The debate about cooking’s role in human evolution is ongoing. Some people may rightly say “Cooking it not a selection pressure.” This is true. However, it doesn’t say much. The advent of cooking was one of the most important events in human history as it released the constraint on brain size due to predigesting our food outside the body. This seminal event in our history here on earth is one of the main reasons we are here today. In the articles I wrote two months ago on how and why we are so intelligent, I forgot to bring up two important things—the thermic effect of food (TEF) and our gut microbiota and its relationship with our brain. The importance of these variables in regards to cooking cannot be overstated. The subject tonight is cooking and how it benefitted us metabolically and our gut microbiota that partly drive our brain and behavior.
Cooking was beneficial to us not only because it released constraints on brain size due to how nutrient-rich meat was as well as other foodstuffs that were then cooked, but because it’s possible to extract more energy out of cooked food compared to non-cooked food. When erectus began controlling fire around 1-1.5 mya (Herculano-Houzel, 2016: 192) this allowed for the digestion of higher-quality foods (meat, tubers, etc) and this is the so-called ‘prime mover’ for the brain size increase in hominids over the past 3my.
The introduction of cooked/mashed foods changed the shape of the ridges on our skull which serve as attachments for the facial muscles responsible for chewing. The saggital crest on the cranium and zygomatic eminences in the cheeks exist in great apes but not us. Further, molars and canine teeth reduced in size while brain size double in erectus. Our jaw bones decreasing in size shows that we didn’t need to have as forceful of a bit due to the introduction of cooked foods 1-1.5 mya (Herculano-Houzel,2016: 193).
Along with the introduction to a diet with softer foods, smaller teeth and intestines then followed. So brain size and teeth size are not correlated per se, neither are brain size and gut size. However, the relationship between all three is cooking: cooking denatures the protein contained in the food and breaks down cell walls, gelatinizing the collagen in the meat allowing for easier chewing and digestion. So the fact that tooth size and brain size do not have a relationship throughout our evolution is not a blow to the cooking hypothesis. The introduction of softer foods is the cause for both the decrease in tooth size and gut size. Cooking is a driver of all three.
Fonseca-Azevedo and Herculano-Houzel (2012) showed that the availability of kcal from a raw diet is so limiting that without a way to overcome this limitation, modern Man would not have been able to evolve. Our brains would not have emerged if not for the advent of cooking. Indeed, Herculano-Houzel and Kaas (2011) showed that the outler is not our brains being bigger than our bodies, great apes have bodies too big for their brains, reversing a long-held belief on our brain-body relationship. Cellular scaling rules apply for all primates, so knowing this, the Colobinae (old-world monkeys) and the Pongidae (gorillas, chimpanzees, and orangutans) favored increases in body size, in line with the ancestor that we share with great apes, while our lineages showed gains in brain size and not body size, possibl due to a metabolic limitation of having both a big brain and body. Indeed, the amount of neurons a brain can hold along with how big a body can realistically get impedes the relationship between the brain and body. You can have either brains or brawns, you can’t have both.
We should then look for when genetic changes in our genome occurred from cooking. Carmody et al (2016) show that these genetic changes occured around 275-765kya. We know that differing nutrients change gene expression, so, over time, if these changes in gene expression were beneficial to the hominin lineage, there would be positive selection for the gene expression. Carmody et al (2016) took 24 mice and fed them either cooked or raw foods for 5 days. Two hours into the 5th day, mice were ‘sacrificed’ (killed) and their liver tissue was harvested and immediately (within 60 seconds of death) were flash frozen for later analysis. They evaluated differential gene expression for cooked/raw food, calorie intake (raw/fed), energy balance of the consusmer (weight gain/loss over 5 days of feeding), and food type (meat/tuber). The diet consisted of either organic lean beaf round eye toast or sweet potato tubers cooked or raw. They gave restricted rations to evaluate the effect of a cooked diet with negative energy status (this is important).
They cooked the meat until it gelatinized (around 70 degress celsius), which is equivalent to medium well-done. They were then given the same diets, cooked/raw, free-fed or restricted sweet potato tubers or meat. The mice were weighed during periods of inactivity and the food they refused to eat was weighed to monitor fresh weight than freeze-fried to monitor dry weight.
The most interesting part of this experiment, in my opinion, was that the mice that were free-fed with cooked diets consumed less kcal than the mice that were free-fed raw diets. They discovered that free-fed cooked diets led to the maintenance of body weight, whereas the free-fed raw diet led to weight loss. This confirms that cooked food gives more energy than raw food, which was itelf a critical driver in our evolution as humans.
When they looked at the livers of the sacrificed mice, they found that the mice that were fed meat showed liver gene expression patterns that were more similar to mice fed a human diet than mice that were fed tuber. The mice that were fed cooked food showed similar gene expression to mice fed a human diet and more similar to the human liver than in the mice fed the raw food. Even more interestingly, the mice fed tuber or raw foods exhibited liver expression patterns more similar to mice fed a chimpanzee diet and gene expression patterns noticed in non-human primates. Their analysis on the gene expression from cooked/raw diets compared to another data set showed that these genes that were expressed went under selection between 275-765kya.
Food type and preparation were associated with significant changes in gene expression, but those related to cooking were shown to have evidence of possible selection in the timeframe state by Carmody et al. These results also show that along with cooking increasing the bioavailability of foods, habitual cooking would have led to less energy spent on immune upregulation. This energy could then be used for other bodily processes—like our increasing brain size/neuronal count.
Carmody et al show that the biological evidence for cooking is 2mya, archaeological evidence 1mya, hearths 300kya, not too many Neanderthals controlled fire until 40 kya, and the earliest direct evidence we have of cooking appears around 50kya. We can obviously look at physiological, metabolic and diet differences between hominins and infer what was eaten. Now with looking at changes in gene expression, we can pinpoint when the positive selection began to occur. The biological evidence, in my opinion, is the best evidence. We don’t need direct physical evidence of cooking, we can make inferences based on certain pieces of knowledge we have. All in all, this new study by Carmody et al show that 1) cooking definitely predated modern humans and 2) many different hominins practiced cooking. This evidence shows that cooking for ancient hominins occurred way earlier than the archaeological record suggest.
Now, remember how the mice free-fed on a cooked meat diet ate less yet maintained their weight? There is a reason for this. Protein is the most filling macro (followed by fat, fiber then CHO). So it’s no surprise that the mice at less of the cooked meat. What was a surprise was that the mice maintained their weight eating less kcal then the mice that ate a raw foods diet. This is yet more evidence that cooking released us from the metabolic constraints of a raw, plant-based diet.
For those who have some knowledge of human metabolism, you may have heard of the thermic effect of food. The thermic effect of food is the amount of energy expenditure above the basal metabolic rate due to the cost of processing food and its storage. So if you’re cooking food before you ingest it, you bypass a lot of the processing that happens internally after digestion, allowing you to extract close to 100 percent of the kcal contained in the food. Due to cooking’s effects on foods, since we our bodies have to use some of the energy we consume to function and process the kcal, getting higher quality food was beneficial to us since we could have more for our bodily functions and to power our growing brains. Since we were able to get higher quality calories from cooked food, the effects of TEF weren’t as large, which was yet another constraint that we bypassed with a cooked diet. A cooked diet is more efficient than a raw one in more ways than one.
One more thing I forgot to mention in my series of articles on the benefits of cooking and human evolution is the effect it had on our microbiome. The completion of the Human Microbome Project (HMP) was imperative to our understanding of the trillions of bacteria that live in our guts. It was commonly stated that the bacteria in our guts outnumbered regular bacteria with a 10:1 ratio. However, Sender, Fuchs, and Milo (2016) showed that on average, there is about a 1:1 ratio with about 30 trillion normal bacteria and 39 trillion gut bacteria, some people possibly having double the amount of gut bacteria in comparison to regular bacteria, but nowhere on the level of 10:1 that has been stated for the past 40 years.
The human microbiome has undergone a substantial change since the divergance of humans and chimpanzees (Moeller et al, 2014). Over the course of our evolutionary history, our microbiome has become specialized to animal-based diets. Wild apes have way more diversity in their gut microbiota than humans do, indicating that we have experienced a depletion in our microbiota since our divergence with chimpanzees. This comes as no surprise. With the introduction to cooked foods, our microbiota became adapted to a new selective pressure. Over time, our gut microbiota became less diverse but more and more specialized to consume the food we were eating. So the introduction to a cooked diet both changed our gut microbiota as well as giving our bodies enough energy to power itself and its processes, the brain and our gut microbiota that are imperative for our development.
All that being said, some people may say “Cooking isn’t a selective pressure; neither is bipedalism nor tool-making”, and they would be correct. However, human tool-making capacities reflect increased information-processing capabilities (Gibson, 2012). So, clearly, there were some changes in our brains before the use of tools. This change was the advent of bipedalism which allowed our bodies to conserve 75 percent more energy in comparison to knuckle-walking (Sockol, Racihlen, and Pontzer, 2007). This was yet another constraint that we bypassed and allowed our brains to grow bigger. When we left the trees, we then became bipedal and that therefore increased the availability of edible foodstuffs for us. This increased our brain size, and as we learned to make tools, that increased our information-processing capabilities.
Cooking, of course, is not a selective pressure. What cooking did, however, was release the use from the metabolic constraints of a raw, plant-based diet and allowed us to extract all of the nutrients from whatever cooked food we ate. This event—one of the most important in human history—would only have been possible with the advent of bipedalism. After we became bipedal we could then manipulate our environement and make tools.
