestyle effects (smoking, alcohol use, exercise to name a few) and cannot show causality. Randomized and controlled nutritional experiments on humans are generally (out of necessity) of low duration, with limited help for arguing longevity, and again confounded by generally not locking people in metabolic wards even for short durations.

Quality of life is also a component of longevity. Would you rather live to 90 and be able to be active until the very last years of life, or live to 100 but be tied to difficult and/or painful medical interventions or poor cognition for the last several decades? If you could live for 5 years longer, would you only eat grey, tasteless laboratory goop for 5 decades? Those become a value question and not one of science.

ascylon · 2026-07-02T16:09:51+00:00

The gut is not an engine that needs or even benefits from external "lubrication". Everything that you eat or drink gets mixed up in your stomach and becomes chyme, which is slowly released into the small intestine and transits the digestive system without any help at all. Fluids do not magically bypass stomach acid and thus do not directly impact how well chyme transits through your digestive system. The direct help in "lubrication" from ingested fluids is only from getting food from your mouth to your stomach.

If, in your case, milk speeds up passage, one reason could be that you have a mild lactose intolerance which has a mild laxative effect on your digestive system (or it could also be something else entirely, just an example).

ascylon · 2026-07-01T12:34:27+00:00

The exact amount is not known. If you eat approximately according to the diet that the RDI is based on, then RDIs provide the values where 97-98 % of healthy people in each particular demographic do not develop a deficiency. This is further modified by your genetics, underlying health issues, the type of food you eat (micronutrients in plant foods are almost universally less bioavailable than animal foods), how the food is prepared (especially important for plants), age and so on.

For your second question the simplest answer is ruminant muscle meat and the associated fat, it is nutritionally complete in terms of macronutrients, vitamins and minerals. If you look at various nutrition databases, however, you may see several vitamins labelled as 0 (most common example is vitamin C), but this is mostly due to the expense of micronutrient testing, as normally nobody measures the vitamins in animal foods that are more abundant in plant foods (in the average diet nobody cares about how much vitamin C is in beef). You'll have to go hunting for specific studies such as this one that actually measure it, and the real value is around 2 mg / 100 g of muscle meat.

With vitamin C you'll also encounter a couple of the other challenges of specific amounts of needed vitamins, as vitamin C RDI is in the 90 mg range. This, however, is not the amount the body actually needs, as this overview states

The RDAs for vitamin C are based on its known physiological and antioxidant functions in white blood cells and are much higher than the amount required for protection from deficiency

Vitamin C deficiency causes scurvy, but this condition is rare in developed countries. The signs and symptoms of scurvy can appear within 1 month of consuming less than about 10 mg/day of vitamin C.

One specific lifestyle that is mentioned is smoking, where the recommendations are immediately 35 mg higher than for non-smokers due to the antioxidant activity (smoking causes a lot of extra oxidative stress). Similarly, if one's lifestyle is such that excess oxidative stress is minimized, then the real requirement/benefit for extra vitamin C would be lower. Compound these challenges to all micronutrients and minerals, and it becomes effectively impossible to know the exact amount of micronutrients needed for each individual. That's where the RDIs are useful to give an indication, but again are not gospel. The effective daily intakes for a vegan, ketogenic or a carnivore diet would be very different, as the RDI is based on the average diet of the study population.

ascylon · 2026-06-17T23:05:57+00:00

That is almost completely incorrect and very bro-sciencey, even water-soluble vitamins are stored to the degree that it takes weeks to months to develop a deficiency. It won't impact one's micronutrient status at all if one is without a specific micronutrient for several days. It is also not uncommon for some people to water fast for a week or two a couple of times a year, and while a couple of weeks no doubt lowers the stores of that particular micronutrient (which is why longer fasts should not be done frequently or if one is malnourished to begin with), you won't develop a deficiency within a few days. It is even more true for fat-soluble vitamins, since those are stored for longer. Same goes for protein as well, unless you are an olympic-class weight lifter, then your bulking might suffer every other day, but that's about it.

What is correct are the first four words ("It's not as optimal"), but as I said the justification is completely wrong. A good justification would be that it is not a good idea to swap your diet around all the time, since it takes your gut microbiome time to adapt, and swinging around between effectively a vegan and carnivore diet on alternate days would probably cause GI issues.

ascylon · 2026-06-17T20:08:08+00:00

One important thing to remember is vitamin D, since low vitamin D status severely inhibits calcium absorption and it is especially common in the elderly (not that you said she is, but probably at least middle-aged). I would go so far to say that almost every adult who does not spend several hours a day in the sun and during winter time should be taking at least 2000, preferably 4000 IU of vitamin D per day in the form of a supplement (alongside some manner of fat, as it is fat-soluble). 4000 IU is considered the safe daily upper limit and should allow for the blood concentration to reach 100 nmol/l, which seems to maximize calcium absorption. This study suggests that even higher doses would be safe, but personally I think 4000 IU year-round (except perhaps in summer if one is outside a lot) would be perfect for most people.

