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Man the Athlete
5450 words
Homo nerdicus or Homo athleticus? Which name more aptly describes Man? Without many important adaptations incurred throughout our evolutionary history, modern Man as you see him wouldn’t be here today. The most important factor in this being our morphology and anatomy which evolved due to our endurance running, hunting, and scavenging. The topics I will cover today are 1) morphological differences between hominin species and chimpanzees; 2) how Man became athletic and bring up criticisms with the model; 3) the evolution of our aerobic physical ability and brain size; 4) an evolutionary basis for sports; and 5) the role of children’s playing in the evolution of human athleticism.
Morphological differences between Man and Chimp
Substantial evolution in the lineage of Man has occurred since we have split from the last common ancestor (LCA) with chimpanzees between 12.1 and 5.3 mya (Moorjani et al, 2016; Patterson et al, 2006). One of the most immediate differences that jump out at you when watching a human and chimpanzee is such stark differences in morphology, in particular, how we walk (pelvic differences) as well as our arm length relative to our torsos. Though we both evolved to be proficient at abilities that had us become evolutionarily successful in the environments we found ourselves in, one species of primate went on to become the apes the took over the world whereas the chimps continued life as the LCA did (as far as we can tell). The evolution of our athleticism is why we have a lean body with the right morphology for endurance running and associated movements. In fact, the evolution of our brain size hinged on a reduction in our fat depots (Navarette, Schaik, and Isler, 2011).
One of the largest differences you can see between the two species is how we walk. Chimps are “specially adapted for supporting weight on the dorsal aspects of middle phalanges of flexed hand digits II–V” (Tuttle, 1967). Meanwhile, humans are specifically adapted for bipedality due to the change in our pelvis over the course of our evolution (Gruss and Schmitt, 2015). Due to staying more arboreal than venturing on the ground, chimp morphology over the course of the divergence became more and more adapted to life in the trees.
Our modern gait is associated with physiologic and anatomic adaptations throughout our evolution, and are not ‘primitive retentions’ from the LCA (Schmitt, 2003). There are very crucial selective pressures that need to be looked at to see which selection pressures caused us to become athletes. Parts of Austripolithicenes still live on in us today, most notably in our lower leg/foot (Prang, 2015). Further, our ancestor, the famous Lucy had the beginnings of a modern pelvis, which was the beginning of the shift to the more energetically efficient bipedality, one thing that fully separates Man from the rest of the animal kingdom.
Of course, no conversation about human evolution would be complete without talking about Erectus. Analysis of 1.5 million-year-old footprints shows that Erectus was the first to have a humanlike weight transfer while walking, confirming “the presence of an energy-saving longitudinally arched foot in H. Erectus.” (Hatala et al, 2016). We have not yet discovered a full Homo erectus foot, but 1.5 million-year-old footprints found in Kenya show that whatever hominin made those prints had a long, striding gait with a full arch (Steudel-Numbers, 2006; Bennett et al, 2009). The same estimates from Steudel-Numbers (2006) show that Erectus nearly halved its travel costs compared to australopithecines. This is due to a longer stride which was much more Manlike than apelike due to a humanlike pelvis and gluteus maximus (Lieberman et al, 2006).
However, the most important adaptations that Erectus evolved was the ability to keep cool while walking long distances. Loss of hair loss specifically allowed individuals to be active in hot climates without overheating. Our ancestors’ hair loss facilitated sweating (Ruxton and Wilkinson, 2011b), which allowed us to become the proficient hunters—the athletes—that we would become. There is also thermoregulatory evidence that endurance running may have been possible for Homo erectus, but not any other earlier hominin (Ruxton and Wilkinson, 2011a) which was the beginnings of our selection to become athletes. The evidence reviewed in Ruxton and Wilkinson (2011a) shows that once hair loss and sweating ability reached human levels, thermoregulation was then possible under the midday sun.
Moreover, our modern gait and bipedalism is 75 percent less costly than quadrupedal/bipedal walking in chimpanzees (Sockel, Raichlen, and Pontzer, 2007), so this extra energy that was conserved with our physiologic and anatomic adaptations due to bipedalism could have gone towards other pertinent metabolic functions—like fueling a bigger brain (more energy could be used to feed more neurons).
Born to run
Before getting into how we are able to run so efficiently, I need to talk about what made it possible for us to be able to have the energy to sustain our distance running. That one thing is eating cooked food (meat). This one seemingly simple thing is the ‘prime mover’ so to speak, of our success as athletes. Eating cooked food significantly increases the amount of energy obtained during digestion. That we could extract more energy out of cooked food—no matter what type of food it was—can not be overstated. This is what gave us the energy to hunt and scavenge. We are, of course, able to hunt/scavenge while fasted, which is an extremely useful evolutionary adaptation which increases important hormones to have us search for food. The hormones released during a fasted state aid in human physiologic/metabolic functioning allowing one who is searching for food more heightened sensibilities.
We are evolutionarily adapted to be endurance runners. Endurance running is defined as the ability to run more than 5 km using aerobic metabolism (Lieberman and Bramble, 2007). Since we are poor sprinters, the idea is that our body has evolved for walking. However, numerous anatomical changes in our phenotypes in comparison to our chimp ancestors have left us some clues. In the previous section, I talked about physical changes that occurred after Man and Chimp diverged, well those evolutionary changes are why we evolved to be athletic.
Endurance running first evolved, most likely due to scavenging and hunting (Lieberman et al, 2009). Through natural selection—survival of the ‘good enough’, those who had better physiologic and anatomic adaptations could reach the animal carcass before other scavengers like vultures and hyenas could get to it. Over time, this substantially changed how we would look. Numerous physiologic changes in our lineage attest to the evolution of our endurance running. The nuchal ligament, as well as the radius of the semicircular canal is larger in Homo sapiens than in chimpanzees or australopithecines. This stabilizes our head while running—something that our ancestors could not do because they didn’t have a canal our size (Bramble and Lieberman, 2004).
Skeletal evidence that points to our evolution as athletes consists of (but not limited to):
- The Nuchal ligament—stabilizes the head
- Shoulder and head stabilization
- Limb length and mass (we have legs longer than our torsos which decreases energy used)
- Joint surface (we can absorb more shock when our feet hit the ground due to a larger surface area)
- Plantar arch (generates spring for running but not walking)
- Calcaneal tuber and Achilles tendon (shorter tuber length leads to a longer Achilles heel stretch, converting more kinetic energy into elastic energy)
So people who had anatomy closer to this in our evolutionary past had more of a success of getting to that animal carcass, divvying it amongst his family/tribe, ensuring the passage of his genes to the next generation. Man had to be athletic in order to be able to run for long distances. Where this would have come in handy the most would have been the Savanna in our ancestral past. Man could now use persistence hunting—chasing animals in the heat of the day—and kill them when they tired out. The evolutionary adaptation sweating due to the loss of our fur is the only reason this is possible.
One of the most important adaptations for endurance running is thermoregulation. All humans are adapted for long range locomotion rather than speed and to dump rather than retain heat (Lieberman, 2015). This is one of the most important adaptations we evolved that had us become successful endurance runners. We could chase down prey and wait for our prey to become exhausted/overheat and then we would move in for the kill. Of course, intelligence and sociality come into play as we needed to create hunting bands, but without our superior endurance running capabilities—that no other animal in the animal kingdom has—we would have gone down a completely different evolutionary path than the one we went down. Our genome has evolved to support endurance running (Mattson, 2012). Since there is an association between too much sitting and all-cause mortality (Biddle et al, 2016), this is yet more evidence that we evolved to be mobile, not sedentary hominins.
Further evidence that we evolved to be athletic is in our hands. When you think about our hands and how we can manipulate our environments with them—what sets us apart from every other species—then, obviously, in our evolutionary past, those who were more successful would have had a higher chance of reproducing. Aggressive clubbing and throwing are thought to be one of the earliest hominin specializations. If true, then those who could club and throw best would have the best chance of passing their genes to the next generation, thusly selecting for more efficient hands (Young, 2003). While we may have evolved more efficient hands over time warring with other hominins, some are more prone to disk herniation.
Plomp et al (2015) propose the ‘ancestral shape hypothesis’ which is derived from studying bipedalism. They propose that those who are more prone to disk herniation preferentially affects those who have vertebrae “towards the ancestral end of the range of shape variation within H. sapiens and therefore are less well adapted for bipedalism” (Plomp et al, 2015). One of the most amazing things they discovered was that humans with signs of intervertebral disc herniation are “indistinguishable from those of chimpanzees.” Of course, due to this, we should then look towards evolutionary biology in regards to a lot of human ailments (which I have also argued here on dietary evolutionary mismatches as well as on obesity).
Of course there are some naysayers arguing that endurance running didn’t drive our evolution. He wrongly states that it’s about what drove the evolution of our bipedalism; however, what the endurance running hypothesis argues is that there are certain physiologic and anatomic changes that only could have occurred from endurance running. Better endurance runners got selected for over time, leading to novel adaptations that stayed in the gene pool and got selected for. One thing is a larger gluteus maximus. A humanlike pelvis is found in the fossil record as far back as 1.9 mya in Erectus (Lieberman et al, 2006). Furthermore, longer toes had a larger mechanical cost, and were thusly selected against, which also helped in the evolution of our endurance running (Rolian et al, 2009). All in all, there are too many adaptations that our bodies have that can only be explained by adapting to endurance running. Just because we may have gotten to the weaker animals sometimes doesn’t falsify the hypothesis; Man still needed to sweat and persist in the hot mid-day temperatures chasing prey.
