Two populations get cited more than any others to defend eating animals. In one, the researcher who built the claim went on to collect the evidence against it. In the other, the claim was never measured at all.

The claim, in its two forms

You have met this argument. It arrives in one of two costumes.

“Early Indigenous coastal Alaskan natives were among the healthiest people in North America. They primarily ate meat and fat. Not tofu or spring salad to get through a brutal Alaskan winter.”

“The Maasai lived on milk, meat, and blood. They were lean, muscular, had low cholesterol, and didn’t get heart disease. Explain that.”

Both deserve a real answer rather than a dismissal. These are resilient peoples who solved food problems most of us would die inside a week attempting, and the researchers who studied them were serious.

Here is what either version needs to be true in order to work:

1. The population must actually have been free of the disease in question.
2. The diet must be the reason.
3. The diet must resemble what modern advocates are proposing.
4. Their biology must be close enough to ours for the result to transfer.
5. The comparison target, a well-planned plant-based diet, must do worse.

Every one of the five fails, in both cases, for closely related reasons. That repetition is the most interesting thing here. This is not two arguments. It is one template with two skins, and once you can see the template you stop needing a separate rebuttal each time somebody produces a new population.

Two ideas from evolutionary medicine sit underneath all of this, and they are worth knowing by name. Antagonistic pleiotropy is the reason a trait can be an evolutionary success and a late-life liability at the same time: selection counts grandchildren, not birthdays, so a gene that pays off at twenty and costs you at seventy gets kept. Evolutionary mismatch is what happens when the environment changes faster than the bodies living in it, so traits well matched to ancestral conditions misfire under conditions nobody was tested against. Both show up repeatedly below, and both are explained properly in The Future Is in Our Hands.

Part 1: Were they actually free of the disease?

Did the Maasai really have no heart disease?

The foundational fieldwork was done by George V. Mann, a Vanderbilt biochemist and former associate director of the Framingham Heart Study who became one of Ancel Keys’s most prominent critics.

Mann et al. (1964) examined four hundred Maasai men. They were lean, hypertension was almost absent, and of the 363 men whose blood was pooled for analysis serum cholesterol averaged about 125 mg/dL, roughly half the American figure of the era. Age-group means ran from about 115 to 130.

The paper also acknowledges support from the National Live Stock and Meat Board. Hold that, because of what Mann did next.

Mann, Spoerry, Gray & Jarashow (1972), in the American Journal of Epidemiology, examined hearts and aortae from fifty Maasai men at autopsy. Verbatim:

Measurements of the aorta showed extensive atherosclerosis with lipid infiltration and fibrous changes but very few complicated lesions. The coronary arteries showed intimal thickening by atherosclerosis which equaled that of old U.S. men. The Masai vessels enlarge with age to more than compensate for this disease.

Coronary atherosclerosis equal to that of old American men. The plaque was there. What was rare was the clinical event, and Mann’s own explanation was that lifelong physical work had enlarged the vessels enough to keep the lumen open around the disease.

So the meat industry funded the study that made the Maasai famous, and the same researcher then collected the evidence that undercut the use his study was being put to. He published it anyway. That is a better man than the argument against him requires.

Two further details from Mann’s own 1964 paper rarely travel with it. Of the four hundred men and boys examined, three were over the age of 55, and coronary events are a disease of older people. And the paper reports hand-dynamometer results showing the Maasai were less powerful than the American comparison group, with a note that the elders seemed sedentary, which complicates the fitness explanation Mann himself would later reach for. He also wrote plainly that there was no autopsy data to confirm the anatomical picture, and called for exactly the material he supplied eight years later.

An earlier and smaller series (Biss et al. 1971, ten consecutive autopsies) had reported a “marked paucity of atherosclerosis.” Mann’s larger series contradicted it and he attributed the discrepancy to omissions in Biss’s selection and methods. So the founding literature is internally contested, and the larger, more rigorous study found abundant disease.

Where did the Inuit paradox come from?

The Inuit version traces to Danish researchers Hans Olaf Bang and Jørn Dyerberg, who in the 1970s reported that Greenland Inuit eating a seal- and whale-blubber diet had remarkably low coronary heart disease. The finding launched the global fish-oil industry.

They never measured it. They inferred low coronary disease from Greenland’s public health records, incomplete death certificates from a population where many deaths were never medically attended.

Two reassessments dismantled it:

• Bjerregaard, Young & Hegele (Atherosclerosis, 2003) concluded the evidence for low ischemic heart disease among the Inuit was “fragile,” resting on unreliable mortality statistics, and noted that stroke mortality was higher among Inuit than in Western comparison populations.
• Fodor et al. (Canadian Journal of Cardiology, 2014) found coronary artery disease prevalence in Inuit populations to be as high or higher than in non-Inuit populations, overall Greenland Inuit mortality roughly twice that of non-Inuit, and stroke death rates very high.

What did CT scans of Arctic mummies find?

The HORUS study (Thompson et al., Lancet, 2013) scanned 137 mummified bodies from four preindustrial populations and found probable or definite atherosclerosis in 47 of them: 29 of 76 ancient Egyptians, 13 of 51 ancient Peruvians, two of five Ancestral Puebloans, and three of five Unangan hunter-gatherers.

Three of five is far too few to rank against groups of 76 and 51, and anyone quoting it as “the highest rate in the study” is making a claim five bodies cannot support. What it does establish is that a marine-mammal diet did not prevent the disease. A 2019 follow-up found calcified arterial plaque in three of four cold-preserved Greenlandic Inuit mummies from around the sixteenth century; its authors point to smoke from indoor fires as one possible contributor (Wann et al. 2019).