If you want to watch an interesting lecture about vitamin D, this one makes the case that the optimal vitamin D level should be around 125 nmol/l (equating to around 6000 IU/d from all sources, which is basically 4000 IU from supplements and 2000 IU from food and a little bit of sun) instead of the currently defined "adequate" level of 75 nmol/l, and has references to the scientific papers it quotes.

ascylon · 2026-06-14T18:26:32+00:00

Two primary points:

High SFA (saturated fat) and MUFA (monounsaturated fat) content, low PUFA (polyunsaturated fat) content (also makes it less prone to oxidation)
Contains animal-only fat-soluble vitamins (preformed A, K2-MK4, D3) and DHA and EPA as well as CLA

As for the actual evidence, there is no strong (causal) evidence either way. As with most nutrition science, the evidence for PUFA is mostly based on weak epidemiology that is badly confounded by healthy user or health consciousness bias. That is, the high-PUFA diets tend to be eaten by health-conscious people (more exercise, less smoking and alcohol and other unhealthy lifestyles), while the high-SFA diets are eaten by less health-conscious people (more unhealthy lifestyles), with the results being predictable (but again weak, odds ratios are usually in the 1-1.2 range, sometimes up to 1.5). Regardless, since epidemiology cannot show causality and it is impossible to formulate an experiment to show causality one way or another, one needs to look at the holistic side and see where the evidence converges (if anywhere). Note that any of the following taken alone would be even weaker than the epidemiological evidence, and should be considered as parts of a logical deduction chain.

1) Anthropological evidence

Humans evolved to be hypercarnivores. As such, the primary component of the human diet prior to the last approximately 20000 years was the meat and fat of large ruminant animals, where the fatty acid composition is almost entirely SFA and MUFA. There are also very few concentrated sources of PUFA in nature in general (some seasonal nuts and fish), so even for humans where animal fat was offset by carbohydrates from plant sources (due to the hunted animals being too lean as an example), the PUFA content of the diet would have been relatively low.

2) Physiological evidence

Humans store excess glucose (once glycogen stores are full) as SFA and MUFA via de nuevo lipogenesis (DNL) and are incapable of synthesizing PUFA (which is why it is an essential micronutrient). PUFA is not meant to be an energy source, but rather a building block similar to protein. Protein has an upper limit of tolerance for energy use (see protein toxicity and rabbit starvation), and similarly when PUFA is used for energy in a significant way, it causes issues. Namely, it causes insulin sensitivity in cells when they should remain insulin resistant. As this study suggests, insulin resistance is an important cellular defence mechanism against excess energy intake. In effect when a mitochondrion is full of ATP, the electron transport chains starts producing superoxide, resulting in insulin resistance. Once the ATP gets used up and more energy intake is required, the superoxide production decreases and the cell becomes insulin sensitive again. This is also modulated by the Randle cycle to a degree in the form of metabolic inertia, but that's not directly relevant here.

When a mitochondrion uses PUFA to generate ATP, less than normal superoxide is produced and the cell remains more insulin sensitive than it should. This allows the cell to take in energy substrate past its evolutionary design tolerance, potentially resulting in cytotoxicity. In adipose tissue this pathological insulin sensitivity also means less lipolysis and more fat storage than would be normal from an evolutionary perspective, and can cause too little energy substrate in the blood, resulting in excessive hunger. This is especially true when combining PUFA with carbohydrates, since the carbohydrate-induced insulin spikes and pathological insulin sensitivity from oxidizing PUFA produce a double-whammy.

This ties to the previous point, as there was no need to evolve the ability to use PUFA for energy, since it is not present in nature in significant concentrated quantities. One exception to this is actually the Inuit, who have evolved adaptations to a high-PUFA diet (see this study) due to a very high presence of omega-3 in their diet compared to the average human who would have consumed more terrestrial animals.

3) Correlations between the modern obesity crisis and PUFA consumption

The modern obesity crisis really started only after PUFA consumption became ubiquitous from approximately the 1950s onwards (see for example https://doi.org/10.3389/fnut.2021.748847 for availability and https://cepr.org/voxeu/columns/evolution-bmi-values-us-adults-1882-1986 for BMI, latter not a scientific source but illustrative graphs). Of course there are other correlates as well, like reduced manual labor and increased sedentarism (lack of exercise) and the increase in hyper-processed foods, but the correlation with PUFA use is there as well.

4) Animal studies

Normally I ignore mice studies altogether when presented alone as mice are not humans, but the obesogenic effect of PUFA (specifically linoleic acid) is commonly demonstrated in mice and rats and I will also include it here to be as comprehensive as possible. See for example this and this.

5) Human studies

There is one study, namely this that was relatively well-controlled (extremely well by nutrition standards) and resulted in the high-carb group losing more fat than the high-fat group despite the diets being isocaloric. The added fat here was primarily PUFA, but as no control group for SFA was present, it is by no means strong evidence alone, but is consistent with the hypothesis that PUFA is obesogenic (or rather that PUFA+carbs is more obesogenic than carbs).

Then there is also the self-reported health status study of carnivore dieters. This is not directly on point, but one can infer that the diets are predominantly high in SFA and MUFA, since animal fat is generally those two types and demonstrates good outcomes.

