By Scott Jameson
670 words
I’ve been active in the blogosphere for around 24 hours now and I’ve already gotten a negative response from someone who happens to be wrong. That’s a win in my book.
The argument we’re having is, as best I can tell, why some populations out there just don’t have obesity as an observed phenotype amongst their members. TL;DR: Pumpkin Person and Robert Lindsay believe that genetics explain why there are no obese New Guineans. But it ain’t so.
The original context is an old Pumpkin Person post. Much of what he’s saying here doesn’t seem too off-base; for example he says that behavioral genetics may explain much of the differences in BMI between individuals within the same population. True. It is possible that some people are genetically inclined to eat more or unhealthier foods, rather than simply being genetically inclined to putting on weight regardless of what they do.
As an aside, genotypes that affect how you digest things also probably explain part of the BMI gap between skinny folks and fat folks within the first world. The APOA2 gene for example has a recessive allele that is associated with higher BMI in people who eat more saturated fats. The interactions between genes and environment which determine BMI are complicated and not yet fully understood, but I’m willing to bet that being genetically worse at processing certain nutrients is a part of the problem, and that being genetically inclined to stuff your face is a part of the problem as well. PP is probably right about that issue.
Where he and Lindsay get it wrong is using examples of people from Podunk, New Guinea as evidence for obesity “being genetic” (relative term). Obesity is a gene-environment interaction such that, without certain environmental inputs, you simply won’t get the phenotype. History tells us that that input is processed carbohydrates.
There was a time when people could have used Australian Aboriginals or Inuit or Pima Indians as examples of groups of people who just don’t have obese folks amongst their numbers, just as Lindsay did with a few populations. Homo sans lardicus. Then the White Devils showed up with their refined Einkorn wheat products and their firewater and so on. Now those populations have fat people in them.
There’s an ongoing debate as to whether some populations are more resistant to the fattening effects of processed carbs or not. My guess is, the answer’s yes (and you’d look at Europeans and East Asians to see the more carb-resistant people, in theory) but that topic would merit its own post. That being said, every population in the world will almost assuredly have obese people in it after you introduce processed carbs. All of the populations that were introduced to this diet, now have fat people in them.
Heritability of BMI is high within the first world because the relevant environmental input is pretty uniform: everybody has access to potatoes, everybody has access to broccoli. As PP points out, which you’re likely to eat and how much you’re likely to eat likely depends on your genetics. As I point out, how your body processes the nutrients also has a likely genetic component. But the environmental contribution to our within-population differences in BMI is low (~20%) because we all have access to roughly the same stuff.
Rural New Guineans, lacking a bunch of processed carbs, could hardly get fat if they tried their best to. That’s a big between-population, nonheritable cause for a phenotypic difference; this means that environment probably explains most of the BMI gap between them and us. If I wanted evidence to refute Lindsay’s assertion that New Guineans are skinnier thanks to genetics, I’d find a population of urbanized New Guineans somewhere with higher average BMI. Such a group would have New Guinean genetics but a “developed” environment vaguely similar to ours; if they were fatter than their rural ken, then Lindsay’s hypothesis that New Guineans are just genetically obesity-free would be falsified.
NotPoliticallyCorrect 
You would be incorrect.
Genetic changes from the gene expression from cooking occurred around 275kya. The biological evidence for fire (which I take to, personally) appears around 2mya. Archaeological evidence 1mya, hearths 300kya, physical evidence from 50 kya and Neanderthals began using fire at 40kya. We don’t need to see actual physical evidence for fire, so we can make inferences based on biological changes between the hominin taxa. (Carmody and Wrangham, 2016)
So since it took so long for positive selection to occur from the gene expression due to cooking, I am hypothesizing that since Man has been split for 50-100kya, there was not enough time for there to be any meaningful changes between the genomes of the races of Man in regards to diet. The most you’d see is differences in gene expression due to different diets (that is, how the genes are expressed due to the diet eaten), but we’d need to be isolated far longer eating different foods before any meaningful changes like this occurred at the biological level. It is very clear that all humans should eat a paleolithic diet if they want to avoid disease and the like; Western-like diets and constant insulin spikes due to evolutionary novel foodstuffs (processed carbohydrates) are the cause for the exploding obesity rates in first world countries.
