Go back 160,000 years and we all share a common ancestor: The emergence of the first Homo sapiens in East Africa. Since then, humans have spread across every environment imaginable and adapted to those environments. Much remains the same. We all breathe oxygen, require protein, produce insulin, oxidize fatty acids. But extended stays in unique environments have created genetic proclivities in different populations. For example, descendants of people who settled in high-altitude areas like the Himalayas, the Andes, and the Ethiopian highlands tend to show greater resistance to low-oxygen environments, while the Greenland Inuit show unique adaptations to cold environments, including increased activity of heat-stimulating brown fat. And among the island-dwellers of Sardinia, where the landscape constrained the amount of available food, there’s considerable evidence of positive selection for short stature.
What other differences exist, and how can we explore them to inform and improve our own diet and lifestyle choices?
One way is to directly test your genes using a service that analyzes your DNA and provides gene-based dietary, exercise, and lifestyle advice. When I got my genes analyzed by DNAFit, my current diet and lifestyle choices—avoiding chronic cardio, eating more fat, taking more vitamin D (or sun) and omega-3s—were vindicated. It turns out that since I’m of Scandinavian stock and my ancestors had steady access to fish rich in omega-3s and vitamin D, I’m adapted to and likely need a diet higher in fish and vitamin D for optimal health. I have the genetic predisposition to excel in endurance athletics, but my genes also predicted I’d be a strong power athlete; that explains why I was an elite marathoner in the old days and more recently have been successful lifting and sprinting.
Another option is to use your ancestral background as a rubric for exploration of different diet modifications.
You can still glean useful info and make realistic inferences from genetic research by examining the regional and ethnic distribution of various alleles (i.e. gene variations) and matching them against your own ancestry. Let’s take a look at some of the alleles for which we have the most data:
There’s a lot of buzz in the alternative health world surrounding MTHFR mutations, so you may have wondered: why is a seemingly wholly negative mutation so prevalent? After all, when folate intake is low, MTHFR mutations cause poor methylation status, numerous health issues, and poor fetal survival. But when folate intake is high, these mutations confer protection against colorectal cancer and acute lymphatic leukemia, and may even augment fetal survival. Populations with sufficiently high intakes of folate would have therefore selected for the MTHFR mutations. So if MTHFR incidence is high in a certain population or ethnic group, that group’s traditional diet was probably rich in folate. If you come from a high-MTHFR population, maybe your diet should be, too.
MTHFR mutations tend to cluster in certain regions and populations. In one major study of newborns spanning 16 regions across the world, Mexicans, Hispanics living in Atlanta, Southern Italians (Campania, Sicily, Veneto), and Northern Han Chinese were more likely than other populations to carry MTHFR mutations that increased the need for dietary folate. Among the other newborns, Spanish whites, Australian whites, northeastern French, Southern Han Chinese, Russians, Israelis, Dutch, Canadian whites, Fins, and blacks living in Atlanta were far less likely to carry the mutation.
You may not have DNA test results confirming your MTHFR status. That’s okay. You can still determine whether your ancestors likely ate folate-rich diets. If you hail from Northern Han Chinese stock, or your grandparents came over from Sicily at the turn of the century, or your dad was Mexican—maybe try eating more folate-rich foods. Eat more leafy greens, chicken liver, pastured egg yolks. Even if it turns out that you don’t carry the MTHFR mutation, your immediate ancestors likely ate a high-folate diet, you may carry unknown alleles that interact with folate status, and eating more folate-rich foods could improve your health and performance.
Salivary amylase predigests starch. AMY1 is the gene coding for salivary amylase production. The more AMY1 copy numbers you have, the more salivary amylase you produce in response to carbohydrate intake. According to population genetics, salivary amylase copy number reflects ancestral starch intake. The more copy numbers you have, the more starch your ancestors ate. If you have fewer, your ancestral diet was likely lower in starch. Chimps and bonobos are our closest ancestors, but because their natural diets are fruit-based and low in starch, they have fewer AMY1 copies than humans.
The fewer copy numbers you carry, the more vulnerable you are to obesity and more likely you are to have insulin resistance. This effect persists across ethnicities and may be more pronounced in females. You have to consider the environmental context of the vast majority of people these days: carbohydrate-based diets. If you’re eating a standard American diet of fast food, sweets, and baked goods and you have a low number of salivary amylase gene copies, you’re more susceptible to obesity. So if you have fewer copies, your ancestors probably ate fewer carbs and, to stay lean and maintain optimal body composition, you should, too.
But it goes the other way, too. People with high copy numbers have a better metabolic response to starch ingestion than the person with fewer copies. How to find out?
The global distribution of AMY1 copy number variation hasn’t received a lot of attention, but we have a few datapoints. High-starch agricultural societies (Japanese and Europeans) and high-starch foragers (Hadza) have all been shown to possess higher average copy numbers than lower-starch societies like the Yakut (a Turkic people indigenous to Siberia), the Mbuti pygmies (a foraging society), the Biaka (foragers in the Congo), and the Datog (a group of pastoralists). Another study found that the mean copy number among Brazilians—a mishmash of European, African, and Native American genetics—was just 2.8 with a range of 1-8 copies of AMY1. That’s pretty low.
If you’ve got a confirmed bead on your number of salivary amylase copies, of if your ethnic background is known for having higher copy numbers—and you’re struggling with your weight—try eating a few more carbs. People with high copy numbers have a better metabolic response to starch ingestion than the person with fewer copies. Fewer copies? Eat fewer carbs. Whatever carbs you do consume, though, make sure they’re high-quality Primal carbs. Potatoes, sweet potatoes, various other roots and tubers, fruit, and low-toxin grains like rice are all great choices.