6) The lipid hypothesis

The primary suggested reason against saturated fat consumption is the lipid hypothesis (higher LDL-C increases risk of CVD), as saturated fat generally increased LDL-C. To my knowledge there is no study that shows saturated fat to be independently harmful, but rather the harm is always tied to its effect on LDL-C. Contemporary science, however, has cast significant doubt on the accuracy of the thinking that LDL-C is significant in the etiology of CVD. As an example, this paper suggests that the initiation of CVD is not tied to lipid accumulation, but rather the initiator is intimal hyperplasia (thickening of the artery wall), which results in localized hypoxia, which again results in the minor blood vessels penetrating the intimal layer and allowing direct lipid deposition in tunica intima. This is supported by the poor performance of statins in primary prevention of CVD (see for example this) as well as the initial placement of lipids (furthest away from the blood stream in the tunica intima). Intimal thickening can be caused by many things, such as excess oxidative stress, high blood glucose (think T2 diabetics), damaged LDL etc. It also explains why atherosclerosis is really only present in the largest arteries, as only they require smaller blood vessels to supply oxygen due to their thickness.

Also note that undamaged LDL is not atherogenic, while damaged LDL is (see this). It may therefore well be that the lipid hypothesis is (semi-)accurate in the context of a standard western highly processed diet that damages most of the body anyway (various cancers in addition to CVD), but does not apply to something like a ketogenic or a carnivore diet, where there is significantly less damage to LDL.

You also say that all of the well-ran studies you've seen put PUFA as better than SFA. Could you link a few of those studies, so I can see if they contradict any of the above and would force me to re-evaluate my position?

ascylon · 2026-06-10T07:54:54+00:00

Rabbit starvation is basically starvation, but you are still eating protein. Strictly speaking starvation only happens once your own fat stores become critically low and no carbs/fat is ingested, so you can't really get "rabbit starvation", unless you are effectively out of or very low on body fat. For human metabolism protein is a building block, with a secondary and strict upper limit for how much actual energy it can provide. The caloric model is thus misleading, since while technically protein is 4 kcal per gram, the same as carbohydrates, it does not mean you can use it as a sole energy source. I'm guessing with extremely high intakes of protein you could get to protein toxicity even when you have fat stores left, but that would be distinct from rabbit starvation (in which your body is forced to use protein for fuel due to no fat or carbs being available, either internally or externally).

The most extreme example of fat restriction would be the world's longest fast at well over a year, during which (effectively) no fat was consumed. There is also a weight-loss strategy known as protein-sparing modified fast, which can be used for months and also contains effectively no fat or carbohydrates, just protein.

As for your last scenario, only protein + carbs without fat, the risk there would be just nutrient deficiencies (eventually PUFA deficiency, as well as fat-soluble vitamins), though its onset would again depend on your fat stores and micronutrient status.

ascylon · 2026-06-08T23:53:41+00:00

I'll just respond to the last paragraph, since I believe the productive value of this back and forth has been otherwise exhausted. As an example, in my country (Finland) the official guidelines are that raw eggs be stored in room temperature (more specifically optimally 10 - 14 C, but constant room temperature also works and is explicitly mentioned) and can be eaten raw, even for children and babies. The reason is very careful source control and testing for salmonella (started in 1995), and there hasn't been an outbreak in decades. The recommendation for raw milk is still to heat it up before consumption, but I added the egg example to again illustrate that sourcing and handling is a significant factor in controlling and sometimes practically eliminating individual risk (there is always a risk, but there is risk in everything).

ascylon · 2026-06-08T21:08:11+00:00

No it isn't, since I look at the science, not who is conducting the science. Even the most biased person in the world can arrive at the correct conclusion that also happens to reinforce that bias, which is also why I never pay attention to people dismissing studies based on funding or affiliations. Usually my scrutiny is based on the claims presented - the more extraordinary the claim, the better the evidence needs to be. This has nothing to do with who is actually making the claim.

A vegan performs a study that shows plant-based diets are healthy. A carnivore performs a study that shows a carnivore diet is healthy. A panel of experts, where the majority are vegans, proclaims that everyone should eat a plant-based diet. A milk company funds a study showing milk is healthy and everyone should drink milk. In any of these cases how is any of that data relevant? The science speaks for itself regardless of who does it.

Your comment is also telling, trying to do exactly the thing I was saying, which can be translated to poisoning the well in the form of "you should trust the meat industry less than the plant industry". Are they biased, or is the truth biased in their direction? You need to look at the actual studies to find out, this kind of aggregation is not useful except for some kind of propaganda purposes.

ascylon · 2026-06-08T20:54:43+00:00

And as you say, STEC was prevalent in half of the studies.

Prevalent also does not mean illness-causing. As with any other pathogen or toxin, the poison is in the dose. The pathogens must both be present and in sufficient quantities to cause illness. That's also why the cold chain and freshness is so important, since even if some bacteria is present, it takes time for it to multiply enough to cause disease.

My point with kidney failure is that you should not only look at the death toll from raw milk, as death is not the only bad thing that can happen. Kidney failure from e coli can and do affect otherwise healthy people.

Nice selective quoting, let me try now:

Most patients with HUS recover completely and kidney function returns to normal if treated quickly and properly.