The HORUS authors themselves read atherosclerosis as having a component intrinsic to human aging rather than being purely a modern artifact. That caveat cuts against everyone’s dietary triumphalism, including the plant-based kind. What it specifically destroys is the claim that these diets conferred arterial immunity.

How big is the population behind the Inuit argument?

Every so often someone plays the Inuit card, so it is worth a moment of perspective. The Inuit Circumpolar Council represents roughly 180,000 Inuit across Alaska, Canada, Greenland and Chukotka, on a planet the United Nations put at 8.2 billion people in 2024. That is about 0.002 percent, which means the rest of the world outnumbers them something like 45,000 to one.

Smallness alone would not disqualify them, and I want to be careful here, because a tiny population can still be enormously informative. The Tsimané are tiny too, and they turn out to be one of the most instructive populations on Earth. So the number is not the argument. The number is the setup.

Here is the argument. The Inuit are the most diet-adapted population in this entire discussion. Generations of natural selection tuned them to a marine, animal-fat diet, and, as Part 3 shows, they carry genetic variants to match that are near-universal among them and essentially absent in everyone else. If any group on Earth were built to thrive on an all-animal diet, it is this one. And as the scans above show, the atherosclerosis turned up anyway. A group that is roughly one part in forty-five thousand, and the single population best genetically equipped for the diet, still was not protected from the disease. That is not the trump card people think they are playing.

How long did these populations actually live?

In the Arctic: circumpolar Inuit populations across Alaska, Canada, Greenland and Chukotka have consistently shown lower life expectancy and up to roughly three times higher infant mortality than their respective national populations; in Nunavut, for example, infant mortality runs three times the Canadian average (Collins et al. 2012).

Among the Maasai: anemia in roughly 39% of children under five and 22% of adult women (Nestel & Geissler 1986); deficiencies documented across vitamins A, C, D, B12, folate and iron (Martin et al. 2014; Goldman et al. 2025); and child stunting in 57% of Maasai children against 21% among the neighboring Meru, 32% Sukuma and 44% Rangi, with about 10% wasted against 2 to 3% in neighboring groups. Lawson et al. (2014) concluded the Maasai were the most disadvantaged of the neighboring ethnic groups studied. Underweight affected 24% of Maasai adults, against 14% of Luo and 21% of Kamba adults in the same rural Kenyan survey (Hansen et al. 2011).

A population where more than half the children are stunted is not the answer to “who were the healthiest people on earth.”

Did the traditional diets cause the short lifespans?

Those short Arctic lifespans were driven overwhelmingly by infectious disease, accident, cold, famine and infant mortality, not by blubber. It is as wrong to say the Inuit died at forty because of their diet as to say they were the healthiest people alive because of it.

And the corollary that rarely gets mentioned: life expectancy in these populations rose as the traditional diet was abandoned, because antibiotics, obstetric care, vaccination and heated housing arrived at the same time. Neither side gets to run that correlation. What the record shows is a mortality profile dominated by causes that have nothing to do with the meat-versus-plants question.

So were the Maasai and the Inuit free of heart disease?

The Maasai had low rates of clinical coronary events alongside documented coronary disease; for the Inuit, a low event rate was never actually established. In the Maasai case the events were suppressed by an extraordinary bundle of factors, none of which is the composition of the diet:

• Physical activity almost no modern person approaches. Mbalilaki et al. (2010) measured Maasai energy expenditure at roughly 2,565 kcal/day above basal requirements, the equivalent of running a marathon daily. The authors concluded the Maasai are protected by activity, not by an unknown genetic factor.
• Chronic calorie restriction. Energy intakes ran at 50 to 80% of recommended levels, and fewer than 5% of Maasai households reported food security (Goldman et al. 2025).
• Leanness, at a mean BMI in the high teens to low twenties.
• Altitude, around 2,000 m, which improves lipid profiles through hypoxia pathways (Goldman et al. 2025).
• Infectious burden, and this one is stronger than it looks. Malaria, tuberculosis and brucellosis all depress cholesterol. So do intestinal worms, which matters here because soil-transmitted helminth prevalence in school-aged children across Maasai areas of Narok County has stayed above 20% even under a national deworming program (Okoyo et al. 2024). A systematic review of 84 studies found helminth-infected people and animals generally carry better lipid profiles than uninfected ones, with lower LDL the most frequently reported finding (Rennie et al. 2023). And a cluster-randomized trial in Uganda tested it the hard way: four years of intensive deworming raised LDL compared with standard treatment, with a dose-response running the other way, so that the more helminth species a person carried, the lower their cholesterol (Sanya et al. 2020). That is interventional evidence, not correlation. Some of the celebrated Maasai low cholesterol is a sickness signal, and the worms were part of it.
• Short lifespan. A 2025 review reports an estimated life expectancy of about 45 years for a twenty-year-old Maasai man, against 58 for Kenyan men in the 1989 census, without making clear whether 45 is remaining years or age at death (Goldman et al. 2025). The plainer figure is Mann’s own: only three of the men he examined were over 55. Few lived long enough to reach the age at which heart disease usually shows itself.

Part 2: They did not eat what you are being sold

Two substitutions do the work in both arguments.

What did the Inuit and the Maasai actually eat?

The Arctic diet was not carbohydrate-free or plant-free. It included berries (crowberries, cloudberries, blueberries, cranberries), roots, tubers and tundra greens, seaweed, fermented preparations, glycogen from freshly killed raw meat and organs, and the partially digested plant contents of caribou stomachs, eaten deliberately.

