How Much Have Human Dietary Requirements Evolved in the Last 10,000 Years?

A hallmark of the Primal Blueprint is that our genetics were shaped by our ancestral environment. That the foods to which we had access, the amount of sun and stress and sleep to which our bodies became accustomed, the movement patterns in which we engaged represented environmental factors that exerted selective pressure on our genetic makeup and phenotypic expression to make us who we are today. As a result, heeding those environmental factors generally results in excellent health. And, even more importantly, many evolutionarily novel environmental factors – like grains, refined sugar, and high omega-6 vegetable oils (plus chronic stress, poor sleep, and all that other good stuff ) – are things to which we’ve only recently been exposed. When we are exposed to them in excess, like in say 21st century America, it generally results in poor health. Hence our current predicament.

But what about genetic variation within a species? After all, it’s not like an entire species suddenly evolves all at once, neatly and cleanly, taking all its members with it into the new genome. Evolution is a messy process. There’s a lot of genetic groundwork laid before a species “becomes” another one. There are tons of mutations that never amount to anything, or that amount to plenty of subtle changes. And we Primals know of a few changes that have occurred within the framework of Homo sapiens in response to dietary pressures.

The first is, of course, lactase persistence. I’ve written about it before, and since its entrance into our diet around 9,000 years ago it’s become an incredibly prevalent mutation – around 35% of human adults worldwide still insist on producing lactase.

Second is salivary amylase production. Salivary amylase predigests starch as you chew it. It’s an enzyme that coats starch in the mouth and stays with it after you swallow it, continuing to break it down. Fruit-eating chimpanzees produce salivary amylase, but far less than humans, who eat more starches and have more copies of the gene. But that’s a whole different species, so it’s not that surprising. However, when you compare traditionally starch-eating human populations to populations with traditionally low-starch diets, the former tend to have more copies of the amylase gene than the latter.

For more intra-species genetic variation, consider the single-nucleotide polymorphism, or SNP. The SNP (or “snip”) is a variation in DNA sequencing, the most common type of genetic variation in humans. Our DNA is comprised of individual nucleotides strung together, and a SNP occurs when a single nucleotide in the genome sequence is altered – say, from AAGCCTA to AAGCTTA (the spot that once held a cytosine nucleotide now has a thymine nucleotide, indicated by bolding and italicizing).

SNPs can affect the way genes work if they fall on a DNA “coding sequence.” When that happens, the slight variation in nucleotides can change the biological function of the particular DNA sequence, effectively altering the way the gene works. Risks for certain diseases might amplify (or decrease), certain energy pathways may be down- or up-regulated, and resistance to climate may change as a result of SNPs. They occur about once in every 300 nucleotides, and, like any component of the evolutionary process examined in isolation, are totally random. They may be beneficial, harmful, or have no effect at all (the vast majority of SNPs do not fall within coding sequences and thus have no discernable effect). What gives them “direction” or “purpose” is how they interact with the environment and whether or not they confer a reproductive or survival advantage.

So, do any SNPs affect the way we process food and metabolize energy? Because, let’s face it: that’s what we’re really interested in here.

There are some, and there’s even evidence that some of them are growing more prevalent in response to dietary pressures. A fairly recent paper examined this very question. The authors took all available SNP data spanning 61 human population data sets, four ecoregion variables (polar, humid temperate, humid tropical, dry), four subsistence variables (agriculture, pastoralism, foraging, horticulture), and three main dietary components (cereal grains, roots and tubers, or fat, meat and milk) and tried to match the prevalence of genic and nonsynonymous SNPs (SNPs that have an effect on the gene and its function) to these variables.

They found some interesting data, but not a ton (in my opinion):

  • That people subsisting on folate-poor roots and tubers for a significant amount of their calories showed greater incidence of a SNP relating to altered folate biosynthesis.
  • That cereal grain eaters showed an alteration in the breakdown of plant fats using a type of pancreatic lipase specific to plant fats (separate from regular pancreatic lipase, which is used for other fats) and a SNP predisposing them to type 2 diabetes.
  • Certainly nothing that makes me reevaluate my dietary choices.