I figure I may as well touch on the Expensive Tissue Hypothesis (ETH; Aiello and Wheeler, 1995) while I’m at it. The ETH states that since our guts are metabolically expensive tissue—as well as our brains—that there was a trade off in our evolutionary history between our brains and guts. However, Navarette, Schaik and Isler (2011) showed that the negative correlation was with fat-free mass and brain size—not with the gut and brain size. However, as I noted earlier in this article, our guts reduced in size due to diet quality, e.g., softer foods. So while the correlation is there for the brain size increase/gut reduction, it is not causal. Diet explains the gut reduction and brain size increase, but the brain size increase did not cause the gut reduction.
In sum, genetic changes from cooking occured between 275-765kya. But we controlled fire and began to cook between 1-2mya (archaeological evidence says 1-1.5 mya while biological evidence says 2 mya). Cooking led to differences in gene expression and then positive selection in the hominin lineage. Mice that were fed a raw diet showed gene expression similar to a chimpanzee fed a raw diet while mice fed a cooked diet showed gene expression like that of a human. This is huge for the cooking hypothesis. What this shows is that while the gene expression occurred while we started cooking, the actual positive selection didn’t occur in our genomes for about 1my after we began cooking. This is more evidence that cooking released us from metabolic constraints, as mice that were fed a cooked diet maintained their weight even when eating less kcal than mice fed raw foods.
When thinking about the evolution of Man and our relationship with fire, we should not forget about how the body uses some of the kcal is ingests for bodily processes. Furthermore, we cannot forget about our microbiome which evolved for an animal-based diet. Those two things both cost caloric energy. The advent of cooking released us from the energetic constraints of a raw, plant-based diet as well as gave our microbiome higher quality energy. When we take both the TEF and our microbiome into account, we can then begin to put 2 and 2 together and state that along with cooking freeing us from the metabolic constraints that apes have to go through due to their diet, it also benefitted our microbiome and gave our bodies higher quality energy to power it.
We would not be here without cooking. Thank cooking for our dominance on this planet.
Aiello, L. C., & Wheeler, P. (1995). The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Current Anthropology,36(2), 199-221. doi:10.1086/204350
Carmody, R. N., Dannemann, M., Briggs, A. W., Nickel, B., Groopman, E. E., Wrangham, R. W., & Kelso, J. (2016). Genetic Evidence of Human Adaptation to a Cooked Diet. Genome Biology and Evolution,8(4), 1091-1103. doi:10.1093/gbe/evw059
Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109
Gibson, K. R. (2012). Human tool-making capacities reflect increased information-processing capacities: Continuity resides in the eyes of the beholder. Behavioral and Brain Sciences,35(04), 225-226. doi:10.1017/s0140525x11002007
Herculano-Houzel, S. (2016). The Human Advantage: A New Understanding of How Our Brains Became Remarkable. doi:10.7551/mitpress/9780262034258.001.0001
Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.
Moeller AH, Li Y, Mpoudi Ngole E, Ahuka-Mundeke S, Lonsdorf EV, Pusey AE, et al. Rapid changes in the gut microbiome during human evolution. Proceedings of the National Academy of Sciences. 2014;111(46):16431–35.
Navarrete, A., Schaik, C. P., & Isler, K. (2011). Energetics and the evolution of human brain size. Nature,480(7375), 91-93. doi:10.1038/nature10629
Sender, R., Fuchs, S., & Milo, R. (2016). Revised estimates for the number of human and bacteria cells in the body. doi:10.1101/036103
Sockol, M. D., Raichlen, D. A., & Pontzer, H. (2007). Chimpanzee locomotor energetics and the origin of human bipedalism. Proceedings of the National Academy of Sciences,104(30), 12265-12269. doi:10.1073/pnas.0703267104
When critics of the mainstream approach towards modern African-American grievance questions the agency of the population to improve their standards of living, they often cite either how minorities such as poor European immigrants of the Early 20th century assimilated better despite discrimination, or how Black immigrants from Africa occupy a higher mode of living.
While multiple factors contribute to the discrepancy, one caught my attention which struck me a paradoxical but soon started to make sense as I dug deeper. That trait being the lack of effective widespread “unity” among not just Black Americans but many other populations, especially those in Africa.
– The Situation
As for my titular use of “chaos” to describe it, I owe it to an Unz commenter who contrasted it from individualism or collectivism. For an intra-regional example, you have riots or protests regarding threats seen as pertaining to the racial mass, yet you have commonly cited the lack of the same regard for those killed by perpetrators of the same race.
From an inter-regional example I refer to the words of my father that, despite the beliefs of some, there is no “Black America” in which the interests or beliefs of blacks due to having comparatively looser connections than others based on a national level. This is noted by regional variance in ideology between blacks during the Progressive Era or better yet modern African conflicts, many of which can be classified as Christians versus Muslims on the larger scale yet can even be observed on a finer, pre-colonial level of identities (Osaghae and Suberu 2005).
“There are numerous examples of pre-colonial migration, usually stimulated by wars or natural disasters, which have continued to generate bitter conflicts today owing to continuing discrimination against the immigrants by the original settlers. These include the eighteenth century mass migration of Oyo Modakeke into Ife in search of a safe haven from the internecine wars of the Oyo empire; the movement of Urhobo and Ijaw into Warri, where the Itsekiri claim to have been the original settlers; the migration of the Jukun-Chamba from Cameroon to parts of the present Taraba state, originally settled by the Kuteb; and the sixteenth century settlement of Hausa merchants in Zangon Kataf within a territory occupied by the Kataf (Isumonah 2003; Mustapha 2000). “
I attribute three reasons why this would be.
One being geography, as these behaviors are most notable with African nations that often overlap in cultural spheres despite living on a huge continent, and also how Black Americans probably covering the largest area relative to other New World African descent populations thus making diversification more enabled.
The second being the process of slavery in New World populations giving various forms of cultural transmission amongst black slaves by region who as well came through different tribes, either producing the typical “Scot-Irish” Black culture or a “Creole” culture, like the Gullah people of the South East. The Third, the Basal reason, being the effects of Genetic interests at hand as put by RR and how African Diversity works.
Here Razib Khan explains that when Foreign Admixture is removed, African diversity is higher among individuals than for major geographical groups.In other words, while geographically diverse, the actual organization of the diversity in the context of cultural boundaries is more stratified due to the lack of breeding, be it outbreeding or replacement involved in nations.
This suggestion is strengthened by famous blogger Jayman attributing this to the lack of large states in Africa to the lack of especially large states in Africa. Granted, you did have relatively large ones in the Sahel but the didn’t last as long as those in Eurasia, falling mainly due to internal struggles.
In the presence of cultural homogeneity, reflecting of a shared lineage, you see improvements in places such as Botswana (Tswana-Sotho) or Ghana (Akan people) partially due to better cultural, and thus likely genetic, unity due to past nationhoods. Apparently, though for short duration, the Tswana formed a political body as large as France,
This is also consistent with the observations made by Sir Harry Hamilton Johnston, a famous colonialist researcher on African and US blacks, on African born blacks on the sea Islands of the South East, which he describes as of “Yoruba Stock” in semblance.
“Also they are when away from white influence inclined to sparsity of clothing-not nowadays a common trait in the United States negro. They are also pure negroes entirely without any infusion of white blood. Crime is very rare among them.” The Negro in the New World by Harry Hamilton Johnston p. 470
A good modern example would be the demographics of West Africa Immigrants, being principally Akan of Ghana and the Yoruba or Igbo of Nigeria, who each come from relatively well constructed precolonial formations. What is also of note is how their prominence seems to be correlated to the extent in which Cousin Marriage is practiced, possibly reflective of the precolonial patterns of cousin marriage
Application for the U.S population in kin networks, where it does not work.
PP, in which he discussed the ethnocentrism of different groups, said this regarding blacks and kin altruism.
“And yet eventually these extremely different tribes mixed, and so you would have parents raising kids who have genetic variants very alien to their own, and this probably contributed to the breakdown of the black family: it’s harder for kin altruism to get selected when the kids you are altruistic to, don’t resemble you that much genetically because their other parent is so unlike you that they don’t inherit your high degree of kin altruism or inherit it as a recessive unexpressed trait. And when kin altruism gets only weakly selected for, racial loyalty (which is probably just an outgrowth of kin loyalty) is probably weakly selected for too.”
Which would be incorrect. Yes, while crossing over does occur, a child would be overall close to their parent’s overall genetic background on the level of relatedness. Leaping from that neglected detail, he assumes from his evidence of “lack of racial loyalty” would that blacks have less ethnic nepotism and thus weaker kin altruism despite not taking into account of selection occurring within subgroups of various constructs like you see in Africa which would apply to families inside them.
If this theory was even supportable, one would expect the opposite that actually occurs with the percentage of Black children to return to relatives compared to White children.
“Of the 94,483 black children discharged from foster care, 12,860, or 13%, were discharged to a relative guardian. Of the 182,941 white children discharged from foster care in 2004, 20,453, or 11%, were discharged to a relative guardian.Of the 15,087 black children adopted from foster care, 4077, or 27%, were adopted by a relative. Of the 29,244 white children adopted from foster care, 5861, or 20%, were adopted by a relative. Of the 279,421 black kids living in foster care for some portion of the year, 69,888 or 25% were living with relatives. Of the 474,734 white children living in foster care for some portion of the year, 101,300, or 21%, were living with relatives.