Vitamin C, the nutrient whose absence should have produced scurvy, came from raw organ meat and muktuk, whale skin and blubber. That detail is almost always dropped, and it matters: the diet worked partly because it was raw and whole-animal. A plate of cooked steak is not the same food.

The Maasai diet was a dairy diet, not a meat diet. In Nestel and Geissler’s fieldwork, dairy supplied about 42% of total calories and meat and animal fat about 9% among adult women (Nestel & Geissler 1993). Biss reported men drinking three to five liters of milk a day. Nestel (1989) found women and children ate meat roughly two to five times a month. Blood was supplemental and seasonal, used mainly when milk supplies fell in the dry months.

So when the Maasai are deployed to defend a steak-and-eggs diet, the citation is to a population whose animal-food calories came overwhelmingly from milk. The argument has the wrong food.

It also has the wrong quantity. This was a calorie-scarce diet in a body doing a marathon’s work. In the largest published survey of carnivore-diet adherents (Lennerz et al. 2021, n=2,029), median LDL cholesterol was 172 mg/dL and median total cholesterol 256. Traditional Maasai total cholesterol, LDL and everything else combined, ran near 125 to 135 (Mann et al. 1964; Biss et al. 1971, as reported by Goldman et al. 2025), so the carnivore group’s LDL alone sat well above the Maasai total.

Is marine fat or fermented milk the same as butter and beef fat?

This is the chemical bait-and-switch, and it runs in both cases, in different ways. In the Arctic the switch is in the class of fat: marine fat traded for ruminant fat. In the Maasai case the fat was already ruminant, so the switch is in the matrix and the amount: raw fermented whole milk in a calorie-short diet, traded for butter, tallow and steak in a calorie-rich one.

Saturated fat is not one molecule. Controlled feeding work maps which fatty acids raise LDL: lauric, myristic and palmitic acids raise it, with myristic and palmitic most potent, while stearic acid is roughly neutral because the body rapidly converts it (Bonanome & Grundy 1988; Mensink et al. 2003).

The Arctic fat was marine fat, dominated by long-chain omega-3s from animals at the top of an algae-based food chain. The fat the argument is used to defend is ruminant fat, and it is a different molecule set:

• Ruminant fat passes through the rumen, where microbes hydrogenate unsaturated fats. The process is incomplete, so beef and dairy fat carry a few percent naturally occurring trans fats.
• Those same microbes saturate omega-3s as readily as omega-6s, which is why even grass-fed beef remains a mediocre omega-3 source, a point covered in Animal fat, plant fat, and your arteries. The “grass-fed is different” defense dies in the rumen.

The Maasai fat was raw fermented zebu milk, in a food matrix. Butter is the myristic-and-palmitic heavyweight plus roughly 3% natural trans fats, generally the worst common fat for LDL in ordinary use. Beef tallow and lard carry less myristic acid and a substantial stearic fraction, so they are less bad than butter and still worse than any liquid plant oil.

The argument runs: a population eating marine omega-3 fat, or raw fermented milk, was healthy, therefore eat butter and feedlot beef. Those are not the same premise.

Note that the food-matrix literature actually cuts against the people who cite it. The matrix argument helps fermented whole dairy and hurts stripped fats like tallow and refined coconut oil, which have no matrix at all.

Did either diet contain much fiber?

The traditional Maasai diet contained essentially no fruits, vegetables or pulses. Fiber is the dietary factor most consistently linked to living longer: a synthesis commissioned for WHO guidelines, pooling 185 prospective studies and 58 trials, found the highest fiber consumers had 15 to 30% lower all-cause and cardiovascular mortality (Reynolds et al. 2019). Meat, milk, eggs and blood contain none.

The Maasai’s documented anemia and vitamin A and C deficiencies are what that structural gap looks like in a real population.

Part 3: The genetics, and why nothing transfers

This is where both arguments fail hardest, because it is not epidemiology. It is allele frequencies.

What is the CPT1A Arctic variant?

The CPT1A p.P479L variant was identified through strong signals of positive selection (Clemente et al. 2014; Fumagalli et al. 2015). CPT1A is the rate-limiting enzyme importing long-chain fatty acids into mitochondria for oxidation. The variant sharply reduces enzyme activity and reshapes circulating fatty-acid profiles.

Allele frequency: roughly 0.68 to 0.85 in Arctic populations. Essentially absent in European, African and East Asian populations.

How do the Maasai digest so much milk?

Adult milk digestion in the Maasai rests on East-African-specific regulatory variants upstream of LCT, chiefly C-14010, plus T/G-13915 and C/G-13907. These arose independently of the European C/T-13910 variant, sit on different haplotype backgrounds, and enhance LCT promoter transcription in vitro (Tishkoff et al. 2007). Haplotype homozygosity extends over 2 Mb, the signature of a hard sweep across roughly 7,000 years.

Separately, Schlebusch et al. (2013) found the LCT-region selection signal is the strongest in the entire Maasai genome, and stronger than the equivalent European signal. The C-14010 allele reaches about 32% in Kenyan Nilo-Saharans and about 58% in the HapMap Maasai sample.

Wagh et al. (2012) scanned Maasai data and found the top genome-wide signal in a region containing LCT/MCM6 and Rab3GAP1, with the highest-Fst non-synonymous SNP in FABP1, which lowers LDL and triglycerides, at about 45% frequency. Combined with Biss’s metabolic finding that the Maasai absorbed roughly twice the cholesterol of white Americans while suppressing their own synthesis by about 50%, against roughly 25% in other populations, this is a genuine population-specific adaptation. As Goldman and colleagues put it, this is not a trainable trait (Goldman et al. 2025).

Why do Inuit and European fat genes point in opposite directions?