Brain size and aerobic physical capacity
When speaking about the increase in our brain size/neuronal count, fire/cooking, the social brain hypothesis, and other theories are brought up first. Erectus had a lot of humanlike qualities, including the ability to control/use fire (Berna et al, 2012), and the appearance of our modern gait/stride which first appeared in Erectus (Steudel-Numbers, 2006; Bennet et al, 2009). This huge change also occurred around the time our lineage began cooking meat/using fire. Without the increased energy from cooking, we wouldn’t be able to hunt for too long. However, we do have very important specific adaptations during a fasted state—the release of hormones such as catecholamines (adrenaline and noradrenaline) which have as react faster to predators/possible prey. Though, a plant-based diet wouldn’t cut it in regards to our daily energy requirements to feed our huge brain with a huge neuronal count (Fonseca-Azevedo and Herculano-Houzel, 2012). Cooked meat is the only way we’d be able to have enough energy required to hunt game.
What kind of an effect did it have on our cranial capacity/evolution?
Four groups of mice selectively bred for high amounts of “voluntary wheel-running”, ran 3 times further than the controls which increased Vo2 max in the mice. Those mice had higher levels of BDNF (Brain Derived Neurotrophic Factor) several days after the experiment concluded as well as also showing greater cell creation in the hippocampus when allowed to run compared to the controls. In two lines of selected mice, the hormone VEGF (Vascular Endothelial Growth Factor) which was correlated with higher muscle capillary density compared to controls. This shows that the evolution of endurance running in mice leads to important hormonal changes which then affected brain growth (Raichlen and Polk, 2012).
The amount of oxygen our brains use increased by 600 percent compared to 350 percent for our brain size over the course of our evolutionary history. This is important. What would cause an increase in oxygen consumption to the brain? Endurance running. There was further selection in our skeleton for endurance running in our morphology such as the semicircular canal radii. The first humanlike semicircular canal radii were found in Erectus (Spoor, Wood, and Zonneveid, 1994). This meant that we had the ability for running and other agile behaviors which were then selected for. There is also little to no activation of the gluteus medius while walking (Lee et al, 2014), implying that it evolved for more efficient endurance running.
Controlling for body mass in humans, extinct hominins and great apes, Raichlen and Polk (2012) found significant positive correlations with encephalization quotient and hindlimb length (0.93), anterior and posterior radii (0.77 and 0.66 respectively), which support the idea that human athletic ability is tied to neurobiological evolution. A man that was a better athlete compared to another would have a better chance to pass on his genes, as physical fitness is a good predictor of biological fitness. Putting this all together, selection improved our aerobic capacity over our evolutionary history by specifically altering signaling systems responsible for metabolism and oxygen intake (BDNF, VEGF, and IGF-1 (insulin-like growth factor 1), responsible for the regulation of growth hormone), which are important for blood flow, increased muscle capillary density, and a larger brain.
Putting this all together, selection improved our aerobic capacity over our evolutionary history by specifically altering signaling systems responsible for metabolism and oxygen intake (BDNF, VEGF, IGF-1). More evidence is needed to corroborate Raichlen and Polk’s (2012) hypothesis. However, with what we know about aerobic capacity and the hormones that drive it and brain size, we can make inferences based on the available data and say, with confidence, that part of our brain evolution was driven by our increased aerobic capacity/morphology, with the catalyst being endurance running. Though with our increased proclivity for athleticism and endurance running, when we became ‘us’, this just shifted the competition and athletic competition—which, hundreds of thousands/millions of years ago would mean life or death, mate or no mate, food or no food.
Clearly, without the evolution of our bipedalism/athleticism we wouldn’t have evolved the brains we have and thus we would be something completely different today.
Sport and evolutionary history
We crowd into arenas to watch people compete against each other in athletic competition. Why? What are the evolutionary reasons behind this? One view is that sport (and along with it playing) was a way for men to get practice hunting game, with playing also affecting children’s ability to assess the strength of others (Lombardo, 2012).
In an evolutionary context, sports developed as a way for men to further develop skills in order to better provide for his family, as well as assessing other men’s physical strength so he can adapt his fighting to how his opponent fights in a possible future situation. Men would then be selected for these advantageous traits. You see people crowd into arenas to watch their favorite sports teams. We are ‘wired’ to like these types of competitions, which then leads to more competition. Since we evolved to be athletes, then it would stand to reason that we would like to watch others be athletic (and hit each other as hard as they can), as a type of modern-day gladiator games.
Better hunters have better reproductive success (Smith, 2004). Further, hunter-gatherer men with lower-pitched voices have more children, while men with higher-pitched voices had higher child mortality rate (Apicella, Feinberg, and Marlowe, 2007). This signals that the H-G men with more children have higher testosterone than others, which then attracts more women to them. Champion athletes, hunters, and warriors all obtain high reproductive success. Women are sexually attracted to certain traits, which events of human athleticism show. However, men follow sports more closely than women (Lombardo, 2012), and for good reason.
Men may watch sports more than women since, in an evolutionary context, they may learn more about potential allies and who to steer clear from because they would get physically dominated. Further, men could watch the actions of others at play and mimic their actions in an attempt to gain higher status with women. Another reason is a man’s character: you can see a man’s character during sports competition and by watching one’s actions closely during, for instance, playing, you can better ascertain their motivations during life or death situations. Men may also derive thrills from watching “idealized men” perform athletic activities. These are consistent with Lombardo’s (2012) male lek hypothesis, “where male physical prowess and the behaviors important in conflict and cooperation are displayed by athletes and evaluated primarily by male, not female, spectators.”
Testosterone changes based on whether one’s favorite sports team wins or loses (Bernhardt et al, 1998). This is important. Testosterone does change under stressful/group situations. Testosterone is also argued to have a role in the search for, and maintenance of social status (Eisenegger, Haushofer, and Fehr, 2011). Testosterone responses to competition in men are also related to facial masculinity (Pound, Penton-Voak, and Surrin, 2009). Male’s physical strength is also signaled through facial characteristics of dominance and masculinity, considered attractive to women (Fink, Neave, and Seydel, 2007). Since testosterone fuels both competition, protectiveness and confidence (Eisenegger et al, 2016), a woman would be attracted to a man’s athleticism/strength, which would then be correlated with his facial structure further signaling biological fitness to possible mates. Testosterone doesn’t cause prostate cancer, as is commonly stated (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Testosterone is a beneficial hormone; you should be worried way more about low T than high T. Further, young men interacting with similar young men increases testosterone while interacting with dissimilar men decreases testosterone (DeSoto et al, 2009). This lends credence to the hypothesis that testosterone raises in response to male-male competition.
Since testosterone is correlated with the above traits, and since athletes have higher testosterone than non-athletes (Wood and Stanton, 2011) then certain types of males would be left in the dust. Athleticism can be looked at as a way to expend excess energy. Those with more excess energy would be more sexually attractive to women and mating opportunities would increase. This is why it’s ridiculous to believe that we evolved to be the ‘nerds’ of the animal kingdom when so much of our evolutionary success has hinged on our athleticism and superior endurance running and other athletic capabilities.
Playing
Child’s play is how children feel out the world in a ‘setting’ in which there are no real-world consequences so they can get a feel for how the world really is. Human babes are born helpless, yet with large heads. Natural selection has lead to large brains to care for children, causing earlier childbirths and making children more helpless, which selected for higher intelligence causing a feedback loop (Piantadosi and Kidd, 2016). They show that across the primate genera, the helplessness of an infant is an extremely strong predictor of adult intelligence.
Indeed, a lot of the crucial shaping of our intelligence and motor capabilities are developed in our infancy and early childhood, which we have over chimpanzees. Blaisdell (2015) defines play as: “an activity that is purposeless in that it tends to be detached from the outcome, is imperfect from the goal-directed form of the activity, and that tends to occur when the individual is in a non-stressed state.” Playing is just a carefree activity that children do to get a feel for the world around them. During this time, skills are honed that, in our ancestral past, allowed us to survive and prosper during times of need (persistence hunting, scavenging, etc).
Anthropological evidence also suggests that the existence of extended childhood in humans adapted to establish the skills and knowledge needed to be a proficient hunter-gatherer. Since there are no real-world outcomes to playing (other than increased/decreased pride), a child can get some physical experience without suffering the real life repercussions of failing. Studies of hunter-gatherers show that play fosters the skills needed to be proficient in tool-making and tool-use, food provisioning, shelter, and predator defense. Play time also hones athletic ability and the brain-body connection so one can be prepared for a stressful situation. In fact, children’s fascination with ‘why’ questions make them ‘little philosophers’, which is an evolutionary adaptation to prepare for possible future outcomes.
Think of play fighting. While play fighting, the outcome has no important real life applications (well, the loser’s pride is hit) and what is occurring is the honing of skills that are useful to survival. During our ancestral evolution, play fighting between brothers could have honed the skills needed during a life our death situation when another band of humans was encountered. As you begin to associate certain movements with certain events, you then become better prepared subconsciously for when novel situations occur. The advantage of an extended childhood with large amounts of play time allow the brain and body to make certain connections between things and when these situations arise during a life or death situation, the brain-body will already have the muscle memory to handle the situation.
Conclusion
Studying our evolution since the divergence between Man and chimp, we can see the types of adaptations that we have incurred over our evolutionary history that have lead to us being specifically adapted for long-term endurance running. The ability to sweat, which, as far as we know began with Erectus, was paramount in our history for thermoregulation. Looking at the evolution of our pelvis, toes, gluteal muscles, heads, shoulders, brains, etc all will point to how they are adapted to a bipedal ape that is born to run—born to be an athlete. Without our athleticism, our intelligence wouldn’t be possible. We have a brain-body connection, our brain isn’t the only thing that drives our body, the two work in concert giving each other information, reacting to familiar and novel stimuli. That’s for another time though.