So black children getting adopted from foster care are somewhat more likely to be adopted by relatives than white kids (27% vs. 20%), black kids exiting foster care are slightly more likely to be discharged to a relative guardian than white kids (13% to 11%), and black kids in foster care are slightly more likely to be living with relatives than white kids (25% vs. 21%). The differences support the hypothesis that blacks are more likely to utilize kinship care networks, but not by a lot, at least in regard to the foster care system.”
From Audacious Epigone, who also notes that despite the higher likelihood of such networks that doesn’t explain disproportion in foster care. Though evidence for IQ is at best moderate, interpersonal indicators were stronger (Azar, Stevenson, and Johnson 2012)).
“SIP problems were associated with direct measures of neglect (e.g., cognitive stimulation provided children, home hygiene, belief regarding causes of child injuries). Further, for the direct measures that were most closely linked to CPS Neglect Status, IQ did not add significant predictive capacity beyond SIP factors in preliminary model testing. Implications for intervention with PID discussed.”
This is possibly linked to EI scores found to differ between Whites and Blacks (Whitman, Kraus, and Rooy 2014)
“The present work examines applicant reactions to a test of emotional intelligence (EI) using an organizational sample of 334 job applicants. Results indicated that Blacks had higher face validity and opportunity to perform perceptions of EI than Whites, but that Whites performed significantly better than Blacks on the EI test. Although exploratory analyses revealed that test performance was positively related to test reactions, we also found that the magnitude of this relationship differed between Blacks and Whites for the opportunity to perform perceptions. We discuss our findings by offering practical advice for organizations considering or using a measure of EI for selection and assessment.”
Evidence for Kin networks is also supported by more data (Taylor 2013).
“Turning first to findings for family support networks, four significant differences were observed in this analysis. African Americans gave assistance to their family members more often than non-Hispanic Whites, were more likely to have daily contact with their extended family members than both non-Hispanic Whites and Black Caribbeans, and had more frequent interactions with their family than Black Caribbeans. Three general conclusions can be drawn from these findings for family assistance and interaction. First, these findings are consistent with prior work indicating that African Americans have similar or higher levels of involvement with kin than non-Hispanic Whites, but are inconsistent with reports that African Americans have lower levels of family support than Whites (e.g., Hogan et al., 1993). As noted in previous reviews of this literature (Sarkisian & Gertsel, 2004), comparisons across studies are problematic given important differences in the dependent variables used. The present study’s investigation of several dimensions of family support relationships (e.g., enacted support, emotional support, contact, negative interaction) in diverse groups of the population and using a common set of sociodemographic correlates clarifies the nature of race/ethnic differences in these relationships.”
It also found, however, weaker ties outside the family, which strengthen my suggestion of finer stratification of kin ties than just simply less selection.
“Several significant differences in friendship networks were observed in this analysis. Non-Hispanic Whites interacted with their friends and gave support to their friends more frequently than African Americans. Additionally, non-Hispanic Whites received support from friends more frequently than both African Americans and Black Caribbeans. Many of the differences between African Americans and non-Hispanic Whites could reflect basic differences in their levels of involvement in friendship networks. For instance, 16.7% of African-Americans, 16.1 % of Black Caribbeans and 9.7% of non-Hispanic Whites report that they never receive help from friends. Similarly, African Americans (11%) were twice as likely as non-Hispanic Whites (4.7%) to indicate that they hardly ever or never interact with friends. Lower levels of involvement with friends among African Americans could be due to estrangement from friends, isolation from friends or exclusive involvement with kinship networks (Ajrouch et al., 2001). Collectively, these results, and previous research (Griffin et al., 2006; Waite & Harrison, 1992), indicate that non-Hispanic Whites are more likely than African Americans to interact with friendship networks and to identify friends as an important source of support.”
This lack of support was not seen, however, with fictive kin or congregational members. So perhaps wither the perception of relationship or differences in genetic similarity may answer some of these questions.
By Scott Jameson
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.
by Scott Jameson
For my first post on this blog, I thought I’d talk about something relevant to the mission of the blog: Political Correctness. I’m very grateful to RaceRealist for inviting me to hop on board here (although I should put out the categorical disclaimer that me posting here is not in and of itself an endorsement of any given thing he’s said over the years).
This is going to be something of an opinion essay about why denying reality is silly: because you still have to live in it. Most of my content is going to be more empirically driven, as you’re used to on this blog. Bear with me.
The SAT’s name change story is a classic case of “Political Correctness,” and is mirrored by KFC’s story of adapting to new nutritional standards. For those out of the loop: after the public realized how unhealthy fried foods are, Kentucky Fried Chicken changed its name to KFC. The point was to make the unhealthy nature of the food one conceptual extrapolation away from the name itself, in hopes that the public would not bother to recall what the “F” stood for.
SAT originally stood for “Scholastic Aptitude Test.” It was (and is) a test to determine how apt you are for scholarly endeavors. Put bluntly, it’s a somewhat sloppy IQ test oriented towards scholarly settings in particular. Of course, that name was too accurate, so it fell out of favor. The public does not want to live in a world wherein poor students are less apt than rich students and Black students are less apt than White students, and so the Scholastic Aptitude Test became the Scholastic Assessment Test. In order to be offended by that, you have to remember that what’s being assessed is aptitude and that nothing has changed. Like “KFC,” it was one conceptual extrapolation away from the reality at hand. Most people were probably too harebrained to see through that.
For some reason, they kept rolling with it. It became an alleged Reasoning Test, and then simply a series of letters that used to be an abbreviation: “the SAT,” no doubt an homage to The Colonel and the chicken he hawks. They’re both just a series of letters now – the unpleasant realities contained therein have been conceptually sterilized. Like the SAT, the nutritional content of the chicken hasn’t changed as much as the name has.
You may suspect that I’m simply flinging excrement in the general direction of The College Board, but there’s a point to what I’m saying here. What we call “Political Correctness” is a pervasive scrubbing of reality out of the consciousness of the public at large, especially the young. There was a time when people were allowed to say things like “I do not enjoy living around Blacks/Whites/Hispanics/whomever.” “Political Correctness” entered from stage left, and then Boomers had to say “bad schools” and “bad neighborhood” instead. Odds are, the Boomers understood the connotative meanings, at least at first. But if you asked millennials what those terms are, I’d bet on most of them actually being ignorant enough to think that the schools are themselves the problem. Nobody ever pointed out to these kids that almost all of the “bad schools” – the schools with low average test scores – are simply full of Hispanics (Mestizos) and African Americans who have low average test scores regardless of what school they’re in, and that the supermajority of all of the “good schools” aren’t. Anyone who doesn’t know this has been deliberately rendered ignorant of a reality that is important to their lives.
What we call “Political Correctness” is in fact the successful, systematic obfuscation of reality, and having reality perpetually hidden from you is dangerous. That is why we at this blog are NotPoliticallyCorrect. As long as I’m here, I can promise you my best attempt at discovering and conveying the truth in the NotPoliticallyCorrect fashion exemplified thus far by RaceRealist: bringing you interesting truths, obscure truths, and of course, controversial truths.
I’m not the first to make the SAT-KFC comparison, by the way. After I wrote this article, I looked around for sources only to dredge this up.
I come across a lot of ridiculous articles from PumpkinPerson, but this has to be one of the most ridiculous. He writes:
Identical twin studies show that obesity has a heritability of almost 80%. Although I generally lean towards nature in most nature-nurture debates, I’ve always had a problem with the idea that obesity is highly genetic, and thus enjoyed this epic rant by blogger Robert Lindsay:
It is 80% genetic[?]
That is why you have whole tribes in South America where not one person has ever been fat.
That is why you have whole towns in Melanesia with 1000’s of people where not one person is fat.
There are fat people in the cities of Solomon Islands. In the study I read, the only man who was fat was one who had gone off to the city for a while and ate salt and processed, packaged food. Do you realize that if you did a genetic study of the fatties in Melanesia, you would find that wonderful 80% “genetic” link you guys are shouting about?
That is why the fatness and obesity rate has exploded in the US and much of the rest of the world. Because it’s 80% genetic!
I do not believe that fatsos act just like the rest of us. Ever known a blimp who ate like a bird? Me either.
I dunno about you, but I have never seen a fat person who wasn’t stuffing their face all the time with lousy food. They are always in restaurants. Always going out to eat. If you go to a restaurant, look around at all the fat people. Those people are fat because fat people like to eat out all the time and restaurant food is fattening. Fat people love to eat. Have you ever noticed that?
It’s 80 percent heritable in first world countries. Obviously the heritability will be lower in the third world. Clearly in first-world countries we have an overabundance of food. We don’t know what to do with it. So instead of having the opposite problem (not enough food) we now have too much food and this is what caused weight to increase (along with added sugars processed carbs).
Look at Melanesia—they still eat an ancestral diet. I can’t tell if Lindsay is being serious or not. He’s comparing people who still eat their ancestral diet to people who live in first-world countries and eat a Western diet. There’s no comparison there. If you want to see why people aren’t fat nor have the same diseases at the same rates (they are low to nonexistent in places like that) read Agriculture and Diseases of Civilization.
This is the study that’s being referred to Elks et al 2012. The heritability of BMI is between .75 and .82. Again: this is in first-world countries.
