I come across a lot of ridiculous articles from PumpkinPerson, but this has to be one of the most ridiculous. He writes:
Identical twin studies show that obesity has a heritability of almost 80%. Although I generally lean towards nature in most nature-nurture debates, I’ve always had a problem with the idea that obesity is highly genetic, and thus enjoyed this epic rant by blogger Robert Lindsay:
It is 80% genetic[?]
That is why you have whole tribes in South America where not one person has ever been fat.
That is why you have whole towns in Melanesia with 1000’s of people where not one person is fat.
There are fat people in the cities of Solomon Islands. In the study I read, the only man who was fat was one who had gone off to the city for a while and ate salt and processed, packaged food. Do you realize that if you did a genetic study of the fatties in Melanesia, you would find that wonderful 80% “genetic” link you guys are shouting about?
That is why the fatness and obesity rate has exploded in the US and much of the rest of the world. Because it’s 80% genetic!
I do not believe that fatsos act just like the rest of us. Ever known a blimp who ate like a bird? Me either.
I dunno about you, but I have never seen a fat person who wasn’t stuffing their face all the time with lousy food. They are always in restaurants. Always going out to eat. If you go to a restaurant, look around at all the fat people. Those people are fat because fat people like to eat out all the time and restaurant food is fattening. Fat people love to eat. Have you ever noticed that?
It’s 80 percent heritable in first world countries. Obviously the heritability will be lower in the third world. Clearly in first-world countries we have an overabundance of food. We don’t know what to do with it. So instead of having the opposite problem (not enough food) we now have too much food and this is what caused weight to increase (along with added sugars processed carbs).
Look at Melanesia—they still eat an ancestral diet. I can’t tell if Lindsay is being serious or not. He’s comparing people who still eat their ancestral diet to people who live in first-world countries and eat a Western diet. There’s no comparison there. If you want to see why people aren’t fat nor have the same diseases at the same rates (they are low to nonexistent in places like that) read Agriculture and Diseases of Civilization.
This is the study that’s being referred to Elks et al 2012. The heritability of BMI is between .75 and .82. Again: this is in first-world countries.
PP then says:
In fact just the other day, I was at the home of someone who was so incredibly fat I thought “it must be genetic.” And then just as I was leaving his house, I noticed a huge empty box of pizza in the kitchen.
“So maybe the answers to be found are in the integration of factors – starting with the physiological, metabolic, and genetic ones and letting them lead us to the environmental triggers. Because the one thing we know for sure is that the laws of thermodynamics, true as they always are, tell us nothing about why we get fat or why we take in more calories than we expend while it’s happening. (emphasis mine) (Taubes, 2011: pg 74, excerpt from Why We Get Fat and What to Do About It)
The fatness itself or the tendency to engage in behaviors that cause fatness such as ordering large pizzas? So while obesity might technically be nearly 80% genetic, the statistic is misleading because it’s not directly genetic in the same was as height is.
If you don’t eat enough, nor get the right nutrients, you don’t hit your genetic height. If you don’t eat enough you don’t hit your genetic weight.
I don’t get why studies like this get generalized to the whole population. This study was done in first-world countries and so this only applies to first-world countries. You’d think that people who think they know science would know that studies are only applicable for the cohort and people they are done on. Guess not.
Of course I don’t deny obesity has some direct genetic component. Some people gain weight a lot easier than others and for some people, it’s virtually impossible to lose weight no matter how well they eat, though this is rare.
Of course some people gain weight easier than others. Some people lose weight easier than others. Much of the biological opposition to sustained weight loss is due to the hormone leptin (Rosenbaum et al, 2010). The more fat you have in your body, the more leptin you have. Moreover, the longer you are at a certain weight, the more likely it is that is your bodyweight set-point and thus you can only move up or down at around a range of 10 to 15 pounds. Also see this quote from neuroscientist Sandra Aamodt’s book Why Diets Make Us Fat (see her Ted Talk here):
Like nearsightedness, environmental influences on weight also mostly affect the genetically vulnerable, although we understand the details of the process in only rare cases. Fitness gains on a standardized exercise program vary from one person to another largely because of differences in their genes. When identical twins, men in their early twenties, were fed an extra thousand calories per day for about three months, each pair showed similar weight gains . In contrast, the gain varied across twin pairs, ranging from nine to twenty-nine pounds, even though the caloric imbalance was the same for everyone. An individual’s genes also influence weight loss. When another group of identical twins burned a thousand more calories per day through exercise while maintaining a stable food intake in an in-patient facility, their losses ranged from two to eighteen pounds and were even more similar within twin pairs than weight gain. (Aamodt, 2016 pg. 138)
The cold, hard truth is that dieting doesn’t have a good track record. See Mann et al (2007) here. People don’t understand the bodies’ biological processes and assume something is easy while being ignorant to how the body reacts under caloric deprivation. This wouldn’t happen if people actually had some knowledge of human physiology. Something that PP and RL lack. They are speaking about a complex problem than they’re too ignorant to really know about.
PP then says:
“Now I have no doubt that if that person has an identical twin raised apart, he too is extremely fat, and thus fatness technically has a high heritability, but what exactly is genetic here?”
Would the identical twin be raised in an obesogenic environment? If so, there’s a high chance that, yes he’d be fat too.
It’s also true that most people who lose weight end up gaining it back, but that’s because they end up returning to their compulsive eating habits.
People should read a few papers and books to see some data and facts before they write what “sounds good” in their head. These two clearly have no idea what they’re talking about and clearly talking from emotion and what sounds good.
Also read Are There Genetic Causes for Obesity?
Diet is the main driver of our evolution. Without adequate energy, we wouldn’t be able to able to have a brain as large as we do that has the number of neurons we have due to how calorically expensive each neuron is (6 kcal per billion neurons). However, as I’m sure everyone can see, our current diets and environment has caused the current obesity crisis in the world. What is the cause of this? Our genomes are adapted for a paleolithic diet and not our modern environment with processed foodstuffs along with an overabundance of energy. With an overabundance of novel food items and situations due to our obesogenic environments, it is easier for a higher IQ person to stay thinner than it is for a lower IQ person. Tonight I will talk about the causes for this, how and what we evolved to eat and, of course, how to reverse this phenomenon.
“Gourmet Sapiens” arose around 1-1.5 mya with the advent of cooking by Homo erectus. Even before then, when we became bipedal our hands were freed which then allowed us to make tools. With these tools, we could mash and cut food which was a sort of pre-digestion outside the body (exactly what cooking is). Over time, our guts shrank (Aiello, 1997) and we became adapted for a certain diet (Eaton, 2006). Over time, we evolved to eat a certain way—that is, we had times of feast and famine. Due to this, eating three meals a day is abnormal from an evolutionary perspective (Mattson et al, 2014). This sets the stage for the acquisition of diseases of civilization along with the explosion of obesity rates.
When looking for the causes—and not symptoms—of the rise of obesity rates, the first thing we should do is look at our current environment. How is it constructed? What type of foodstuffs are in it? What kinds of foods get advertised to us and how does this have an effect on our psyche and what we eventually buy? All three of these questions are extremely important to think of when talking about why we are so obese as a society. First-world environments are obesogenic (Galgani and Ravussin, 2008) due to being evolutionarily novel. Our genomes are adapted to a paleolithic diet, and so the introduction of the neolithic diet and agriculture reduced our quality of life, with a marked decrease in the quality of skeletal remains discovered after the advent of agriculture. However, agriculture is obviously responsible for the population boom that allowed us to become the apes the took over the world, cause being the population boom that followed the agricultural revolution (Richards, 2002).