We didn’t evolve to be Homo nerdicus, we evolved to be Homo athleticus. This can be seen with how exercise has such a huge impact on cognition. We can further see the relationship between our athletic ability and our cognition/brain size. Without the way our evolution happened, Man—along with everything else you see around you—would not be here today. In a survival situation—one in which society completely breaks down—one who has better control over his body and motor functions/capabilities will outlast those who do not. Ultimate and conscious control over our bodies, reacting to stimuli in the environment is fostered in our infancy during our play time with others. Playing allows an individual to get experience in a simulated event, getting important muscle memory to react to future situations. The brain itself, of course, is being molded during playing as well. This just attests to the large part that playing has on cognition, survival skills and athletic ability over our evolutionary history.
Aerobic capacity throughout our evolutionary history beginning with Erectus was paramount for what we have become today. Without the evolution of certain muscles like our gluteus maximus along with certain appendages that gave us the ability to trek/run long distances, we would have lost a very important variable in our brain evolution. Aerobic activity increases blood flow to the brain and so the more successful endurance runners/hunters would increase their biological fitness (as seen in Smith, 2004) and thusly those who were more athletically successful would have more children, increasing selection for important traits for endurance running/athleticism throughout our evolutionary history.
We still play sports today since we love competition. Testosterone fuels the need for competition and sports is the best way to engage in competition in the modern day. Women are much more attracted to men with higher levels of testosterone which in turn means a more masculinized face which signals dominance and testosterone levels during competition. Women are attracted to men with higher levels of testosterone and a more masculinized face. This just so happens to mirror athletes, who have both of these traits. However, being in top physical condition is not enough; an athlete must also have a strong mental background if, for instance, they wish to break world records (Lippi, Favaloro, and Guidi, 2008).
The evolution of human playing ties this together. These sports competitions that we have made hearken back to our evolutionary past and show who would have fared best in the past. When we play, we are feeling our competition and who we can possibly make allies with/watch out for due to their actions during playing. One would also see who he would likely need to avoid and form an alliance with as to not get on his bad side and prevent a loss of status in his band. This is what it really comes down to—loss of status. Higher-status men do have higher levels of testosterone, and by one losing to a more capable person, they show that they aren’t fit to lead and they fall in the social hierarchy.
To fully understand human evolution and how we became ‘us’ we need to understand the evolution of our morphology and how it pertains to things such as our cognition and overall brain size and what advantages/disadvantages it afforded us. Whatever the case may be, it’s clear that we have evolved to be athletic and any change in that makeup will lead to a decrease in quality of life.
Homo athleticus, not Homo nerdicus, best describes Man.
References
Apicella, C. L., Feinberg, D. R., & Marlowe, F. W. (2007). Voice pitch predicts reproductive success in male hunter-gatherers. Biology Letters,3(6), 682-684. doi:10.1098/rsbl.2007.0410
Biddle, S. J., Bennie, J. A., Bauman, A. E., Chau, J. Y., Dunstan, D., Owen, N., . . . Uffelen, J. G. (2016). Too much sitting and all-cause mortality: is there a causal link? BMC Public Health,16(1). doi:10.1186/s12889-016-3307-3
Bennett, M. R., Harris, J. W., Richmond, B. G., Braun, D. R., Mbua, E., Kiura, P., . . . Gonzalez, S. (2009). Early Hominin Foot Morphology Based on 1.5-Million-Year-Old Footprints from Ileret, Kenya. Science,323(5918), 1197-1201. doi:10.1126/science.1168132
Berna, F., Goldberg, P., Horwitz, L. K., Brink, J., Holt, S., Bamford, M., & Chazan, M. (2012). Microstratigraphic evidence of in situ fire in the Acheulean strata of Wonderwerk Cave, Northern Cape province, South Africa. Proceedings of the National Academy of Sciences,109(20). doi:10.1073/pnas.1117620109
Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4
Blaisdell, A. P. (2015). Play as the Foundation of Human Intelligence: The Illuminating Role of Human Brain Evolution and Development and Implications for Education and Child Development. Journal of Evolution and Health,1(1). doi:10.15310/2334-3591.1016
Bramble, D. M., & Lieberman, D. E. (2004). Endurance running and the evolution of Homo. Nature,432(7015), 345-352. doi:10.1038/nature03052
Desoto, M. C., Hitlan, R. T., Deol, R. S., & Mcadams, D. (2010). Testosterone Fluctuations in Young Men: The Difference between Interacting with like and Not-Like others. Evolutionary Psychology,8(2), 147470491000800. doi:10.1177/147470491000800203
Eisenegger, C., Haushofer, J., & Fehr, E. (2011). The role of testosterone in social interaction. Trends in Cognitive Sciences,15(6), 263-271. doi:10.1016/j.tics.2011.04.008
Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011
Fink, B., Neave, N., & Seydel, H. (2006). Male facial appearance signals physical strength to women. American Journal of Human Biology,19(1), 82-87. doi:10.1002/ajhb.20583
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
Gruss, L. T., & Schmitt, D. (2015). The evolution of the human pelvis: changing adaptations to bipedalism, obstetrics and thermoregulation. Philosophical Transactions of the Royal Society B: Biological Sciences,370(1663), 20140063-20140063. doi:10.1098/rstb.2014.0063
Hatala, K. G., Roach, N. T., Ostrofsky, K. R., Wunderlich, R. E., Dingwall, H. L., Villmoare, B. A., . . . Richmond, B. G. (2016). Footprints reveal direct evidence of group behavior and locomotion in Homo erectus. Scientific Reports,6, 28766. doi:10.1038/srep28766
Lee, S., Lee, S., & Jung, J. (2014). Muscle Activity of the Gluteus Medius at Different Gait Speeds. Journal of Physical Therapy Science,26(12), 1915-1917. doi:10.1589/jpts.26.1915
Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255
Lieberman, D. E., & Bramble, D. M. (2007). The Evolution of Marathon Running. Sports Medicine,37(4), 288-290. doi:10.2165/00007256-200737040-00004
Lieberman, D. E., Bramble, D. M., Raichlen, D. A., & Shea, J. J. (2009). Brains, Brawn, and the Evolution of Human Endurance Running Capabilities. Vertebrate Paleobiology and Paleoanthropology The First Humans – Origin and Early Evolution of the Genus Homo, 77-92. doi:10.1007/978-1-4020-9980-9_8
Lieberman, D. E. (2015). Human Locomotion and Heat Loss: An Evolutionary Perspective. Comprehensive Physiology, 99-117. doi:10.1002/cphy.c140011
Lippi, G., Favaloro, E. J., & Guidi, G. C. (2008). The genetic basis of human athletic performance. Why are psychological components so often overlooked? The Journal of Physiology,586(12), 3017-3017. doi:10.1113/jphysiol.2008.155887
Lombardo, M. P. (2012). On the Evolution of Sport. Evolutionary Psychology.
Mattson, M. P. (2012). Evolutionary aspects of human exercise—Born to run purposefully. Ageing Research Reviews,11(3), 347-352. doi:10.1016/j.arr.2012.01.007
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
Moffit, D. M., & Swanik, C. B. (2011). The Association between Athleticism, Prenatal Testosterone, and Finger Length. Journal of Strength and Conditioning Research,25(4), 1085-1088. doi:10.1519/jsc.0b013e3181d4d409
Moorjani, P., Amorim, C. E., Arndt, P. F., & Przeworski, M. (2016). Variation in the molecular clock of primates. doi:10.1101/036434
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
Patterson, N., Richter, D. J., Gnerre, S., Lander, E. S., & Reich, D. (2006). Genetic evidence for complex speciation of humans and chimpanzees. Nature,441(7097), 1103-1108. doi:10.1038/nature04789
Piantadosi, S. T., & Kidd, C. (2016). Extraordinary intelligence and the care of infants. Proceedings of the National Academy of Sciences,113(25), 6874-6879. doi:10.1073/pnas.1506752113
Pound, N., Penton-Voak, I. S., & Surridge, A. K. (2009). Testosterone responses to competition in men are related to facial masculinity. Proceedings of the Royal Society B: Biological Sciences,276(1654), 153-159. doi:10.1098/rspb.2008.0990
Plomp, K. A., Viðarsdóttir, U. S., Weston, D. A., Dobney, K., & Collard, M. (2015). The ancestral shape hypothesis: an evolutionary explanation for the occurrence of intervertebral disc herniation in humans. BMC Evolutionary Biology,15(1). doi:10.1186/s12862-015-0336-y
Prang, T. C. (2015). Rearfoot posture of Australopithecus sediba and the evolution of the hominin longitudinal arch. Scientific Reports,5, 17677. doi:10.1038/srep17677
Raichlen, D. A., & Polk, J. D. (2012). Linking brains and brawn: exercise and the evolution of human neurobiology. Proceedings of the Royal Society B: Biological Sciences,280(1750), 20122250-20122250. doi:10.1098/rspb.2012.2250
Rolian, C., Lieberman, D. E., Hamill, J., Scott, J. W., & Werbel, W. (2009). Walking, running and the evolution of short toes in humans. Journal of Experimental Biology,212(5), 713-721. doi:10.1242/jeb.019885
Ruxton, G. D., & Wilkinson, D. M. (2011). Avoidance of overheating and selection for both hair loss and bipedality in hominins. Proceedings of the National Academy of Sciences,108(52), 20965-20969. doi:10.1073/pnas.1113915108
Ruxton, G. D., & Wilkinson, D. M. (2011). Thermoregulation and endurance running in extinct hominins: Wheeler’s models revisited. Journal of Human Evolution,61(2), 169-175. doi:10.1016/j.jhevol.2011.02.012
Schmitt, D. (2003). Insights into the evolution of human bipedalism from experimental studies of humans and other primates. Journal of Experimental Biology,206(9), 1437-1448. doi:10.1242/jeb.00279
Schulkin, J. (2016). Evolutionary Basis of Human Running and Its Impact on Neural Function. Frontiers in Systems Neuroscience,10. doi:10.3389/fnsys.2016.00059
Smith, E. A. (2004). Why do good hunters have higher reproductive success? Human Nature,15(4), 343-364. doi:10.1007/s12110-004-1013-9
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
Spoor, F., Wood, B., & Zonneveld, F. (1994). Implications of early hominid labyrinthine morphology for evolution of human bipedal locomotion. Nature,369(6482), 645-648. doi:10.1038/369645a0
Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572
Steudel-Numbers, K. L. (2006). Energetics in Homo erectus and other early hominins: The consequences of increased lower-limb length. Journal of Human Evolution,51(5), 445-453. doi:10.1016/j.jhevol.2006.05.001
Tuttle, R. H. (1967). Knuckle-walking and the evolution of hominoid hands. American Journal of Physical Anthropology,26(2), 171-206. doi:10.1002/ajpa.1330260207
Wood, R. I., & Stanton, S. J. (2012). Testosterone and sport: Current perspectives. Hormones and Behavior,61(1), 147-155. doi:10.1016/j.yhbeh.2011.09.010
Young, R. W. (2003). Evolution of the human hand: the role of throwing and clubbing. Journal of Anatomy,202(1), 165-174. doi:10.1046/j.1469-7580.2003.00144.x
Racial Differences in Muscle Fiber Typing Cause Differences in Elite Sporting Competition
1050 words
Blacks are, on average, better at sports than whites. Why? The answer is very simple: muscle fiber typing. Most individuals have an even proportion of muscle fibers, skewing about 5 to 10 percent less on type II fibers. However, when it comes to elite competition, race—and along with it muscle fiber typing—come into play more. Who is stronger? Why? Who is faster? Why? Who is better at endurance running? Why? The answers to these questions lie in muscle fiber typing, somatype, and, of course, grit and determination. Today I will provide yet more evidence for my argument that whites are stronger than blacks.