The FADS gene cluster builds long-chain fatty acids. In Greenlandic Inuit, selection favored variants that suppress that pathway, sensible when your food already delivers abundant EPA and DHA (Fumagalli et al. 2015). Buckley et al. (2017) showed that selection on FADS in Europeans ran the opposite direction, favoring variants that increase production of long-chain fats from the short-chain precursors you get from plants.

The same gene cluster. Two populations. Opposite directions. The European story is not simple, since the alleles under selection shifted before and after the arrival of farming, but the contrast with the Arctic holds.

Meanwhile AMY1, the salivary amylase gene, has been multiplying in our lineage for a very long time. Two 2024 analyses dated the first duplication to possibly 800,000 years ago and found hunter-gatherers 45,000 years ago already carrying four to eight copies, with European farmers rising from around four to around seven in roughly four thousand years (Yilmaz et al. 2024; Bolognini et al. 2024).

Milk in East Africa. Marine fat in the Arctic. Plant fat in Europe. Starch nearly everywhere. These are convergent, independent, local adaptations to different foods, which is evidence against a single ancestral human diet, not for one. Every time an advocate reaches for another population, they add a data point to the pile showing that humans adapt locally and that no local adaptation generalizes.

Did these genetic adaptations have costs?

This is the part that should end the “look how healthy the adaptation made them” framing.

The CPT1A variant impairs fasting ketogenesis, putting homozygous infants at risk of hypoglycemia and seizures during illness or fasting:

• Gessner et al. (2016), 110 Alaska Native infant deaths against 395 controls: among western and northern Alaska residents, homozygosity carried an adjusted odds ratio of 2.5 (95% CI 1.3–5.0) for infant death.
• Sinclair et al. (2012): in British Columbia First Nations, homozygotes were overrepresented in unexpected infant deaths, OR 3.92 (95% CI 1.69–9.00).
• Collins et al. (2021), 2,225 Nunavut Inuit children: homozygosity associated with lower respiratory tract infection admission (aOR 2.5) and otitis media (aOR 3.0).

Causality is debated, but the signal is strong enough that some jurisdictions screen newborns. The Inuit FADS alleles carry costs too, with effect sizes on the order of two centimeters of height and four kilograms of weight.

This is antagonistic pleiotropy in a real population: selection drove an allele to near-fixation because of what it did for adults processing a high-fat diet, and it carried a cost paid by infants, which selection was in no position to weigh against the benefit.

The concept is unpacked in the companion piece. The honest summary here is that the adaptation which made an extreme diet metabolically survivable is entangled with a higher-risk infant phenotype, in the adapted population. In everyone else, the adaptation is simply absent.

Did lactase persistence spread because milk is healthy?

Evershed et al. (2022) analyzed pottery lipid residues across European prehistory and found that people were drinking milk for thousands of years before lactase persistence became common, and that the gene’s rapid spread was probably driven by famine and disease, periods when milk-induced diarrhea in a lactase-non-persistent person turned lethal.

Lactase persistence did not spread because milk is optimal. It spread because during famine, not being able to digest it could kill you. That is a survival adaptation to scarcity, the same category as the Arctic diet, not a demonstration of dietary optimum.

Does drinking more milk over a lifetime help you live longer?

Bergholdt et al. (2018) ran a Mendelian randomization study in the Danish general population using lactase-persistence genotype as an instrument for lifelong milk intake. Mendelian randomization sidesteps confounding, because genotype is assigned at conception, before any lifestyle choice.

The result: no effect of genetically predicted lifelong higher milk intake on mortality. It is one study in a young literature, and I am not going to overstate it.

But notice what it does. The strongest natural experiment available on lifelong milk drinking, using the very gene the Maasai argument rests on, finds no survival benefit.

Part 4: The sampling error, and the population both arguments lose to

Step back from the specifics and look at the shape.

The Arctic is the coldest, least plant-accessible environment any human population has inhabited. East African pastoralism is a specific ecological solution to semi-arid savanna. Neither is a claim about optimal human nutrition.

The sampling problem is the same one that inflates meat in the archaeological record: bone collagen survives best in cold dry caves, so the isotope record over-represents glacial Europe, and isotopes see protein rather than calories. A forager who got her protein from reindeer and half her calories from cooked roots reads as a carnivore. It is like sampling only the Inuit and concluding humans are seal-eaters, a bias taken apart in full in how humans evolved to eat, or sampling only the Maasai and concluding humans are milk-drinkers.

When Pontzer and Wood (2021) reviewed the forager evidence, they found the plant-to-animal balance varies widely and tracks climate and economy rather than anything about human nature. A roughly even split prevails among warm-climate hunter-gatherers; cold-climate societies and those relying on fishing or herding eat more meat; warm-climate foragers and part-time farmers eat more plants. Paleolithic diets, they concluded, would have been remarkably variable across time and space. What foragers share is a pattern, whole foods and enormous variety and a great deal of fiber and constant physical work, not a ratio.

One more constraint explains the Arctic diet’s shape better than any story about optimality: there is a ceiling on how much protein a human can eat, somewhere around 35 to 40 percent of calories, beyond which rabbit starvation sets in with nausea, diarrhea and eventually death, a phenomenon Arctic explorers documented well (Speth & Spielmann 1983; Bilsborough & Mann 2006). Any all-meat human diet has to be a high-fat diet. That is not a preference. It is the only shape a viable diet can take with those ingredients and this body.

Which population has the healthiest arteries ever measured?

Kaplan et al. (Lancet, 2017) CT-scanned 705 Tsimané adults in the Bolivian Amazon: 85% had no detectable coronary artery calcium, against 14% of American adults of similar age. Their arteries were estimated to have aged roughly 28 years behind a comparable US population. Their diet is about 72% carbohydrate and 14% fat, and their mean LDL is around 91 mg/dL. The paper’s own conclusion leads with a lifetime of very low LDL.

