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Genetic Changes from Cooking
2600 words
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.
References
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
An Evolutionary Look At Obesity
2050 words
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
References
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
Our Vampiric Brains
1100 words
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.
References
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
Happy Darwin Day, Heathens
1650 words
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.
PP says:
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.
Which of the great cabbage races will survive? He used race as a term for varieties.
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.
Ironic….
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?
Out of FACTfrica
1650 words
Ever since Chris Stringer and Peter Andrews (1988) discovered that the genetic and archaeological evidence confirms OoA, there has been uproar in some of the less intellectually inclined and ideological sects of the Internet. These people emphatically deny—without evidence (using their emotions like a leftist, ironic…)—that the OoA hypothesis is wrong, because ‘I can’t be related to Africans, my skin is white and theirs is black—black skin cannot turn white!’ (one of the more ridiculous statements I’ve come across in my time). The fact of the matter is, people who deny OoA have ideological reasons to do so, which are not backed by science. I will provide the best (and most recent) data pointing to the OoA hypothesis, as well as go through the main paper that OoA-deniers may bring up.
OoA was first proposed by archaeologist Christ Stringer in the late 1980s (Stringer and Andrews, 1988). The totality of genetic and archaeological evidence points to Africa as the home for Anatomically Modern Humans (AMH). One of the best points of evidence is that Africans have the highest level of genetic diversity amongst humans on the planet (Campbell and Tishkoff, 2008; Gomez, Hirbo and Tishkoff, 2014; Ashraf and Galor, 2014). Furthermore, Tattersall (2009) showed that a “radical reorganization of gene expression that underwrote the distinctive physical appearance of H. sapiens was probably also responsible for the neural substrate that permits symbolic cognition.” Here are the first signs of behavioral modernity that PumpkinPerson speaks about. What people do not understand (nor grasp), is that most of our modern-day behaviors originated in Africa (see comments by Jm8 here).
Proving OoA, nowadays, is pretty ‘easy’. I say ‘easy’, because nothing ever really gets ‘proven’ in science; as any theory can be uprooted when new evidence is available. However, there are a few key data points that point to OoA being a fact:
- Melanesians and Australoids share genetic affinities linked to the OoA exodus 50kya.
- OoA was only really in dispute due to the lack of AMH fossil evidence in Melanesia/Australia (at the time of the exodus they were a conjoined landmass (the landbridge becoming submerged underwater around 8kya).
- Minor secondary gene flow into the area, but after the disappearance of the land bridge, they became more homogeneous. So any differences in the archaeological record are due to isolation from the landbridge disappearing. Hudjasov et al (2007)
Further, genetic evidence also attests to the appearance of AMH in Africa. Nei (1995) provides evidence that AMH arose 100-200 kya with all humans alive today being descendants of migrations that began ~100 kya (around 70 kya). Further, since genetic diversity decreases as the distance from Africa increases shows the OoA hypothesis to be true. Bottlenecks and founder effects reduce genetic diversity. There is also recent data that suggests that the population bottleneck coming OoA along with deleterious alleles that introgressed from Neanderthal to Eurasians caused a 1 percent decrease in historic fitness respectively (Harris and Nielson, 2016). This is further evidence that AMH began in Africa: the main piece of evidence is the population bottleneck. Since population bottlenecks and founder effects reduce genetic diversity, and the further you go from Africa, more and more populations show less and less genetic diversity from Africans, this is one major clue.
Furthermore, a human skull discovered in South Africa further attests to the truth of OoA. This skull shows similarities with skulls found in Europe at that same time period; predicting that AMH would have been found in Europe about 40 kya. This is true, and yet another piece of evidence for the OoA hypothesis. Why would two skulls separated by tens of thousands of miles be similar? Because they have the same origins, obviously.
For a solid review of the OoA hypothesis vs. the multiregional hypothesis see Edwards (2012). The preponderance of evidence points to Africa as the origin for AMH. (This article will be frequently updated with new information).
OoA Denial
Referring back to what I stated at the beginning of this piece, many people will deny OoA due to ideological reasons. When they hear of people pushing (what is currently archaeologically/genetically true) OoA, they get upset. “How could I be descended from people with dark skin, I am white!” Clearly, people don’t understand the mechanisms of evolution, nor how people adapt to climate through natural selection (obviously drift, migration and mutation plays a role here as well). I will present and go through two pieces of ‘evidence’ that OoA deniers cite when attempting to show the OoA hypothesis wrong.
No, Not Africa, RUSSIA!
This one is ridiculous. It is also the most cited study from OoA deniers. In 2012, researchers Klyosov and Rozhanskii reportedly ‘debunked’ the OoA hypothesis. Their most major claims are: AMH arose on the ‘Russian plain’ which extends from Russia to Germany and France (WOW what a huge ground for them! Seems like he ‘posited’ this large area so he ‘may be right by chance—a fat chance); that the AMH spoke a proto-Slavic language (….); Indo-Europeans being synonomous with Slavs etc. It’s ridiculous. A comment from the abstract of the article:
The earliest anatomically modern humans outside Africa and the Middle East very close to Africa, (there are some 100,000 year old specimens in Israel), are 60,000 years old-and they didn’t come near Russia. The next oldest anatomically modern humans in Europe and most of Asia are 46,000 years old. So the very concept of the first anatomically modern humans first coming into being in Russia is hilarious.
And now we have this article: Jewish-Academic subversive, malicious ‘Out of Africa Hypothesis’ annihilated which uses the Kysolov study, as well as misrepresenting another in order to ‘prove’ that the OoA hypothesis is false.
One of the largest claims he makes is that Kysolov’s paper proves there is no link to Australia from Africa. However, Hudjasov (2007) showed that Melanesians and Australoids do show affinities to Africans.
His main point is that it’s not Out of Africa—it’s Out of Australia. “Humans weren’t one coherent group”, except Homo Sapiens dispersed OoA, spreading maternal haplotype L3 all around the world between 50,000-100,000 ya (Moreno, 2011; Pagani et al, 2015; Stock, 2008; Klein, 2009). The dispersal of the L3 haplogroup confirms OoA (Rito et al, 2013).
Finally, we have the evolution of white skin. The allele that codes for white skin, SLC24A5, evolved around 7500 ya (Malick et al, 2013). This allele has the greatest effect on skin color in Europeans and neighboring populations (Cochran and Harpending, 2009). This throws a wrench into that theory; the phenotypes we racially code are recent (Mathieson et al, 2015). This is why peoples can ‘look similar’ despite being geographically separated: because the races we see today are new. Europeans are an amalgamation of three populations: the Yamna, West-European hunter-gatherers and Anatolian Farmers. I’m not saying that racial categories aren’t meaningful; just saying that they’re recent (which attests to the recent how fast racial differences have been occurring). Furthermore, faster evolution means more racial differences due to genetic isolation.
In sum, the preponderance of evidence points to Africa as being the birthplace of AMH. People can deny it for ideological reasons due to ignorance of how the evolutionary process works, but just because people don’t believe something doesn’t mean it’s not true. In my opinion, one of the best pieces of evidence for the dispersal of Man out of Africa is, as Darwin first noticed, apes and gorillas evolved in Africa. It’s only logical to posit that Man also evolved in Africa, from a primate with a common ancestor. Multiregional hypotheses don’t make sense with the genetic data.
References
Ashraf, Q., & Galor, O. (2011). The “Out of Africa” Hypothesis, Human Genetic Diversity, and Comparative Economic Development. doi:10.3386/w17216
Campbell, M. C., & Tishkoff, S. A. (2008). African Genetic Diversity: Implications for Human Demographic History, Modern Human Origins, and Complex Disease Mapping. Annual Review of Genomics and Human Genetics,9(1), 403-433. doi:10.1146/annurev.genom.9.081307.164258
Cochran, G., & Harpending, H. (2009). The 10,000 year explosion: how civilization accelerated human evolution. New York: Basic Books.