PP then says:
In fact just the other day, I was at the home of someone who was so incredibly fat I thought “it must be genetic.” And then just as I was leaving his house, I noticed a huge empty box of pizza in the kitchen.
“So maybe the answers to be found are in the integration of factors – starting with the physiological, metabolic, and genetic ones and letting them lead us to the environmental triggers. Because the one thing we know for sure is that the laws of thermodynamics, true as they always are, tell us nothing about why we get fat or why we take in more calories than we expend while it’s happening. (emphasis mine) (Taubes, 2011: pg 74, excerpt from Why We Get Fat and What to Do About It)
The fatness itself or the tendency to engage in behaviors that cause fatness such as ordering large pizzas? So while obesity might technically be nearly 80% genetic, the statistic is misleading because it’s not directly genetic in the same was as height is.
If you don’t eat enough, nor get the right nutrients, you don’t hit your genetic height. If you don’t eat enough you don’t hit your genetic weight.
I don’t get why studies like this get generalized to the whole population. This study was done in first-world countries and so this only applies to first-world countries. You’d think that people who think they know science would know that studies are only applicable for the cohort and people they are done on. Guess not.
Of course I don’t deny obesity has some direct genetic component. Some people gain weight a lot easier than others and for some people, it’s virtually impossible to lose weight no matter how well they eat, though this is rare.
Of course some people gain weight easier than others. Some people lose weight easier than others. Much of the biological opposition to sustained weight loss is due to the hormone leptin (Rosenbaum et al, 2010). The more fat you have in your body, the more leptin you have. Moreover, the longer you are at a certain weight, the more likely it is that is your bodyweight set-point and thus you can only move up or down at around a range of 10 to 15 pounds. Also see this quote from neuroscientist Sandra Aamodt’s book Why Diets Make Us Fat (see her Ted Talk here):
Like nearsightedness, environmental influences on weight also mostly affect the genetically vulnerable, although we understand the details of the process in only rare cases. Fitness gains on a standardized exercise program vary from one person to another largely because of differences in their genes. When identical twins, men in their early twenties, were fed an extra thousand calories per day for about three months, each pair showed similar weight gains . In contrast, the gain varied across twin pairs, ranging from nine to twenty-nine pounds, even though the caloric imbalance was the same for everyone. An individual’s genes also influence weight loss. When another group of identical twins burned a thousand more calories per day through exercise while maintaining a stable food intake in an in-patient facility, their losses ranged from two to eighteen pounds and were even more similar within twin pairs than weight gain. (Aamodt, 2016 pg. 138)
The cold, hard truth is that dieting doesn’t have a good track record. See Mann et al (2007) here. People don’t understand the bodies’ biological processes and assume something is easy while being ignorant to how the body reacts under caloric deprivation. This wouldn’t happen if people actually had some knowledge of human physiology. Something that PP and RL lack. They are speaking about a complex problem than they’re too ignorant to really know about.
PP then says:
“Now I have no doubt that if that person has an identical twin raised apart, he too is extremely fat, and thus fatness technically has a high heritability, but what exactly is genetic here?”
Would the identical twin be raised in an obesogenic environment? If so, there’s a high chance that, yes he’d be fat too.
It’s also true that most people who lose weight end up gaining it back, but that’s because they end up returning to their compulsive eating habits.
People should read a few papers and books to see some data and facts before they write what “sounds good” in their head. These two clearly have no idea what they’re talking about and clearly talking from emotion and what sounds good.
Also read Are There Genetic Causes for Obesity?
Diet is the main driver of our evolution. Without adequate energy, we wouldn’t be able to able to have a brain as large as we do that has the number of neurons we have due to how calorically expensive each neuron is (6 kcal per billion neurons). However, as I’m sure everyone can see, our current diets and environment has caused the current obesity crisis in the world. What is the cause of this? Our genomes are adapted for a paleolithic diet and not our modern environment with processed foodstuffs along with an overabundance of energy. With an overabundance of novel food items and situations due to our obesogenic environments, it is easier for a higher IQ person to stay thinner than it is for a lower IQ person. Tonight I will talk about the causes for this, how and what we evolved to eat and, of course, how to reverse this phenomenon.
“Gourmet Sapiens” arose around 1-1.5 mya with the advent of cooking by Homo erectus. Even before then, when we became bipedal our hands were freed which then allowed us to make tools. With these tools, we could mash and cut food which was a sort of pre-digestion outside the body (exactly what cooking is). Over time, our guts shrank (Aiello, 1997) and we became adapted for a certain diet (Eaton, 2006). Over time, we evolved to eat a certain way—that is, we had times of feast and famine. Due to this, eating three meals a day is abnormal from an evolutionary perspective (Mattson et al, 2014). This sets the stage for the acquisition of diseases of civilization along with the explosion of obesity rates.
When looking for the causes—and not symptoms—of the rise of obesity rates, the first thing we should do is look at our current environment. How is it constructed? What type of foodstuffs are in it? What kinds of foods get advertised to us and how does this have an effect on our psyche and what we eventually buy? All three of these questions are extremely important to think of when talking about why we are so obese as a society. First-world environments are obesogenic (Galgani and Ravussin, 2008) due to being evolutionarily novel. Our genomes are adapted to a paleolithic diet, and so the introduction of the neolithic diet and agriculture reduced our quality of life, with a marked decrease in the quality of skeletal remains discovered after the advent of agriculture. However, agriculture is obviously responsible for the population boom that allowed us to become the apes the took over the world, cause being the population boom that followed the agricultural revolution (Richards, 2002).
Evolutionary mismatches occur when the rate of cultural or technological change is far faster than the genome can change to adapt to the new pressure. These dietary mismatches occur when cultural and technological change which can vastly outstrip biological evolution. The two big events that occurred in human history that have vastly outstripped biological evolution are the agricultural and Industrial Revolution. Contrary to Ryan Faulk’s belief, East Asians are not ‘less sensitive to carbohydrates’ and he did not “solve Gary Taubes’ race problem” in regards to diabesity rates. The rate of cultural and technological change has had large deleterious effects on our quality of life, and our increasing obesity rates have a lot to do with it.
Cofnas (2016) showed that mice taken off of their ancestral diet lead to worse healthy outcomes. The results of Lamont et al (2016) show that we, as animals, are adapted for ancestral diets, not the diets of the environment we have currently made for ourselves. This is a big point to take home from this. All organisms are adapted/evolved for what occurred in the ancestral past, not any possible future events. Therefore, to be as healthy as possible, it stands to reason you should eat a diet that’s closer to the ones your ancestors ate, especially since it can reverse type II diabetes and reverse bad blood markers (Klonoff, 2009). Even a short-term switch to a paleo diet “improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.” (Frassetto et al, 2009) Since we evolved for a past environment and not any possible future ones, then eating a diet that’s as close as possible to our paleolithic ancestors looks like a smart way to beat the evolutionary mismatch in terms of our new, current obesogenic environment.
In one extremely interesting study, O’dea (1984) took ten middle-aged Australian Aborigines with type 2 diabetes and had them return to their ancestral hunter-gatherer lifestyle. With seven weeks of an ancestral diet and exercise, the diabetes had almost completely reversed! Clearly, when the Aborigines were taken off of our Western diet and put back in their ancestral environment with their ancestral diet, their diabetes disappeared. If we went back to a more ancestral eating pattern, the same would happen with us. This one small study lends credence to my claim that we need to eat a diet that’s more ancestral to us for us to ameliorate diseases of civilization (Eaton, 2006).
Further, looking at obesity from an evolutionary perspective can and will help us understand the disease of obesity (Ofei, 2005) better. Speakman (2009) reviewed three different explanations of the current obesity epidemic and assessed their usefulness in explaining the epidemic. The thrifty gene hypothesis states that obesity is an adaptive trait, that people who carry so-called ‘thrifty genes’ would be at an adaptive advantage. And since we have an explosion of obesity today from the 70s to today, this must explain a large part of the variance, right? There is evidence pointing in this direction, however (Southam et al, 2009). The second cause that Speakman looks at is the adaptive viewpoint—that obesity may have never been advantageous in our history, but genes that ultimately predispose us to obesity become “selected as a by-product of selection on some other trait that is advantageous.” (Speakman, 2009) The third and final perspective he proposes is that it’s due to random genetic drift, called ‘drifty genes’, predisposing some—and not others—to obesity. Whatever the case may be, there is some truth to their being genetic factors involved in the acquisition of fat storage. Though drifty genes and the adaptive viewpoint on obesity make more sense than any thrifty gene hypothesis.
For there to be any changes in the rate of obesity in the world, we need to begin to change our obesogenic environments to environments that are more like our ancestral one in terms of what foods are available. Once we alter our obesogenic environment into one that is more ancestrally ‘normal’ (since we are adapted for our past environments and not any possible future ones) then and only then will we see a reduction in obesity around the world. We are surrounded and bombarded with ads since we are children, which then effects our choices later in life; children consume 45 percent more when exposed to advertising (Harris et al, 2009). Clearly, advertisements can have one eat more, and the whole environmental mismatch in regards to being surrounded by foodstuffs not ancestral to us causes the rate of obesity to rise.