Evolutionary mismatches occur when the rate of cultural or technological change is far faster than the genome can change to adapt to the new pressure. These dietary mismatches occur when cultural and technological change which can vastly outstrip biological evolution. The two big events that occurred in human history that have vastly outstripped biological evolution are the agricultural and Industrial Revolution. Contrary to Ryan Faulk’s belief, East Asians are not ‘less sensitive to carbohydrates’ and he did not “solve Gary Taubes’ race problem” in regards to diabesity rates. The rate of cultural and technological change has had large deleterious effects on our quality of life, and our increasing obesity rates have a lot to do with it.
Cofnas (2016) showed that mice taken off of their ancestral diet lead to worse healthy outcomes. The results of Lamont et al (2016) show that we, as animals, are adapted for ancestral diets, not the diets of the environment we have currently made for ourselves. This is a big point to take home from this. All organisms are adapted/evolved for what occurred in the ancestral past, not any possible future events. Therefore, to be as healthy as possible, it stands to reason you should eat a diet that’s closer to the ones your ancestors ate, especially since it can reverse type II diabetes and reverse bad blood markers (Klonoff, 2009). Even a short-term switch to a paleo diet “improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.” (Frassetto et al, 2009) Since we evolved for a past environment and not any possible future ones, then eating a diet that’s as close as possible to our paleolithic ancestors looks like a smart way to beat the evolutionary mismatch in terms of our new, current obesogenic environment.
In one extremely interesting study, O’dea (1984) took ten middle-aged Australian Aborigines with type 2 diabetes and had them return to their ancestral hunter-gatherer lifestyle. With seven weeks of an ancestral diet and exercise, the diabetes had almost completely reversed! Clearly, when the Aborigines were taken off of our Western diet and put back in their ancestral environment with their ancestral diet, their diabetes disappeared. If we went back to a more ancestral eating pattern, the same would happen with us. This one small study lends credence to my claim that we need to eat a diet that’s more ancestral to us for us to ameliorate diseases of civilization (Eaton, 2006).
Further, looking at obesity from an evolutionary perspective can and will help us understand the disease of obesity (Ofei, 2005) better. Speakman (2009) reviewed three different explanations of the current obesity epidemic and assessed their usefulness in explaining the epidemic. The thrifty gene hypothesis states that obesity is an adaptive trait, that people who carry so-called ‘thrifty genes’ would be at an adaptive advantage. And since we have an explosion of obesity today from the 70s to today, this must explain a large part of the variance, right? There is evidence pointing in this direction, however (Southam et al, 2009). The second cause that Speakman looks at is the adaptive viewpoint—that obesity may have never been advantageous in our history, but genes that ultimately predispose us to obesity become “selected as a by-product of selection on some other trait that is advantageous.” (Speakman, 2009) The third and final perspective he proposes is that it’s due to random genetic drift, called ‘drifty genes’, predisposing some—and not others—to obesity. Whatever the case may be, there is some truth to their being genetic factors involved in the acquisition of fat storage. Though drifty genes and the adaptive viewpoint on obesity make more sense than any thrifty gene hypothesis.
For there to be any changes in the rate of obesity in the world, we need to begin to change our obesogenic environments to environments that are more like our ancestral one in terms of what foods are available. Once we alter our obesogenic environment into one that is more ancestrally ‘normal’ (since we are adapted for our past environments and not any possible future ones) then and only then will we see a reduction in obesity around the world. We are surrounded and bombarded with ads since we are children, which then effects our choices later in life; children consume 45 percent more when exposed to advertising (Harris et al, 2009). Clearly, advertisements can have one eat more, and the whole environmental mismatch in regards to being surrounded by foodstuffs not ancestral to us causes the rate of obesity to rise.
Finally, one thing we need to look at is the n-3 to n-6 ratio of our diets. As I covered last month, the n-6/n-3 is directly related to cognitive ability (Lassek and Gaulin, 2011). Our obesogenic environments cause our n-3/n-6 levels to be thrown out of whack. Our hunter-gatherer ancestors had a 1:1 level of n-3 and n-6 (Kris-Etherton, 2000). However, today, our diets contain 14 to 25 times more n-6 than n-3!! Still wondering why we are getting stupider and fatter? Further, Western-like diets (high in linolic acid; an n-6 fatty acid) induces a general fat mass enhancement, which is in line with the observation of increasing obesity in humans (Massiera et al, 2010). There is extreme relevance to the n-3/n-6 ratio on human health (Griffin, 2008), so to curb obesity and illness rates, we need to construct environments that promote a healthy n-3/n-6 ratio, as that will at least curb the intergenerational transmission of obesity. Lands (2015) has good advice: “A useful concept for preventive nutrition is to NIX the 6 while you EAT the 3.” Here is a good list to help balance n-6 to n-3 levels.
In sum, obesity rates are a direct product of obesogenic environments. These environments cause obesity since we are surrounded by evolutionary novel situations and food. The two events in human history that contribute to this is the agricultural and Industrial Revolution. We have paleolithic genomes in a modern-day world, which causes a mismatch between our genomes and environment. This mismatch can be ameliorated if we construct differing environments—ones that are less obesogenic with less advertisement of garbage food—and we should see rates of obesity begin to decline as our environment becomes more and more similar to our ancestral one (Genné-Bacon, 2014).
The study on mice showed that for them to be healthy they need to eat a diet that is ancestral to them. We humans are no different.The evidence from the study on Australian Aborigines and the positive things that occur after going on a paleo diet for humans—even for sedentary people—shows that for us to be as healthy as possible in these obesogenic environments that we’ve made for ourselves, we need to eat a diet that matches with our paleolithic genome. This is how we can begin to fight these diseases of civilization and heighten our quality of life.
Note: Diet and exercise only under Doctor’s supervision, of course
Aiello, L. C. (1997). Brains and guts in human evolution: The Expensive Tissue Hypothesis. Brazilian Journal of Genetics,20(1). doi:10.1590/s0100-84551997000100023
Cofnas, N. (2016). Methodological problems with the test of the Paleo diet by Lamont et al. (2016). Nutrition & Diabetes,6(6). doi:10.1038/nutd.2016.22
Eaton, S. B. (2006). The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proceedings of the Nutrition Society,65(01), 1-6. doi:10.1079/pns2005471
Frassetto, L. A., Schloetter, M., Mietus-Synder, M., Morris, R. C., & Sebastian, A. (2009). Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. European Journal of Clinical Nutrition,63(8), 947-955. doi:10.1038/ejcn.2009.4
Galgani, J., & Ravussin, E. (2008). Energy metabolism, fuel selection and body weight regulation. International Journal of Obesity,32. doi:10.1038/ijo.2008.246
Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99–112, 2014
Griffin, B. A. (2008). How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP study. Current Opinion in Lipidology,19(1), 57-62. doi:10.1097/mol.0b013e3282f2e2a8
Harris, J. L., Bargh, J. A., & Brownell, K. D. (2009). Priming effects of television food advertising on eating behavior. Health Psychology,28(4), 404-413. doi:10.1037/a0014399
Klonoff, D. C. (2009). The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and other Risk Factors for Cardiovascular Disease. Journal of Diabetes Science and Technology,3(6), 1229-1232. doi:10.1177/193229680900300601
Kris-Etherton PM, Taylor DS, Yu-Poth S, et al. Polyunsaturated fatty acids in the food chain in the United States. Am J Clin Nutr, 2000, vol. 71 suppl(pg. 179S-88S)
Lamont, B. J., Waters, M. F., & Andrikopoulos, S. (2016). A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. Nutrition & Diabetes,6(2). doi:10.1038/nutd.2016.