Lactase persistence allows safe digestion of the milk sugar lactose well into adulthood. The ability to digest lactose as an adult without gastrointestinal distress and watery bowel vacations allowed access to a versatile, dependable source of fat, protein, carbs, calories, and important micronutrients. The raising of dairy livestock and spread of pastoralism explain the pockets of lactase persistence that appear in otherwise lactose-intolerant areas, like Asia—where almost everyone but the Mongolians, the central Asian steppe peoples, and the inhabitants of the Indian subcontinent are entirely intolerant of lactose—or Africa—where only a few isolated pastoral groups, like the Masai, still produce lactase as adults. Clearly, lactase persistence is beneficial enough to have arisen independently in many different regions and populations. The nutrients in dairy are just too important to pass up.
If you’re Northern European (Scandinavian, British Isles) or Western European (France, Germany, etc), you’re probably lactose tolerant. Among Eastern and Southern Europeans, lactase persistence appears in 15-54% of the population. In Northern Indians, it’s 63%. In Southern Indians, it’s 23%. Hail from East Asia or have Native American ancestry, you probably aren’t.
The science is still young here. Even when researchers identify a genetic variant that interacts with diet and lifestyle, we need to know its distribution across populations and ethnicities to hypothesize about how it’ll affect us. Until we have more detailed data on these and other genetic variants, we’ll have to get speculative:
Read the ethnographical literature. It’s not always empirical. It may not even be accurate. Most often, you’ll be reading one person’s anecdotal observations, an outsider’s perspective. But they typically include frank descriptions of the traditional diet and lifestyle practices of the people and cultures being studied.
Northern European/German? Read Caesar’s accounts of the German tribes his legions faced. “They do not pay much attention to agriculture, and a large portion of their food consists in milk, cheese, and flesh.”
His observations of the Celtic Britons are also interesting. “They consider it contrary to divine law to eat the hare, the chicken, or the goose,” yet “do not sow grain but live on milk and flesh.”
Weston A Price’s Nutrition and Physical Degeneration may be the most helpful examples of ethnographic literature. Price focused on isolated populations eating their native diets free of modern processed food, people like the Masai, Swiss villagers living in a remote alpine valley, Australian aborigines, South Pacific islanders, American Indians, Arctic Inuit, and Scottish fishermen. The diets are quite representative—almost everyone can find something that applies to their ethnic context—so read the sections most relevant to your ethnicity.
If the ethnographical literature turns out to be erroneous, so what? It’s not dangerous to try eating more kale with your food. Most people can get away with eating fermented dairy for a couple weeks to see how it affects them. You’ll get past it. You’ll learn something.
Focus on staple foods. Staples may be boring but human diets are based on them; they’re likely nutritionally significant. The Hadza prefer meat and honey to the fibrous tubers that comprise a large chunk of their diet, but the tubers provide important prebiotics that shape their microbiome. Look at the foods that consistently appear in the traditional cuisine of your ethnicity and consider implementing it.
Focus on the “defining ingredients” of your ethnic cuisine. Unique foods may be uniquely important. If you’re Thai, import and regularly eat some galangal, a variety of ginger. If you come from several generations of Americans, eat apples. If you’re a black American, try some collard greens (and pot liquor!) instead of kale and pork trotters instead of chicken breast. Korean? Keep a jar of kimchi in your fridge (your mom will probably be proud). Polish? Get on that borscht. You probably won’t ever see diet studies into the effects of adherence to traditional ethnic cuisines on members of that ethnicity. You’ll have to run the “study” yourself.
Watch out for big, recent shifts. Traditions that go back only a generation or two aren’t enshrined in your genetics. Take the traditional Indian diet, which went from using highly-saturated butter-based ghee as the basis for its cooking to using vegetable oil-based trans-fat rich vegetable ghee. If you’re Indian and go back home, “traditional food” swimming in vegetable oil actually isn’t all that traditional—or suitable for your biology.
Look for apparent paradoxes. Eastern and Southern Europeans may not have the highest rates of lactase persistence, but that doesn’t mean they abstain from dairy. For instance, though lactase persistence is uncommon among native inhabitants of Sardinia, they eat a lot of dairy. This is possible because they primarily eat aged cheeses, which are very low in lactose. Same goes for other populations in “low-to-moderate” lactase persistence category, like Greeks, Turks, or Polish, who take advantage of dairy nutrients via low-lactose alternatives like yogurt and/or cheese.
Speculate based on geography. If you come from a coastal people with lots of fish available year round—Northern Europe, the Arctic, the Mediterranean, the South Pacific, any coast, really—try eating more fish. If your people were landlocked, maybe don’t eat ten fish oil caps a day.
As you can see, it’s messy. It’s far from settled science. Very few ethnic groups have rock-solid, linear, stable genetics. No one’s ancestry is a straight line and there’s a lot of admixture from other groups. White Brits, for example, have about 30% German blood thanks to early Saxon incursions; the later Viking raids and Norman conquest further complicated the gene pool. The original Britons, the Celts, likely came from a group of Spanish hunter-gatherers. So the truth is—despite the title of this article—there’s no “definitive guide” to using your recent ancestry to determine your optimal diet, because everyone’s ancestry is different and will follow different threads. However, through synthesis of ethnography literature, allele distribution frequency, genetic testing, asking your grandma about how she ate growing up, and a little creative thinking, we can make a few educated inferences and start playing around with things.
Even if you get it terribly wrong, if your family hails from Britain but has very little actual Celtic blood or if you follow the native Maori diet despite being a white New Zealander, you’re still eating real whole foods. Anything is better than the industrial food diet.
Thanks for reading, everyone. Where do you come from and how does it inform your current diet? How are you going to play with your diet after reading this post?
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