Edwards, S. (n.d.). (2012) ANTHROJOURNAL Analysis of Two Competing Theories on the Origin of Homo sapiens sapiens: Multiregional Theory vs. the Out of Africa 2 Model. Retrieved February 08, 2017, from http://anthrojournal.com/issue/october-2011/article/analysis-of-two-competing-theories-on-the-origin-of-homo-sapiens-sapiens-multiregional-theory-vs-the-out-of-africa-2-model
Gomez, F., Hirbo, J., & Tishkoff, S. A. (2014). Genetic Variation and Adaptation in Africa: Implications for Human Evolution and Disease. Cold Spring Hanrbor Perspectives in Biology,6(7). doi:10.1101/cshperspect.a008524
Harris, K., & Nielsen, R. (2015). The Genetic Cost of Neanderthal Introgression. Genetics, 2016 doi:10.1101/030387
Hudjashov, G., Kivisild, T., Underhill, P. A., Endicott, P., Sanchez, J. J., Lin, A. A., . . . Forster, P. (2007). Revealing the prehistoric settlement of Australia by Y chromosome and mtDNA analysis. Proceedings of the National Academy of Sciences,104(21), 8726-8730. doi:10.1073/pnas.0702928104
Klein, R. G. (2009). Darwin and the recent African origin of modern humans. Proceedings of the National Academy of Sciences,106(38), 16007-16009. doi:10.1073/pnas.0908719106
Klyosov, A. A., & Rozhanskii, I. L. (2012). Re-Examining the “Out of Africa” Theory and the Origin of Europeoids (Caucasoids) in Light of DNA Genealogy. Advances in Anthropology,02(02), 80-86. doi:10.4236/aa.2012.22009
Mathieson, I., Lazaridis, I., Rohland, N., Mallick, S., Patterson, N., Roodenberg, S. A., . . . Reich, D. (2015). Genome-wide patterns of selection in 230 ancient Eurasians. Nature,528(7583), 499-503. doi:10.1038/nature16152
Nei, M. (1995). Genetic support for the out-of-Africa theory of human evolution. Proceedings of the National Academy of Sciences,92(15), 6720-6722. doi:10.1073/pnas.92.15.6720
Mallick, C. B., Iliescu, F. M., Mã¶Ls, M., Hill, S., Tamang, R., Chaubey, G., . . . Kivisild, T. (2013). The Light Skin Allele of SLC24A5 in South Asians and Europeans Shares Identity by Descent. PLoS Genetics,9(11). doi:10.1371/journal.pgen.1003912
Moreno, E. 2011. The society of our ‘out of Africa’ ancestors (1). Communicative & Integrative Biology, 4, 163e170
Pagani, L., Schiffels, S., Gurdasani, D., Danecek, P., Scally, A., Chen, Y., . . . Tyler-Smith, C. (2015). Tracing the Route of Modern Humans out of Africa by Using 225 Human Genome Sequences from Ethiopians and Egyptians. The American Journal of Human Genetics,96(6), 986-991. doi:10.1016/j.ajhg.2015.04.019
Rito, T., Richards, M. B., Fernandes, V., Alshamali, F., Cerny, V., Pereira, L., & Soares, P. (2013). The First Modern Human Dispersals across Africa. PLoS ONE,8(11). doi:10.1371/journal.pone.0080031
Stock, J. T. (2008). Are humans still evolving? Technological advances and unique biological characteristics allow us to adapt to environmental stress. Has this stopped genetic evolution? EMBO reports,9. doi:10.1038/embor.2008.63
Stringer, C., & Andrews, P. (1988). Genetic and fossil evidence for the origin of modern humans. Science,239(4845), 1263-1268. doi:10.1126/science.3125610
Tattersall, I. (2009). Human origins: Out of Africa. Proceedings of the National Academy of Sciences,106(38), 16018-16021. doi:10.1073/pnas.0903207106
Human Mating and Aggression—An Evolutionary Perspective
1650 words
One of the many oft-repeated statements from feminists is “Who commits over 80 percent of all violent crime?! MEN!!!!” This is true. No one denies this. Is this stark disparity due to biology or culture? Anyone who reads this blog knows the answer to that question, however, a lot of people (mostly feminists and other radical leftists) disagree and, of course, believe that all differences within and between people are explainable by environmental factors.
Men commit 80 percent of all crimes. Feminists may point to this stat and say that men are more dangerous than men, and, for instance, use the crime argument for separation from men the way some people use the black crime argument as a point to argue for separation. It’s clear that people who say these things don’t understand biology, because things such as this are easily explainable.
Men average 270-1,070 ng/dl on average compared to women’s 15-70 ng/dl.This large variation in testosterone between men and women is an indication that the testosterone ‘gap’ (which should be there, biologically speaking) is the main factor in explaining the crime disparities between males and females (Dabbs et al, 1995; Batrinos, 2012).
Testosterone regulates morphological traits which are then sexually selected for (Hillgarth, Ramenofsky and Wingfield, 1997). So, in a way, testosterone itself was being selected for, as it is the mediator of all of the morphological characteristics that make Men men.
These same differences in testosterone between men and women also explain the huge variation in muscle mass and strength between men and women. Muscle mass was, potentially, a way to attract mates. Though muscle mass itself is a sexually selected trait, in terms of natural selection it is a negative. This is because the more muscle mass you have, the more calories you need to consume. Men have 61 percent more upper body strength than women and 75 percent more arm mass, which translates to 90 percent greater upper body strength in men. 99.9 percent of females fall below the male mean here, which is to be expected with what we know about anatomy and physiology in regards to the human sexes. The effect was almost as large when it came to lower body mass, with men having 50 percent more muscle mass while being 65 percent stronger than women (Lassek and Gaulin, 2009). Muscle mass is also a feature in men that gets sexually selected for (Puts, 2016)
When women are ovulating, they “show a weakness” for men with “good genes” when they are at their most fertile. This shows a causal mechanism through sexual selection for high levels of testosterone to be selected for in men, which then causes the differences in fat-free mass and aggression rates, among other variables. Indeed, we do know that, on average, women want a mate that is successful, good looking, has money, has a desire for home and children, and being a loving partner. Women, obviously, secure a man’s genes when she bears his child. So a woman would always attempt to secure the best combination of these traits in the same man (Buss and Shackelford, 2008). Sexual selection explains sex differences in aggression (Archer, 2009). So, as you can see (evolutionarily speaking), it’s women that are the cause for the so-called aggression that feminists complain about—they sexually selected us for higher levels of aggression and testosterone, then complain about it in the modern world.
Sexual and natural selection are the causes for increased aggression/testosterone rates in men when compared to women. These traits were clearly advantageous during in our ancestral habitat, as a more aggressive mate would provide better protection and food acquisition. When organisms compete for scarce, nutritious food, mates, and space, competition increases between organisms. This can lead to injury or death (the less-able being naturally selected out of the gene pool); chronically elevated levels of testosterone associated with aggressive competition may suppress the immune system and have negative effects for health and fitness (elevated cortisol levels, which triggers fight or flight is also a negative); it may increase risk of predation since a high testosterone organism won’t notice predators around them; aggressive contests tend to be physically demanding, sapping energy; and it may damage social relationships, for instance if a male is aggressive to a female that male won’t mate and thus get selected out of the gene pool (Georgiev et al, 2013).
A study in Sweden looked at the frequency and how often men committed acts of violent crime compared to women (Trägårdh et al, 2016). They discovered that in the two decades from 1990 to 2010, there were 1,570 cases of deadly violence with men accounting for 1,420 of the cases (90.4 percent) while 150 women committed violent crime (9.6 percent). Women accounted for one-third of crimes committed against children, however, which has its basis in evolutionary psychology as well.
The risk of being killed is highest in your first year of life (Friedman and Resnick, 2007). Why? Infanticide. The mean age that mothers commit filicide at is 29.5 while the mean age of the babe is 3.5 years (Rouge-Maillart et al, 2005). The evolutionary explanation for this is that the mother still has time to conceive more children, so the fitness hit is not too large. Further, women are more likely to commit filicide if they have a second child under the age of 20 (Bourget, Grace, and Whitehurts, 2007). So obviously, the older a woman is the less of a chance there is that filicide will be committed since it would be a fitness hit since older women have less of a chance to conceive children, along with a higher chance for the child to have birth defects (Stein and Susser, 2000; Lampinen, Vehviläinen-Julkunen and Kankkunen, 2009; Jolly et al, 2000). So from an evolutionary perspective, it doesn’t make sense for a woman to kill her child if she’s about to hit the age-40 wall (Reproductive Endocrinology Infertility Committee et al, 2011; O’Reilly-Green and Cohen, 1993; van Katwjk and Peeters, 1998; Yaniv et al, 2010).