Lands, B. (2015). Choosing foods to balance competing n-3 and n-6 HUFA and their actions. Ocl,23(1). doi:10.1051/ocl/2015017
Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005
Massiera, F., Barbry, P., Guesnet, P., Joly, A., Luquet, S., Moreilhon-Brest, C., . . . Ailhaud, G. (2010). A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. The Journal of Lipid Research,51(8), 2352-2361. doi:10.1194/jlr.m006866
Mattson, M. P., Allison, D. B., Fontana, L., Harvie, M., Longo, V. D., Malaisse, W. J., . . . Panda, S. (2014). Meal frequency and timing in health and disease. Proceedings of the National Academy of Sciences,111(47), 16647-16653. doi:10.1073/pnas.1413965111
O’dea, K. (1984). Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes,33(6), 596-603. doi:10.2337/diabetes.33.6.596
Ofei F. Obesity- a preventable disease. Ghana Med J 2005;39: 98-101
Richards, M. P. (2002). A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence. European Journal of Clinical Nutrition,56(12), 1270-1278. doi:10.1038/sj.ejcn.1601646
Southam, L., Soranzo, N., Montgomery, S. B., Frayling, T. M., Mccarthy, M. I., Barroso, I., & Zeggini, E. (2009). Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants? Diabetologia,52(9), 1846-1851. doi:10.1007/s00125-009-1419-3
Speakman, J. R. (2013). Evolutionary Perspectives on the Obesity Epidemic: Adaptive, Maladaptive, and Neutral Viewpoints. Annual Review of Nutrition,33(1), 289-317. doi:10.1146/annurev-nutr-071811-150711
The relationship between exercise and cognitive ability is important, but often not spoken about. Exercise releases many endorphins (Harber and Sutton, 1984) that help to further positive mood, have one better handle stress since sensitivity to stress is reduced after exercise; and after exercise, depression, and anxiety also decrease (Salmon, 2001). Clearly, if you’re attempting to maximize your cognition, you want to exercise. However, a majority of Americans don’t exercise (49 percent of Americans over the age of 18 do aerobic exercise whereas only 20 percent of Americans do both aerobic and muscle-strengthening exercise). The fact that we do not exercise as a country is proof enough that our life expectancy is declining (Olshansky et al, 2005), and we need to exercise—as a country—to reverse the trend.
Regular readers may know of my coverage of obesity on this blog. Understandably, a super majority of people will disregard my views on obesity and its causes as ‘pseudoscience’ or ‘SJW-ness’, that however says nothing to the data (and if anyone would like to discuss this, they can comment on the relevant articles). Since the average American hardly gets any exercise, this can lead to a decrease in cognitive functioning as less blood flows to the brain. Thus, everyone—especially the obese—needs to exercise to reach maximum genetic brain performance, lest they degenerate in cognitive function due a low-quality diet, such as a diet high in n-6 (the SAD diet), which is correlated with decreased cognition. Further, contrary to popular belief, the obese have lower IQs since around age three; obesity does not itself lower genotypic IQ, their IQ is ALREADY LOW which leads to obesity later in life due to a non-ability to delay gratification. Clearly, exercise education needs to be targeted at those with lower IQs since they have a higher chance of becoming obese in comparison to those with lower IQs (Kanazawa, 2013; 2014).
Clearly not eating well and not exercising can have negative effects on cognition. But what are the positives?
As mentioned previously, exercise releases endorphins that cause good mood and block pain. However, the importance of exercise does not stop there. Exercise also leads to faster reaction times on memory tasks and “increased levels of high-arousal positive affect (HAP) and decreased levels of low-arousal positive affect (LAP).” Exercise has important effects on people of all age groups (Hogan, Mata and Carstensen, 2013; Chodzko-Zajko et al, 2009). Further, physical exercise protects against age-related diseases and cognitive decline in the elderly by modifying “metabolic, structural, and functional dimensions of the brain that preserve cognitive performance in older adults.” (Kirk-Sanchez and McGough, 2014). Exercise is, clearly, a brain protectant during both adolsence and old age, so no matter your age if you want a high QoL living the best life possible, you need to supplement an already healthy lifestyle with strength training/cardio (of course, under doctor’s supervision).
Another important benefit to exercise is that it increases blood flow to the brain (Querido and Steele, 2007; Willie and Ainslie, 2011); however, changes in cerebral blood flow (CBF) during exercise are not associated with higher cognition (Ogoh et al, 2014). During prolonged exercise, cognition was improved when blood flow to the middle cerebral artery (MCA) was decreased. Thusly, exercise-induced changes in CBF do not preserve cognitive performance. Exercise to get blood to the brain is imperative for proper brain functioning. Our brains are vampiric, so we need to ‘feed it’ with blood and what’s the best way to ‘feed’ the brain in this context? Exercise!
Exercise also protects against cognitive degeneration in the elderly (Bherer, Erikson and Lie-Ambrose, 2013; Carvalho et al, 2014; Paillard, 2015). Further, longitudinal studies show an association between exercise and a decrease in dementia (Blondell, Hammersley-Mather and Veerman, 2014). The evidence is currently piling up showing that exercise at all ages is good cognitively, reduces mortality as well as a whole slew of other age-related cognitive diseases. The positive benefits of exercise need to be shown to elderly populations since exercise—mainly strength training—reduces the chance of osteoporosis (Layne and Nelson, 1999; Gray, Brezzo, and Fort, 2013). Moreover, elderly people who exercise live longer (Gremeaux et al, 2012). Now, if you don’t exercise, now’s looking like a pretty good time to start, right?
Finally, lack of exercise causes a myriad of deleterious diseases (Booth, Roberts, and Laye, 2014). This is due, in large part to our evolutionary novel environment (Kanazawa, 2004) which leads to evolutionary mismatches. An evolutionary mismatch, in this instance, is our obesogenic environment (Lake and Townshend, 2006). In terms of our current environment, it is evolutionary novel in comparison to our ancestral land (the Savanna; re: Kanazawa, 2004). Modern-day society is ‘evolutionarily novel’. In this case, we haven’t fully adapted (genetically) to our new lifestyles as, Gould said in Full House, our rate of cultural change has vastly exceeded Darwinian selection. Thusly, our environments that we have made for ourselves (and that we assume that heighten our QoL) actually cause the reverse, all the while top researchers are scratching their heads to figure out the answer, the problem while it’s staring them right in the face.
Our obesogenic environments have literally created a mismatch with our current eating habits and our ancestral one (Krebs, 2009). Moreover, dietary mismatches occur when cultural and technological change vastly outstrip biological evolution (Logan and Jacka, 2009). Clearly, we need to lessen the impact of our obesogenic environment we have made for ourselves so that we can live as long as possible, as well as be as cognitively sharp as possible. Thusly, if our environment causes a mismatch with our genome which in turn causes obesity, then by changing our environment to one that matches our genome, so to speak, levels of obesity should decline as our environment becomes less obesogenic while becoming like our ancestral environment (Genne-Bacon, 2014).