Finally, one thing we need to look at is the n-3 to n-6 ratio of our diets. As I covered last month, the n-6/n-3 is directly related to cognitive ability (Lassek and Gaulin, 2011). Our obesogenic environments cause our n-3/n-6 levels to be thrown out of whack. Our hunter-gatherer ancestors had a 1:1 level of n-3 and n-6 (Kris-Etherton, 2000). However, today, our diets contain 14 to 25 times more n-6 than n-3!! Still wondering why we are getting stupider and fatter? Further, Western-like diets (high in linolic acid; an n-6 fatty acid) induces a general fat mass enhancement, which is in line with the observation of increasing obesity in humans (Massiera et al, 2010). There is extreme relevance to the n-3/n-6 ratio on human health (Griffin, 2008), so to curb obesity and illness rates, we need to construct environments that promote a healthy n-3/n-6 ratio, as that will at least curb the intergenerational transmission of obesity. Lands (2015) has good advice: “A useful concept for preventive nutrition is to NIX the 6 while you EAT the 3.” Here is a good list to help balance n-6 to n-3 levels.
In sum, obesity rates are a direct product of obesogenic environments. These environments cause obesity since we are surrounded by evolutionary novel situations and food. The two events in human history that contribute to this is the agricultural and Industrial Revolution. We have paleolithic genomes in a modern-day world, which causes a mismatch between our genomes and environment. This mismatch can be ameliorated if we construct differing environments—ones that are less obesogenic with less advertisement of garbage food—and we should see rates of obesity begin to decline as our environment becomes more and more similar to our ancestral one (Genné-Bacon, 2014).
The study on mice showed that for them to be healthy they need to eat a diet that is ancestral to them. We humans are no different.The evidence from the study on Australian Aborigines and the positive things that occur after going on a paleo diet for humans—even for sedentary people—shows that for us to be as healthy as possible in these obesogenic environments that we’ve made for ourselves, we need to eat a diet that matches with our paleolithic genome. This is how we can begin to fight these diseases of civilization and heighten our quality of life.
Note: Diet and exercise only under Doctor’s supervision, of course
Aiello, L. C. (1997). Brains and guts in human evolution: The Expensive Tissue Hypothesis. Brazilian Journal of Genetics,20(1). doi:10.1590/s0100-84551997000100023
Cofnas, N. (2016). Methodological problems with the test of the Paleo diet by Lamont et al. (2016). Nutrition & Diabetes,6(6). doi:10.1038/nutd.2016.22
Eaton, S. B. (2006). The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proceedings of the Nutrition Society,65(01), 1-6. doi:10.1079/pns2005471
Frassetto, L. A., Schloetter, M., Mietus-Synder, M., Morris, R. C., & Sebastian, A. (2009). Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. European Journal of Clinical Nutrition,63(8), 947-955. doi:10.1038/ejcn.2009.4
Galgani, J., & Ravussin, E. (2008). Energy metabolism, fuel selection and body weight regulation. International Journal of Obesity,32. doi:10.1038/ijo.2008.246
Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99–112, 2014
Griffin, B. A. (2008). How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP study. Current Opinion in Lipidology,19(1), 57-62. doi:10.1097/mol.0b013e3282f2e2a8
Harris, J. L., Bargh, J. A., & Brownell, K. D. (2009). Priming effects of television food advertising on eating behavior. Health Psychology,28(4), 404-413. doi:10.1037/a0014399
Klonoff, D. C. (2009). The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and other Risk Factors for Cardiovascular Disease. Journal of Diabetes Science and Technology,3(6), 1229-1232. doi:10.1177/193229680900300601
Kris-Etherton PM, Taylor DS, Yu-Poth S, et al. Polyunsaturated fatty acids in the food chain in the United States. Am J Clin Nutr, 2000, vol. 71 suppl(pg. 179S-88S)
Lamont, B. J., Waters, M. F., & Andrikopoulos, S. (2016). A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. Nutrition & Diabetes,6(2). doi:10.1038/nutd.2016.
Lands, B. (2015). Choosing foods to balance competing n-3 and n-6 HUFA and their actions. Ocl,23(1). doi:10.1051/ocl/2015017
Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005
Massiera, F., Barbry, P., Guesnet, P., Joly, A., Luquet, S., Moreilhon-Brest, C., . . . Ailhaud, G. (2010). A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. The Journal of Lipid Research,51(8), 2352-2361. doi:10.1194/jlr.m006866
Mattson, M. P., Allison, D. B., Fontana, L., Harvie, M., Longo, V. D., Malaisse, W. J., . . . Panda, S. (2014). Meal frequency and timing in health and disease. Proceedings of the National Academy of Sciences,111(47), 16647-16653. doi:10.1073/pnas.1413965111
O’dea, K. (1984). Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes,33(6), 596-603. doi:10.2337/diabetes.33.6.596
Ofei F. Obesity- a preventable disease. Ghana Med J 2005;39: 98-101
Richards, M. P. (2002). A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence. European Journal of Clinical Nutrition,56(12), 1270-1278. doi:10.1038/sj.ejcn.1601646
Southam, L., Soranzo, N., Montgomery, S. B., Frayling, T. M., Mccarthy, M. I., Barroso, I., & Zeggini, E. (2009). Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants? Diabetologia,52(9), 1846-1851. doi:10.1007/s00125-009-1419-3
Speakman, J. R. (2013). Evolutionary Perspectives on the Obesity Epidemic: Adaptive, Maladaptive, and Neutral Viewpoints. Annual Review of Nutrition,33(1), 289-317. doi:10.1146/annurev-nutr-071811-150711
The relationship between exercise and cognitive ability is important, but often not spoken about. Exercise releases many endorphins (Harber and Sutton, 1984) that help to further positive mood, have one better handle stress since sensitivity to stress is reduced after exercise; and after exercise, depression, and anxiety also decrease (Salmon, 2001). Clearly, if you’re attempting to maximize your cognition, you want to exercise. However, a majority of Americans don’t exercise (49 percent of Americans over the age of 18 do aerobic exercise whereas only 20 percent of Americans do both aerobic and muscle-strengthening exercise). The fact that we do not exercise as a country is proof enough that our life expectancy is declining (Olshansky et al, 2005), and we need to exercise—as a country—to reverse the trend.
Regular readers may know of my coverage of obesity on this blog. Understandably, a super majority of people will disregard my views on obesity and its causes as ‘pseudoscience’ or ‘SJW-ness’, that however says nothing to the data (and if anyone would like to discuss this, they can comment on the relevant articles). Since the average American hardly gets any exercise, this can lead to a decrease in cognitive functioning as less blood flows to the brain. Thus, everyone—especially the obese—needs to exercise to reach maximum genetic brain performance, lest they degenerate in cognitive function due a low-quality diet, such as a diet high in n-6 (the SAD diet), which is correlated with decreased cognition. Further, contrary to popular belief, the obese have lower IQs since around age three; obesity does not itself lower genotypic IQ, their IQ is ALREADY LOW which leads to obesity later in life due to a non-ability to delay gratification. Clearly, exercise education needs to be targeted at those with lower IQs since they have a higher chance of becoming obese in comparison to those with lower IQs (Kanazawa, 2013; 2014).
Clearly not eating well and not exercising can have negative effects on cognition. But what are the positives?
As mentioned previously, exercise releases endorphins that cause good mood and block pain. However, the importance of exercise does not stop there. Exercise also leads to faster reaction times on memory tasks and “increased levels of high-arousal positive affect (HAP) and decreased levels of low-arousal positive affect (LAP).” Exercise has important effects on people of all age groups (Hogan, Mata and Carstensen, 2013; Chodzko-Zajko et al, 2009). Further, physical exercise protects against age-related diseases and cognitive decline in the elderly by modifying “metabolic, structural, and functional dimensions of the brain that preserve cognitive performance in older adults.” (Kirk-Sanchez and McGough, 2014). Exercise is, clearly, a brain protectant during both adolsence and old age, so no matter your age if you want a high QoL living the best life possible, you need to supplement an already healthy lifestyle with strength training/cardio (of course, under doctor’s supervision).
Another important benefit to exercise is that it increases blood flow to the brain (Querido and Steele, 2007; Willie and Ainslie, 2011); however, changes in cerebral blood flow (CBF) during exercise are not associated with higher cognition (Ogoh et al, 2014). During prolonged exercise, cognition was improved when blood flow to the middle cerebral artery (MCA) was decreased. Thusly, exercise-induced changes in CBF do not preserve cognitive performance. Exercise to get blood to the brain is imperative for proper brain functioning. Our brains are vampiric, so we need to ‘feed it’ with blood and what’s the best way to ‘feed’ the brain in this context? Exercise!
Exercise also protects against cognitive degeneration in the elderly (Bherer, Erikson and Lie-Ambrose, 2013; Carvalho et al, 2014; Paillard, 2015). Further, longitudinal studies show an association between exercise and a decrease in dementia (Blondell, Hammersley-Mather and Veerman, 2014). The evidence is currently piling up showing that exercise at all ages is good cognitively, reduces mortality as well as a whole slew of other age-related cognitive diseases. The positive benefits of exercise need to be shown to elderly populations since exercise—mainly strength training—reduces the chance of osteoporosis (Layne and Nelson, 1999; Gray, Brezzo, and Fort, 2013). Moreover, elderly people who exercise live longer (Gremeaux et al, 2012). Now, if you don’t exercise, now’s looking like a pretty good time to start, right?