Muscle fiber typing by race
I’ll be quick here since I’ve covered this extensively.
Blacks have more type II muscle fibers in comparison to whites who have more type I muscle fibers. This difference in fiber typing causes differences in aerobic capacity which lead to higher rates of cardiorespiratory diseases such as type II diabetes, heart disease, and hypertension.
There are two types of muscle fibers with two divisions: Type I and Type II with the divisions being in the slow twitch fiber, further broken down into Type IIa and Type II x. Type I fibers fire slowly and possess greater aerobic metabolic capacity due to higher levels of lipid, myoglobin, mitochondrial and capillary content. Type II fibers, on the other hand, fire faster, have reduced aerobic capacity (and all that comes with it) and are better equipped for anaerobic activity (explosive sports). Type IIa possesses more aerobic potential than IIx, but less anaerobic potential than type I fibers. Some evidence exists showing that it’s possible to train type II fibers to have a similar aerobic capacity to type I, but I don’t really buy that. It is possible to make aerobic capacity similar to the aerobic capacity that type I fibers have, but type II will not be fully like them.
Blacks have more type II fibers while whites have more type I fibers. Type II fibers predispose people to a myriad of cardiometabolic diseases which are also associated with grip strength.
Differences in fiber typing in elite athletes
Now comes the fun part. How do muscle fibers differ between elite athletes? A few studies have been done but, as expected in physiology studies, they have a low n, but they still do show physiologic differences when compared to the control subjects, physiologic differences that were predicted due to what we know about muscle fiber typing.
Type IIa fibers possess more aerobic potential than IIx, therefore, power lifters have a higher proportion of IIa fibers compared to IIx fibers. It should also be noted that powerlifters have the same amount of type I fibers as the general population (Fry et al, 2003a), so knowing this fact, since blacks have a lower proportion of type I muscle fibers as noted in Caeser and Hunter (2015), this explains why there are very few black power lifters: they have the opposite type II fiber type while having less type I fiber.
Furthermore, Olympic lifters also use a higher percentage of type IIa fibers (Fry et al, 2003b). This also explains the lower amount of blacks in weight lifting as well. Fiber types don’t explain everything, but at elite levels, they do mean a lot and looking at the racial variation explains racial differences in elite sporting competition.
Explaining racial differences in sprinting competitions is easy as well. Type IIx fibers combined with the ACTN3 gene=elite human performance (Mills et al, 2001). The gene ACTN3 was discovered to explain explosive power, and it just so happened to vary by race. William Saletan writes:
the relative frequency of the X allele is 0.52 in Asians, 0.42 in whites, 0.27 in African-Americans, and 0.16 in Africans. If you break out the data further, the frequency of the XX genotype is 0.25 in Asians, 0.20 in European whites, 0.13 in African-Americans, and 0.01 in African Bantu. Conversely, the frequency of RR (the genotype for speed and power) is 0.25 in Asians, 0.36 in European whites, 0.60 in African-Americans, and 0.81 in African Bantu. Among Asians, you can expect to find one RR for every XX. Among whites, you can expect nearly two RRs for every XX. Among African-Americans, you can expect more than four RRs for every XX.
This allele is responsible for explosive power. Explosive power is needed to excel in events such as sprinting, football, basketball and other sports where power is needed in short bursts. However, where blacks have an advantage in explosive power sports, the advantage is lost once events like swimming, power lifting (described above), Olympic lifting (differing fiber type) etc.
Conclusion
Racial differences in elite sporting competition come down to a lot of genetic factors, largely influenced by hormones, genes, and muscle fiber typing. Population variation between known fiber typings/hormones/genes that affect certain types of athletic performance explains a lot of the variation within, and especially between populations. Due to anatomical differences, blacks excel at some sports and suffer at others. The same also holds for whites; there is considerable variation in somatype, some somatypes are better for strongman/powerlifting competitions than others. These differences affect the outcomes of elite sporting competition as well.
Blacks have a higher amount of type II fibers, which accounts for a lot of their disease acquisition (Caesar et al, 2015). Due to this physiologic difference, this is why blacks excel at some sports, and not others.
Once again: Blacks are not stronger than whites.
(Note: Click here for discussion on Kenyan distance running.)
References
Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7
Fry, A. C., Webber, J. M., Weiss, L. W., Harber, M. P., Vaczi, M., & Pattison, N. A. (2003). Muscle Fiber Characteristics of Competitive Power Lifters. The Journal of Strength and Conditioning Research,17(2), 402. doi:10.1519/1533-4287(2003)017<0402:mfcocp>2.0.co;2
Fry, A. C., Schilling, B. K., Staron, R. S., Hagerman, F. C., Hikida, R. S., & Thrush, J. T. (2003). Muscle Fiber Characteristics and Performance Correlates of Male Olympic-Style Weightlifters. Journal of Strength and Conditioning Research,17(4), 746-754. doi:10.1519/00124278-200311000-00020
Mills, M., Yang, N., Weinberger, R., Vander Woude, D., Beggs, A., Easteal, S., & North, K. (2001). Differential expression of the actin-binding proteins, alpha-actinin-2 and -3, in different species: implications for the evolution of functional redundancy. Human Molecular Genetics,10(13), 1335-1346. doi:10.1093/hmg/10.13.1335
Racial Differences in Grip Strength
1700 words
Strength differences between the races are of big interest to me. Not only due to the evolutionary perspective, but also due to how it relates to health and disease. Hand grip strength (HGS) in men is a good predictor of: Parkinson’s disease (Roberts et al, 2015); lower cardiovascular health profile (Lawman et al, 2016); Alzheimer’s disease (Buchman et al, 2007) and other chronic diseases in men, not in women (Cheung et al, 2013). HGS also predicts diabetes and hypertension (Mainous 3rd et al, 2015), as well as death from all causes, cardiovascular disease (CVD) and cancer in men (Gale et al, 2006). Due to these associations, the study of HGS in men is well warranted. However, here too, we find racial differences and they just so happen to follow trends and corroborate with other data on the mortality of men with lower grip strength.
Araujo et al (2010) obtained data from the Boston Community Health/Bone (BACH/Bone) Survey which included 1,219 randomly selected black, white and ‘Hispanic’ men to assess lean mass, muscle strength, and physical function. Though out of this sample, 10 men didn’t have a DXA performed and 49 men missing data on lean mass, fat mass and Physical Activity for the Elderly (PASE), which left 1,157 men to be analyzed. These studies, however, leave a lot to be desired in how they measure strength (for the purposes that I’m interested in) but they will have to do, for now. Unlike the bench pressing study I wrote about yesterday in which calipers were used to assess body fat, in this study they measured body fat with the DXA scan to assess lean mass. That way, there won’t be any potential confounds, possibly skewing lean mass/fat comparisons. The age of the cohort ranged from 30 to 79 with a mean age of 48.
Table 1 shows the results of the DXA scan, anthropometric data and lean and fat mass. Blacks’ mean lean mass of 124 pounds (mean weight 193 pounds), ‘Hispanics” lean mass was 114 pounds (mean weight 179 pounds) and whites had a mean lean mass of 122 pounds (mean weight 196 pounds). Blacks had a mean grip strength of 89.826 pounds while ‘Hispanics’ had a mean grip strength of 82.698 pounds and whites had a mean grip strength of 88.528 pounds. Blacks had a higher lean mass index than whites by 5 percent, but had a composite physical function score 20 percent lower than whites.
White men had a 25 percent higher average composite physical functioning score, which, when indexed by lean mass and grip, white men had grips 10 percent stronger. White men also scored higher on physical function and lean mass. White men had lower levels of lean muscle mass than blacks and ‘Hispanics’ after controlling for confounding factors, yet whites were still stronger. Since lean mass is related to strength, blacks and ‘Hispanics’ should have had a stronger grip, yet they didn’t. Why?