In sum, the evidence for the positive benefits for exercise is ever-mounting (not like you need Pubmed studies to know that exercise is beneficial). However, due to our obesogenic environments, this makes it hard for people with higher time preference to resist their urges and the result is what you see around you today. The evidence is clear: exercise leads to increased blood flow to our vampiric brains; thus it will have positive effects on memory and other cognitive faculties. So, in order to live to a ripe, old age as a healthy man/woman, hit the gym and treadmill and try staying away from evolutionarily novel things as much as possible (i.e., like processed food). When we, as a country recognize this, we can then be smarter, healthier and, above all else, have a high QoL while living a longer life. Is that not what we all want? Well hit the gym, start exercising and change your diet to one that matches our ancestors. Don’t be that guy/gal (we all know who that guy is) that jumps on the exercise train late and misses out on these cognitive and lifestyle benefits!
Note: Only with Doctor supervision, of course
Bherer, L., Erickson, K. I., & Liu-Ambrose, T. (2013). A Review of the Effects of Physical Activity and Exercise on Cognitive and Brain Functions in Older Adults. Journal of Aging Research,2013, 1-8. doi:10.1155/2013/657508
Blondell, S. J., Hammersley-Mather, R., & Veerman, J. L. (2014). Does physical activity prevent cognitive decline and dementia?: A systematic review and meta-analysis of longitudinal studies. BMC Public Health,14(1). doi:10.1186/1471-2458-14-510
Booth, F. W., Roberts, C. K., & Laye, M. J. (2013). Lack of Exercise Is a Major Cause of Chronic Diseases. Comprehensive Physiology. doi:10.1002/cphy.c110025
Carvalho, A., Cusack, B., Rea, I. M., & Parimon, T.,. (2014). Physical activity and cognitive function in individuals over 60 years of age: a systematic review. Clinical Interventions in Aging, 661. doi:10.2147/cia.s55520
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Gray M., Di Brezzo R., I.L. Fort (2013) The effects of power and strength training on bone mineral density in premenopausal women. J Sports Med Phys Fitness, 53, pp. 428–436
Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99–112, 2014
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Harber VJ, Sutton JR. (1984) Endorphins and exercise. Sports Medicine 1: 154–174, 1984
Hogan, C. L., Mata, J., & Carstensen, L. L. (2013). Exercise holds immediate benefits for affect and cognition in younger and older adults. Psychology and Aging,28(2), 587-594. doi:10.1037/a0032634
Kanazawa, S. (2004). The Savanna Principle. Managerial and Decision Economics,25(1), 41-54. doi:10.1002/mde.1130
Kanazawa, S. (2013). Childhood intelligence and adult obesity. Obesity,21(3), 434-440. doi:10.1002/oby.20018
Kanazawa, S. (2014). Intelligence and obesity. Current Opinion in Endocrinology & Diabetes and Obesity,21(5), 339-344. doi:10.1097/med.0000000000000091
Krebs, J. R. (2009). The gourmet ape: evolution and human food preferences. American Journal of Clinical Nutrition,90(3). doi:10.3945/ajcn.2009.27462b
Lake, A., & Townshend, T. (2006). Obesogenic environments: exploring the built and food environments. The Journal of the Royal Society for the Promotion of Health,126(6), 262-267. doi:10.1177/1466424006070487
Layne, J. E., & Nelson, M. E. (1999). The effects of progressive resistance training on bone density: a review. Medicine & Science in Sports & Exercise,31(1), 25-30. doi:10.1097/00005768-199901000-00006
Kirk-Sanchez, N., & Mcgough, E. (2014). Physical exercise and cognitive performance in the elderly: current perspectives. Clinical Interventions in Aging, 51. doi:10.2147/cia.s39506
Ogoh, S., Tsukamoto, H., Hirasawa, A., Hasegawa, H., Hirose, N., & Hashimoto, T. (2014). The effect of changes in cerebral blood flow on cognitive function during exercise. Physiological Reports,2(9). doi:10.14814/phy2.12163
Olshansky, S. J., Passaro, D. J., Hershow, R. C., Layden, J., Carnes, B. A., Brody, J., . . . Ludwig, D. S. (2005). A Potential Decline in Life Expectancy in the United States in the 21st Century. New England Journal of Medicine,352(11), 1138-1145. doi:10.1056/nejmsr043743
Paillard, T. (2015). Preventive effects of regular physical exercise against cognitive decline and the risk of dementia with age advancement. Sports Medicine – Open,1(1). doi:10.1186/s40798-015-0016-x
Querido, J. S., & Sheel, A. W. (2007). Regulation of Cerebral Blood Flow During Exercise. Sports Medicine,37(9), 765-782. doi:10.2165/00007256-200737090-00002
Salmon, P. (2001). Effects of physical exercise on anxiety, depression, and sensitivity to stress. Clinical Psychology Review,21(1), 33-61. doi:10.1016/s0272-7358(99)00032-x
Willie, C. K., & Ainslie, P. N. (2011). Cool head, hot brain: cerebral blood flow distribution during exercise. The Journal of Physiology,589(11), 2657-2658. doi:10.1113/jphysiol.2011.209668
Much has been written in the scientific literature on our brain size increase, which has doubled in the timespan of about 3 million years. It is assumed that our brains became bigger so we could become smarter. However, recent data shows that the amount of blood our brains use dramatically increased over the course of human evolution—the amount of blood our brains use increased some 600 percent over the course of human evolution, substantially more than our brain size increase (350 percent).
Seymour, Bosiocic, and Snelling (2016) showed that while there was a 3.5-fold increase in brain size while there was a 6-fold increase in total cerebral blood flow rate. This is due to increased interneuron connectivity, synaptic activity and cognitive function which all depend on the cerebral metabolic rate. This is yet another reason why cooking was so important during our brain evolution. If the brain has a higher metabolic rate, only a high-quality diet will allow it to function. This can only occur if and only if there is a high-quality diet in the first place.
The metabolic intensity of cerebral tissue in our lineage could only be satisfied by a high-quality cooked diet. Clearly, the evolution of the human brain most always goes back to nutrition and the quality of the human diet. Without erectus’ control of fire around 1.5 mya, our brains wouldn’t have been able to grow this big, nor would we have the cerebral blood flow we eventually had. The below picture is figure 1 from the paper. The left slide is Australopithecus Afarensis, the middle is a Neanderthal, and the right is archaic Homo Sapiens.
They measured the lumen radius of the internal carotid arteries and were able to deduce that there were large changes in cerebral blood flow in hominin evolution due to the increasing size of the ICAs. Arterial size, blood flow rate and metabolic rate are tightly related. So if there are bigger ICAs, then that hominin had more blood flow to feed a bigger brain. This is clear evidence that as our brain size increased that we needed more blood to feed our growing brain.
Kilroy et al (2013) hypothesize that due to widespread anatomical differences in the anterior cingulate cortex (ACC), PFC and insula and subcortical cortices, those regions must be a “central node of the brain’s network underlying individual differences in intellectual development throughout childhood and adolescence.” Cerebral blood flow in the subgenual/ACC correlates the highest with IQ. They also showed that it’s possible to delineate “where CBF is modulated by IQ.” More blood flow in these regions means a higher IQ. Since the ICAs grew larger over the course of hominin brain evolution to increase intelligence, it’s no surprise that more blood flow to certain parts of the brain is related to higher intelligence in children and adolescents.