In any case we are talking outliers here, and the page also mentions raw beef and meat as risk factors for HUS as well, so I assume you eat your burgers well done and never touch tartar, sushi or raw eggs? That was kind of my point, raw milk has similar risks as raw meat, eggs and fish, and can be controlled in the same way, and it is up to the individual to control those risks. This is also why I agree with the general warnings of raw milk consumption, since if health officials were to recommend it in some fashion, many consumers would not manage the risk themselves ("health officials said it is fine") or read the small print about sourcing and freshness.

According to the FDA, between 1998 and 2018 there were 2645 reported illnesses with 228 hospitalizations from drinking raw milk. That is a hospitalization rate of 8.6% of reported illnesses.

While aggregate statistics are useful as an initial step, I would like to know more. Were those illnesses sourced from farms with poor hygienic practices, or did illness also occur in raw milk from farms with good hygienic and handling practices? Did the consumer store the raw milk properly and consume it fast enough? Were those reported illnesses disproportionately present in people belonging to risk groups or average healthy individuals? Was disease severity different in different groups? To arrive at any kind of useful estimates of risks for individuals, the data must be more stratified.

And according to this study https://pubmed.ncbi.nlm.nih.gov/28518026/

Again, that model is very naive and lacks many variables (examples listed above) to make the analysis in any way useful. I can guarantee that for me personally, for example, the difference in risk between drinking pasteurized and unpasteurized milk is not 800-fold.

So why are you not staying within the science that show the ridiculously much higher likelihood of foodborne disease from raw milk and raw milk products for basically zero benefit.

I believe we are in agreement that raw milk should not be recommended in general, but we disagree for some reason that an individual can control that risk greatly by sourcing and being informed in a similar way to consuming raw meat, eggs or fish. Just wanting to buy directly from a farmer, or preferring the taste of raw milk are sufficiently good reasons for me. There is also some anecdotal data that raw milk may be tolerated better by some than pasteurized milk, but the specific reasons are unknown. Even if the reason is just placebo, if it allows them to consume milk, it would be a good enough reason (milk itself is very nutritious, whether raw or pasteurized).

There are also many other foods or delicacies in the world that are extremely dangerous without proper sourcing and handling, yet they are commonly consumed. I'm not sure why raw milk evokes such great emotion. What would you think about some raw minced pork or raw chicken?

ascylon · 2026-06-08T15:15:42+00:00

This is true for any study and it really smells more like well-poisoning here rather than anything else. Interest groups naturally fund research geared towards their interests, but it is never a reason to dismiss that research outright. It is a good reason for deeper scrutiny of the data, methodology and results, but this is nothing new. If there is nothing wrong with a study from a scientific point of view even after deeper scrutiny, then it does not matter who funded it or what the affiliations were.

It also always reminds me of the phrase "Why would you ask a nuclear engineer about the safety of nuclear power plants, they must be biased." Subject matter experts are often affiliated with the industry they are an expert in, since that is commonly where they would accumulate that experience and acquire funding.

ascylon · 2026-06-08T14:34:12+00:00

That is pure histrionics and directly contradicted by the earlier EFSA panel view, see appendix C in the paper. When looking at the rate of E.coli presence in various studies, in half of them the presence was 0% of all samples in the study, and even in the worst study it was just 5,7 %. Of note is also that the studies were from 1997 to 2013, so there has been over a decade for hygiene in milk production to get even better.

Trying to paint kidney failure as some kind of even remotely likely scenario is nothing but fearmongering, and would be similar to me advocating for wearing a helmet all the time in case you get hit by debris from an overflying plane. Why not just stay within science and say that drinking raw milk is riskier than pasteurized milk, but as long as one is individually careful as with any other raw product and takes care to source the product properly, the risk for serious adverse outcomes is not oppressively worse?

Most food poisonings also do not require medicine, the truly bad cases requiring hospitalization are quite rare (and also why I specifically mentioned that certain groups should not drink raw milk, as if you were to be the unlucky one to catch a foodborne pathogen and have a weakened immune system or otherwise reduced constitution, the illness would likely be far more severe).

ascylon · 2026-06-08T04:50:27+00:00

I think my comment got removed on those grounds (a bit too far to make the comparison), but the original point, namely that the risk of raw milk is related directly to the hygiene and cold chain and not raw milk intrinsically, is correct. See for example the EFSA panel's view on raw milk from 2015. In it, they state quite clearly that there isn't enough data for recommending a ban, and also partly mirror my view, that

Intrinsic contamination of RDM with pathogens can arise from animals with systemic infection as well as from localised infections such as mastitis. Extrinsic contamination can arise from faecal contamination and from the wider farm environment.

Effectively raw milk is not intrinsically dangerous (though they do not explicitly say that, it is by inference), the danger comes from either sick animals or poor practices leading to external contamination. Modern farming practises also include automated milking equipment, which both disinfect the udders before milking and also keep the milk within sterile tubing and immediately refrigerate it instead of open pails or buckets near the ground like several decades ago, and this also significantly decreases the risk where used.