Finally, lack of exercise causes a myriad of deleterious diseases (Booth, Roberts, and Laye, 2014). This is due, in large part to our evolutionary novel environment (Kanazawa, 2004) which leads to evolutionary mismatches. An evolutionary mismatch, in this instance, is our obesogenic environment (Lake and Townshend, 2006). In terms of our current environment, it is evolutionary novel in comparison to our ancestral land (the Savanna; re: Kanazawa, 2004). Modern-day society is ‘evolutionarily novel’. In this case, we haven’t fully adapted (genetically) to our new lifestyles as, Gould said in Full House, our rate of cultural change has vastly exceeded Darwinian selection. Thusly, our environments that we have made for ourselves (and that we assume that heighten our QoL) actually cause the reverse, all the while top researchers are scratching their heads to figure out the answer, the problem while it’s staring them right in the face.
Our obesogenic environments have literally created a mismatch with our current eating habits and our ancestral one (Krebs, 2009). Moreover, dietary mismatches occur when cultural and technological change vastly outstrip biological evolution (Logan and Jacka, 2009). Clearly, we need to lessen the impact of our obesogenic environment we have made for ourselves so that we can live as long as possible, as well as be as cognitively sharp as possible. Thusly, if our environment causes a mismatch with our genome which in turn causes obesity, then by changing our environment to one that matches our genome, so to speak, levels of obesity should decline as our environment becomes less obesogenic while becoming like our ancestral environment (Genne-Bacon, 2014).
In sum, the evidence for the positive benefits for exercise is ever-mounting (not like you need Pubmed studies to know that exercise is beneficial). However, due to our obesogenic environments, this makes it hard for people with higher time preference to resist their urges and the result is what you see around you today. The evidence is clear: exercise leads to increased blood flow to our vampiric brains; thus it will have positive effects on memory and other cognitive faculties. So, in order to live to a ripe, old age as a healthy man/woman, hit the gym and treadmill and try staying away from evolutionarily novel things as much as possible (i.e., like processed food). When we, as a country recognize this, we can then be smarter, healthier and, above all else, have a high QoL while living a longer life. Is that not what we all want? Well hit the gym, start exercising and change your diet to one that matches our ancestors. Don’t be that guy/gal (we all know who that guy is) that jumps on the exercise train late and misses out on these cognitive and lifestyle benefits!
Note: Only with Doctor supervision, of course
Bherer, L., Erickson, K. I., & Liu-Ambrose, T. (2013). A Review of the Effects of Physical Activity and Exercise on Cognitive and Brain Functions in Older Adults. Journal of Aging Research,2013, 1-8. doi:10.1155/2013/657508
Blondell, S. J., Hammersley-Mather, R., & Veerman, J. L. (2014). Does physical activity prevent cognitive decline and dementia?: A systematic review and meta-analysis of longitudinal studies. BMC Public Health,14(1). doi:10.1186/1471-2458-14-510
Booth, F. W., Roberts, C. K., & Laye, M. J. (2013). Lack of Exercise Is a Major Cause of Chronic Diseases. Comprehensive Physiology. doi:10.1002/cphy.c110025
Carvalho, A., Cusack, B., Rea, I. M., & Parimon, T.,. (2014). Physical activity and cognitive function in individuals over 60 years of age: a systematic review. Clinical Interventions in Aging, 661. doi:10.2147/cia.s55520
Chodzko-Zajko WJ, Proctor DN, Fiatarone Singh MA, Minson CT, Nigg CR, Salem GJ, Skinner JS: American College of Sports Medicine position stand. Exercise and physical activity for older adults. Med Sci Sports Exerc. 2009, 41: 1510-1530. 10.1249/MSS.0b013e3181a0c95c.
Gray M., Di Brezzo R., I.L. Fort (2013) The effects of power and strength training on bone mineral density in premenopausal women. J Sports Med Phys Fitness, 53, pp. 428–436
Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99–112, 2014
Gremeaux V, Gayda M, Lepers R, Sosner P, Juneau M, Nigam A. Exercise and longevity. Maturitas. 2012;73(4):312–7.
Harber VJ, Sutton JR. (1984) Endorphins and exercise. Sports Medicine 1: 154–174, 1984
Hogan, C. L., Mata, J., & Carstensen, L. L. (2013). Exercise holds immediate benefits for affect and cognition in younger and older adults. Psychology and Aging,28(2), 587-594. doi:10.1037/a0032634
Kanazawa, S. (2004). The Savanna Principle. Managerial and Decision Economics,25(1), 41-54. doi:10.1002/mde.1130
Kanazawa, S. (2013). Childhood intelligence and adult obesity. Obesity,21(3), 434-440. doi:10.1002/oby.20018
Kanazawa, S. (2014). Intelligence and obesity. Current Opinion in Endocrinology & Diabetes and Obesity,21(5), 339-344. doi:10.1097/med.0000000000000091
Krebs, J. R. (2009). The gourmet ape: evolution and human food preferences. American Journal of Clinical Nutrition,90(3). doi:10.3945/ajcn.2009.27462b
Lake, A., & Townshend, T. (2006). Obesogenic environments: exploring the built and food environments. The Journal of the Royal Society for the Promotion of Health,126(6), 262-267. doi:10.1177/1466424006070487
Layne, J. E., & Nelson, M. E. (1999). The effects of progressive resistance training on bone density: a review. Medicine & Science in Sports & Exercise,31(1), 25-30. doi:10.1097/00005768-199901000-00006
Kirk-Sanchez, N., & Mcgough, E. (2014). Physical exercise and cognitive performance in the elderly: current perspectives. Clinical Interventions in Aging, 51. doi:10.2147/cia.s39506
Ogoh, S., Tsukamoto, H., Hirasawa, A., Hasegawa, H., Hirose, N., & Hashimoto, T. (2014). The effect of changes in cerebral blood flow on cognitive function during exercise. Physiological Reports,2(9). doi:10.14814/phy2.12163
Olshansky, S. J., Passaro, D. J., Hershow, R. C., Layden, J., Carnes, B. A., Brody, J., . . . Ludwig, D. S. (2005). A Potential Decline in Life Expectancy in the United States in the 21st Century. New England Journal of Medicine,352(11), 1138-1145. doi:10.1056/nejmsr043743
Paillard, T. (2015). Preventive effects of regular physical exercise against cognitive decline and the risk of dementia with age advancement. Sports Medicine – Open,1(1). doi:10.1186/s40798-015-0016-x
Querido, J. S., & Sheel, A. W. (2007). Regulation of Cerebral Blood Flow During Exercise. Sports Medicine,37(9), 765-782. doi:10.2165/00007256-200737090-00002
Salmon, P. (2001). Effects of physical exercise on anxiety, depression, and sensitivity to stress. Clinical Psychology Review,21(1), 33-61. doi:10.1016/s0272-7358(99)00032-x
Willie, C. K., & Ainslie, P. N. (2011). Cool head, hot brain: cerebral blood flow distribution during exercise. The Journal of Physiology,589(11), 2657-2658. doi:10.1113/jphysiol.2011.209668
Much has been written in the scientific literature on our brain size increase, which has doubled in the timespan of about 3 million years. It is assumed that our brains became bigger so we could become smarter. However, recent data shows that the amount of blood our brains use dramatically increased over the course of human evolution—the amount of blood our brains use increased some 600 percent over the course of human evolution, substantially more than our brain size increase (350 percent).
Seymour, Bosiocic, and Snelling (2016) showed that while there was a 3.5-fold increase in brain size while there was a 6-fold increase in total cerebral blood flow rate. This is due to increased interneuron connectivity, synaptic activity and cognitive function which all depend on the cerebral metabolic rate. This is yet another reason why cooking was so important during our brain evolution. If the brain has a higher metabolic rate, only a high-quality diet will allow it to function. This can only occur if and only if there is a high-quality diet in the first place.
The metabolic intensity of cerebral tissue in our lineage could only be satisfied by a high-quality cooked diet. Clearly, the evolution of the human brain most always goes back to nutrition and the quality of the human diet. Without erectus’ control of fire around 1.5 mya, our brains wouldn’t have been able to grow this big, nor would we have the cerebral blood flow we eventually had. The below picture is figure 1 from the paper. The left slide is Australopithecus Afarensis, the middle is a Neanderthal, and the right is archaic Homo Sapiens.
They measured the lumen radius of the internal carotid arteries and were able to deduce that there were large changes in cerebral blood flow in hominin evolution due to the increasing size of the ICAs. Arterial size, blood flow rate and metabolic rate are tightly related. So if there are bigger ICAs, then that hominin had more blood flow to feed a bigger brain. This is clear evidence that as our brain size increased that we needed more blood to feed our growing brain.
Kilroy et al (2013) hypothesize that due to widespread anatomical differences in the anterior cingulate cortex (ACC), PFC and insula and subcortical cortices, those regions must be a “central node of the brain’s network underlying individual differences in intellectual development throughout childhood and adolescence.” Cerebral blood flow in the subgenual/ACC correlates the highest with IQ. They also showed that it’s possible to delineate “where CBF is modulated by IQ.” More blood flow in these regions means a higher IQ. Since the ICAs grew larger over the course of hominin brain evolution to increase intelligence, it’s no surprise that more blood flow to certain parts of the brain is related to higher intelligence in children and adolescents.