Even CBF at rest is correlated with higher intelligence and creativity (Takeuchi et al, 2011). They showed that gray and white matter in the brain is correlated with CBF at rest and significantly and positively with psychometric intelligence. Further, the Raven’s Advanced Progressive Matrices (RAPM) and scores on the creativity test that were administered to the cohort correlated positively with white matter and cerebral blood flow. They also noticed that there was an association between negative mood and increased cerebral blood flow. Grey and white matter CBF at rest were both correlated with the RAPM and the creativity test administered. This is yet more evidence that blood flow to certain parts of the brain dictates intelligence (and most likely individual differences in intelligence as well).
The more vampiric a brain is (especially in certain regions), the higher one’s intelligence will be, on average. By looking back at the fossil skulls of our hominin ancestors and the radius of the ICA, we can infer that as hominin evolution ‘progressed’ through time, the ICA radius increased which meant increased blood flow to the brain. This is directly related to brain metabolism and could only be afforded with a high-quality diet which started with the advent of tool-making and the use of fire to cook by erectus. Cerebral blood flood in the anterior cingulate cortex is significantly and positively correlated with IQ. CBF at rest is also correlated with IQ and certain regions of the brain. This shows that a brain with a higher metabolic rate will be, on average, more intelligent than a brain that has a lower one. The current data on intelligence and CBF points to increased blood flow in certain parts of the brain is related to higher levels of intelligence. This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with more cerebral blood flow due to larger arteries and a higher metabolic rate.
This does make sense, as our blood flow to the brain increased by 600 percent over the course of human evolution. So, in a way, we can say that along with our brain size increasing for expertise capacity (which was most definitely needed over the course of hominin evolution) (Skoyles, 2009) along with the need for more blood to the brain to increase intelligence (as blood will also shuttle oxygen to the brain). This is yet another reason why our not-so-special brains are remarkable compared to the rest of the animal kingdom—the one variable that gives us our cognitive superiority over other animals is the ability to cook and use fire. A lot of our physiologic, anatomic and brain evolution can be explained simply as: no cooking, fire, and meat, no big brains (and as a consequence, everything you see around you today would not be here), and the only thing that can drive such a metabolically demanding brain is cooking and eating high-quality foods. The outstanding number of neurons crowded into our cerebral cortex along with much blood our vampiric brain guzzles explains our cognitive superiority over other animals.
Kilroy, E., Yan, L., Wang, D. J., Dapretto, M., Mendez, M. F., Liu, C. Y., & Kim, Y. C. (2011). Relationships between Cerebral Blood Flow and IQ in Typically Developing Children and Adolescents. Journal of Cognitive Science,12(2), 151-170. doi:10.17791/jcs.2011.12.2.151
Seymour, R. S., Bosiocic, V., & Snelling, E. P. (2016). Fossil skulls reveal that blood flow rate to the brain increased faster than brain volume during human evolution. Royal Society Open Science,3(8), 160305. doi:10.1098/rsos.160305
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002)
Takeuchi, H., Taki, Y., Hashizume, H., Sassa, Y., Nagase, T., Nouchi, R., & Kawashima, R. (2011). Cerebral Blood Flow during Rest Associates with General Intelligence and Creativity. PLoS ONE,6(9). doi:10.1371/journal.pone.0025532
Today is Darwin’s 208th birthday and the 158th year since the publication of On the Origin of Species by Means of Natural Selection or the Preservation of Favoured Races in the Struggle of Life. So many people get Darwin wrong. They either have never read his books, or are taking a secondhand account. You can tell who has never read his writings in his own words and who takes snippets of his writings to use them for ideological purposes. I was going to wait until I finished The Descent of Man (Darwin, 1871) until I wrote this article but Darwin Day seems like the best time to do it.
People call themselves ‘Darwinists’ when it’s clear they’ve never read his writings. And due to this, people have large misconceptions on cherry-picked quotes and then use it for their pet ideology—not even attempting to understand the context around what he wrote. One large misquotation you may see around the Internet may put charges of ‘racism’ on Darwin since he ‘believed’ that the ‘higher’ races of Man will one day exterminate the ‘lower’ races. PumpkinPerson is guilty of this, writing in his article Darwin’s terrifying prediction:
Sadly, if HBD is correct, I think there probably will be natural selection favoring higher IQ populations, in fact it’s already happening. In sub-Saharan Africa, we see the more primitive cultures like pygmies and Bushmen losing more and more territory and their populations declining.
Which is based on a (misinterpreted) Darwin quote from his book Descent of Man (1871 (2004): 132-3); note: I have the Barnes n Noble edition):
The great break in the organic chain between man and his nearest allies, which cannot be bridged over by any extinct or living species, has often been advanced as a grave objection to the belief that man is descended from some lower form; but this objection will not appear of much weight to those who, convinced by general reasons, believe in the general principle of evolution. Breaks incessantly occur in all parts of the series, some being wide, sharp and defined, others less so in various degrees; as between the orang and its nearest allies—between the Tarsius and the other Lemuridae—between the elephant and in a more striking manner between the Ornithorhynchus or Echidna, and other mammals.
But all these breaks depend merely on the number of related forms which have become extinct. At some future period, not very distant as measured by centuries, the civilised races of man will almost certainly exterminate and replace throughout the world the savage races. At the same time the anthropomorphous apes, as Professor Schaaffhausen has remarked, will no doubt be exterminated. The break will then be rendered wider, for it will intervene between man in a more civilised state, as we may hope, than the Caucasian, and some ape as low as a baboon, instead of as at present between the negro or Australian and the gorilla.
This is the big quote. The quote that supposedly what paints Darwin as a ‘racist’ and one of the many, many instances of quote-mining from Creationists attempting to discredit his theory of evolution through natural selection. But here’s the thing that people fail to realize: without the rest of the context, you won’t know what he’s saying because the very next paragraph writes (pg 132):
With respect to the absence of fossil remains, serving to connect man with his ape-like progenitors, no one will lay much stress on this fact who reads Sir C. Lyell’s discussion, where he shows that in all the vertebrate classes the discovery of fossil remains has been a very slow and fortuitous process. Nor should it be forgotten that those regions which are the most likely to afford remains connecting man with some extinct ape-like creature, have not as yet been searched by geologists.
So, the whole quote taken in context, it seems he was defending his theory showing that even though no there was an “absence of fossil remains” connecting us to our apelike ancestors.
This book was written 12 years after On the Origin, so knowing that and then seeing the rest of the omitted context behind the controversial quote (and, of course, how Creationists quote-mine and attempt to twist and turn words), what do you think he was saying? To me, it looks like he was defending his theory and addressing critics who said that the fossil record does not support his claims. In fact, Darwin and other Naturalists of the time didn’t separate culture and biology and thus used a blend of both. Darwin was simply observing that a slight advantage between races of men would, after time, lead to the creation of a new species. You’d have to have actually read his books to know that, though.
PP’s other post on Darwin, Did Darwin believe in HBD? he writes (referring to the previous quote-mine):
What it looks like is Darwin describing an evolutionary hierarchy: Caucasian > negro/Australoid > gorilla > baboon.
If you’re looking for something, you’re going to find it. Complete misrepresentation of Darwin’s words, and just reading Descent of Man will let you know how grossly incorrect this interpretation really is.
Darwin only meant that Caucasians would replace savage races because of their cultural superiority; biological superiority had nothing to do with it. And are we also supposed to believe that Darwin’s predicted demise of gorillas was also for cultural, not biological reasons?