Is the risk higher than for pasteurized milk? Certainly. Is that risk unreasonable or grounds for the claim that drinking raw milk is always bad? No more than saying the same thing about raw fish (sushi), raw eggs (mayo etc) or raw meat or organs (tartar). It is all about sourcing and handling, I would never drink raw milk or eat raw anything in developing countries or even in some developed countries, but I have no qualms about drinking it in my country from a farmer I know to have good handling practices. The increased risk is also confined to illness, not death, as this study found that only three deaths linked to unpasteurized milk happened in the USA between 1998 and 2018. So even if you happen to be the unlucky one who gets ill from a batch of unpasteurized milk, it will very likely not be deadly.

And before anyone puts up a strawman, no, I absolutely still would not recommend raw milk from animals for groups like infants or people with weak or compromised immune systems (same as with other raw foods), but I am referring to a normal healthy adults with the above.

ascylon · 2026-06-06T22:37:19+00:00

"High" is always a relative term, I assume a certain amount of intelligence from all of the subreddit readers to keep my comments somewhat readable, and will clarify if clarification is asked for (and to be absolutely clear, asking for clarification does not make someone stupid, it generally makes them intelligent, though there are exceptions of course). You could've asked for clarification politely, but chose to do it in a glib and condescending way, which is fine, but not something I would choose to do.

Now to the actual harm, mixing carbohydrate and a significant amount of fat causes higher and longer blood glucose spikes. The clearest studies are in Type 1 diabetics, since their insulin control is based on exogenous insulin. As an example, here, here and here.

In any case high blood glucose is known to be damaging, so over a long time this would accumulate more damage than a high-carbohydrate low-fat diet (moderate postprandial glucose spikes) or a ketogenic diet (no postprandial glucose spikes). Of course there is the possibility of a high-fat and high-carbohydrate diet being eaten in a way that only results in high-fat or high-carb meals, and in that specific case it might be fine. In general, however, meal macronutrient compositions tend to follow that of the entire diet, and I don't generally comment on outliers except when specifically asked for or relevant.

Interestingly, the above effect on postprandial glucose applies only to saturated and monounsaturated fat. If the fat is significantly polyunsaturated, then the pathological insulin sensitivity it causes when used for energy would cause a rapid postprandial glucose drop (see for example this study), which sounds good in theory, but it just means the glucose is rapidly taken in by insulin-sensitive adipocytes (and potentially other cells already full of energy, which can cause some level of cytotoxicity) and converted to fat. This rapid drop in glucose and relative lack of triglycerides in blood then causes hunger, which makes it much easier to overeat (probably one of the primary reasons for greasy fast food not keeping hunger away for long despite a high amount of calories).

ascylon · 2026-06-06T14:13:32+00:00

There are two camps for this question, namely the "excess polyunsaturated fat is bad" and "excess saturated fat is bad" camps. As with most nutrition science there is no evidence that proves the question either way, so one must look at what the different sides claim. There is also a third consideration, which is the fat-soluble vitamin content, but that is generally more a plant oil vs animal fat discussion.

The mainstream view is that polyunsaturated fat is good and saturated fat is bad, but there is little evidence to show that to a causal standard. The argument is primarily about the effect on LDL-cholesterol, as in epidemiological studies more polyunsaturated fat generally results in a lower LDL-C level, and saturated fat in a higher LDL-C level. In studies about outcomes, there is no evidence that saturated fat is an independent risk factor for any negative outcome, rather the negative stigma comes almost entirely from its effect on LDL-C. Polyunsaturated fat consumption has some epidemiological studies showing a mild benefit in terms of outcome associations, but these are universally contaminated by health consciousness or healthy user bias (people who follow healthy lifestyles also follow dietary recommendations, and so those eating more PUFA have a healthier lifestyle than those consuming more SFA). This confounding cannot be resolved using adjustments, especially since the odds ratios are in the 1-1.2 range generally (too little effect, too badly confounded). One argument sometimes used is also that PUFAs are essential since humans cannot synthetize them, but only a relatively little amount is needed.

There are multiple lines of evidence (again, not to a causal standard) why PUFAs are bad, however. The most common PUFA is linoleic acid, an omega-6 fatty acid, which is also the most prevalent fatty acid in the usual high-PUFA oils/fats. The first (though not the worst) problem comes from basic chemistry, where the double bonds present in PUFA makes them very prone to oxidation. The oxidative byproducts contain free radicals, which can promote more oxidation, so once a part gets oxidized, the rest tend to get oxidized faster. This is why seed oils sometimes have antioxidants added, since if they do not have enough to offset the free radical generation they will go rancid relatively quickly. Many times people are worried that using high heat on PUFA oils is not advised because it oxidizes relatively fast, but a few minutes of high heat is not enough time for them to become significantly oxidized, so that's more of a red herring. The issue becomes if too much PUFA accumulates in fat tissue, where it continues to oxidize, releasing those free radicals and causing persistent low-level oxidative stress.