Male infanticide is associated with social monogamy in primates; male infanticide may be what causes females to stay and mate with one male (Opie et al, 2013). This is caused by females choosing to stay faithful to mates, which then drives monogamous relationships. Serial and social monogamy is the norm for humans (Brandon, 2016). This, then, goes back to what a woman looks for in a man, and has her want to stay with that one man who has all of the qualities necessary to be a good mate and father.
In sum, when feminists complain about male aggression and crime, there are substantial evolutionary underpinnings behind them. They do not even realize that even when they are fighting for ‘equality’ between the sexes, that they are directly helping our arguments that there are inherent biological, physiological and morphological differences between the sexes—driven by sexual selection—which is then a cause for a large amount of the variation in crime (and other variables) between men and women. These intrinsic differences between men and women are why we are so different from each other.The sexes also differ in the brain. There are numerous biological explanations between differences in aggression between men and women, and they come down to sexual selection and what propagated our species in during our ancestral evolution. A large cause for these differences is mate selection—which would, technically, make women the culprits, as they selected us for these traits. The fact that these differences are still so profound in modern-day society is not at all surprising.
References
Archer, J. (2009). Does sexual selection explain human sex differences in aggression? Behavioral and Brain Sciences,32(3-4), 249. doi:10.1017/s0140525x09990951
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Reproductive E, Infertility C. Family physicians advisory C, maternal-fetal medicine C, executive, council of the society of O et al. Advanced reproductive age and fertility. Journal of obstetrics and gynaecology, Canada : JOGC. Journal d’obstetrique et gynecologie du Canada : JOGC. 2011;33(11):1165–75.
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Psychology, Anti-Hereditarianism, and HBD
3800 words
Abstract
The denial of human nature is extremely prevalent, most noticeably in our institutions of higher learning. To most academics, the fact that there could be population differences that are genetic in nature is troubling for many people. However, denying genetic/biological causes for racial differences is 1) intellectually dishonest; 2) will lead to negative health outcomes for populations due to the assumption that all human populations are the same; and 3) the ‘lie of equality’ will not allow all human populations to reach their ‘potential’ to be as good as they can be due to the fact that implicit assumption that all human populations are the same. Anti-hereditarians fully deny any and all genetic explanations for human differences, believing that human brain evolution somehow halted around 50-100 kya. Numerous studies show that race is a biological reality; it doesn’t matter what we call the clusters as those are the social constructs. The contention is that ‘all brains are the same color’ (Nisbett, 2007; for comment see my article Refuting Richard Nisbett), and that evolution in differing parts of the world for the past 50,000 years was not enough for any meaningful population differences between people. But to accept that means you must accept the fact that the brain is the only organ that is immune to natural selection. Does that make any sense? I will show that these differences do exist and should be studied, as free of any bias as possible, with every possible hypothesis being looked at and not discarded.
Evolution is true. It’s not ‘only a theory’ (as some anti-evolutionists contend). Anti-evolutionists do not understand the definition of the word ‘theory’. Richard Dawkins (2009) wrote that a theory is a scheme or system of ideas or statements held as an explanation or account of a group of facts or phenomena. This is in stark contrast to the layperson’s definition of the word theory, which means ‘just a guess’. Evolution is a fact. What biologists argue with each other about is the mechanisms behind evolution, for any quote-mining Creationists out there.
We know that evolution is a fact and it is the only game in town (Dawkins, 2009) to explain the wide diversity and variation we see on our planet. However, numerous scholars deny the effect of evolution on human behavior (most residing in the social sciences, but other prominent biologists have denied (or implied there were no differences between us and our ancestors) the effect of human evolution on behavior and cognition; Gould 1981, 1996, for a review of Gould 1996, see my article Complexity, Walls, 0.400 Hitting and Evolutionary “Progress” and Stephen Jay Gould and Anti-Hereditarianism; Mayr 1963; see Cochran and Harpending 2009). A prominent neuroscientist, who I have written about here, Herculano-Houzel, implied that Neanderthals and Antecessor may have been just as intelligent as we are due to a neuronal count in a similar range to ours (Herculano-Houzel 2013). This raises an interesting question (which I have tackled here and will return to in the future): did our recent hominin ancestors at least have the capacity for similar intellect to ours (Villa and Roebroeks, 2014; Herculano-Houzel and Kaas, 2011)? It is interesting that neuronal scaling rules hold for our extinct ancestors, and this question is most definitely worth looking into.
Whatever the case may be in regards to recent human evolution and our extinct hominin ancestors, human evolution has increased in the past 10,000 years (Cochran and Harpending, 2009; Wade, 2014). This is due to the dispersal of Anatomical Modern Humans (AMH) OoA around 70 kya; and with this geographical isolation, populations began to diverge with no interbreeding with each other. However, this is noticed most in ‘Native’ Americans, who show no gene flow with other populations due to being genetically isolated (Villena et al, 2000). Who’s to say that evolution stops at the neck, and no further evolution occurs on the brain? Is the brain itself exempt from the laws of natural selection? We know that there is no/hardly any gene flow between populations before the advent of modern-day technology and vehicles; we know that humans differ on morphological and anatomical traits, why are genetic differences out of the question, especially when genetic differences may explain, in part, some of the variation between populations?
We know that evolution is true, without a reasonable doubt. So why, do some researchers contend, is the human brain exempt from such selective pressures?
A theoretical article by Winegard, Winegard, and Boutwell (2017) was just released on January 17th. In the article, they argue that social scientists should integrate HBD into their models. Social scientists do not integrate genetics into their models, and the longer one studies social sciences, the more likely it is they will deny human nature, regardless of political leaning (Perry and Mace, 2010). This poses a problem. By completely ignoring a huge variable (possible genetic differences), this has the potential to harm people’s health, as race is a very informative marker when discussing diseases acquisition as well as whether certain drugs will work on two individuals of different races (Risch et al, 2002; Tang et al, 2005; Wade, 2014). People who deny the usefulness of race, even in a medical context, endanger the lives of individuals from different races/ethnies since they assume that all humans are the same inside, despite ‘superficial differences’ between populations.
The notion that all human populations—genetic isolation and evolution in differing ecosystems/climates/geographic locales be damned—is preposterous to anyone who has a true understanding of evolution. Why should man’s brain be the only organ on earth exempt from the forces of natural selection? Why do egalitarians assume that all humans are the same and have the same psychological faculties compared to other humans, despite the fact that rapid evolution has occurred within the human species within the last 10,000 years?
To see some of the most obvious ways to see natural selection in action in human populations, one should look to the Inuits (Fumagalli, 2015; Daanen and Lichtenbelt, 2016; NIH, 2015; Cardona et al, 2014; Tishkoff, 2015; Ford, McDowell, and Pierce, 2015; Galloway, Young, and Bjerregaard, 2012; Harper, 2015). Global warming is troubling to some researchers, with many researchers suggesting that global warming will have negative effects on the health and food security of the Inuit (Ford et al, 2014, 2016; Ford, 2012, 2009; Wesche, 2010; Furgal and Seguin, 2006; McClymont and Myers, 2012; Petrasek et al, 2015; Rosol, Powell-Hellyer, and Chan, 2016; Petrasek, 2014; WHO, 2003). I could go on and on citing journal articles for both claims, but you get the point already. The main point is this: we know the Inuit have evolved for their climate, and a (possible) climate change would then have a negative effect on their quality of life due to their adaptations to the cold weather climate. However, egalitarians still contend, with these examples and numerous others I could cite, that any and all differences within and between human populations can be explained by socio-cultural factors and not any genetic ones.
One of the best examples of genetic isolation in a geographic locale that is the complete opposite from the environment of evolutionary adaptedness (EEA; Kanazawa, 2004), the African savanna in which we evolved in. I did entertain the idea of the Savanna hypothesis, and while I do believe that it could explain a lot of the variance in IQ between countries (Kanazawa, 2007), his hypothesis doesn’t make sense with what we know about human evolution over the past 10,000 years.