Before anyone runs that as an ancestral argument, it deserves the same scrutiny the other two just got. The Tsimané are also extraordinarily active, lean and non-smoking, and each of those independently lowers cardiovascular risk, so diet is not the only thing keeping their arteries clean. But the scrutiny cuts differently here. They also carry a heavy burden of infection and inflammation, which pushes cardiovascular risk up rather than down, and they have the clean arteries anyway. That makes the Tsimané not a confounded story to wave off, but a population that should have had the disease on every count except diet and activity, and did not.

Which is exactly the point. The ancestral appeal is unfalsifiable by selection: whichever population you name, someone names another. Here are the three populations this argument turns on, with what imaging and autopsy actually found:

Population	Diet	Arteries
Maasai	~42% of calories from dairy, ~9% meat (adult women), no fiber	Coronary atherosclerosis “equal to old U.S. men” (Mann 1972)
Unangan / Inuit	Marine mammal fat and fish	Atherosclerosis in three of five Unangan mummies; calcification in three of four Greenlandic Inuit
Tsimané	~72% carbohydrate, plant-based staples	85% with zero coronary calcium, the best ever measured

The two populations invoked to defend animal foods are the two with documented arterial disease. That is not cherry-picking. These are the populations the argument itself chooses.

Part 5: What happened when the diets changed

The Maasai. Government ranching programs from the 1960s and 70s pushed toward processed foods, refined grain and sugar. Per Pressler et al. (2022), the shift brought a 14 to 19% calorie increase, more smoking and alcohol, less activity, a BMI rise of about 2 kg/m², and rising glucose intolerance. Diabetes went from no evidence among rural Maasai in 1931 to impaired glucose tolerance or diabetes in 5.2% of rural men and 7.8% of rural women by 2006, rising to 11.8% and 26% in urban samples that also included people from other groups.

Even relatively traditional communities now show substantial risk. Diarz et al. (2020) surveyed 894 adults in the Ngorongoro Conservation Area and found hyperlipidemia in 23.7%, pre-hypertension in 37.0% and hypertension in 9.8%, with higher red-meat consumption significantly associated with hyperlipidemia.

The Arctic. Pressler and colleagues’ review also reports that obesity among Inuit was infrequent, under 6%, in 1955 to 1959, and that by 2007 it affected 15.8% of Inuit men and 25.5% of Inuit women. Diabetes rates in Alaska and Greenland Inuit rose almost threefold between the 1960s and 1970s, and arterial calcification increased fivefold in families that gave up a nomadic life (Pressler et al. 2022).

What both transitions document is evolutionary mismatch: a genome that stayed put while the world around it changed inside a generation. The Arctic and Maasai cases are two of the cleanest natural experiments in it, and several more, including the Pima, the Tarahumara and Japanese migrants, are laid out in The Future Is in Our Hands.

Two things must be said honestly about this.

First, the Pressler review, looking across the four populations it reviewed systematically and seven more it examined for bias, concluded that the outcomes cannot be attributed to saturated fat or total fat consumption. What it implicates is refined carbohydrate and sugar; Maasai carbohydrate intake rose 39% in men and 362% in women. Anyone using this section to argue “see, plants did it” is misreading it, and anyone using it to exonerate saturated fat is over-reading it. Population transitions cannot isolate saturated fat, because saturated fat moves in lockstep with calories, processing, sugar and inactivity. Ruling it in or out requires controlled feeding trials and genetic evidence, which is a different literature.

Second, and decisively for the argument at hand: there is no permanent dietary immunity here. When activity fell and calories became available, both populations got what everyone else gets. And within the Maasai’s own population, more meat tracked with worse lipids.

Part 6: The five errors, and how to answer each version

Laid out plainly, both arguments commit:

1. An outdated-and-misread-evidence error. The Maasai version cites Mann’s 1964 clinical snapshot and ignores Mann’s own 1972 autopsies. The Arctic version rests on the Inuit paradox, which specialists retired two decades ago and which the mummy data contradict directly.
2. A naturalistic fallacy. A survival adaptation to plant scarcity, or to famine, is not a demonstration of dietary optimum. Especially not for populations with 57% child stunting, widespread anemia, and few men surviving past 55.
3. A genetic-generalization error. CPT1A, LCT C-14010, FABP1 and the Inuit FADS alleles are population-specific sweep-selected variants, absent from most of humanity, and European FADS selection ran the opposite way. The adaptations do not transfer, and they carry costs even where they exist.
4. A bait-and-switch on the food. Marine omega-3 fat from raw whole animals, or raw fermented milk at 42% of women’s calories against 9% from meat, is not butter, cheese, tallow and feedlot beef.
5. A strawman of plant-based eating. “Tofu or spring salad” is not a well-planned plant-based diet, and nobody proposes salad as Arctic winter provisioning.

What is the short answer to the Inuit argument?

The Inuit paradox was retired by the specialists who later examined it. The original claim came from unreliable death records, and when CT scanners were pointed at actual Arctic mummies they found atherosclerosis in three of five Unangan hunter-gatherers and three of four Greenlandic Inuit. These populations also had higher stroke mortality, shorter life expectancy, and up to three times the infant mortality of their national populations. They also weren’t eating “meat and fat”: they ate berries, roots, seaweed and raw organs, which is where their vitamin C came from. And they carried genetic variants, CPT1A and FADS, that are near-universal in the Arctic and essentially absent in everyone else, with European FADS selection running the opposite direction toward plant-fat processing. The CPT1A variant is itself associated with elevated infant mortality, though whether it causes the deaths is contested. Meanwhile the population with the healthiest arteries ever measured is the Tsimané of Bolivia, 85% with zero coronary calcium, on a diet about 72% carbohydrate.