PP, read the whole context and tell me if that’s how you still interpret it. It is worth noting that the quotes are taken from a part of the book that has the subsection: On the Birthplace and Antiquity of Man, which lends more credence to the fact that he was defending his theory from detractors (due to the names he brought up and his prose, in context) who needed to see ‘transitional’ fossils between ape and man.
Further, since PP is using a Creationist quotation, then a Creationist rebuttal is apt here:
First of all, Darwin is making a technical argument as to the “reality” of species, particularly Homo sapiens in this case, and why there should still be apparently distinct species, if all the different forms of life are related by common descent through incremental small changes. His answer is that competition against those forms with some, even small, advantage tends to eliminate closely related forms, giving rise to an apparent “gap” between the remaining forms. Whether or not Darwin was right about that is irrelevant to the use of this quote mine, of course, since that is part of the context that the creationists using it have assiduously removed.
Irony aside that an atheist is using a Creationist quote-mine to prove biological differences, this shows how people who’ve never read his writing can misinterpret what he really meant.
Darwin was also a huge abolitionist, which is never brought up in these discussions. He argued, for his whole life, that slavery should be abolished. He also came from an extremely abolitionist family, so any charges of ‘racism’ to Darwin seem pretty far off the mark.
According to liberals, Darwin only meant that Caucasians would replace savage races because of their cultural superiority; biological superiority had nothing to do with it. And are we also supposed to believe that Darwin’s predicted demise of gorillas was also for cultural, not biological reasons?
According to people that know what they’re talking about, Darwin meant that closely related organisms even will a small advantage will replace the other, and that will give rise to a ‘gap’ between organisms. Learn the context behind the whole quote, instead of what Creationists quote-mine. And biological superiority doesn’t exist.
Never mind that Darwin’s theory of natural selection was actually based on biology, not culture.
Can natural selection NOT occur because of cultural differences? Say, two genetically similar populations and one has the native culture and the other with a new, alien culture and they have to use it to adapt to a new environment. Would that be an example of culture and its effect on natural selection?
Never mind that Darwin’s own cousin (Francis Galton) was the father of HBD.
Nothing to do with Darwin himself.
Never mind that Darwin’s own book on natural selection was subtitled The Preservation of Favoured Races in the Struggle for Life.
Why let facts get in the way of a convenient rationalization.
Why don’t you tell me?
They just come up with increasingly creative rationalizations to deny the truth, and the effort this takes makes them more and more psychologically invested in denying inconvenient realities.
People who quote Darwin should most definitely read his works, as if they’re quoting him—especially in these contexts—they should really know the whole context behind the quote and not rely on a Creationist quote-mine which is easily dismantled.
And the way it’s going now, the savage races are outbreeding the civilized races—so how do you see (your interpretation of) Darwin’s theory coming to pass? How will your race war fantasy with each of the macro-races genociding the rest of the ethnies in their group and form one ethnicitu of that racial group? PP believes that eventually it’ll be Ashkenazi Jews vs. East Asians for East Asia. Except Ashkenazi Jews frequently breed with gentiles, and in 100 years there will be very few Ashkenazi Jews left. Japan is having a huge population decline, which is partly biological and partly cultural/environmental in nature. One of the so-called ‘most evolved’ ethnies isn’t able to reign superior over the rest of the inferior ethnies/races due to low birthrates? As I said last night: civilization is dysgenic and leads to low birth rates. So how will the civilized races exterminate the savage races, if the civilized races hardly breed because they get too civilized?
PumpkinPerson’s most recent article Are muscular guys genetically inferior? is a joke. He makes huge assumptions and attempts to this ‘social experiment’ as evidence that women find ‘nerds’ more attractive. The logic here is that since East Asians are the ‘most evolved’ race and (in his world) they have the least testosterone along with the highest intelligence, that this is some kind of apex of human evolution. However the conclusions he makes off of this one video are very erroneous and I will explain why.
They are simply genetically inferior because the muscular body type branched off the evolutionary tree pre-maturely.
…No idea what he’s talking about. No source that the ‘muscular body type branched off the evolutionary tree prematurely.’ This is just an assumption because Africans supposedly have higher testosterone than both Europeans and East Asians, except East Asians have the highest testosterone out of all of all three traditional races, not Africans.
After watching this video I feel like starving my muscles off (not that I recommend that).
Good luck with that.
I realize not everyone agrees with the progressive model of evolution, but real scientists do. For example, check out this phys.org article:
This article has nothing to do with progressive evolution at all. In fact, this article is basically a summary of Full House (Gould, 1996) in which Gould argues that since life began at the left wall of complexity—where no organism can get simpler—that a right-tail distribution of complexity was inevitable. I have covered this here. This is not evidence for progressive evolution. It is, in fact, the opposite. He’s never read Gould’s books so he wouldn’t know that.
Now, PP’s contention that women find nerds more attractive has no basis. When I think of a ‘nerd’, I think of a scrawny pencil-neck, buck teeth, person with thick-rimmed black glasses. This, obviously, isn’t true. If it were, then why do East Asians—Japan specifically—have the lowest birthrates? Of course, social factors have a lot to do with it—birthrates decline in developed countries (Nargund, 2009; Sinding, 2009), as well as genetic ones (Harris and Nielson, 2016). So, clearly, the more intelligent, more developed countries don’t have more children, which then, of course implies that either higher IQ people are less desirable from a reproductive point of view (plausible), or they forgo having children until around 28 years of age (Lange, Rinderu and Bushman, 2016). Whatever the case may be, those with higher IQs do not conceive as many children as those with lower IQs, signifying something about their fitness aspects.
Further, women, evolutionarily speaking, sexually selected men for high levels of testosterone, which leads to bigger muscles, more defined facial features, higher levels of aggression (good for protecting genetic interests) and so on. The fact that some people may think that nerds have better prospects than non-nerds, evolutionarily speaking, had no basis in reality and for one to believe as much, it has to be driven by ideology.
Dixson et al (2010) showed that women prefer men with the mesomorphic somatype and ‘average’ body type, then prefer ectomorphs (a skinnier body type) and finally endomorph (a heavier build) ranging from most attractive to least. This study shows that, at least when it comes to European females, they prefer mesomorphic somatypes, which, more often than not, one who is over 6 feet tall will have. Does that seem like a ‘nerd’ to you? I don’t think so. Someone who has the potential ability to control a room with his presence doesn’t seem like a nerd to me. These are the same people who are CEOs.
Journalist Malcolm Gladwell showed that on average, CEOs averaged just under 6 foot tall. Since the average American is 5 foot 9, the average CEO has a three-inch height advantage over the average man in America. However, when looking at those who are 6 feet tall and up, for average Joe the percentage is a paltry 3.9 percent while, in Gladwell’s sample, 30 percent were over 6’2″. So, Gladwell states, the lack of minorities and women in high positions has a plausible explanation: height. Men are, on average taller than women. Tall men earn more money than their shorter counterparts. Taller children also perform better on cognitive tests, taller men earn more money in Mexico, and taller children do better on learning tests in India (Lawson and Spears, 2016).
Women want taller men more than men want taller women (Stulp, Buunk, and Pollet, 2012). Tall men are also more likely to have a mesomorphic somatype. Those somatypes are seen as the most attractive. Does that seem like a nerd somatype to you? An athletic somatype? On the other hand, women aren’t attracted to short men (Nettle, 2002). East Asians—the so-called ‘most evolved race’—are the shortest race. Doesn’t look too good for them.