The authors stated that the reason was unknown since they didn’t test for muscle quality or strength exerted for each unit of muscle. I have proven that whites, on average, are stronger than blacks. If the it were true that blacks were stronger, which is what you see upon first glance viewing table 1 of Araujo et al (2010), then the black population would have lower rates of morbidity and mortality due to higher levels of strength. The black population doesn’t have lower levels of morbidity or mortality. Therefore blacks are not stronger than whites.
Muscular strength is associated with mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015), so if the strongest race of men has lower incidences of the above diseases mentioned above along with a higher life expectancy, then there is a good chance that muscular strength is a good predictor of disease within and between race and ethnicity as well. Muscular strength is inversely associated with death from all causes and cancer in men even after adjusting for cardiorespiratory factors. The findings from Ruiz et al (2008) are valid for young and old men (aged 20-82), as well as normal and overweight men.
There are clear associations between muscular strength/hand grip strength and mortality. These differences in mortality are also seen in the United States between race. In 2012, the death rate for all cancer combined was 24 percent higher in black men than in white men. Life expectancy is lower for blacks at 72.3 years compared to 76.7 years for white men (American Cancer Society, 2016). As shown above, men with lower levels of muscular strength have a higher risk of mortality.
As I have asserted in the past, blacks have differing muscle fiber typing (type II) on average when compared to whites (who have type I fibers). Type II muscle fibers are associated with a reduced Vo2 max, which has implications for the health of black Americans. Blacks have lower aerobic capacity along with a greater percentage of type II skeletal muscle fiber (Caesar and Hunter, 2015).
Slow twitch fibers fire through aerobic pathways. Fast twitch (Type II) fibers fire through anaerobic pathways and tire quicker than slow twitch. 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.
Differences in muscle fiber typing explain why whites had a stronger grip than non-whites in the BACH/Bone survey. Testing the fiber typings of the three ethnies would have found a higher percentage of type II fibers in blacks, which would account for the lower grip strength despite having higher levels of lean mass when compared to whites.
The apparent ‘paradox’ seen in Araujo et al (2010) is explained by basic physiology. However, in our politically correct society, such differences may be suppressed and thusly people won’t be able to receive the help they need. Race is an extremely useful marker in regards to medicine. By denying average racial differences in numerous anatomical/metabolic/physiologic traits, we deny people the right help they need. Common sense dictates that if such relationships are found, then further research must occur in order to find the cause and a possible solution to the problem.
This study by Araujo et al shows that we need to pay more attention to race when it comes to disease. By denying racial differences we are dooming people to a lower quality of life due to the implicit assumption that we are all the same on the inside (farrrrr from the truth). These average differences in metabolism, anatomy, and physiology do account for some of the variation in disease between race and ethnicity, so this warrants further research. If only we, as a country, can acknowledge racial differences and get people the correct help. Maybe one day we can stop assuming that all races are equal on the inside and when you notice a trend within a particular racial group you find out the cause and whether or not there is any way to ameliorate it.
Muscular strength adds to the protective effect of cardiorespiratory fitness and risk of death in men. That blacks have lower levels of strength than whites, have different muscle fiber typing than whites on average, a lower life expectancy than whites, and higher rates of cancer show that they do not have the physical strength that whites do. What really seals the deal is the fact that blacks have more type II muscle fibers (Caesar and Hunter, 2015). Muscular strength/grip strength is a great predictor of disease in men. Since blacks have lower grip strength yet higher levels of lean mass compared to whites, this show that the difference is due to muscle fiber typing, which, as I have covered in the past, are also associated with cardiometabolic disease and obesity.
Blacks have the highest rate of obesity in America. Looking at obesity rates in America, we see that 69 percent of black men are overweight or obese (remember that black Americans with more African ancestry are less likely to be obese), 71.4 percent of white men are overweight or obese, and 78.6 percent of ‘Hispanic’ men are overweight or obese (Ogden et al, 2016).
Blacks are not stronger than whites. I have compiled enough data to prove that fact. This adds further support for my contention.
References
American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.
Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508
Buchman, A. S., Wilson, R. S., Boyle, P. A., Bienias, J. L., & Bennett, D. A. (2007). Grip Strength and the Risk of Incident Alzheimer’s Disease. Neuroepidemiology,29(1-2), 66-73. doi:10.1159/000109498
Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7
Cheung, C., Nguyen, U. D., Au, E., Tan, K. C., & Kung, A. W. (2013). Association of handgrip strength with chronic diseases and multimorbidity. Age,35(3), 929-941. doi:10.1007/s11357-012-9385-y
Gale, C. R., Martyn, C. N., Cooper, C., & Sayer, A. A. (2006). Grip strength, body composition, and mortality. International Journal of Epidemiology,36(1), 228-235. doi:10.1093/ije/dyl224
Lawman, H. G., Troiano, R. P., Perna, F. M., Wang, C., Fryar, C. D., & Ogden, C. L. (2016). Associations of Relative Handgrip Strength and Cardiovascular Disease Biomarkers in U.S. Adults, 2011–2012. American Journal of Preventive Medicine,50(6), 677-683. doi:10.1016/j.amepre.2015.10.022
Mainous, A. G., Tanner, R. J., Anton, S. D., & Jo, A. (2015). Grip Strength as a Marker of Hypertension and Diabetes in Healthy Weight Adults. American Journal of Preventive Medicine,49(6), 850-858. doi:10.1016/j.amepre.2015.05.025
Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.
Roberts, H. C., Syddall, H. E., Butchart, J. W., Stack, E. L., Cooper, C., & Sayer, A. A. (2015). The Association of Grip Strength With Severity and Duration of Parkinson’s. Neurorehabilitation and Neural Repair,29(9), 889-896. doi:10.1177/1545968315570324
Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439
Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013
Muscular Strength By Gender and Race
2000 words
It’s a known fact that men are stronger, but how much stronger are we really than women? Strength does vary by race as I have covered here extensively. However, I took another look at the only paper that I can find in the literature on black/white strength on the bench press and found one more data point that lends credence to my theory on racial differences in strength.
Strength and gender
Men are stronger than women. No one (sane) denies this. There are evolutionary reasons for this, main reason being, women selected us for higher levels of testosterone, along with differences in somatype. Now, what is not known by the general public is just how much stronger the average man is compared to the average woman.
Miller et al (2008) studied the fiber type and area and strength of the biceps brachii and vastus lateralis in 8 men and 8 women. They were told to do two voluntary tests of strength, using elbow flexion (think biceps curl) and knee extension. (Note: I am assuming they are exercises similar to biceps curls and knee extension, as the authors write that they had custom-made equipment from Global Gym.) They also measured motor unit size, number, and activation during both movements.
The women had 45 percent smaller muscle cross-section area (CSA) in the brachii, 41 percent in the total elbow flexor, 30 percent in the vastus laterus, and 25 percent smaller knee extensors. The last point makes sense, since women have stronger lower bodies compared to their upper bodies (as you can see).
Men were significantly stronger in both upper and lower body strength. In the knee extension, women was 62 and 59 percent of male 1RM and maximal voluntary isometric contraction (MVC) respectively. As for elbow strength, women were 52 percent as strong as men in both 1RM and MVC. Overall, women were 70 and 80 percent as strong as men in the arms and the legs. This is attributed to either men’s bigger fibers or men putting themselves into more physical situations to have bigger fibers to be stronger (…a biological explanation makes more sense). However, no statistical difference between muscle fibers was found between gender, lending credence to the hypothesis that men’s larger fibers are the cause for greater overall upper-body strength.
The cause for less upper-body strength in women is due the distribution of women’s lean tissue being smaller. Women, as can be seen in the study, are stronger in terms of lower limb strength and get substantially weaker when upper-body strength is looked at.
Other studies have shown this stark difference between male and female strength. Men have, on average, 61 percent more total muscle mass than women, 75 percent more arm muscle mass, which translates approximately into a 90 percent greater upper body strength in men. 99.9 percent of females fall below the male mean, meaning that sex accounts for 70 percent of human variation in muscle mass and upper-body strength in humans (Lassek and Gaulin, 2009). Women select men for increased muscular size, which means increased testosterone, but this is hard to maintain so it gets naturally selected against. There is, obviously, a limit to muscle size and how many kcal you can intake and partition enough kcal to your growing muscles. However, women are more attracted to a muscular, mesomorphic phenotype (Dixson et al, 2009) so selection will occur by women for men to have a larger body type due to higher levels of testosterone.
Strength and race
The only study I know of comparing blacks and whites on a big three lift (bench pressing) is by Boyce et al (2014). They followed a sample of 13 white female officers, 17 black female officers, 41 black male officers and 238 white male officers for 12.5 years, assessing bench pressing strength at the beginning and the end of the study. The average age of the sample was 25.1 for the 41 black males and 24.5 for the 237 white males. The average age for the black women was 24.9 and the average for white women was 23.9. This is a longitudinal study, and the methodology is alright, but I see a few holes.
An untrained eye looking at the tables in the study would automatically think that blacks are stronger than whites at the end of the study. At the initial recruitment, the black mean weight was 187 pounds and they benched 210 pounds. They benched 1.2 times their body weight. Whites weighed 180 pounds and benched 185 pounds. They benched 1.02 times their body weight. Black women weighed 130 pounds at initial recruitment and benched 85 pounds, benching .654 times their body weight. White women weighed 127 pounds at initial recruitment and bench 82 pounds, benching .646 times their body weight. Right off the bat, you can see that the difference between black and white women is not significant, but the difference between blacks and whites is.
At the follow-up, the black sample weighed 224 pounds and benched 240 pounds while the whites weighed 205 pounds benching 215 pounds. Looking at this in terms of strength relative to body weight, we see that black males benched 1.07 times their body weight while whites benched 1.04 times their body weight. A very slight difference favoring black males. However, there were more than 5 times the amount of whites in comparison to blacks (41 compared to 238), so I can’t help but wonder if the smaller black sample compared to the white sample may have anything to do with it.