The most obvious differences we can see between populations is differences in skin color. Skin color does not signify race, per se, but it is a good indicator. Skin color is an adaptation to UV radiation (Jablonski and Chaplin, 2010, 2000; Juzenienne et al, 2009; Jeong and Rienzo, 2015; Hancock, et al, 2010; Kita and Fraser, 2016; Scheinfeldt and Tishkoff, 2013), and is therefor and adaptation based on climate. Dark skin is a protectant from skin cancer (Brenner and Hearing, 2008; D’Orazio et al, 2010; Bradford, 2009). Skin cancer is a possible selective force in black pigmentation of the skin in early hominin evolution (Greaves, 2014). With these adaptations in skin color between genetically and geographically isolated populations, are changes in the brain, however small, really out of the question?
A better population to bring up in regards to geographic isolation having an effect on human evolution is the Tibetans. For instance, Tibetans have higher total lung capacities in comparison to the Han Chinese (Droma et al, 1991). There are even differences in lung capacity between Tibetans and Han Chinese who live at the same altitude (Yangzong et al, 2013), with the same thing noticed for peoples living in the Andean mountains (Beall, 2007). Tibetans evolved in a higher elevation than the Han Chinese who lived closer to sea level, so it makes sense that they would be selected for the ability to take deeper inhales They also have a larger chest circumference and greater capacity than the Han Chinese who live at lower altitudes (Gilbert-Kawai et al, 2014).
Admittedly, the acceptance of the usefulness of race in regards to human differences is a touchy subject. So much so, that social scientists do not take genetics into account in their models. However, researchers in the relevant fields accept the usefulness of race (Risch et al, 2002; Tang et al, 2005; Wade, 2014; Sesardic, 2010), so the fact that social scientists do not is to be ignored. Race is a social construct, yes. But no matter what we call these clusters, clines, demes, races, ethnies—whatever name you want to use to describe them—this does not change the fact that race is a useful category in biomedical research. Race is an issue when talking about bone marrow transplants, so by treating all populations as the same with no variation between them, people are pretty much saying that differences between people in a biomedical context do not exist, with there being other explanatory factors behind population differences, in this case, bone marrow transplants. Ignoring heritable human variation will lead to disparate health outcomes for all human populations with the assumption that all humans are the same. Is that what we want? Is that what race-deniers want?
So there are anatomical and physiological differences between human populations (Wagner and Hayward, 2000), with black Americans having a different morphology and lower fat-free body mass on average in comparison to white Americans. This, then, is one of the variables that dictates racial differences in sports, along with muscle fiber explaining a large portion of the variance, in my opinion. No one denies that blacks and whites differ at elite levels in baseball, football, swimming and jumping, and bodybuilding and strength sports. Though, accepting the fact that these morphological and anatomical differences between the races come down to evolution, one would then have to accept the fact that different races/ethnies differ in the brain, thusly destroying their egalitarian fantasy in their head of all genetically isolated human populations being the same in the brain. Wade (2014) writes on page 106:
“… brain genes do not lie in some special category exempt from natural selection. They are as much under evolutionary pressure as any other category of gene”
This is a hard pill to swallow for race-deniers, especially those who emphatically deny any type of selection pressure on the human brain within the past 10,000 to 100,000 years.
Winegard, Winegard, and Boutwell (2017) write:
Consider an analogy that might make this clear while simultaneously illuminating the explanatory importance of population differences. Most cars are designed from the same basic blueprint and consist of similar parts—an internal combustion engine, a gas tank, a chassis, tires, bearings, spark plugs, et cetera. Cars as distinct as a Honda Civic and a Subaru Outback are built from the same basic blueprint and comprised of the same parts; so, in this sense, there is a “universal car nature” (Newton 1999). However, precise, correlated changes in these parts can dramatically change the characteristics of a car.
Humans, like cars, are built from the same basic body plan. They all have livers, lungs, kidneys, brains, arms, and legs. And these structures are built from the same basic building blocks, tissues, which are built of proteins, which are built of amino acids, et cetera. However, small changes in the structures of these building blocks can lead to important and scientifically meaningful differences in function.
Put in this context, yes, there is a ‘universal human nature’, but the application of that human nature will differ depending on what a population has to do to survive in that climate/ecosystem. And, over time, populations will diverge away from each other, both physically and mentally. The authors also argue that societal differences between Eurasians (Europeans and East Asian) can be explained partly by genetic differences. Indeed, the races do differ on the Big Five Personality traits, with heritable components explaining 40 to 60 percent of the variation (Power and Pluess, 2015). So some of the cultural differences between European and East Asians must come down to some biological variation.
One of the easiest ways to see the effects of cultural/environmental selective pressures in humans is to look at Ashkenazi Jews (Cochran et al, 2006). Due to Ashkenazi Jews being barred from numerous occupations, they were confined to a few cognitively demanding occupations. Over time, only the Jews that could handle these occupations would prosper, further selecting for higher intelligence due to the cognitive demands of the jobs they were able to acquire. Thus, Ashkenazi Jews who could handle the few occupations they were allowed to do would breed more and pass on variants for higher intelligence to their offspring, whereas those Jews who couldn’t handle the cognitive demands of the occupation were selected out of the gene pool. This is one situation in which natural selection worked swiftly, and is why Ashkenazi Jews are so overrepresented in the fields of academia today—along with nepotism.
Winegard, Winegard, and Boutwell (2017) lay out six basic principles for a new Darwinian paradigm, as follows:
- Variation is the grist for the mill of natural selection and is ubiquitous within and among human populations.
- Evolution by natural selection has not stopped acting on human traits and has significantly shaped at least some human traits in the past 50,000 years.
- Current hunter-gatherer groups might be slightly different from other modern human populations because of culture and evolution by natural selection acting to influence the relative presence, or absence, of trait-relevant alleles in those groups. Therefore, using extant hunter-gatherers as a template for a panhuman nature is problematic.
- It is probably more accurate to say that, while much of human nature is universal, there may have been selective tuning on various aspects of human nature as our species left Africa and settled various regions of the planet (Frost 2011).
- The human brain is subject to selective forces in the same way that other organ systems are. Natural selection does not discriminate between genes for the body and genes for the brain (Wade 2014).
- The concept of a Pleistocene-based environment of evolutionary adaptedness (EEA) is likely unhelpful (Zuk 2013). Individual traits should be explored phylogenetically and historically. Some human traits were sculpted in the Pleistocene (or before) and have remained substantially unaltered; some, however, have been further shaped in the past 10,000 years, and some probably quite recently (Clark 2007). It remains imperative to describe what selection pressures might have been actively shaping human nature moving forward from the Pleistocene epoch, and how those ecological pressures might have differed for different human populations.
No stone should be left unturned when attempting to explain population differences between geographically isolated peoples, and these six principles are a great start, which all social scientists should introduce into their models.
As I brought up earlier, Kanazawa’s (2004b) hypothesis doesn’t make sense in regards to what we know about the evolution of human psychology. Thus, any type of proposed evolutionary mismatch in regards to our societies do not make much sense. However, one mismatch that does need to be looked into is the negative mismatch we have with our modern-day Western diets. Agriculture was both a gift and a negative event in human history. Yes, without the advent of agriculture 10,000 years ago we would not have the societies we have today. However, on the other hand, we have higher rates of disease compared to our hunter-gatherer ancestors. This is one evolutionary mismatch that cannot and should not go ignored as it has devastating effects on our populations that consume a Western diet—which we did not evolve to eat.
Winegart, Winegart, and Boutwell (2017) then discuss how their new Darwinian paradigm could be used by researchers: 1) look for differences among human populations; 2) after population differences are found, causal analyses should be approached neutrally; 3) researchers should consider a broad range of data to consider whether or not the trait or traits in question are heritable; and 4) researchers should test the posited biological cause more indepth. Without understanding—and using—biological differences between human populations, the quality of life for some populations will be diminished, all for the false notion of ‘equality’ between human races.