Furthermore, while East Asian men see themselves as attractive and dateable, they don’t believe society sees it that way. Forty-six percent of the sample said they could recall one instance where they hear someone state that they do not date Asian men, while eleven percent of Asian men have heard it at least six times. For Okcupid’s 2009 race/dating data, 18 percent of Asian women (3,381 yes) would date someone of their own background/skin color while 82 percent (17,227) wouldn’t! So much for the ‘most evolved’ race having dating prospects in their own race. East Asian men said yes to the question at a rate of 24 percent (7,965 yes) and no 76 percent of the time (25,358).
To further put this into perspective, white women would said yes to the question at a rate of 54 percent (154,595) and no at a rate of 46 percent (132,497) while white men said yes at a 40/60 yes/no rate (183,360/277,827 respectively). In total, 45 percent of whites would prefer to date someone of their skin color/ethnicity while 55 percent wouldn’t (337,955/410,324) while non-whites said yes to the question 20 percent of the time while they said no 80 percent of the time (56,080/222,484).
A 2014 follow-up found the same thing, however with Asian women showing some positive ratings toward Asian males (while all races of men didn’t find black women particularly attractive). However, Asian men were seen as the least attractive throughout the whole sample. Asian males are also seen as less attractive than males of other races (Fisman et al, 2008). In their sample, they found even after running regressions that Asian women found white, black, and ‘Hispanic’ men. They also show that even Asian men find white, black and ‘Hispanic’ females more attractive than Asian females.
In sum, PP’s contentions and reaches in his article are wrong. ‘Nerds’ (in the way I’m defining the word) are not more successful than the alpha CEOs who are over 6’2”. PP seems to have an aversion to testosterone (believes that it is the cause for racial differences in prostate cancer differences, but vitamin D deficiencies are a more likely culprit). East Asian men—the so-called ‘most evolved’ men of the ‘most evolved’ race do not fair well in terms of physical attractiveness, and this may be a reason why the Japanese birthrate is declining, with the average Japanese woman having only one child during her lifetime (Nomura and Koizumi, 2016). PP’s theory makes no sense, because women favor mesomorphic somatypes. Mesomorphs are more likely to be CEOs of 500 companies, more likely to be more cognitively adept and make more money than their shorter counterparts. Making evolutionary theories off of one (obviously fake) ‘social experiment’ is ridiculous. East Asian men, the so-called ‘most evolved man’ fall short in the dating game, due to being seen as less attractive.
Dixson, B. J., Dixson, A. F., Bishop, P. J., & Parish, A. (2009). Human Physique and Sexual Attractiveness in Men and Women: A New Zealand–U.S. Comparative Study. Archives of Sexual Behavior,39(3), 798-806. doi:10.1007/s10508-008-9441-y
Fisman, R. J., Iyengar, S. S., Kamenica, E., & Simonson, I. (2008) (n.d.). Racial Preferences in Dating: Evidence from a Speed Dating Experiment. SSRN Electronic Journal. doi:10.2139/ssrn.610589
Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.
Harris, K., & Nielsen, R. (2016). The Genetic Cost of Neanderthal Introgression. Genetics, 2016 doi:10.1101/030387
Lange, P. A., Rinderu, M. I., & Bushman, B. J. (2016). Aggression and Violence Around the World: A Model of CLimate, Aggression, and Self-control in Humans (CLASH). Behavioral and Brain Sciences, 1-63. doi:10.1017/s0140525x16000406
Nargund G. (2009) Declining birth rate in Developed Countries: A radical policy re-think is required. F.V & V in ObGyn. 2009;1:191-3
Nettle, D. (2002). Women’s height, reproductive success and the evolution of sexual dimorphism in modern humans. Proceedings of the Royal Society B: Biological Sciences,269(1503), 1919-1923. doi:10.1098/rspb.2002.2111
Nomura, K., & Koizumi, A. (2016). Strategy against aging society with declining birthrate in Japan. Industrial Health INDUSTRIAL HEALTH,54(6), 477-479. doi:10.2486/indhealth.54-477
Sinding S.(2009) Population, poverty and economic development. Phil. Trans. R. Soc. B 364.
Stulp, G., Buunk, A. P., & Pollet, T. V. (2013). Women want taller men more than men want shorter women. Personality and Individual Differences,54(8), 877-883. doi:10.1016/j.paid.2012.12.019
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).
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.
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.
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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.
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I just came across this video on YouTube published yesterday called “White people are not 100% human (Race differences) (I.Q debunked)“, with, of course, outrageous claims (the usual from Afrocentrists). I already left a comment proving his nonsense incorrect, but I thought I’d further expound on it here.
His first ‘evidence’ that whites aren’t 100 percent human is showing some individuals who are born with tails. Outliers are meaningless, of course. The cause of the human tail is due to the unsuccessful inhibition of the Wnt3-a gene. When this gene isn’t successful in signaling the cell death of the tail in early embryonic development, a person is then born with a small vestigial tail. This doesn’t prove anything.
His next assertion is that since “94 percent of whites test positive for Rh blood type” and that “as a result, they are born with a tail”, then whites must have interbred with rhesus monkeys in the past. This is ridiculous. This blood type was named in error. The book Blood Groups and Red Cell Antigens sums it up nicely:
The Rh blood group is one of the most complex blood groups known in humans. From its discovery 60 years ago where it was named (in error) after the Rhesus monkey, it has become second in importance only to the ABO blood group in the field of transfusion medicine. It has remained of primary importance in obstetrics, being the main cause of hemolytic disease of the newborn (HDN).
It was wrongly thought that the agglutinating antibodies produced in the mother’s serum in response to her husbands RBCs were the same specificity as antibodies produced in various animals’ serum in response to RBCs from the Rhesus monkey. In error, the paternal antigen was named the Rhesus factor. By the time it was discovered that the mother’s antibodies were produced against a different antigen, the rhesus blood group terminology was being widely used. Therefore, instead of changing the name, it was abbreviated to the Rh blood group.
As you can see, this is another ridiculous and easily debunked claim. One only needs to do a bit of non-biased reading into something to get the truth, which some people are not capable of.
What he says next, I don’t really have a problem with. He just shows articles stating that Neanderthals had big brains to control their bodies and that they had a larger, elongated visual cortex. However, there is archeological evidence that our cognitive superiority over Neanderthals is a myth (Villa and Roebroeks, 2014). What he shows in this section is the truest thing he’ll say, though.
Then he shows how African immigrants to America have a higher educational achievement than whites and immigrant East Asians. However, it’s clear he’s not heard of super-selection. The people with the means to leave will, and, most likely, those with the means are the more intelligent ones in the group. We also can’t forget about ‘preferential treatment’, AKA Affirmative Action.
The concept of ‘multiple intelligences’ is then brought up. The originator of the theory, Howard Gardner, rejects general intelligence, dismisses factor analysis, doesn’t defend his theory with quantitative data, instead, drawing on anthropology to zoology findings for his claims, being completely devoid of any psychometric or quantitative data (Herrnstein and Murray, 1994: 18). The Alternative Hypothesis also has a thorough debunking of this claim.
He then makes the claim that hereditarians assume that environment/experience play no factor in performance on IQ tests/life success. We know that both the individual heritability is 80/20 genetics and environment, with the black-white gap being the same (Rushton and Jensen 2005: 279). Another easily refuted claim.
The term ‘inferior’ is brought up due to whites’ supposed ‘inferiority’, though we know that terms such as those have no basis in evolutionary biology.