Some other interesting, diet-related SNPs include:

  • Rs1800562(A:A), which codes for hemachromatosis, or excessive iron accumulation. For Northern European folks (in whom the SNP most often appears) moving from an iron-heavy, meat-rich hunting and gathering diet to a Neolithic diet of mineral-binding cereal grains, an enhanced uptake of dietary iron may have been helpful. This is probably worth knowing, because iron accumulation is indicated in several illnesses.
  • Rs7501331, which codes for conversion of (plant-based) beta-carotene into the (animal-based) usable form. Heterozygous and homozygous female carriers have poor conversion. Not surprisingly, this SNP appears most often in European populations, ancestors of whom could generally depend on steady access to animal retinol (liver and animal fat).
  • Rs2291725, which codes for incretin (hormones that release insulin) secretion in response to dietary glucose. People with the “ancestral,” or original allele, have lower fasting blood glucose, while people with the “Neolithic,” or derived allele, have higher fasting blood glucose. The derived allele was positively selected for in Asian populations about 8,100 years ago, presumably because it allowed more efficient use of dietary carbohydrates when fewer were available during lean times. In today’s grain and carb-heavy environment of endless abundance, it’s a risk factor for diabetes. Highly prevalent in Asians, somewhat so in Europeans, barely present in Africans.

But the emergence of SNPs across the human DNA mosaic does not mean “humans have evolved beyond our hunter-gatherer beginnings, rendering them immaterial, so bring on the bagels!” It simply confirms that humans indeed respond to dietary and environmental pressures with genetic changes. It means that what we have access to eat changes who we are and shapes the genome of our species.

Have human genetics – especially the genetics influencing energy metabolism, also known as eating – undergone enough selective pressure in the last 10,000-odd years to justify a reexamination of our basic premise? That is, are our dietary recommendations couched in evolutionary biology now on shaky ground? Should we start reaching for the whole wheat bagels after all?

To the first question, I’d say kinda. We should always reexamine our premises – any and every premise that we hold dear. That goes without saying. It keeps us honest and, most importantly, it helps us make sure the advice we follow and dole out to others actually works.

To the second question, I’d say no. The basics still hold true. The vast majority of people are better off without grains (especially wheat), sugar (especially refined sugar and HFCS), and omega-6 vegetable oils and trans fats. I don’t think you’ll find a single person who suffers from a soybean oil or gluten deficiency. And some evidence suggests that SNPs associated with hyper-assimilation of dietary glucose are partly responsible for type 2 diabetes in today’s environment, even though they were advantageous 8,100 years ago. Like I said before, it’s a dirty, murky, confusing business, evolution, with lots of fits, starts, and backtracking.

And to the third, I’ll say never.

So, in response to the title question – we just don’t know. Changes are definitely happening right now at the population level, but they’re not earth-shattering and by the very definition of evolution, they must accumulate before any real conclusions can be drawn. At any rate, you, yourself, are not going to suddenly develop a tolerance for industrial foods and an intolerance for grass-fed meat within your lifetime. And even if someone did develop a genetic adaptation to trans fats, it doesn’t mean the longstanding genetic adaptation to real dietary animal fat would disappear. That’s not how it works.

What we do know is that people seem to do really well eating this way, and if they don’t, if they move beyond strict Primal to include some rice or some properly prepared grains or legumes, the point is that they used evolutionary reasoning as a jump off point. And really, that’s the point: it’s a foundation upon which we can build a pretty diverse, fairly all-inclusive diet that appeals to just about everyone. In fact, when I look at a lot of people’s Primal journeys, it kind of resembles human dietary evolution. They begin with the basics – meat, poultry, vegetables, nuts, some fruit, the traditional Primal Blueprint eating plan – and it goes very well. Weight is lost, effortlessly, health is regained. As time goes on, they might experiment with different additions or subtractions. They add some tubers. It works out, their workouts improve. They try some dairy. Fermented dairy agrees with them, but regular does not. They switch out some chicken for more seafood and red meat. They lean out and blood lipids improve. They remove all chicken and replace with shellfish. They improve even more. They – gasp! – add a bit of wild rice after big workouts. Strength gains continue, leanness persists. So on and so forth. And, of course, every person’s path is unique.

That tells me that humans vary, that dietary recommendations can be fine-tuned and tailored to the individual’s situation, that this person will tolerate more carbs than this or that person. Genetic variation most likely plays a role in all of this, but I’m not sure we know enough to start basing our diets on it. It also tells me that the basics – eating animals and plants while avoiding industrial, refined carb-heavy foods – is never going to stop working. Not in our lifetime, at least.

Thanks for reading and let me know what you think in the comment board!

About the Author

Mark Sisson is the founder of Mark’s Daily Apple, godfather to the Primal food and lifestyle movement, and the New York Times bestselling author of The Keto Reset Diet. His latest book is Keto for Life, where he discusses how he combines the keto diet with a Primal lifestyle for optimal health and longevity. Mark is the author of numerous other books as well, including The Primal Blueprint, which was credited with turbocharging the growth of the primal/paleo movement back in 2009. After spending three decades researching and educating folks on why food is the key component to achieving and maintaining optimal wellness, Mark launched Primal Kitchen, a real-food company that creates Primal/paleo, keto, and Whole30-friendly kitchen staples.

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