There are huge barriers in place to studying human differences, however. Hayden (2013) documents differing taboos in genetics, with intelligence having a high taboo rating. Of course, we HBDers know that intelligence is a highly heritable trait, largely genetic in nature, and so studying these differences between human populations may lead to some uncomfortable truths for some people. On the 200th anniversary of Darwin’s On the Origin of Species, Ceci and Williams (2009) said that “the scientific truth must be pursued” and that researchers must study race and IQ, much to the chagrin of anti-hereditarians (Horgan, 2013). He does write something very troubling in regards to this research, and free speech in our country as a whole:
Some readers may wonder what I mean by “ban,” so let me spell it out. I envision a federal prohibition against speech or publications supporting racial theories of intelligence. All papers, books and other documents advocating such theories will be burned, deleted or otherwise destroyed. Those who continue espousing such theories either publicly or privately (as determined by monitoring of email, phone calls or other communications) will be detained indefinitely in Guantanamo until or unless a secret tribunal overseen by me says they have expressed sufficient remorse and can be released.
Whether he’s joking or not, that’s besides the point. The point is, is that these topics are extremely sensitive to the lay public, and with these articles being printed in popular publications, the reader will get an extremely biased look into the debate and their mind will already be made up for them. This is the definition of intellectual dishonesty, attempting to sway a lay-readers’ opinion on a subject they are ignorant of with an appeal to emotion. Shouldn’t all things be studied scientifically, without any ideological biases?
Speaking about the ethics of putting this information out to the general public, Winegard, Winegard, and Boutwell (2017) write:
If researchers do not responsibly study and discuss population differences, then they leave an abyss that is likely to be filled by the most extreme and hateful writings on population differences. So, although it is understandable to have concerns about the dangers of speaking and writing frankly about potential population differences, it is also important to understand the likely dangers of not doing so. It is not possible to hide the reality of human variation from the world, not possible to propagate a noble lie about human equality, and the attempt to do so leaves a vacancy for extremists to fill.
This is my favorite quote in the whole paper. It is NOT possible to hide the reality of HBD from the world; anyone with eyes can see that humans do differ. Attempting to continue the feel-good liberal lie of human equality will lead to devastating effects in all countries/populations due to the implicit assumption that all human groups are the same in their cognitive and mental faculties.
The denial of genetic human differences, could, as brought up earlier in this article, lead to negative effects in regards to health outcomes between populations. Black Americans have higher rates of hypertension than white Americans (Fuchs, 2011; Ferdinand, 2007; Ortega, Sedki, and Nayer, 2015; Nesbitt, 2009; Wright et al, 2005). To overlook possible genetic differences as a causal factor in regards to racial differences will mean the deaths of many people since people truly believe that people are the same and that all differences come down to the environment. This, however, is not true and believing so is extremely dangerous to the health of all populations in the world.
Epigenetic signatures of ethnicity may be biomarkers for shared cultural experiences. Seventy-six percent of the genetic alteration between Mexicans and Puerto Ricans in this study was due to DNA methylation—which is an epigenetic mechanism used by cells to control gene expression. Therefore, 24 percent of the effect is due to an unknown factor, probably regarding environmental, social, and cultural differences between the two ethnies (Galanter et al, 2017). This is but one of many effects that culture can have on the genome, leading to differences between two populations, and is good evidence for the contention that the different races/ethnies evolved different psychological mechanisms due to genetic isolation in different environments.
We must now ask the question: what if the hereditarian hypothesis is true (Gottfredson, 2005)? If the hereditarian hypothesis is true, Gottfredson argues, special consideration should be given to those found to have a lower IQ, with better training and schooling that specifically target those individuals at risk to be less able due to their lower intelligence. This is one way the hereditarian hypothesis can help race relations in the country: people will (hopefully) accept intrinsic differences between the races. What Gottfredson argues in her paper will hopefully then pacify anti-hereditarians, as less able people of all races/ethnicities will still get the extra help they need in regards to finding work and getting schooling/training/jobs that accommodate their intelligence.
Conclusion
People accept genetic causes for racial differences in sports, yet emphatically deny that human races/ethnies differ in the brain. The denial of human nature—racially and ethnically—is the next hurdle for us to jump over. Once we accept that these differences in populations can, in part, be explained by genetic factors, we can then look to other avenues to see how and why these differences exist between populations occur and if anything can be done to ameliorate them. However, ironically, anti-hereditarians do not realize that their policies and philosophy is actively hindering their goals, and by accepting biological causes—if only to see them researched and held against other explanations—will lead to further inequality, while they scratch their heads without realizing that the cause is the one variable that they have discarded: genetics. Still, however, I see this won’t happen in the future and the same non-answers will be given in response to findings on how the human races differ psychologically (Gottfredson, 2012). The races do differ in biologically meaningful ways, and denying or disregarding the truth will not make these differences disappear. Social scientists must take these differences into account in their models, and seriously entertain them like any other hypothesis, or else they will never fully understand human nature.
Is General Intelligence Domain-Specific?
1600 words
Is the human brain ‘special’? Not according to Herculano-Houzel; our brains are just linearly scaled-up primate brains. We have the number of neurons predicted for a primate of our body size. But what does this have to do with general intelligence? Evolutionary psychologists also contend that the human brain is not ‘special’; that it is an evolved organ just like the rest of our body. Satoshi Kanazawa (2003) proposed the ‘Savanna Hypothesis‘ which states that more intelligent people are better able to deal with ‘evolutionary novel’ situations (situations that we didn’t have to deal with in our ancestral African environment, for example) whereas he purports that general intelligence does not affect an individuals’ ability to deal with evolutionarily familiar entities and situations. I don’t really have a stance on it yet, though I do find it extremely interesting, with it making (intuitive) sense.
Kanazawa (2010) suggests that general intelligence may both be an evolved adaptation and an ‘individual-difference variable’. Evolutionary psychologists contend that evolved psychological adaptations are for the ancestral environment which was evolved in, not in any modern-day environment. Kanazawa (2010) writes:
The human brain has difficulty comprehending and dealing with entities and situations that did not exist in the ancestral environment. Burnham and Johnson (2005, pp. 130–131) referred to the same observation as the evolutionary legacy hypothesis, whereas Hagen and Hammerstein (2006, pp. 341–343) called it the mismatch hypothesis.
From an evolutionary perspective, this does make sense. A perfect example is Eurasian societies vs. African ones. you can see the evolutionary novelty in Eurasian civilizations, while African societies are much closer (though obviously not fully) to our ancestral environment. Thusly, since the situations found in Africa are not evolutionarily novel, it does not take high levels of g to survive in, while Eurasian societies (which are evolutionarily novel) take much higher levels of g to live and survive in.
Kanazawa rightly states that most evolutionary psychologists and biologists contend that there have been no changes to the human brain in the last 10,000 years, in line with his Savanna Hypothesis. However, as I’m sure all readers of my blog know, there were sweeping changes in the last 10,000 years in the human genome due to the advent of agriculture, and, obviously, new alleles have appeared in our genome, however “it is not clear whether these new alleles have led to the emergence of new evolved psychological mechanisms in the last 10,000 years.”
General intelligence poses a problem for evo psych since evolutionary psychologists contend that “the human brain consists of domain-specific evolved psychological mechanisms” which evolved specifically to solve adaptive problems such as survival and fitness. Thusly, Kanazawa proposes in contrast to other evolutionary psychologists that general intelligence evolved as a domain-specific adaptation to deal with evolutionary novel problems. So, Kanazawa says, our ancestors didn’t really need to think inorder to solve recurring problems. However, he talks about three major evolutionarily novel situations that needed reasoning and higher intelligence to solve:
1. Lightning has struck a tree near the camp and set it on fire. The fire is now spreading to the dry underbrush. What should I do? How can I stop the spread of the fire? How can I and my family escape it? (Since lightning never strikes the same place twice, this is guaranteed to be a nonrecurrent problem.)
2. We are in the middle of the severest drought in a hundred years. Nuts and berries at our normal places of gathering, which are usually plentiful, are not growing at all, and animals are scarce as well. We are running out of food because none of our normal sources of food are working. What else can we eat? What else is safe to eat? How else can we procure food?
3. A flash flood has caused the river to swell to several times its normal width, and I am trapped on one side of it while my entire band is on the other side. It is imperative that I rejoin them soon. How can I cross the rapid river? Should I walk across it? Or should I construct some sort of buoyant vehicle to use to get across it? If so, what kind of material should I use? Wood? Stones?