Black women weighed 150 pounds at the follow-up, benching 99 pounds while white women weighed 140 pounds benching 90 pounds. So black women benched .66 times their body weight while white women benched .642 times their body weight.
Another thing we have to look at is black body weight compared to bench press decreased in the 12 years while white body weight compared to bench press was diverging with the black bench press compared to body weight.
Furthermore, this study is anomalous as the both cohorts gained strength into their late 30s (testosterone begins to decline at a rate of 1-2 percent per year at age 25). It is well known in the literature that strength begins to decrease at right around 25 years of age (Keller and Englehardt, 2014).
Another pitfall is that, as they rightly point out, they used skin caliper measuring on the black cohort. It has been argued in the literature that blacks should have a different BMI scale due to differing levels of fat-free body mass (Vickery et al, 1988). Remember that black American men with more African ancestry are less likely to be obese, which is due to levels of fat-free body mass. Since fat-free mass is most likely skewed, I shouldn’t even look at the study. I do believe that black Americans should have their own BMI scale; they’re physiologically different enough from whites—though the differences are small—they lead to important medical outcomes. This is why race most definitely should be implemented into medical research. The authors rightly state that when further research is pursued the DXA scan should be used to assess fat-free body mass.
Unfortunately, the authors did not have access to the heights of the cohort due to an ongoing court case on the department for discrimination based on height. So, unfortunately, this is the only anthropometric value that could not be assessed and is an extremely important variable. Height can be used to infer somatype. Somatype can then be used to infer limb length. Longer limbs increase the ROM, in turn, decreaseing strength. The missing variable of height is a key factor in this study.
Finally, and perhaps most importantly, they assessed the strength of the cohort on a Smith Machine Bench Press.
- The Smith Machine is set on a fixed range of motion; not all people have the same ROM, so assessing strength on a smith machine makes no sense.
- To get into position for the Smith Machine, since the bar path is the same, you need to get in pretty much the same position as everyone else. I don’t need to explain the anatomical reasons why this is a problem in regards to testing a 1RM.
- An Olympic bar weighs 45 pounds, but numerous Smith Machines decreases the weight by 10-20 pounds.
- Since the individual is not able to stabilize the bar due to the machine, the chest, triceps, and biceps are less activated during the Smith Machine lift (Saeterbakken et al, 2011)
Due to all of these things wrong with the study, especially the Smith Machine bench press, it’s hard to actually gauge the true strength of the cohort. Depending on the brand, Smith Machines can decrease the load by 10-30 pounds. Combined with the unnatural, straight-line bar path of the movement, it’s not ideal for a true strength test.
Conclusion
Gender differences in strength have a biological basis (obviously) and are why women shouldn’t be able to serve in the military and transgendered people shouldn’t be able to compete with ‘the gender they feel that they are’ (coming in the future).
The more interesting topic is the one on racial differences in strength. The untrained eye may read that paper and walk away assuming that the average black person is somehow stronger than the average white person. However, this study is anomalous since the cohort gained strength into their 30s when the literature shows otherwise. The biggest problem with the study is the Smith Machine bench press. It is not a natural movement and decreases muscle activation in key areas of the chest and triceps which aid in power while doing a regular bench press. Due to this, and the other problems I pointed out, I can’t accept this study.
Of course, height not being noted is not the fault of the researchers, but more questions would be answered if we knew the heights of the officers—which is an extremely critical variable. White males also gained more lean mass over the course of the study compared to blacks—47 percent and 44 percent respectively—which, as I pointed out, is anomalous.
There is more to HBD than IQ differences. I contend that somatype differences between the races are much more interesting. I will be writing about that more in the future.
Furthermore, for anyone with any basic physiology and anatomy knowledge, they’d know that different leverages affect strength. The races differ in somatype on average and thusly have different leverages. This is one out of many reasons why there are racial differences in strength and elite sports. Leverages and muscle fiber typing.
My points on racial differences in strength still hold; the anthropmetric data backs me up, elite sporting events back me up. My theory as a whole to racial differences in sports is sound, and this study does nothing to make me think twice about it. There are way too many confounds for me to even take it seriously when reevaluating my views on racial differences in strength. This study was garbage to assess absolutely strength due to the numerous things wrong with it. I await a more robust study with actual strength exercises, not one done on an assisted machine.
References
Boyce, R. W., Willett, T. K., Jones, G. R., & Boone, E. L. (2014). Racial Comparisons in Police Officer Bench Press Strength over 12.5 Years. Int J Exerc Sci 7 (2), 140-151.
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
Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. MLTJ. 2013;3(4):346–350.
Lassek, W. D., & Gaulin, S. J. (2009). Costs and benefits of fat-free muscle mass in men: relationship to mating success, dietary requirements, and native immunity. Evolution and Human Behavior,30(5), 322-328. doi:10.1016/j.evolhumbehav.2009.04.002
Miller, A. E., Macdougall, J. D., Tarnopolsky, M. A., & Sale, D. G. (1993). Gender differences in strength and muscle fiber characteristics. European Journal of Applied Physiology and Occupational Physiology,66(3), 254-262. doi:10.1007/bf00235103
Saeterbakken, A. H., Tillaar, R. V., & Fimland, M. S. (2011). A comparison of muscle activity and 1-RM strength of three chest-press exercises with different stability requirements. Journal of Sports Sciences,29(5), 533-538. doi:10.1080/02640414.2010.543916
Vickery SR, Cureton KJ, Collins MA. Prediction of body density from skinfolds in black and white young men. Hum Biol 1988;60:135–49.
Brain Size Increased for Expertise Capacity, not IQ
2000 words
One of the HBD’s supposed biggest findings is that IQ increases as a function of distance from the equator. The theory holds that those groups who experienced colder winters were selected for levels of higher g and they passed on their high IQ genes. Cold winter theory is supposed to explain why some races have higher levels of achievement and IQ than others. However, after a conversation with PumpkinPerson about cold winter theory and tool use, something clicked in my head: the real reason for the increase in brain size in peoples further from the equator wasn’t for IQ, but expertise capacity. I will go through the reasons how and why our brain size increased for the capacity for expertise and not IQ and hopefully put the cold winter theory to rest for good.
Tool complexity/use and brain size
PumpkinPerson is one of the biggest champions of the cold winter theory, writing: “I don’t even understand how one can believe in racially genetic differences in IQ without also believing that cold winters select for higher intelligence because of the survival challenges of keeping warm, building shelter, and hunting large game.” He wrongly assumes that climate theories are the only explanation for racial gaps in intelligence when other theories (such as differing types of sexual selection) could explain the gap just as well. However, since Rushton and Lynn have pushed this theory for 30+ years, it’s still engrained in the minds of some people. It is hard to change your views in the face of contrary data, but for those of my readers who are proponents of cold winters increasing IQ, I hope tonight I can sway you into believing that brain size increased as a function of climate and tool-making, not for IQ.
In his article he cites Richard Lynn (2006: 148), saying:
… hunter-gatherer peoples in tropical and subtropical latitudes such as the Amazon basin and New Guinea typically have between 10 and 20 different tools, whereas those in the colder northern latitudes of Siberia, Alaska, and Greenland have between 25 and 60 different tools. In addition, peoples in cold northern environments make more complex tools, involving the assembly of components, such as hafting a sharp piece of stone or bone onto the end of a spear and fixing a stone axe head onto a timber shaft.
I, of course, don’t doubt that peoples in cold northern environments need more (and complex) tools compared to those in tropical climes. But I look at it from a different point of view.
This is based on the research of Terrence (1983) and his study on time budgeting and hunter-gathering technology. The data does show that the number of tools correlates to latitude, but he leaves out that it also correlates with mobile and immobile and diet. That’s a pretty big factor. Of course, the type of animals around and what you need to do to kill/extract the meat involves a certain type of complex tool. In northern environments, a few more tools are needed to survive, so what? That doesn’t really mean anything. The whole brain-size/IQ latitude cold winter theory can be explained in another way.
Tool use increased our brain size throughout our evolutionary history, so with Arctic peoples living in cold climes where having a bigger brain is advantageous, they already had more neural columns for expertise capacity. The construction of complex tools increased brain size along with the colder climate. If tool use can explain part of the increase in our brain size over 3 million years, why can’t it partly explain why Arctic peoples—who use more (and complex) tools—larger brains over those further from the Arctic? Because brain size increased for expertise capacity, not IQ. Since they had bigger brains they were able to master the creation of complex tools, which further increased their brain size along with colder climates. Those who could make better tools could pass their genes, selecting for bigger brains.
Brain size increased for expertise capacity, not IQ
Table 3.1 in Torrence (1983) makes reference to technounits, a way to gauge the complexity of a particular item (Collard et al, 2011). Those in northerly climes do have tools with higher technounits, however, that’s showing that what is needed to construct the tools is a high capacity for expertise.
Skoyles (1999) posits that brain size increased for expertise capacity, not IQ. Bigger brains cause extreme complications during birth, calling for Caesarian sections (which is driving the evolution of bigger heads), so selection for bigger brains must have been advantageous in another way. Skoyles cites studies showing that microcephalics have brains in the average range of Erectus while having IQs in the normal/above average range. This implies that Erectus could have had IQs in our range, and that selection for bigger heads was caused by something else—the need for expertise.
Even then, the correlation between brain size and IQ cannot be invoked here. A .33-.4 correlation between brain size and IQ still leaves a lot of room for people to have brain sizes in the range of Erectus and still have above average IQs. Assuming a correlation of .51, that leaves 74 percent of the brain size/IQ correlation unexplained. This leaves a lot of room for other explanations for the remaining variance.