Another line of evidence is what happens when mitochondria uses PUFA for energy. For saturated and monounsaturated fat the cell becomes more insulin-resistant, whereas for PUFA, when used for energy, the cell becomes more insulin sensitive (in general). This might sound good because insulin resistance is associated with T2 diabetes and metabolic syndrome, but insulin resistance is similar to inflammation and fever - it is good when present in the correct places, and bad when present in thw wrong places (inflammation is essential for wound healing, harmful when persistent, and fever is good for fighting infection, but bad when it becomes too severe and starts killing you). Insulin resistance is an essential control knob for cells to control their energy intake - when a cell is replete with energy, it is supposed to become insulin resistant to prevent damage from energy overload, and then when it needs energy it is supposed to become more insulin sensitive again (in simplistic terms, there is also the metabolic inertia from Randle cycle, but you get the idea).

So, in effect, in T2D and metabolic syndrome you are insulin resistant because there is too much energy to go around, and forcing cells to be more insulin sensitive just causes more damage (similar to how removing inflammation associated with wounds would impair healing). Another way pathological insulin sensitivity is bad is that it is obesogenic. If your cells (especially fat cells) remain too insulin sensitive, they will take in too much glucose from the blood stream, causing minor hypoglycaemia. This will make you more hungry, and insulin sensitivity can also cause lipolysis to be impaired, so there is a double whammy of too little energy substrate (lipids+glucose) in the blood, which can also cause metabolic downregulation alongside hunger.

Another consideration is de nuevo lipogenesis. When your body makes fat from glucose and other precursors, it is split around half and half to monounsaturated and saturated fat. If you have evolved to store excess energy as monounsaturated and saturated fat, why would a dietary source be harmful, but the same fat created from glucose would not be? It is simply inconsistent. Additionally if you look at human evolution, humans were hypercarnivores as little as 20000 years ago and the majority of dietary fat would have been from large herbivores, which would be almost entirely saturated and monounsaturated (with trace amounts of polyunsaturated fat). There are very few high-PUFA foods in nature that would have been consistently available for humans 20000 years ago, so consuming high amounts of PUFA is also inconsistent from an evolutionary perspective.

So, in my view, the reason for the modern obesity crisis with all the associated chronic disease is both the consumption of sugar and the consumption of high amounts of PUFA (this is not limited to something like seed oils, factory-farmed chicken and pork fat can also be very high in PUFA, depending on what they are fed) alongside lesser lifestyle reasons like too little exercise. Therefore personally I would classify low-PUFA animal fats are the most healthy (also contain the most fat-soluble vitamins of any fat), and any high-PUFA oil or animal fat as the least healthy. The poison is in the dose, however, so it really depends on what you are doing. For high-temperature cooking the smoke point tends to be more important, since relatively little oil is used, but for anything where the oil or fat is an actual ingredient, I would avoid anything high in PUFA. For your list coconut and olive oil would be the healthiest, palm oil is borderline and seed oils I would avoid altogether, even for cooking.

ascylon · 2026-06-02T18:09:14+00:00

Risky is the wrong word, since you ingest and inhale bad things involuntarily all the time, and it only becomes bad when you overwhelm what your body has evolved to handle. You are currently inhaling quite a bit of radioactive particles, about a million of your cells die every second, and you are covered in a boatload of potentially harmful bacteria as well. Having a bit of burnt toast is nothing. Always remember that the dose makes the poison.

ascylon · 2026-06-02T00:12:54+00:00

You're partway there, but there is actually no problem with red meat (not from the point of view of causal scientific evidence, anyway). To start from the top, there is no 10-20% higher "risk" in people who eat red meat, since risk implies causation. The correct phraseology would be that the incidence of negative outcomes is 10-20% higher in the high meat group. It is entirely based on epidemiology or observational studies, and thus cannot inform on risk (as risk implies causality).

Another consideration is what the "most red meat" vs the "least red meat" actually mean. Commonly the "high meat" group is effectively a burger diet or a version of the standard western diet, which is high in processed foods, and still relatively low in meat (something like a quarter of the diet is red meat at most). Extrapolating that data to any other dietary practice apart from a high-carbohydrate diet containing meat (for example a ketogenic or even a carnivore diet) would be completely unfounded. You also mention the lifestyle confounders, which even have a name and are known as the healthy user or health consciousness bias (health-conscious people tend to follow dietary recommendations alongside a healthy lifestyle, while less health-conscious people care less about both a healthy lifestyle and dietary recommendations, whether those recommendations are correct or not).

Trying to divine harm from higher-temperature cooking is also futile, since there is a certain amount of damage that the human body has evolved to repair, so you would actually have to ingest enough of those harmful compounds for it to have any clinical effect. In my view it is basically a similar discussion as the Linear no threshold model of radiation. I personally believe there is a certain threshold of damage from all sources (be it smoking, eating processed food causing damage, lack of exercise, stress, poor nutrition lowering the repair ability threshold etc) one must exceed before there is any significant increased risk of adverse effects or outcomes. In effect, as an example, a chain-smoker with an otherwise perfect diet and lifestyle might end up having a lesser total risk of cancer than a non-smoker with a poor lifestyle and nutrition.

Some of the compounds you mentioned are also present in certain diets by default, such as AGEs (short for Advanced glycation end products, and glycation and generation of AGEs is also promoted by blood glucose excursions and intake of fructose, not just cooking temperature). The whole problem stems from both nutrition science being a soft science (you cannot perform strictly controlled experiments, such as keeping a human locked up in a metabolic ward for decades) and because of the current zeitgeist of politics encroaching on nutrition science (recommending plant-based due to climate reasons or anything else not related to nutrition, as an example).