These are great examples of ‘novel’ situations that may have arisen, in which our ancestors needed to ‘think outside of the box’ in order to survive. Situations such as this may be why general intelligence evolved as a domain-specific adaptation for ‘evolutionarily novel’ situations. Clearly, when such situations arose, our ancestors who could reason better at the time these unfamiliar events happened would survive and pass on their genes while the ones who could not die and got selected out of the gene pool. So general intelligence may have evolved to solve these new and unfamiliar problems that plagued out ancestors. What this suggests is that intelligent people are better than less intelligent people at solving problems only if they are evolutionarily novel. On the other hand, situations that are evolutionarily familiar to us do not take higher levels of g to solve.
For example, more intelligent individuals are no better than less intelligent individuals in finding and keeping mates, but they may be better at using computer dating services. Three recent studies, employing widely varied methods, have all shown that the average intelligence of a population appears to be a strong function of the evolutionary novelty of its environment (Ash & Gallup, 2007; D. H. Bailey & Geary, 2009; Kanazawa, 2008).
Who is more successful, on average, over another in modern society? I don’t even need to say it, the more intelligent person. However, if there was an evolutionarily familiar problem there would be no difference in figuring out how to solve the problem, because evolution has already ‘outfitted’ a way to deal with them, without logical reasoning.
Kanazawa then talks about evolutionary adaptations such as bipedalism (we all walk, but some of us are better runners than others); vision (we can all see, but some have better vision than others); and language (we all speak, but some people are more proficient in their language and learn it earlier than others). These are all adaptations, but there is extensive individual variation between them. Furthermore, the first evolved psychological mechanism to be discovered was cheater detection, to know if you got cheated while in a ‘social contract’ with another individual. Another evolved adaptation is theory of mind. People with Asperger’s syndrome, for instance, differ in the capacity of their theory of mind. Kanazawa asks:
If so, can such individual differences in the evolved psychological mechanism of theory of mind be heritable, since we already know that autism and Asperger’s syndrome may be heritable (A. Bailey et al., 1995; Folstein & Rutter, 1988)?
A very interesting question. Of course, since it’s #2017, we have made great strides in these fields and we know these two conditions to be highly heritable. Can the same be said for theory of mind? That is a question that I will return to in the future.
Kanazawa’s hypothesis does make a lot of sense, and there is empirical evidence to back his assertions. His hypothesis proposes that evolutionarily familair situations do noot take any higher levels of general intelligence to solve, whereas novel situations do. Think about that. Society is the ultimate evolutionary novelty. Who succeeds the most, on average, in society? The more intelligent.
Go outside. Look around you. Can you tell me which things were in our ancestral environment? Trees? Grass? Not really, as they aren’t the same exact kinds as we know from the savanna. The only thing that is constant is: men, women, boys and girls.
This can, however, be said in another way. Our current environment is an evolutionary mismatch. We are evolved for our past environments, and as we all know, evolution is non-teleological—meaning there is no direction. So we are not selected for possible future environments, as there is no knowledge for what the future holds due to contingencies of ‘just history’. Anything can happen in the future, we don’t have any knowledge of any future occurences. These can be said to be mismatches, or novelties, and those who are more intelligent reason more logically due to the fact that they are more adept at surviving evolutionary novel situations. Kanazawa’s theory provides a wealth of information and evidence to back his assertion that general intelligence is domain-specific.
This is yet another piece of evidence that our brain is not special. Why continue believing that our brain is special, even when there is evidence mounting against it? Our brains evolved and were selected for just like any other organ in our body, just like it was for every single organism on earth. Race-realists like to say “How can egalitarians believe that we stopped evolving at the neck for 50,000 years?” Well to those race-realists who contend that our brains are ‘special’, I say to them: “How can our brain be ‘special’ when it’s an evolved organ just like any other in our body and was subject to the same (or similar) evolutionary selective pressures?”
In sum, the brain has problems dealing with things that were not in its ancestral environment. However, those who are more intelligent will have an easier time dealing with evolutionarily novel situations in comparison to people with lower intelligence. Look at places in Africa where development is still low. They clearly don’t need high levels of g to survive, as it’s pretty close to the ancestral environment. Conversely, Eurasian societies are much more complex and thus, evolutionarily novel. This may be one reason that explains societal differences between these populations. It is an interesting question to consider, which I will return to in the future.
Fatty Acids and PISA Math Performance
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There are much more interesting theories of the evolution of hominin intelligence other than the tiring (yawn) cold winter theory. Last month I wrote on why men are attracted to a low waist-to-hip ratio in women. However, the relationship between gluteofemoral fat (fat in the thighs and buttocks) is only part of the story on how DHA and fatty acids (FAs) drove our brain growth and our evolution as a whole. Tonight I will talk about how fatty acids predict ‘cognitive performance’ (it’s PISA, ugh) in a sample of 28 countries, particularly the positive relationship between n-3 (Omega-3s) and intelligence and the negative relationship between n-6 and intelligence. I will then talk about the traditional Standard American Diet (the SAD diet [apt name]) and how it affects American intelligence on a nation-wide level. Finally, I will talk about the best diet to maximize cognition in growing babes and women.
Lassek and Gaulin (2013) used the 2009 PISA data to infer cognitive abilities for 28 countries (ugh, I’d like to see a study like this done with actual IQ tests). They also searched for studies that showed data providing “maternal milk DHA DHA values as percentages of total fatty acids in 50 countries”. Further, to control for SES influences on cognitive performance, they controlled for GDP/PC (gross domestic product per country) and “educational expenditures per pupil.” They further controlled for the possible effect of macronutrients on maternal milk DHA levels, they included estimates for each country of the average amount of kcal consumed from protein, fat, and carbohydrates. To explore the relationship between DHA and cognitive ability, they included foodstuffs high in n-3—fish, eggs, poultry, red meat, and milk which also contain DPA depending on the type of feed the animal is given. There is also a ‘metabolic competition’ between n-3 and n-6 fatty acids, so they also included total animal and vegetable fat as well as vegetable oils.
Lassek and Gaulin (2013) found that GDP/PC, expenditures per student and DHA were significant predictors of (PISA) math scores, whereas macronutrient content showed no correlation.
The predictive value of milk DHA on cognitive ability is only weak when either two of the SES variables are added in the multiple regression. When milk arachidonic (a type of Omega-6 fatty acid) is added to the regression, it is negatively correlated with math scores but not significantly (so it wasn’t added to the table below).
So countries with lower maternal milk levels of DHA score lower on the maths section of the PISA exam (not an IQ test, but it’s ‘good enough’). Knowing what is known about the effects of DHA on cognitive abilities, countries who have higher maternal milk levels of DPA do score higher on the maths section of the PISA exam.
Table 2 shows the correlations between grams per capita per day of food consumption in the data set they used and maternal milk DHA. As you can see, total fish and seafood consumption are substantially correlated with total milk DHA, while foods that are high in n-6 show medium negative correlations with maternal milk DHA. The combination of foods that explain the most of the variance in maternal milk DHA is total fat consumed and total fish consumed. This explained 61 percent of the variance in maternal milk DHA across countries.
Not surprisingly, foodstuffs high in n-6 showed significant negative correlations on maternal milk DHA. “Any regression including total fish or seafood, and vegetable oils, animal fat or milk consistently explains at least half of the variance in milk DHA, with fish or seafood having positive beta coefficients and the remainder having negative beta coefficients.”
The study showed that a country’s balance of n-3 and n-6 was strongly related to the students’ math performance on the PISA. This relationship between milk DHA and cognitive performance remains sufficient even after controlling for national wealth, macro intake and investment in education. The availability of DHA in populations is a better predictor of test scores than are SES factors (which I’ve covered here on Italian IQ), though SES explains a considerable portion of the variance, it’s not as much as the overall DHA levels by country. Furthermore, maternal DHA levels are strongly correlated to per capita fish and seafood consumption while a negative correlation was noticed with the intake of more vegetable oils, fat, and beef, which suggests ‘metabolic competition’ between the n-3 and n-6 fatty acids.