Even CBF at rest is correlated with higher intelligence and creativity (Takeuchi et al, 2011). They showed that gray and white matter in the brain is correlated with CBF at rest and significantly and positively with psychometric intelligence. Further, the Raven’s Advanced Progressive Matrices (RAPM) and scores on the creativity test that were administered to the cohort correlated positively with white matter and cerebral blood flow. They also noticed that there was an association between negative mood and increased cerebral blood flow. Grey and white matter CBF at rest were both correlated with the RAPM and the creativity test administered. This is yet more evidence that blood flow to certain parts of the brain dictates intelligence (and most likely individual differences in intelligence as well).
The more vampiric a brain is (especially in certain regions), the higher one’s intelligence will be, on average. By looking back at the fossil skulls of our hominin ancestors and the radius of the ICA, we can infer that as hominin evolution ‘progressed’ through time, the ICA radius increased which meant increased blood flow to the brain. This is directly related to brain metabolism and could only be afforded with a high-quality diet which started with the advent of tool-making and the use of fire to cook by erectus. Cerebral blood flood in the anterior cingulate cortex is significantly and positively correlated with IQ. CBF at rest is also correlated with IQ and certain regions of the brain. This shows that a brain with a higher metabolic rate will be, on average, more intelligent than a brain that has a lower one. The current data on intelligence and CBF points to increased blood flow in certain parts of the brain is related to higher levels of intelligence. This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with more cerebral blood flow due to larger arteries and a higher metabolic rate.
This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with the need for more blood to the brain to increase intelligence (as blood will also shuttle oxygen to the brain). This is yet another reason why our not-so-special brains are remarkable compared to the rest of the animal kingdom—the one variable that gives us our cognitive superiority over other animals is the ability to cook and use fire. A lot of our physiologic, anatomic and brain evolution can be explained simply as: no cooking, fire, and meat, no big brains (and as a consequence, everything you see around you today would not be here), and the only thing that can drive such a metabolically demanding brain is cooking and eating high-quality foods. The outstanding number of neurons crowded into our cerebral cortex along with much blood our vampiric brain guzzles explains our cognitive superiority over other animals.
Kilroy, E., Yan, L., Wang, D. J., Dapretto, M., Mendez, M. F., Liu, C. Y., & Kim, Y. C. (2011). Relationships between Cerebral Blood Flow and IQ in Typically Developing Children and Adolescents. Journal of Cognitive Science,12(2), 151-170. doi:10.17791/jcs.2011.12.2.151
Seymour, R. S., Bosiocic, V., & Snelling, E. P. (2016). Fossil skulls reveal that blood flow rate to the brain increased faster than brain volume during human evolution. Royal Society Open Science,3(8), 160305. doi:10.1098/rsos.160305
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002)
Takeuchi, H., Taki, Y., Hashizume, H., Sassa, Y., Nagase, T., Nouchi, R., & Kawashima, R. (2011). Cerebral Blood Flow during Rest Associates with General Intelligence and Creativity. PLoS ONE,6(9). doi:10.1371/journal.pone.0025532
Today is Darwin’s 208th birthday and the 158th year since the publication of On the Origin of Species by Means of Natural Selection or the Preservation of Favoured Races in the Struggle of Life. So many people get Darwin wrong. They either have never read his books, or are taking a secondhand account. You can tell who has never read his writings in his own words and who takes snippets of his writings to use them for ideological purposes. I was going to wait until I finished The Descent of Man (Darwin, 1871) until I wrote this article but Darwin Day seems like the best time to do it.
People call themselves ‘Darwinists’ when it’s clear they’ve never read his writings. And due to this, people have large misconceptions on cherry-picked quotes and then use it for their pet ideology—not even attempting to understand the context around what he wrote. One large misquotation you may see around the Internet may put charges of ‘racism’ on Darwin since he ‘believed’ that the ‘higher’ races of Man will one day exterminate the ‘lower’ races. PumpkinPerson is guilty of this, writing in his article Darwin’s terrifying prediction:
Sadly, if HBD is correct, I think there probably will be natural selection favoring higher IQ populations, in fact it’s already happening. In sub-Saharan Africa, we see the more primitive cultures like pygmies and Bushmen losing more and more territory and their populations declining.
Which is based on a (misinterpreted) Darwin quote from his book Descent of Man (1871 (2004): 132-3); note: I have the Barnes n Noble edition):
The great break in the organic chain between man and his nearest allies, which cannot be bridged over by any extinct or living species, has often been advanced as a grave objection to the belief that man is descended from some lower form; but this objection will not appear of much weight to those who, convinced by general reasons, believe in the general principle of evolution. Breaks incessantly occur in all parts of the series, some being wide, sharp and defined, others less so in various degrees; as between the orang and its nearest allies—between the Tarsius and the other Lemuridae—between the elephant and in a more striking manner between the Ornithorhynchus or Echidna, and other mammals.
But all these breaks depend merely on the number of related forms which have become extinct. At some future period, not very distant as measured by centuries, the civilised races of man will almost certainly exterminate and replace throughout the world the savage races. At the same time the anthropomorphous apes, as Professor Schaaffhausen has remarked, will no doubt be exterminated. The break will then be rendered wider, for it will intervene between man in a more civilised state, as we may hope, than the Caucasian, and some ape as low as a baboon, instead of as at present between the negro or Australian and the gorilla.
This is the big quote. The quote that supposedly what paints Darwin as a ‘racist’ and one of the many, many instances of quote-mining from Creationists attempting to discredit his theory of evolution through natural selection. But here’s the thing that people fail to realize: without the rest of the context, you won’t know what he’s saying because the very next paragraph writes (pg 132):
With respect to the absence of fossil remains, serving to connect man with his ape-like progenitors, no one will lay much stress on this fact who reads Sir C. Lyell’s discussion, where he shows that in all the vertebrate classes the discovery of fossil remains has been a very slow and fortuitous process. Nor should it be forgotten that those regions which are the most likely to afford remains connecting man with some extinct ape-like creature, have not as yet been searched by geologists.
So, the whole quote taken in context, it seems he was defending his theory showing that even though no there was an “absence of fossil remains” connecting us to our apelike ancestors.
This book was written 12 years after On the Origin, so knowing that and then seeing the rest of the omitted context behind the controversial quote (and, of course, how Creationists quote-mine and attempt to twist and turn words), what do you think he was saying? To me, it looks like he was defending his theory and addressing critics who said that the fossil record does not support his claims. In fact, Darwin and other Naturalists of the time didn’t separate culture and biology and thus used a blend of both. Darwin was simply observing that a slight advantage between races of men would, after time, lead to the creation of a new species. You’d have to have actually read his books to know that, though.
PP’s other post on Darwin, Did Darwin believe in HBD? he writes (referring to the previous quote-mine):
What it looks like is Darwin describing an evolutionary hierarchy: Caucasian > negro/Australoid > gorilla > baboon.
If you’re looking for something, you’re going to find it. Complete misrepresentation of Darwin’s words, and just reading Descent of Man will let you know how grossly incorrect this interpretation really is.
Darwin only meant that Caucasians would replace savage races because of their cultural superiority; biological superiority had nothing to do with it. And are we also supposed to believe that Darwin’s predicted demise of gorillas was also for cultural, not biological reasons?
PP, read the whole context and tell me if that’s how you still interpret it. It is worth noting that the quotes are taken from a part of the book that has the subsection: On the Birthplace and Antiquity of Man, which lends more credence to the fact that he was defending his theory from detractors (due to the names he brought up and his prose, in context) who needed to see ‘transitional’ fossils between ape and man.
Further, since PP is using a Creationist quotation, then a Creationist rebuttal is apt here:
First of all, Darwin is making a technical argument as to the “reality” of species, particularly Homo sapiens in this case, and why there should still be apparently distinct species, if all the different forms of life are related by common descent through incremental small changes. His answer is that competition against those forms with some, even small, advantage tends to eliminate closely related forms, giving rise to an apparent “gap” between the remaining forms. Whether or not Darwin was right about that is irrelevant to the use of this quote mine, of course, since that is part of the context that the creationists using it have assiduously removed.
Irony aside that an atheist is using a Creationist quote-mine to prove biological differences, this shows how people who’ve never read his writing can misinterpret what he really meant.
Darwin was also a huge abolitionist, which is never brought up in these discussions. He argued, for his whole life, that slavery should be abolished. He also came from an extremely abolitionist family, so any charges of ‘racism’ to Darwin seem pretty far off the mark.
According to liberals, Darwin only meant that Caucasians would replace savage races because of their cultural superiority; biological superiority had nothing to do with it. And are we also supposed to believe that Darwin’s predicted demise of gorillas was also for cultural, not biological reasons?
According to people that know what they’re talking about, Darwin meant that closely related organisms even will a small advantage will replace the other, and that will give rise to a ‘gap’ between organisms. Learn the context behind the whole quote, instead of what Creationists quote-mine. And biological superiority doesn’t exist.
Never mind that Darwin’s theory of natural selection was actually based on biology, not culture.
Can natural selection NOT occur because of cultural differences? Say, two genetically similar populations and one has the native culture and the other with a new, alien culture and they have to use it to adapt to a new environment. Would that be an example of culture and its effect on natural selection?
Never mind that Darwin’s own cousin (Francis Galton) was the father of HBD.
Nothing to do with Darwin himself.
Never mind that Darwin’s own book on natural selection was subtitled The Preservation of Favoured Races in the Struggle for Life.
Why let facts get in the way of a convenient rationalization.
Why don’t you tell me?