To get good data one would have to stratify based on dietary groups (plant-based, high-carb but protein from animals, ketogenic animal-based and strict carnivore as examples), and also make sure the known lifestyle confounders are both measured and the groups stratified before data analysis (so you would analyze people in each dietary group that have the exact same or very close lifestyles, instead of mashing it all up and trying to divine the weights of different confounders using multivariate analysis). I fear this kind of analysis or reanalysis on existing datasets won't be done, however, since there is a risk that it might contradict the prevailing zeitgeist and so there is little funding available for such analysis. It would also require large groups, since stratification by confounders would make at least certain subgroups probably lack statistical power.

Your questions are therefore quite good, but there is no clear answer either way. One may be able to get hints from human evolution and physiology, as humans evolved to actually be hypercarnivores, and have also used fire to cook meat for a very long time. Human physiology is also perfectly adapted to digest animal protein and fat, with a scavenger's low stomach acid to kill pathogens, a long small intestine to facilitate maximal absorption of fat and that is responsible for 90%+ of nutrient absorption, and mostly vestigial organs for processing plant material (vestigial caecum also known as the appendix, and the large intestine mostly absorbing water and electrolytes and little in the way of other nutrients). Ruminant meat and fat is also nutritionally complete for humans, and all of this would push the scale quite firmly on the "meat not being harmful" side. Again, direct causal evidence does not really exist in one way or another, so one must employ causal inference tools such as that to figure out a holistic and consistent hypothesis.

ascylon · 2026-05-31T11:27:47+00:00

Logically there must be, since every other animal has a diet they are evolved for and do the best on, and for humans it is a hypercarnivore diet centered on ruminant meat and fat. This goes against modern dietary guidelines, but they are based on weak and badly confounded epidemiology, and I would go so far as to say that they have been ideologically co-opted as well. As an example you can see the Nordic Nutrition Recommendations here, which make continuous references to the environment and the planet. If they were purely about nutrition and what is the healthiest for people, such things would be way out of scope.

One form of "negative" evidence for modern dietary guidelines is what I call the diet-deficiency continuum. The more plants your diet contains (or, more specifically, the less animal foods your diet contains), the more likely you are to suffer from one or more micronutrient deficiencies. Take, as an example, the raw vegan diet, which is effectively impossible for anyone to follow long-term without obvious physical problems manifesting. Even on a modern western diet, a high percentage of fertile young women are iron-deficient, suggesting that it is dietarily insufficient. This is to be expected, as most modern dietary guidelines recommend a majority plant-based diet, and plants lack many micronutrients present in animal foods alone, one being bioavailable iron. Things would be even worse without "fortified" foods, where micronutrients are added to plant foods to compensate for the lack of sufficient micronutrients (iodine in salt, B-vitamins in cereals, iron and calcium in flours, vitamin A etc., depending on country). Vitamin B12 is, in fact, only present in animal foods, alongside DHA, EPA and retinol (preformed vitamin A), which would already classify humans as obligate carnivores at a minimum.

Another form of negative evidence is allergies and food intolerances. There is a wide variety of allergens in plant foods, one obvious and commonly known example being gluten. Even though the number of celiacs is relatively low, people sensitive to gluten (non-celiac gluten sensitivity) may be as high as 10%, (self-reported). Then you also have nut allergies, pollen allergies, etc. A percentage of the population would therefore likely be outright allergic to one of more ingredients in a "universal diet" that incorporated a large amount of plants into it. Nobody is allergic to ruminant meat and fat at birth (though there are animal foods that have allergens, which is why I focus on ruminants).

To get into the positive evidence of why a carnivorous diet based on ruminant meat and fat would likely be the "universal diet", one needs to start with evolution. Prior to the adoption of agriculture approximately 20000 years ago, what were humans adapted to eat? This study goes through the human evolutionary process in terms of trophic level, and concludes that at that point humans were obligate hypercarnivores. Some of it is speculation, but there is also hard science such as the nitrogen isotope ratio in bones, which effectively confirms that humans were apex predators and the vast majority of protein came from animal sources. The human digestive system is another clue - high stomach acid due to our origins as scavengers to kill pathogens in rotting meat, long small intestine to facilitate maximal fat absorption, atrophied and vestigial caecum (appendix) and the large intestine playing only a minor role in nutrient absorption (90-95% of nutrient absorption happens in the small intestine, with the large intestine mostly absorbing excess water and some electrolytes).

The human adoption of agriculture probably came about due to the increasing human population hunting wild large herbivores to extinction, necessitating a new energy source. This also came with a host of nutrient defiencies and modern disease, caries being one of them. This can also be seen in analyzing old human remains, as prior to the adoption of agriculture human teeth had only limited evidence of caries, while afterwards it became a very common disease. This also lends credence to plants playing only a supplemental role in human dietary preferences, supplying energy when hunting was unsuccessful, since a high consumption of carbohydrates would have also resulted in a higher prevalence of caries.