There are, of course, many possible errors with the study such as maternal milk DHA values not reflecting the total DHA in that population as a whole; measures of extracting milk fatty acids differed between studies; test results being due to sampling error; and finally the per capita consumption of foods is based on food disappearance, not amount of food consumed. However, even with the faults of the study, it’s still very interesting and I hope they do further work with actual measures of cognitive ability. Despite the pitfalls of the study (the main one being the use of PISA to test ‘cognitive abilities’), this is a very interesting study. I eventually hope that a study similar to this one is undertaken with actual measures of cognitive ability and not PISA scores.
We now know that n-6 is negatively linked with brain performance, and that n-3 is positively linked. What does this say about America?
As I’m sure all of you are aware of, America is one of the fattest nations in the world. Not surprisingly, Americans consume extremely low levels of seafood (very high in DPA) and more foods high in n-6 (Papanikolaou et al, 2014). High levels of n-3 (which we do not get enough of in America) and n-6 are correlated with obesity (Simopoulos, 2016). So not only do we have a current dysgenic effect in America due to decreased fertility of the more intelligent (which is also part of the reason why we have the effect of dysgenic fertility in America), obesity is also driven by high levels of n-6 in the Western diet, which then causes obesity down the generations (Massiera et al, 2010).
I also previously wrote on agriculture and diseases of civilization. Our hunter-gatherer ancestors were all around healthier than we were. This, clearly, is due to the fact that they ate a more natural diet and not one full of processed, insulin-spiking carbohydrates, among other things. Our hunter-gatherer ancestors consumed n-3 and n-6 at equal amounts (1:1) (Kris-Etherson, et al 2000). As I documented in my article on agriculture and disease, HGs had low to nonexistent rates of the diseases that plague us in our modern societies today. However, around 140 years ago, we entered the Industrial Revolution. The paradigm shift that this caused was huge. We began consuming less n-3 (fish and other assorted seafood and nuts among other foods) while n-6 intake increased (beef, grains, carbohydrates) (Kris-Etherson, et al 2000). Moreover, the ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 2013). We Americans also consume 20 percent of our daily kcal from one ‘food’ source—soybean oil—with almost 9 percent of the total kcal coming from n-6 linoleic acids (United States Department of Agriculture, 2007). The typical American diet contains about 26 percent more n-6 than n-3, and people wonder why we are slowly getting dumber (which is, obviously, a side effect of civilization). So our n-6 consumption is about 26 percent higher than it was when we were still hunter-gatherers. Does anyone still wonder why diseases of civilization exist and why hunter-gatherers have low to nonexistent rates of the diseases that plague us?
The bioavailability of n-6 is dependent on the amount of n-3 in fatty tissue (Hibbeln et al, 2006). This goes back to the ‘metabolic competition’ mentioned earlier. N-3 also makes up 10 percent of the overall brain weight since the first neurons evolved in an environment high in n-3. N-3 fatty acids were positively related to test scores in both men and women, while n-6 showed the reverse relationship (with a stronger effect in females). Furthermore, in female children, the effect of n-3 intake were twice as strong in comparison to male children, which also exceeded the negative effects of lead exposure, suggesting that higher consumption of foods rich in n-3 while consuming fewer foods rich in n-6 will improve cognitive abilities (Lassek and Gaulin, 2011).
The preponderance of evidence suggests that if parents want to have the healthiest and smartest babes that a pregnant woman should consume a lot of seafood while avoiding vegetable oils, total fat and milk (fat, milk and beef moreso from animals that are grain-fed) Grassfed beef has higher levels of n-3, which will balance out the levels of n-6 in the beef. So if you want your family to have the highest cognition possible, eat more fish and less grain-fed beef and animal products.
In sum, if you want the healthiest, most intelligent family you can possibly have, the most important factor is…diet. Diets high in n-3 and low in n-6 are extremely solid predictors of cognitive performance. Due to the ‘meatbolic competition’ between the two fatty acids. This is because n-6 accumulates in the blood and tissue lipids exacerbating the competiiton between linolic acid (the most common form of n-6) and n-3 for metabolism and acylation into tissue lipds (Innis, 2014). Our HG ancestors had lower rates of n-6 in their diets than we do today, along with low to nonexistent disease rates. This is due to the availability of n-6 in the modern diet, which was unknown to our ancestors. Yes, seafood intake had the biggest effect on the PISA math scores, which, in my opinion (I need to look at the data), is due in part to poverty. I’m very critical of PISA, especially as a measure of cognitive abilities, but this study is solid, even though it has pitfalls. I hope a study using an actual IQ test is done (and not Richard Lynn IQ tests that use children, a robust adult sample is the only thing that will satisfy me) to see if the results will be replicated.
I also think it’d be extremely interesting to get a representative sample from each country studied and somehow make it so that all maternal DHA levels are the same and then administer the tests. This way, we can see how all groups perform with the same amounts of DHA (and to see how much of an effect that DHA really does have). Furthermore, nutritonally impoverished countries will not have access to the high-quality foods with more DHA and healthy fatty acids that lead to higher cognitive function.
It’s clear: if you want the healthiest family you could possibly have, consume more seafood.
Expounding On My Theory for Racial Differences In Sports
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In the past, I’ve talked about why the races differ—at the extremes—(and the general population, but the extremes put the picture into focus) in terms of what sports they compete and do best in. These differences come down to morphology somatype, physiology. People readily admit racial differences in sports and—rightly say—that these differences are largely genetic in nature. Why is it easier for people to accept racial differences in sports and not accept other truisms, like racial IQ differences?
I’ve muscle fiber typing and how the variances in fiber typing dictate which race/ethny performs best at which sport. I’ve also further evidence that blacks have type II fibers (responsible for explosive power), which leads to a reduced Vo2 max. This lends yet more credence to my theory of racial differences in sports—black Americans (West African descendants) have the fiber typing that is associated with explosive power, less so with endurance activities. Since I’ve documented evidence on the differences in sports such as baseball, football, swimming and jumping, bodybuilding, and finally strength sports, tonight I will talk about the evolutionary reasons for muscle fiber and somatype differences that will have us better understand the evolutionary conditions in which these traits evolved and why they got selected for.
Most WSM winners are from Nordic countries or have Nordic ancestry. There’s a higher amount of slow twitch fibers in Nordics and East Asians (and Kenyans) which is more conducive to strength and less conducive to ‘explosive’ sports. West Africans and their descendants dominate in sprinting competitions. Yea yea yea white guy won in 1960. So they will be less likely to be in strength comps and more likely to win BBing and physique comps. This is what we see.
Only three African countries have placed in the top ten in the WSM (Kenya, Namibia, and Nigeria, however, one competitor from Namibia I was able to find has European ancestry). Here is a video of a Nigerian Strongest Man competition (notice how his chest isn’t up and his hips rise before the bar reaches his knees, horrible form). Fadesere Oluwatofunmi is Nigeria’s Strongest Man, competing in the prestigious Arnold Classic, representing Nigeria. However, men such as Fadesere Olutaofunmi are outliers.
Now for a brief primer on muscle fibers and which pathways they fire through. Understanding this aspect of the human body is paramount to understanding how and why the races differ in elite competition.
Life history and muscle fiber typing
Slow twitch fibers fire through aerobic pathways. Breaking down fats and proteins takes longer through aerobic respiration. Moreover, in cold temperatures, the body switches from burning fat to burning carbohydrates for energy, which will be broken down slower due to the aerobic perspiration. Slow twitch (Type I) fibers fire through aerobic pathways and don’t tire nearly as quickly as type II fibers. Also, CHO reserves will be used more in cold weather. The body’s ability to use oxygen decreases in cold weather as well, so having slow twitch fibers is ideal (think about evolution thousands of years ago). Type I fibers fire off slower so they’ll be able to be more active for a longer period of time (studies have shown that Africans with Type II fibers hit a ‘wall’ after 40 seconds of explosive activity, which is why there are so few West-African descended marathon runners, powerlifters, Strongmen, etc). Those who possess these traits will have a higher chance to survive in these environments. Those with slow twitch fibers also have to use more oxygen. They have larger blood vessels, more mitochondria and higher concentrations of myoglobin which gives the muscles its reddish color.