They just come up with increasingly creative rationalizations to deny the truth, and the effort this takes makes them more and more psychologically invested in denying inconvenient realities.
People who quote Darwin should most definitely read his works, as if they’re quoting him—especially in these contexts—they should really know the whole context behind the quote and not rely on a Creationist quote-mine which is easily dismantled.
And the way it’s going now, the savage races are outbreeding the civilized races—so how do you see (your interpretation of) Darwin’s theory coming to pass? How will your race war fantasy with each of the macro-races genociding the rest of the ethnies in their group and form one ethnicitu of that racial group? PP believes that eventually it’ll be Ashkenazi Jews vs. East Asians for East Asia. Except Ashkenazi Jews frequently breed with gentiles, and in 100 years there will be very few Ashkenazi Jews left. Japan is having a huge population decline, which is partly biological and partly cultural/environmental in nature. One of the so-called ‘most evolved’ ethnies isn’t able to reign superior over the rest of the inferior ethnies/races due to low birthrates? As I said last night: civilization is dysgenic and leads to low birth rates. So how will the civilized races exterminate the savage races, if the civilized races hardly breed because they get too civilized?
PumpkinPerson’s most recent article Are muscular guys genetically inferior? is a joke. He makes huge assumptions and attempts to this ‘social experiment’ as evidence that women find ‘nerds’ more attractive. The logic here is that since East Asians are the ‘most evolved’ race and (in his world) they have the least testosterone along with the highest intelligence, that this is some kind of apex of human evolution. However the conclusions he makes off of this one video are very erroneous and I will explain why.
They are simply genetically inferior because the muscular body type branched off the evolutionary tree pre-maturely.
…No idea what he’s talking about. No source that the ‘muscular body type branched off the evolutionary tree prematurely.’ This is just an assumption because Africans supposedly have higher testosterone than both Europeans and East Asians, except East Asians have the highest testosterone out of all of all three traditional races, not Africans.
After watching this video I feel like starving my muscles off (not that I recommend that).
Good luck with that.
I realize not everyone agrees with the progressive model of evolution, but real scientists do. For example, check out this phys.org article:
This article has nothing to do with progressive evolution at all. In fact, this article is basically a summary of Full House (Gould, 1996) in which Gould argues that since life began at the left wall of complexity—where no organism can get simpler—that a right-tail distribution of complexity was inevitable. I have covered this here. This is not evidence for progressive evolution. It is, in fact, the opposite. He’s never read Gould’s books so he wouldn’t know that.
Now, PP’s contention that women find nerds more attractive has no basis. When I think of a ‘nerd’, I think of a scrawny pencil-neck, buck teeth, person with thick-rimmed black glasses. This, obviously, isn’t true. If it were, then why do East Asians—Japan specifically—have the lowest birthrates? Of course, social factors have a lot to do with it—birthrates decline in developed countries (Nargund, 2009; Sinding, 2009), as well as genetic ones (Harris and Nielson, 2016). So, clearly, the more intelligent, more developed countries don’t have more children, which then, of course implies that either higher IQ people are less desirable from a reproductive point of view (plausible), or they forgo having children until around 28 years of age (Lange, Rinderu and Bushman, 2016). Whatever the case may be, those with higher IQs do not conceive as many children as those with lower IQs, signifying something about their fitness aspects.
Further, women, evolutionarily speaking, sexually selected men for high levels of testosterone, which leads to bigger muscles, more defined facial features, higher levels of aggression (good for protecting genetic interests) and so on. The fact that some people may think that nerds have better prospects than non-nerds, evolutionarily speaking, had no basis in reality and for one to believe as much, it has to be driven by ideology.
Dixson et al (2010) showed that women prefer men with the mesomorphic somatype and ‘average’ body type, then prefer ectomorphs (a skinnier body type) and finally endomorph (a heavier build) ranging from most attractive to least. This study shows that, at least when it comes to European females, they prefer mesomorphic somatypes, which, more often than not, one who is over 6 feet tall will have. Does that seem like a ‘nerd’ to you? I don’t think so. Someone who has the potential ability to control a room with his presence doesn’t seem like a nerd to me. These are the same people who are CEOs.
Journalist Malcolm Gladwell showed that on average, CEOs averaged just under 6 foot tall. Since the average American is 5 foot 9, the average CEO has a three-inch height advantage over the average man in America. However, when looking at those who are 6 feet tall and up, for average Joe the percentage is a paltry 3.9 percent while, in Gladwell’s sample, 30 percent were over 6’2″. So, Gladwell states, the lack of minorities and women in high positions has a plausible explanation: height. Men are, on average taller than women. Tall men earn more money than their shorter counterparts. Taller children also perform better on cognitive tests, taller men earn more money in Mexico, and taller children do better on learning tests in India (Lawson and Spears, 2016).
Women want taller men more than men want taller women (Stulp, Buunk, and Pollet, 2012). Tall men are also more likely to have a mesomorphic somatype. Those somatypes are seen as the most attractive. Does that seem like a nerd somatype to you? An athletic somatype? On the other hand, women aren’t attracted to short men (Nettle, 2002). East Asians—the so-called ‘most evolved race’—are the shortest race. Doesn’t look too good for them.
Furthermore, while East Asian men see themselves as attractive and dateable, they don’t believe society sees it that way. Forty-six percent of the sample said they could recall one instance where they hear someone state that they do not date Asian men, while eleven percent of Asian men have heard it at least six times. For Okcupid’s 2009 race/dating data, 18 percent of Asian women (3,381 yes) would date someone of their own background/skin color while 82 percent (17,227) wouldn’t! So much for the ‘most evolved’ race having dating prospects in their own race. East Asian men said yes to the question at a rate of 24 percent (7,965 yes) and no 76 percent of the time (25,358).
To further put this into perspective, white women would said yes to the question at a rate of 54 percent (154,595) and no at a rate of 46 percent (132,497) while white men said yes at a 40/60 yes/no rate (183,360/277,827 respectively). In total, 45 percent of whites would prefer to date someone of their skin color/ethnicity while 55 percent wouldn’t (337,955/410,324) while non-whites said yes to the question 20 percent of the time while they said no 80 percent of the time (56,080/222,484).
A 2014 follow-up found the same thing, however with Asian women showing some positive ratings toward Asian males (while all races of men didn’t find black women particularly attractive). However, Asian men were seen as the least attractive throughout the whole sample. Asian males are also seen as less attractive than males of other races (Fisman et al, 2008). In their sample, they found even after running regressions that Asian women found white, black, and ‘Hispanic’ men. They also show that even Asian men find white, black and ‘Hispanic’ females more attractive than Asian females.
In sum, PP’s contentions and reaches in his article are wrong. ‘Nerds’ (in the way I’m defining the word) are not more successful than the alpha CEOs who are over 6’2”. PP seems to have an aversion to testosterone (believes that it is the cause for racial differences in prostate cancer differences, but vitamin D deficiencies are a more likely culprit). East Asian men—the so-called ‘most evolved’ men of the ‘most evolved’ race do not fair well in terms of physical attractiveness, and this may be a reason why the Japanese birthrate is declining, with the average Japanese woman having only one child during her lifetime (Nomura and Koizumi, 2016). PP’s theory makes no sense, because women favor mesomorphic somatypes. Mesomorphs are more likely to be CEOs of 500 companies, more likely to be more cognitively adept and make more money than their shorter counterparts. Making evolutionary theories off of one (obviously fake) ‘social experiment’ is ridiculous. East Asian men, the so-called ‘most evolved man’ fall short in the dating game, due to being seen as less attractive.
Dixson, B. J., Dixson, A. F., Bishop, P. J., & Parish, A. (2009). Human Physique and Sexual Attractiveness in Men and Women: A New Zealand–U.S. Comparative Study. Archives of Sexual Behavior,39(3), 798-806. doi:10.1007/s10508-008-9441-y
Fisman, R. J., Iyengar, S. S., Kamenica, E., & Simonson, I. (2008) (n.d.). Racial Preferences in Dating: Evidence from a Speed Dating Experiment. SSRN Electronic Journal. doi:10.2139/ssrn.610589
Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Harris, K., & Nielsen, R. (2016). The Genetic Cost of Neanderthal Introgression. Genetics, 2016 doi:10.1101/030387
Lange, P. A., Rinderu, M. I., & Bushman, B. J. (2016). Aggression and Violence Around the World: A Model of CLimate, Aggression, and Self-control in Humans (CLASH). Behavioral and Brain Sciences, 1-63. doi:10.1017/s0140525x16000406
Nargund G. (2009) Declining birth rate in Developed Countries: A radical policy re-think is required. F.V & V in ObGyn. 2009;1:191-3
Nettle, D. (2002). Women’s height, reproductive success and the evolution of sexual dimorphism in modern humans. Proceedings of the Royal Society B: Biological Sciences,269(1503), 1919-1923. doi:10.1098/rspb.2002.2111
Nomura, K., & Koizumi, A. (2016). Strategy against aging society with declining birthrate in Japan. Industrial Health INDUSTRIAL HEALTH,54(6), 477-479. doi:10.2486/indhealth.54-477
Sinding S.(2009) Population, poverty and economic development. Phil. Trans. R. Soc. B 364.
Stulp, G., Buunk, A. P., & Pollet, T. V. (2013). Women want taller men more than men want shorter women. Personality and Individual Differences,54(8), 877-883. doi:10.1016/j.paid.2012.12.019