So if you think of the implications of Skoyles’ (1999) paper in regards to human races and the quote provided from Lynn (2006), you can look at it as Arctic peoples needed to be able to learn how to make complex tools which required a certain amount of expertise. Acquiring certain types of expertise does lead to certain local changes in the brain due to environmental demands, for instance in racecar drivers (Bernardi et al, 2013) and in taxi drivers in London who were “on The Knowledge” (Maguire et al, 2000). Tool use did cause increases in our brain size in our ancestral past, so the fact that Arctic peoples have bigger brains but lower IQs is explained by brain size being selected for expertise (their expertise to make their numerous tools) and cold climates but cold temperatures do NOT explain intelligence differences between the races.
Expertise
Indeed, there is evidence that ‘chunks’ form in the brain due to certain types of expertise (Gobet and Simon, 1998). In their study, Gobet and Simon showed that Chess masters used significantly more chunks, extending the chunking theory ” to take account of the evidence for large retrieval structures (templates) in long-term memory.” This study is direct evidence for Skoyles’ contention on “informational chunks (Skoyles, 1999) lending credence to the claim that people who master something have more information stored in their ‘chunks’.
Furthermore, high and low skill employees organize their conceptual knowledge about a problem differently (Lamberti and Newsome, 1989). Low-skilled workers performed much faster on the tasks that needed concrete information organization whereas high-skilled workers were better on the more abstract concepts. Overall, both high- and low-skilled workers processed the same information differently. This study has nothing to do with IQ itself, just how high- and low-skilled workers process information differently (which may come down to ‘chunks’ in the brain).
Chase and Simon (1973) show that the amount of information extracted during a memory and perception task is directly related to the amount of time the individual has played chess. They state that chess skill is “reflected in the speed with which chunks are perceived in the perception task and the size of the chunks in the memory task.” Of course, you can’t just throw anyone into a chess game who has never played before—IQ be damned—and expect them to do well. You need to hone your strategy and skill over time by noticing all types of moves, thinking ahead and guessing what your opponent will do ahead of time. This all takes time playing the game, and since people who have played longer can more easily tap into the ‘chunks’, this shows that chess skill is largely a function of time spend playing (note: IQ is still important, of course. Just, practice makes perfect and one with practice and a low IQ will beat someone with no/little practice and a high IQ).
Expertise does, indeed, take deliberate practice. Practice DOES make perfect.
Conclusion
Our brains increased evolutionarily speaking as to acquire more expertise. Bigger brains (and therefore bigger heads) cause problems with childbirth and so natural selection must have selected bigger brains since they increase expertise capacity. The fact that there are numerous people in the world with Erectus-sized brains and IQs in the normal/above average range lends credence to the claim. Erectus could have possibly had intelligence level near our own. But what really needs to be thought about here is this: It just so happens that the brain size increase corresponds with the beginnings of our modern gait and pelvis (Lieberman et al, 2006). The beginnings of cultural acquisition and transference began around that time (Herculano-Houzel and Kaas, 2011) and so our brain size would have increased due to cooking allowing us to have the energy for a bigger brain with more neurons.
Of course Erectus would need to become an expert with the new-found technology he acquired. Over time, the more ‘expert’ Erectus would have passed their genes on, both for increased brain size and expertise, and the hominin brain size then increased.
Looking at racial differences in brain size while thinking about how expertise capacity increases brain size and thinking about tool use/complexity of Arctic peoples is an alternate (and in my opinion) better theory of explaining racial differences in brain size. I obviously don’t believe that brain size differences cause IQ differences, the brain size differences are a function of climate and tool use/complexity. To make complex tools you need a sort of ‘expertness’, which, as Skoyles argues, causes brain size to increase. This explains the so-called anomalous Inuits with a brain size equal to that of East Asians but with an IQ in the low 90s.
Put simply, complex tools+cold winters+ cooked food=big brains. Cold climates DO NOT by themselves CAUSE higher levels of g. It’s just a correlation, it does not mean that it is causal. Big brains retain heat better in the cold whereas smaller heads cool better. That’s the reason for racial brain size differences, but climate and brain size in and of themselves do not CAUSE racial differences in IQ.
I now believe that sexual selection is a cause for racial differences in IQ, but that’s for another day.
References
Bernardi, G., Ricciardi, E., Sani, L., Gaglianese, A., Papasogli, A., Ceccarelli, R., . . . Pietrini, P. (2013). How Skill Expertise Shapes the Brain Functional Architecture: An fMRI Study of Visuo-Spatial and Motor Processing in Professional Racing-Car and Naïve Drivers. PLoS ONE,8(10). doi:10.1371/journal.pone.0077764
Chase, W. G., & Simon, H. A. (1973). Perception in chess. Cognitive Psychology,4(1), 55-81. doi:10.1016/0010-0285(73)90004-2
Collard, M., Buchanan, B., Morin, J., & Costopoulos, A. (2011). What Drives the Evolution of Hunter–Gatherer Subsistence Technology? A Reanalysis of the Risk Hypothesis with Data from the Pacific Northwest. Culture Evolves, 341-358. doi:10.1093/acprof:osobl/9780199608966.003.0020
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Gobet, F., & Simon, H. A. (1998). Expert Chess Memory: Revisiting the Chunking Hypothesis. Memory,6(3), 225-255. doi:10.1080/741942359
Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.
Lamberti, D. M., & Newsome, S. L. (1989). Presenting abstract versus concrete information in expert systems: what is the impact on user performance? International Journal of Man-Machine Studies,31(1), 27-45. doi:10.1016/0020-7373(89)90031-x
Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255
Lynn, R. (2006). Race differences in intelligence: An evolutionary analysis. Augusta, Ga.: Washington Summit Publishers.
Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences,97(8), 4398-4403. doi:10.1073/pnas.070039597
Torrence, R. (1983). Time budgeting and hunter-gatherer technology. In G. Bailey (Ed.). Hunter-Gatherer Economy in Prehistory: A European Perspective. Cambridge, Cambridge University Press.
Testosterone and Society
1050 words
In my last post on testosterone, I showed how the alarmism against having high testosterone is blown out of proportion. The hormone testosterone was extremely important in our evolutionary history, with skull changes that are affected by testosterone changing, indicating that it’s a cause of the rise of civilization. By looking at the skulls and skeletons of our hominin ancestors, we can infer how high the testosterone was due to changes in their skeletons over time. It seems that a decrease in testosterone was partly responsible for the advent of civilization, but too low of a dip is causing problems in the West.
Testosterone on its own is very important for male fertility, and confidence with there being no evidence showing causation in regards to prostate cancer. There are, however, large increases and dips and testosterone throughout evolutionary history. This can be inferred from looking at the skeletal remains of our ancestors.
One such study was completed by Cieri et al (2014). Cieri et al found that there was substantial feminization of Homo sapiens facial anatomy. Most notably there were reductions in average brow projection and the shortening of the upper facial skeleton. If you have knowledge of testosterone and its effects on the body, this is not surprising. Relaxing either testosterone or androgen sensitivity will cause softer, more feminized facial features over time. They argue that changes in craniofacial morphology reflects reduction in circulating levels of testosterone, “or reduced androgen receptor densities”, which, they argue “reflect the evolution of enhanced social tolerance since the Middle Pleistocene.”
The reduction in human craniomorphology coincides with larger populations from the Agricultural Revolution, which meant greater social tolerance and reduced aggression towards the group. Due to this, people were more altruistic to each other. Men that were more altruistic and had more pro-social behaviors, for instance, would be able to trade with other men in the band, which became sort of a fallback when they couldn’t forage any food. Over time, those men who could cooperate better (and had more feminized craniomorphology due to less circulating testosterone/androgen receptors).
Due to the selection of more pro-social behaviors, humans started becoming less aggressive and facial features became more feminized (due to less circulating testosterone/androgen receptors). Testosterone itself is correlated with aggressive behavior (Olweus et al, 1988) so with the selection against testosterone due to people who were more altruistic makes sense in this evolutionary context.
Cieri et al argue a good case—that the beginnings of behavioral modernity was due to selection against aggressive behavior, shifted towards pro-sociality. The fact that this began to occur around the Agricultural Revolution is no coincidence, in my opinion.
However, there seems to be a level of testosterone that a civilization needs to remain standing. Testosterone levels have reduced in the past two decades. Men are becoming more feminized, partly due to the environments we have constructed for ourselves. It’s in part due to the foods we eat/what we eat out of that is causing the drop. For instance, imagine being in an environment that destroys human testosterone levels. For instance, let’s say that a lot of the food we eat is made with/stored in a lot of BPA-containing storage. Over time, this would cause differing gene expression. People who are eating these testosterone-lowering foods will have children and, theoretically, pass on the genetically expressed genes to their children, in an epigenetic transference. Since those genes would then be advantageous in the environments we have constructed for ourselves, they would then get selected for. Once enough people get the gene in the population then it will reach fixation. That gene will then get selected in that population. If that gene is one that lowers testosterone, you will then begin to have a more feminized population (like we are seeing now, with men having lower levels of testosterone now than we did twenty years ago).
As I argued in my previous article on testosterone, what Rushton described in his 1988 paper was the Graeco-Roman elite did not breed due to having less circulating testosterone. As I have covered, low testosterone is correlated with having fewer children. As Rushton hypothesized, the elite did not breed while the lower classes did. We can look at it today and look at the ‘elite’ as upper-middle/upper class and look at the lower class, as, well the lower class. We do see the testosterone/class relationship today, with higher classes having lower levels of testosterone, vice versa for lower classes (Dabbs and Morris, 1990).
When looking at testosterone changes over time, fertility rates need to be looked at. Testosterone is down across the board all over the Western hemisphere, and it just so happens that the West is in a fertility crisis (with Europe having the lowest fertility in the world). Not surprisingly, testosterone is taking a dip in the West which is then having a negative effect on testosterone levels. This is due, partly, to the anti-testosterone environments that we have unknowingly (?) constructed for ourselves. To mediate these problems, we need to construct environments that keep testosterone levels raised as to side-step all of the horrible health problems associated with low testosterone, especially later in life.