Each fiber fires off through different pathways, whether they be anaerobic or aerobic. The body uses two types of energy systems, aerobic or anaerobic, which then generate Adenosine Triphosphate, better known as ATP, which causes the muscles to contract or relax. Depending on the type of fibers an individual has dictates which pathway muscles use to contract which then, ultimately, dictate if there is high muscular endurance or if the fibers will fire off faster for more speed.
Type I fibers lead to more strength and muscular endurance as they are slow to fire off, while Type II fibers fire quicker and tire faster. Slow twitch fibers use oxygen more efficiently, while fast twitch fibers do not burn oxygen to create energy. Slow twitch muscles delay firing which is why the endurance is so high in individuals with these fibers whereas for those with fast twitch fibers have their muscles fire more explosively. Slow twitch fibers don’t tire as easily while fast twitch fibers tire quickly. This is why West Africans and their descendants dominate in sprinting and other competitions where fast twitch muscle fibers dominate in comparison to slow twitch.
Paleolithic Europeans who had more stamina spread more of their genes to the next generation as their genotype was conducive to reproductive success in Ice Age Europe. Conversely in Africa, those who could get away from predators and could hunt prey more efficiently survived. Over time, frequencies of genes related to what needed to be done to survive in those environments increased, along with the frequencies of muscle fibers in the races.
Racial differences in anatomy and physiology
Along with muscle fiber differences, blacks and whites also have differences in fat-free body mass, bone density, distribution of subcutaneous fat, length of limbs relative to the trunk, and body protein contents (Wagner and Heyward, 2000). These differences are noticed and talked about in the scientific literature, even in University biology and anatomy textbooks. However, in terms of University textbooks, authors who recognize the concept of race do so in spite of what other authors write (Hallinan, 1994). Furthermore, Strkalj and Solyali (2010) analyzed 18 English textbooks on anatomy and concluded that discussion of race was ‘superficial’ and the content ‘outdated’, i.e., using the ‘Mongoloid, Caucasoid, Negroid terminology (I still do out of habit). They conclude that most mentions of race are either not mentioned in anatomy textbooks or are only ‘superficially accounted for in textbooks’. Clearly, though they are outdated, some textbooks do talk about human biological diversity, though the information needs to be updated (especially now). The center of mass in blacks is 3 percent higher than in whites, meaning whites have a 1.5 percent speed advantage in swimming while blacks have a 1.5 percent speed difference in sprinting. East Asians that are the same height as whites are even more favored in swimming, however, they are shorter on average so that’s why they do not set world records (Bejan, Jones, and Charles, 2010).
For another hand grip strength (HGP) test, see Leong et al (2016). Most studies on HGS are done on Caucasian populations with little data for non-Caucasoid populations. They found that HGS values were higher for North America and Europe, intermediate in China, South America and the Middle East, and the lowest in South Asia, Southeast Asia, and Africa. These are, most likely, average Joes and not elite BBers or strength trainers. This is one of the best papers I’ve come across on this matter (though I would kill to have a nice study done on the three classical races and their performance on the Big 3 lifts: squat, bench press and deadlift; I’m positive it would be Asian/white and blacks as the tail end).
Among other physical differences is brain size and hip width. Blacks have narrower hips than whites who have narrower hips than Asians (Rushton, 1997: 163). Bigger-brained babes are more than likely born to women who have wider hips. If you think about athletic competition, one with wide hips will get decimated by one with narrower hips as he will be better able to move. People with big crania, in turn, have the hip structure to birth big brains. This causes further division between racial groupings in sports competition.
Some people may dispute a genetic causation and attribute the success of, say, Kenyan marathoners (the Kalenjin people) and attribute the effects to the immediate environment (not ancestral), training and willpower (see here for discussion). This Kenyan subpopulation also has the morphology conducive to success in marathons (tall and lengthy), as well as type II muscle fibers (which is why Kenya placed in the WSM).
I would also like to see a study of men in their prime (age 21 to 24) from European, Africans, and East Asian backgrounds with a high n (for a study like this it’d be 20 to 30 participants for each race), with good controls. You’d see, in my opinion, East Asians slightly nudge out whites who destroy blacks. The opposite would occur in sports that use type II fibers. West Africans also have the gene variant ACTN3 which is associated with explosive sports.
For a better (less ethical study) we can use a thought experiment.
We take two babes fresh out of the womb (one European, the other West African) and keep them locked in a metabolic chamber for their whole entire lives. We keep them in the chamber until they die and monitor them, feeding them the same exact diet and giving them the same amount of attention. They start training at age 15. Who will be stronger in their prime (the European man)? Who will have more explosive power (the West African man)? A simple thought experiment can have one thinking about intrinsic racial differences in things the average American watches in their everyday lives. The subject of racial differences in sports is a non-taboo subject, however, the subject of racial differences in intelligence is a big no-no.
Think about that for a second. People obviously accept racial differences in sports, yet they have some kind of emotional attachment to the blank slate narrative. We don’t hear that you can nurture athletic success. We do, however, hear that ‘we can succeed at anything we put out minds to’. That’s not in dispute; that’s a fact. But it’s twisted in a way that genetics and ancestry has no bearing on it, when it explains a lot of the variance. People accept racial differences when they’re cheering on their favorite football team or basketball team. For instance, NFL announcer Gus Johnson said during a broadcast of a Titans and Jaguars game “He’s [Chris Johnson] got gettin’ away from the cops speed!”
Pro-sports announcers, as well as college recruiters, know what the average person doesn’t who is not exposed to these differences daily for decades on end. People in these types of professions, especially collegiate sports recruiters, must get the low-down on average racial differences and then use what they know to make their choices on who to draft for their team.
For more (anecdotal) evidence, you can look up the race/ethnicity of the winners in competitions where peoples from all over the world compete in. More West African descendants place higher in physique, BBing comps, etc; more Caucasians and East Asians (and Kenyans) place higher in strength comps. A white man has won the WSM every year since its inception. West African descended blacks dominate BBing and physique comps. Eurasians (and Kenyans) dominate in marathon running.
All of this talk of racial differences in sports (which largely has to do with whites vs. blacks, though Asians are included in my overall analysis), I’ve hardly cited anything on East Asians directly. In regards to sports that take extreme dexterity or flexibility (and high reaction), East Asians shine. They shine in diving, ping-pong, skating and gymnastics events. They usually have long torsos and small limbs. I theorize that this was an evolutionary adaptation for the East Asians, as shorter people have less surface area to keep warm. Taller people would have died out quicker than one who’s smaller and can cover up and get warmer faster. They also have quicker reaction times (Rushton and Jensen, 2005) and it has been hypothesized that this is why they dominate in ping pong.
Conclusion
We don’t need any tests to show that there are racial differences in sports; the test is the competition itself. On average, A white will be stronger than an Asian who will be stronger than a black. Conversely, a Kenyan will be a better marathoner than a West African, European or Asian. West Africans will be more likely to beat all three groups in a sprint. These differences come down to morphology, but they start inside the muscles with the muscle fibers. Some anatomy textbooks acknowledge the existence of race, however, they have old and outdated information. It’s a good thing that anatomy textbooks talk about racial differences in physiology and anatomy, now we need to start doing heavy research into racial differences in the brain. The races evolved their fiber typing depending on what they had to do to survive along with their immediate environment, i.e., high elevation like the Kalenjin people.
The evolution of differing muscle fiber types in different races is easily explainable: Europeans have slow twitch fibers. In cold temperatures, the body switches from burning fat to burning carbs for energy. Furthermore, the average person would need to have a higher lung capacity and not tire out during long hunts on megafauna. Over time, selection occurred on the individuals with more type I fibers. Conversely, West Africans and their descendants have the ACTN3 gene, which is associated with elite human athletic performance (Yang et al, 2003). Africans who could get away from predators survived and passed on the genes and fiber typing for elite athletic performance.
In sum, the races differ in terms of entrants to elite athletic competition. These differences are largely genetic in nature. Evolutionary processes explain racial differences in sports. These same selection processes that explain racial differences in elite sports competitions also explain racial differences in intelligence. I await the day that we can freely speak about racial differences in intelligence just like we speak about racial differences in sports. Denying human variation makes no sense, especially in today’s world where we have state of the art testing.
NotPoliticallyCorrect 