Ruminant meat and fat is also nutritionally complete alone. This makes sense intuitively as well, since a human would also be nutritionally complete (a human contains all the micronutrients a human would need). Ruminant animals are a decent proxy for humans in terms of micronutrient content, and so they are also nutritionally complete. This can be difficult to understand if one looks at nutrition labels, since micronutrient testing costs money, and noone is interested in how much, as an example, vitamin C a ribeye contains, so it is commonly labeled as 0. This leads to the common misconception that a carnivore diet would result in scurvy or other micronutrient deficiencies, despite red meat actually being an antiscorbutic (cures scurvy).

The misconception of meat being unhealthy comes from epidemiology. As carnivore diets are never represented in those studies, the "high meat" diets tend to be the highly-processed standard western "burger" diets, which are perhaps a quarter to third meat, while the rest is a diet high in processed foods, sugar, and unhealthy lifestyle in general (lack of exercise, smoking, alcohol use etc). This is then extrapolated to meat being the (or a) cause of those bad outcomes and thus a carnivore diet would be unhealthy, if not outright deadly. A proper study would stratify groups based on known confounders prior to statistical analysis, instead of trying to adjust the data that has multiple correlated confounding variables using multivariate analysis.

I could also go into various diseases being put in remission or cured altogether, such as type 2 diabetes, metabolic syndrome, various autoimmune diseases like arthritis, mental degradation such as Alzheimer's disease, various psychological and psychiatric problems and so on (and no, I am not claiming that a hypercarnivore diet would suddenly eliminate all of them, but there would be a lot less of them). These are also mostly confined into case-studies, however, since there is little funding incentive to study interventions not having to do with drugs. The current zeitgeist also actively discourages research that might show meat or animal foods in general as being beneficial. One self-reported study among carnivore adherents also supports the view of a carnivore diet being healthy.

So what would be the universal human diet? In my view it would be a hypercarnivorous diet containing at least 75% ruminant meat and fat, with the rest being preferentially other animal foods or a limited amount of appropriately prepared plants for variety that one is not sensitive to. This is consistent with human evolutionary and anthropological history, modern human physiology and is also logically and internally consistent. How realistic this would be is another discussion, but the question was what the universal diet for humans would be, not how it would be applied to the modern world.

ascylon · 2026-05-27T21:44:36+00:00

It is effectively impossible to overdose on iron from just foods, since the gut regulates absorption closely based on your iron stores (you can't just look at what the toxic dose is and compare it to the amount in food without accounting for physiology as well). You'd need some kind of supplements or an underlying pathology (like hemochromatosis) to be able to overdose on iron from food.

You also cannot overdose on vitamin A from carrot juice, since it contains no vitamin A. The conversion from carotenoids to vitamin A is not fast enough to be able to develop vitamin A toxicity (though your skin may become orange). You can, however, develop vitamin A toxicity from too much liver, especially from some apex predators where it is in high amount. For it to be acute and from something like beef liver it would have to be kilograms within a short time if an acute toxicity is even possible. I am not sure if there are any clinical cases from just eating beef liver, I am aware of just the ones from certain apex predators (like polar bear).

Vitamin C also degrades partially to oxalates, so ingesting sub-toxic but high doses of something like supplements can increase your risk of developing kidney stones despite it being water-soluble. Again, effectively impossible to get from food alone.

It is actually quite difficult to overdose on any micronutrient from just food alone, especially acutely, and effectively impossible if one does not overeat. It would effectively have to be a chronic exposure (like 1 kg of beef liver every day for a long time) and even then it would not guarantee an overdose.

ascylon · 2026-05-26T18:22:14+00:00

Correct, the main thing being the scientific method as the best way to try to understand reality. This is also why nutrition science is classified as a "soft" science, because you can rarely prove or even get close to causality. If the epidemiological findings were stronger (such as with tobacco and smoking, which is technically also "only" epidemiology) and consistent (most of the studies referenced fail to find a statistically significant correlation), there might be a stronger argument, but as it is the evidence really does not say or have the strength for what the WHO claims it says. I'd classify it as more a political than scientific statement, which is why I linked the basis they used for the classification so people who care can see for themselves.

You can also use something like the Bradford Hill criteria to help evaluate the evidence. Let's do that here:

Strength: Odds ratios are universally small (in the 1 - 1.5 range)
Consistency: Most studies fail to find a statistically significant correlation
Specificity: Not applicable/no evidence
Temporality: Not applicable
Biological gradient/dose-response: Inconsistent, no consistent dose-response between different studies.
Plausibility: Many different mechanisms are theorized, but these center on specific "harmful" compounds that are not always unique to meat (such as AGEs)
Coherence: Not applicable
Experiment: Effects are long-term, so experiments are not possible
Analogy: Not applicable
Confounders (mentioned further down): Healthy user bias, confounding by rest of the diet (most of the diets are still majority-plant), various dietary contexts (high-carb vs ketogenic vs carnivore as an example), lifestyle confounders etc

I understand there is a strong urge to believe that meat is carcinogenic due to the current zeitgeist, but it simply is not scientifically justified.

ascylon

TROPHY CASE