What is the short answer to the Maasai argument?

The man who made the Maasai famous, George Mann, also did the autopsies, and his 1964 study was funded in part by the National Live Stock and Meat Board. In 1972 he opened fifty Maasai men and found “intimal thickening by atherosclerosis which equaled that of old U.S. men.” They had the plaque. They were protected from events by burning about 2,565 calories a day above basal, a marathon’s worth, while eating 50 to 80 percent of recommended calories, staying very lean, living at 2,000 meters with endemic malaria and TB lowering their lipids, and few of the men living past 55. Their diet also wasn’t what you think: among women, dairy was about 42 percent of calories and meat about 9, they ate meat two to five times a month, and 57 percent of their children were stunted. Their milk digestion runs on an East African LCT variant absent from most of humanity, and when researchers used that exact gene as a natural experiment in Denmark, lifelong higher milk intake showed no mortality benefit.

What the argument is actually being used to defend

One more thing worth saying, because it is usually left implicit.

Arctic subsistence hunting and Maasai pastoralism are low-input systems on land that grows little else. Whatever you think of them, they are not what the argument is deployed to protect. It is deployed to protect an industrial system in which animal products occupy about 83% of the world’s farmland and generate 56 to 58% of food’s emissions while supplying 37% of protein and 18% of calories (Poore & Nemecek 2018). Producing 100 g of protein from beef raised in dedicated beef herds emits roughly 50 kg CO₂-equivalent on average, and even the lowest-impact animal products typically exceed the average impacts of plant proteins.

Citing seal hunters and nomadic cattle herders to defend feedlots is its own category of error, separate from the five above. That ledger is taken up in Rewilding the Plate and The 86% meme, debunked.

So what does the evidence support?

This post is about what these two populations do and do not show. If you have decided the science will never be settled to your satisfaction, there is a short version of the argument written for exactly that position. The positive case for how to eat is a different piece, and it lives in the full evidence review and in The Future Is in Our Hands. The short version, stated no more strongly than the evidence allows:

Shifting toward whole plant foods and away from red and processed meat is well supported. That rests on LDL’s established causal role, on substitution analyses, on a diet gradient inside single cohorts, on an identical-twin trial, on a formal carcinogen review, and on the structural fact that fiber exists in one kingdom and not the other.

A well-planned vegan diet is a defensible endpoint of that gradient, conditional on B12 without exception and attention to calcium, vitamin D, iodine and protein. The support for that is weaker and takes the form of an absence: no study identifies a level of animal food whose addition to a well-planned plant-based diet improves a hard outcome.

The countersignals are real and are handled in full elsewhere. The stroke association in EPIC-Oxford is unresolved. Part of the vegan fracture signal resists the calcium explanation, and the same cohort found elevated hip fracture in fish eaters, which no vegan-nutrient account explains. Those belong in the record, and they are covered in do vegans have weaker bones? and The Great B12 Gamble.

None of that is what the Maasai or the Inuit establish. What they establish is that human populations adapt locally, at a cost, to whatever their environment offers, and that the adaptation does not travel.

Whether any of this reaches the next generation, and the one after that, is a separate question with its own evidence, taken up in The Future Is in Our Hands.

What to actually do with this

1. Cut ultra-processed food. The least contested finding here, and the actual lesson of both nutrition transitions.
2. Eat a whole-food, plant-forward pattern. Legumes daily if you take one instruction from this page.
3. If going fully plant-based, plan it. B12 without exception, then vitamin D, iodine, calcium, iron with vitamin C, zinc, selenium, adequate protein, daily ALA.
4. Move like it matters. The most defensible lesson from the Maasai is not dietary. A marathon a day covers a multitude of sins, and most of us are not running one.

What would change this conclusion: a well-powered study showing that people without these adaptations achieve equal or better outcomes on a high-animal-product diet at matched modern activity levels; evidence that the Maasai cholesterol-suppression phenotype is inducible in non-adapted people; or a long-duration trial with hard endpoints favoring animal-based eating. None exists.

Caveats

• The foundational data on both populations are 50+ years old, using mid-century methods, with the cardiovascular work resting mainly on men and the dietary detail mainly on women and children. Read effect sizes cautiously in both directions.
• Biss (1971) and Mann (1972) genuinely disagreed on atherosclerosis severity. I have weighted Mann’s larger series and his stated critique of Biss, but the disagreement is real.
• The relative contributions of genetics, activity, leanness, altitude and infection to Maasai lipid levels have never been precisely partitioned. Mbalilaki’s group argued activity dominates; Biss’s metabolic data argue genetics contributes. Both are probably right.
• Three of five mummies is a proportion of five. It establishes presence, not rate.
• The CPT1A infant-mortality association is contested as to causality, though strong enough to prompt newborn screening in some jurisdictions.
• Fermented whole dairy does appear less atherogenic than red-meat fat, and the fermented-dairy food-matrix literature is a live scientific position, not a talking point.
• The nutrition-transition literature implicates refined carbohydrate and sugar as primary drivers. Do not overread it in either direction.
• Some prevalence figures trace to older primary sources verified through secondary citation. The Martin/Petrucka/Buza micronutrient study appeared in a lower-tier open-access journal; treat those specific numbers as suggestive.
• The 2025 narrative review of Maasai dietary practices was written by authors with plant-based nutrition affiliations. Its individual claims are sourced to primary literature, but the orientation should be named, as should the fact that most sources on the other side are commercial books and blogs rather than peer-reviewed work.
• Wagh et al. (2012) used a modest sample and identifies candidate loci under selection, not proven causal variants.
• “Healthiest people in North America” is an unquantified claim. This post evaluates it against measurable endpoints: cardiovascular disease, mortality, life expectancy, infant mortality.
• None of this addresses the ethical or environmental case, which stands or falls independently.