He claims that a black man named Jesse Russel invented the cell phone, when in reality a white man named Martin Cooper did. He claims that Lewis Latimer invented the filament lightbulb, when a man named Joseph Swan obtained the patent in the UK in 1860. Of course, individual outliers are meaningless to group success, as they don’t reflect the group average as a whole, so these discussions are meaningless.
He finally claims that the “black Moors civilized Europe”. Europeans didn’t need to “be civilized”, I guess people don’t understand that empires/kingdoms rise and fall and go through highs and lows. That doesn’t stop people from pushing a narrative, though. Further, the Moors were not black. People love attempting to create their own fantasy history in which their biases are a reality.
I don’t know why people have to make these idiotic and easily refuted videos. Lies that push people further from the truth of racial differences, genetics, and history as a whole. Biases such as these just cloud people’s minds to the truth, and when the truth is shown to them, refuting their biases and twisting of history, genetics, and IQ, they then look at it as an attack on what they deem to be true despite all of the conflicting, non-biased evidence shown to them. Afrocentric loons need to be refuted, lest people believe their lies, misconceptions and twistings of history.
What gave us the ability to become the apes that took over the world comes down to three things: bipedalism, tool-making, and fire use and acquisition. Those three things catapulted our evolution and brain size (number of neurons) and made it possible for us to be human. The cause of our extraordinary cognitive abilities is the number of neurons in our brain in total—16 billion in all. The only thing that could power a brain so energy-demanding is a diet of cooked meat and other foods. This acts as a predigestion outside of the body so more nutrients can get extracted more efficiently, to power a growing brain due to other selective pressures. Clearly, without cooking, our brains we wouldn’t have the cognitive capacity to take over the world.
In 2001 a huge finding was made in Africa, that of an ape with the beginnings of a bipedal pelvis. Soon after, footprints were discovered where the skeleton was found. A huge debate broke out, with researchers wondering how this new finding fit in with our evolution. Since Lucy had the beginnings of a bipedal pelvis, this conserved about 75 percent more energy than walking on all fours did (Sockol, Raichlen, and Pontzer, 2007). Since the human brain is our most costly organ, the advent of bipedalism freed up an immense amount of energy to power our soon to be big brains.
After the advent of bipedalism, we could then manipulate our environment which called for the need for tools. To have the ability to make tools—and make them efficiently—our ancestors needed to have hands and opposable thumbs. Since we are primates just like them, we just happen to have this evolutionary trait. To create a usable stone tool for the right situation, one needed a certain expertise in making that tool. There is evidence that our brain size increased since we needed the expertise to survive in our ancestral past (Skoyles, 2007).
Soon after, our ancestor Homo erectus appeared on the scene. The fossil record shows that our brain size really began to increase around 2 million years ago, (Herculano-Houzel, 2016). What could have driven such a rapid increase in brain size? The advent of cooking. Herculano-Houzel (2016) defines cooking as things cooked with fire, as well as foodstuffs mashed with the stone tools we could now create with our newly freed hands. After these two discoveries, brain size then nearly doubled in size. However, when the neuronal composition of the brain is looked at, it has the number of neurons expected for a brain its size (Herculano-Houzel, 2009). The human brain is not special in its neuronal composition.
Erectus began controlling fire between 1-1.5 mya (Berna et al, 2012). The use of fire softened food, making it easier to chew, decreasing our jaw muscles and size of our teeth which also allowed for our big brains with large amount of cerebral neurons—16 billion in all, the most out of any animal in the animal kingdom, and is the cause of our superior cognitive abilities (Herculano-Houzel, 2016).
Since the human brain is a primate brain, it has some key features that aren’t available in other brains. The most important being that we have the most neurons crowded into our cerebral cortex than other animals. That is the cause for our cognitive superiority over other animals, but not Neanderthals (Villa and Roebroeks, 2014). There is anthropological evidence that our so-called cognitive superiority over the Neanderthals may be a myth, since they discovered no data inferring that we had any ‘superiority’ over Neanderthals in terms of technology, social structure or cognitively.
Without our ability to control and create fire, starting with erectus (Berna et al, 2012), our brains wouldn’t have had the ability to power such a large brain, and thus our brains would have stayed erectus-sized. We can look at the evolution of great apes’ brains (Herculano-Houzel and Kaas, 2011) and say, with confidence, that if our hominin ancestors never would have controlled fire and passed down the useful skill down through the generations then we would not be here today. Looking at it in this way, we can thank the beginnings of cultural transference and acquisition for a large part of the reason why we are here today (mass extinctions and decimations aside). If we would have continued to eat our plant-based diet than our brains would have stayed around 600-800 cc, a size with nowhere near enough neurons for our outstanding cognitive abilities. So, Stephen Jay Gould may be on his way to vindication, as he wrote in his book Full House (1996): “We have no evidence that the modal form of human bodies or brains has changed at all in the past 100,000 years—a standard phenomenon of stasis for successful and widespread species, and not (as popularly misconceived) an odd exception to an expectation of continuous and progressive change.” There is now some evidence to corroborate his theorizing.
When talking about how we evolved to become the ape that took over the world, three things cannot be overlooked: 1) Bipedalism. We know that Lucy was the first hominin to have a pelvis close to our modern one (Harcourt-Smith and Aiello, 2004); 2) we could now stand upright, acquiring kcal was easier and more efficient (Lieberman, 2013); and 3) walking bipedally conserves 75 percent more energy compared to knuckle-walking (Sockol, Raichlen, and Pontzer, 2007). Bipedalism then freed our hands so we could use tools (Marzke, 2011). Furthermore, there are biomechanical reasons for the acquisition of bipedalism: one main factor being that every development of typical human morphology can be explained as adaptations to conserve energy walking long distances (Preuschoft, 2004). Bipedal walking may be one of the most important events in our evolution—for without that, every other great thing you see around you today would not be here since we then would not have the ability to manipulate the environment in which we live.
Just like our capacity for expertise may have increased our brain size, there is evidence that tool making increased our brain size as well (Stout et al, 2015). So this further increased our brain size, and when our brains reached around 800 cc with erectus, the ‘discovery’ of fire was able to occur due to the ability expertise capacity gained from becoming experts with creating tools and learning how to survive. This crude form of cooking (mashing/smashing foodstuffs to extract nutrients) allowed our brains to be fueled by the coming wave of nutrients. Furthermore, since the food was already ‘predigested’, so to speak, it was easier to chew. The softened foods then weakened our jaw muscles (Organ et al, 2011). So, in a way, you can say that human evolution is driven by dietary changes (Luca, Perry and Di Rienzo, 2010).
The advent of bipedalism allowed for the ability to make stone tools, which was one of the first cases of cultural transference. To see how important the use of fire was, one only needs to look at gorillas. Metabolic limitations resulting from the number of hours available to feed along with the low caloric yield of raw foods imposed a limitation on brain size for great apes and gorillas—imposing a tradeoff between the total neuronal amount and body size, making them the outlier in terms of body size (Fonseca-Azevedo and Herculano-Houzel, 2012). Thus, you can see the benefits of cultural transference and acquisition, which gave us the ability to have us become the ape that took over the world with our superior cognitive abilities primarily caused by the advent of cultural transference and acquisition beginning with the advent of bipedalism which allowed us to increase our foraging range, allowing us to consume higher-quality kcal to power our soon-to-be big brains, tool-making, and fire-use.
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