Pick up the book The Story of the Human Body: Health, Evolution, and Disease when you get a chance.
It is higher in low SES populations due to food insecurity (Drewnowski and Specter, 2004). See my refutation on Ryan Faulk’s video on agriculture and evolution. I talk about that a bit. But what you need to realize is that, for instance, as Faulk claims, East Asians are not ‘more sensitive to carbohydrates’, they just eat less percentage of their kcal from processed carbs. This explains the East Asian rice eater paradox.
People should really get a clue on diet and nutrition before they talk about it.
That is a great study you cited.
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“I am hypothesizing that since Man has been split for 50-100kya, there was not enough time for there to be any meaningful changes between the genomes of the races of Man.”
What? You run an HBD blog. There’s been signs of selection in alleles for height, skin color, immune genes, eye color, lactose tolerance, fat digestion. And, of course, intelligence.
“A variety of genes involved in carbohydrate metabolism have evidence for recent selection, including genes involved in metabolizing mannose (MAN2A1 in Yoruba and East Asians), sucrose (SI in East Asians), and lactose (LCT in Europeans).”
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0040072#s2
The genetic architecture for risk factors in Type 2 diabetes is pretty different around the globe: the risk factors in East Asians are much more rare in South Asian Indians
http://download.springer.com/static/pdf/803/art%253A10.1186%252F1471-2350-12-18.pdf?originUrl=http%3A%2F%2Fbmcmedgenet.biomedcentral.com%2Farticle%2F10.1186%2F1471-2350-12-18&token2=exp=1487994501~acl=%2Fstatic%2Fpdf%2F803%2Fart%25253A10.1186%25252F1471-2350-12-18.pdf*~hmac=b8fd53a24e533fc086c2ee342960d70411bbdf9ef3e68b74f8ea74815cbdfa94
I remember reading that South Asian Indians have a separate risk factor, though, I’ll see if I can dig it up.
There have definitely been changes in how we metabolize stuff, big changes which differ between races across the globe. Lactose tolerance is the simplest to point out.
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I meant in regards to diet.
Sure. CHO metabolism is lower in African-American women than in white women. Fat oxidation is also lower in African-American man compared to white men. This is why blacks have a lower fat-free body mass when compared to other races.
Energy metabolism in African Americans: potential risk factors for obesity
In regards to lactose for Europeans, see the ecological niche theory.
Dairy farming is apparently an instance of human cultural niche construction that is mediated by cultural processes. There are no genes for dairy farming (using “genes for” in the sense of Dawkins 1976). Genes do not constitute the appropriate level of analysis to explain why individuals in some societies farm cattle and others do not— this is a cultural phenomenon. Yet in spite of the fact that dairy farming is not caused by genes and is not a product of natural selection, it has clearly had evolutionary consequences. Recent findings of mutations that allow lactase persistence in some non-dairying African groups does not fundamentally change this logic (Tishkoff et al. 2006).
Conceptual Barriers to Progress Within Evolutionary Biology
So I spoke too soon. However everyone should stay away from CHO, it leads to nothing but insulin resistance and metabolic diseases.
I wish I knew the dietary composition of the cohort in the study you cited. Because Western diets have exploded in India over the past few decades.
But table 1 has a pretty incredible difference.
Fact of the matter is, novel food items spike insulin which lead to obesity. Insulin literally causes weight gain.
Our findings suggest that the genetic background of Africans and East Asians makes them more and differentially susceptible to diabetes than Caucasians. This ethnic stratification could be implicated in the different natural courses of diabetes onset.
Ethnic Differences in the Relationship Between Insulin Sensitivity and Insulin Response: A systematic review and meta-analysis
Fact of the matter is, one of the main causes of diabetes is a high CHO diet. What ameliorates that is a low-carb diet. All people should be eating a low-carb diet, one that is as close as an ancestral one as possible (with a doctor’s supervision of course).
As Western diets get introduced to people who eat ancestral diets (or ones like them), rates of diabesity will explode in those areas. My main thesis still stands: disease rates explode to the introduction of Western diets and high consumption of processed foods. Even then, milk has a high level of n-6 fatty acids, a risk factor for obesity. Diabesity rates have exploded in India recently, for example, due to the introduction of a Western diet.
Rates of diabesity are also exploding in China.
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