References

The Maasai

1. Mann GV, Shaffer RD, Anderson RS, Sandstead HH. Cardiovascular disease in the Masai. J Atheroscler Res. 1964;4:289–312. https://doi.org/10.1016/S0368-1319(64)80041-7
2. Mann GV, Spoerry A, Gray M, Jarashow D. Atherosclerosis in the Masai. Am J Epidemiol. 1972;95(1):26–37. https://academic.oup.com/aje/article-abstract/95/1/26/167903
3. Biss K, Ho KJ, Mikkelson B, Lewis L, Taylor CB. Some unique biologic characteristics of the Masai of East Africa. N Engl J Med. 1971;284:694–9. https://www.nejm.org/doi/abs/10.1056/NEJM197104012841304
4. Nestel PS. Food intake and growth in the Maasai. Ecol Food Nutr. 1989;23:17–30. https://doi.org/10.1080/03670244.1989.9991085
5. Nestel PS, Geissler CA. Lipid intakes of Maasai women and children. Ecol Food Nutr. 1993;29:155–65. https://doi.org/10.1080/03670244.1993.9991299
6. Nestel PS, Geissler C. Potential deficiencies of a pastoral diet: a case study of the Maasai. Ecol Food Nutr. 1986;19:1–10. https://doi.org/10.1080/03670244.1986.9990941
7. Mbalilaki JA, Masesa Z, Strømme SB, et al. Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians. Br J Sports Med. 2010;44(2):121–6. https://doi.org/10.1136/bjsm.2007.044966
8. Goldman DM, Waterfall TJ, Nagra M. Traditional Maasai dietary practices and their inapplicability to modern carnivore diets: a narrative review. Cureus. 2025;17(2):e78448. https://doi.org/10.7759/cureus.78448 Authors report ties to the Game Changers Institute and other nutrition companies.
9. Lawson DW, Borgerhoff Mulder M, Ghiselli ME, et al. Ethnicity and child health in northern Tanzania. PLOS ONE. 2014;9(10):e110447. https://doi.org/10.1371/journal.pone.0110447
10. Hansen AW, Christensen DL, Larsson MW, et al. Dietary patterns, food and macronutrient intakes among adults in three ethnic groups in rural Kenya. Public Health Nutr. 2011;14:1671–9. https://doi.org/10.1017/S1368980010003782
11. Diarz EJ, Leyaro BJ, Kivuyo SL, et al. Red meat consumption and its association with hypertension and hyperlipidaemia among adult Maasai pastoralists. PLOS ONE. 2020;15(6):e0233777. https://doi.org/10.1371/journal.pone.0233777
12. Rennie C, Fernandez R, Donnelly S, McGrath KC. The impact of helminth infection on cardiometabolic disease and risk factors: a systematic review. PLOS Neglected Tropical Diseases. 2023;17(2):e0011022. https://doi.org/10.1371/journal.pntd.0011022
13. Sanya RE, Webb EL, Zziwa C, et al. The effect of helminth infections and their treatment on metabolic outcomes: results of a cluster-randomized trial. Clinical Infectious Diseases. 2020;71(3):601-613. https://doi.org/10.1093/cid/ciz859
14. Okoyo C, et al. Epidemiology of soil-transmitted helminthiasis among school-aged children in pastoralist communities of Kenya: a cross-sectional study. PLOS ONE. 2024;19(5):e0304266. https://doi.org/10.1371/journal.pone.0304266
15. Martin H, Petrucka P, Buza J. Determination of vitamins A, C and D status among Maasai women of reproductive age. Open Access Libr J. 2014;1(8):e893. https://doi.org/10.4236/oalib.1100893

The Arctic

1. Bjerregaard P, Young TK, Hegele RA. Low incidence of cardiovascular disease among the Inuit: what is the evidence? Atherosclerosis. 2003;166(2):351–7. https://doi.org/10.1016/S0021-9150(02)00364-7
2. Fodor JG, Helis E, Yazdekhasti N, Vohnout B. “Fishing” for the origins of the “Eskimos and heart disease” story. Can J Cardiol. 2014;30(8):864–8. https://doi.org/10.1016/j.cjca.2014.04.007
3. Thompson RC, Allam AH, Lombardi GP, et al. Atherosclerosis across 4000 years of human history: the Horus study. Lancet. 2013;381:1211–1222. https://doi.org/10.1016/S0140-6736(13)60598-X
4. Gessner BD, Wood T, Johnson MA, Richards CS, Koeller DM. Evidence for an association between infant mortality and homozygosity for the Arctic variant of CPT1A. Genet Med. 2016;18:933–939. https://doi.org/10.1038/gim.2015.197
5. Sinclair GB, et al. Carnitine palmitoyltransferase I and sudden unexpected infant death in British Columbia First Nations. Pediatrics. 2012;130(5):e1162–9. PubMed title search
6. Collins SA, Surmala P, Osborne G, et al. Causes and risk factors for infant mortality in Nunavut, Canada 1999-2011. BMC Pediatr. 2012;12:190. DOAJ record
7. Collins SA, Edmunds S, Akearok GH, et al. Association of the CPT1A p.P479L metabolic gene variant with childhood respiratory and other infectious illness in Nunavut. Front Pediatr. 2021;9:678553. https://doi.org/10.3389/fped.2021.678553
8. Wann LS, Narula J, Blankstein R, et al. Atherosclerosis in 16th-century Greenlandic Inuit mummies. JAMA Netw Open. 2019;2(12):e1918270. https://doi.org/10.1001/jamanetworkopen.2019.18270 Funded by the Paleocardiology Foundation, a charity unrelated to industry.
9. Inuit Circumpolar Council. About ICC: representing approximately 180,000 Inuit across Alaska, Canada, Greenland and Chukotka. inuitcircumpolar.com
10. United Nations Department of Economic and Social Affairs. World Population Prospects 2024: Summary of Results. Press release, July 11, 2024. un.org

Genetics and adaptation

1. Clemente FJ, Cardona A, Inchley CE, et al. A selective sweep on a deleterious mutation in CPT1A in Arctic populations. Am J Hum Genet. 2014;95:584–589. https://doi.org/10.1016/j.ajhg.2014.09.016
2. Fumagalli M, Moltke I, Grarup N, et al. Greenlandic Inuit show genetic signatures of diet and climate adaptation. Science. 2015;349:1343–1347. https://doi.org/10.1126/science.aab2319
3. Buckley MT, Racimo F, Allentoft ME, et al. Selection in Europeans on fatty acid desaturases associated with dietary changes. Mol Biol Evol. 2017;34:1307–1318. https://doi.org/10.1093/molbev/msx103
4. Tishkoff SA, Reed FA, Ranciaro A, et al. Convergent adaptation of human lactase persistence in Africa and Europe. Nat Genet. 2007;39:31–40. https://doi.org/10.1038/ng1946
5. Schlebusch CM, Sjödin P, Skoglund P, Jakobsson M. Stronger signal of recent selection for lactase persistence in Maasai than in Europeans. Eur J Hum Genet. 2013;21:550–553. https://doi.org/10.1038/ejhg.2012.199
6. Wagh K, Bhatia A, Alexe G, et al. Lactase persistence and lipid pathway selection in the Maasai. PLOS ONE. 2012;7(9):e44751. https://doi.org/10.1371/journal.pone.0044751
7. Evershed RP, et al. Dairying, diseases and the evolution of lactase persistence in Europe. Nature. 2022;608:336–345. https://doi.org/10.1038/s41586-022-05010-7
8. Bergholdt HKM, et al. Lactase persistence, milk intake, and mortality in the Danish general population: a Mendelian randomization study. Eur J Epidemiol. 2018;33(2):171–181. https://doi.org/10.1007/s10654-017-0328-x
9. Yilmaz F, Karageorgiou C, Kim K, et al. Reconstruction of the human amylase locus reveals ancient duplications seeding modern-day variation. Science. 2024;386:eadn0609. https://doi.org/10.1126/science.adn0609
10. Bolognini D, et al. Recurrent evolution and selection shape structural diversity at the amylase locus. Nature. 2024;634:617–625. https://doi.org/10.1038/s41586-024-07911-1
11. Pontzer H, Wood BM. Effects of evolution, ecology, and economy on human diet. Annu Rev Nutr. 2021;41:363–385. https://doi.org/10.1146/annurev-nutr-111120-105520

Comparison populations and transitions

1. Kaplan H, Thompson RC, Trumble BC, et al. Coronary atherosclerosis in indigenous South American Tsimane. Lancet. 2017;389:1730–1739. https://doi.org/10.1016/S0140-6736(17)30752-3
2. Pressler M, Devinsky J, Duster M, et al. Dietary transitions and health outcomes in four populations: a systematic review. Front Nutr. 2022;9:748305. https://doi.org/10.3389/fnut.2022.748305

Fat chemistry, fiber and diet evidence

1. Bonanome A, Grundy SM. Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels. N Engl J Med. 1988;318:1244–1248. https://doi.org/10.1056/NEJM198805123181905
2. Mensink RP, Zock PL, Kester ADM, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol. Am J Clin Nutr. 2003;77:1146–1155. https://doi.org/10.1093/ajcn/77.5.1146
3. Reynolds A, Mann J, Cummings J, et al. Carbohydrate quality and human health: a series of systematic reviews and meta-analyses. Lancet. 2019;393:434–445. https://doi.org/10.1016/S0140-6736(18)31809-9
4. Lennerz BS, Mey JT, Henn OH, Ludwig DS. Behavioral characteristics and self-reported health status among 2029 adults consuming a “carnivore diet.” Curr Dev Nutr. 2021;5(12):nzab133. https://doi.org/10.1093/cdn/nzab133
5. Speth JD, Spielmann KA. Energy source, protein metabolism, and hunter-gatherer subsistence strategies. J Anthropol Archaeol. 1983;2(1):1–31. https://doi.org/10.1016/0278-4165(83)90006-5
6. Bilsborough S, Mann N. A review of issues of dietary protein intake in humans. Int J Sport Nutr Exerc Metab. 2006;16(2):129–152. https://doi.org/10.1123/ijsnem.16.2.129
7. Poore J, Nemecek T. Reducing food’s environmental impacts through producers and consumers. Science. 2018;360:987–992. https://doi.org/10.1126/science.aaq0216 PMID 29853680. Erratum: Science. 2019;363(6429):eaaw9908, https://doi.org/10.1126/science.aaw9908; it does not change the figures cited here.

This is health information, not medical advice. Anyone with questions about their own diet should consult a physician or registered dietitian, ideally one who practices lifestyle medicine, since that field puts the evidence first and respects a person’s values.

Last updated: October 6, 2026, 2:04 PM ET