So, since testosterone is the dominance/confidence/stress hormone, it’s clear that most men don’t put themselves into situations where the hormone would be heightened by the body. Testosterone levels do change throughout the day and depending on events that occur. If you’re around a lot of rowdy people, your testosterone will raise in response to the action around you. Testosterone rises significantly when in large groups and others around are committing violence and being destructive. This is natural, though. When this occurs, you’ll be at the ready for anything that happens, there will be no surprises. It’s a stress hormone, in that it rises mostly in stressful situations.
For society to form, there needed to be somewhat of a testosterone reduction throughout our evolutionary history. This allowed us to trade with each other and so, altruistic behaviors then were selected for. However, too much of a testosterone reduction within single populations leads to lower fertility, and, eventually, the fall of societies due to lower fertility rates. The key here is that we need to construct environments that encourage higher levels of testosterone. If something is not done, then Western society will fall sooner, rather then later (all things eventually come to an end; nothing lasts forever).
Evolution and IQ Linkfest II
1000 words
Why Grit Is More Important Than IQ When You’re Trying To Become Successful (Psychologist Angela Duckworth states that what matter for future life success isn’t IQ, SAT scores, or even graduating from a top college. What matters most for life success is a blend of perseverance and passion that she calls ‘grit’, in her book Grit: The Power of Passion and Perseverance. According to Duckworth, grittiness is passion, and being passionate about something will make you successful is persevering in the face of adversity; i.e., something not working out in your favor and you continue to go at it. She thought of two equations: talent x effort=skill, skill x effort=achievement. Talent is how quickly skills improve when effort is invested, whereas achievement occurs when you take the skills you acquired and put them to use. I’ll buy the book and read it and see what else she says.)
How Skill Expertise Shapes the Brain Functional Architecture: An fMRI Study of Visuo-Spatial and Motor Processing in Professional Racing-Car and Naïve Drivers (Brain functional architecture sustaining visuo-motor processing in racecar drivers “undergoes both ‘quantitative’ and ‘qualitative’ modifications that are evident even when the brain is engaged in relatively simple, non-demanding tasks.” Pretty much, get good at something, like really good, and your brain will change in size and mass.)
Acquiring ‘‘the Knowledge’’ of London’s Layout Drives Structural Brain Changes (Specific and enduring structural brain changes in adults “can be induced by biologically relevant behaviors engaging higher cognitive functions such as spatial memory.” Yet more evidence that becoming an ‘expert’ in something leads to substantial brain changes—which are permanent.)
Autism genes conserved during human evolution to make us smarter, say scientists (We were selected to be autistes since it was beneficial in our ancestral past. Autism is also associated with intellectual achievement.)
A model for brain life history evolution (As adult brain mass increases, so does skill, assumming the costs of maintaining brain mass and memories stay constant. This could be a cause for our larger brains. We know that our brains consume 20 ro 25 percent of our daily kcal, so in our evolutionary past, those who couldn’t amass the kcal to power the ever-growing brain would have died. González-Forero says that as we became proficient with tools, then our brain size began to increase. I have cited a few studies saying that over the past month.)
Lessons from Making Brain Soup (Learn about Herculano-Houzel and Lent’s 2005 Isotropic Fractionator—a machine that allows single cells in ‘brain soup’ to be counted as to get an accurate estimate of neurons.)
Numbers of neurons as biological correlates of cognitive capability (Body mass is a poor predictor of neurons, number of brain stem neurons estimates the capacity for processing bodily signals, mass of the cortex is a poor predictor of neuronal amount, the bird pallium packs more neurons than primate cortices of similar mass and finally the number of neurons in the cortex or pallium correlate directly with intelligence. Herculano-Houzel is blazing a new path in the field of neuroscience, with a novel way of looking at the brain showing that our brains are only scaled-up primate brains in terms of its neuronal composition.)
Creative People Have Better-Connected Brains, Scans Reveal (Highly creative people have more connections on the right and left sides of their brains, suggesting that creativity is biological in nature.)
Genetics Play a Role in Social Anxiety Disorder, Study Finds (Like most disorders, genetics plays a role. Whether it’s small or large, more often than not, genetics will always have at least a bit to say.)
Peer-review activists push psychology journals towards open data (An APA editor will not step down for stating that he won’t publish papers in which the authors don’t let their dataset become public. This is a great move. Why publish something that may possibly be garbage?)
We Look Like Our Names: The Manifestation of Name Stereotypes in Facial Appearance. (This is an interesting one, and one I’ve wondered my whole life since people have told me that ‘I don’t physically look’ how my name is. The researchers state that “facial appearance represents social expectations of how a person with a specific name should look.” Social tags influence one’s facial appearance.)
Greater insight into basic biology of pain will reveal non-addictive remedies (We need to better understand pain physiology, drug development and the individual response to pain in order to develop non-addictive drugs.)
Researchers Discover How Animals Measure Annual Time to Reproduce (The pituitary gland mediates when some mammals start reproducing. The length of the day is noticed in most animals by the pineal gland in the brain.
Does Cannabis Use Lower Your IQ? (No it does not. Recent longitudinal studies show that smoking marijuana does not lead to cognitive decline.
Reader’s Corner: Do we really understand animal intelligence? “Are We Smart Enough to Know How Smart Animals Are?” (We do not understand animal intelligence and we are not smart enough to know how smart animals are. We have an anthropocentric view of evolution, and thusly, we attempt to put our cognitive traits onto other animals when they are adapted for other areas. Herculano-Houzel’s research will begin to detangle this.)
Can Animals Acquire Language? (Evidence says no. However, I’m sure a few readers have heard of Koko the gorilla. She’s able to do sign language and has an estimated IQ of 75 to 95 on the Cattell Infant Intelligence Scale (pg. 99))
Dogs, toddlers show similarities in social intelligence (There is a g factor for dogs. The authors state that the similarities between child and dog intelligence could come down to ‘survival of the friendliest’. I’ll write about this soon.)
How Humans Became Intelligent (Cognitive neuroscientist and philosopher Daniel Dennet sees human consciousness as memetics and genetics. That is, we learn from others and what we are able to learn from others comes down to our genes. I will buy this book as well.)
The Testosterone and Fertility Conundrum: A Western Perspective
2750 words
Some people are scared of testosterone. This is no surprise, since a super-majority of people have no background in the human sciences. I’m sure plenty men know what it’s like to have low testosterone, just like some men know what it’s like to have higher T levels than average. What is the optimum level of testosterone? Why are some people scared of this hormone?
Rushton (1997) posited that r/K Selection Theory could be used to classify the races of Man on a spectrum, going from r-selection (having many children but showing little to no parental care) to K-selection (having fewer children but showing a lot of parental care). He stated that the traits of the races were also on the r/K spectrum, with the races having stark differences in morphology. Rushton’s application of r/K theory to humans isn’t completely wrong, though I do have some problems with some of his claims, such as his claims that the races differ in average penis size. He contends that testosterone is the cause for higher crime rates for black Americans and higher rates of prostate cancer in black Americans compared to white Americans.
However, in 2014, Richard et al showed that when controlling for age, blacks had 2.5 to 4.9 percent more testosterone than whites, on average. This cannot explain racial differences in prostate cancer. However, some people may emphatically claim that the races differ in average testosterone, with blacks having 13 percent higher free testosterone than whites on average. The citation that gets used the most to prove that blacks supposedly have higher testosterone than whites is Ross et al (1986), which is based on a sample of 100 people (50 black, 50 white). He claims that it’s when T levels are higher, so it’s a ‘better study’ even though the sample leaves a lot to be desired. A much more robust study showed that the difference was negligible, and not enough to account for the differential prostate cancer rates between the races.
Rohrmann et al (2007) show that there are no differences in circulating testosterone between blacks and whites in a nationally representative sample of American men. Mexicans had the highest levels. There were, however, B-W differences in estradiol production. They couldn’t confirm the other studies that stated that blacks had higher testosterone, possibly due to variations in age or using non-representative samples (that’s the culprit). Their nationally representative sample showed there was no difference in testosterone between blacks is whites, while the meta-analysis showed by Richard et al (2014) showed the difference was negligible at 2.5 to 4.9 percent higher rate of testosterone which doesn’t explain why blacks have a higher rate of acquiring prostate cancer.
The much more likely culprit for blacks having higher rates of prostate cancer, as I have written about before, are environmental factors. The two main factors are receiving less sunlight and diet. There is no evidence that higher levels of testosterone lead to prostate cancer (Michaud, Billups, and Partin, 2015). Contrary to those who say that higher levels of T cause prostate cancer, there is growing evidence that lower levels of T lead to prostate cancer (Park et al, 2015). Put simply, there is no evidence for testosterone’s supposed impact on the prostate (Stattin et al, 2013).
Differences in androgen/androgen receptors have been explained as a cause for racial differences in prostate cancer (Pettaway, 1999), however, these results haven’t been consistent (Stattin et al, 2003) and these differences in circulating androgen may possibly be explained by differences in obesity between the two populations (Gapstur et al, 2002; also see my posts on obesity and race).
Due to the ‘testosterone scare’, some people may believe that having low T is a ‘good thing’, something that’s preferred over being a high T savage. However, testosterone and the androgen receptor gene polymorphism are both associated with competitiveness and confidence in men (Eisenegger et al, 2016) and a reduced risk of cardiovascular disease in elderly men (Ohlsson et al, 2011). Obviously, lower testosterone is related to less overall confidence. People who have the thought in their head that testosterone is a ‘bad hormone’ will believe the negativity about it in the media and popular headlines.
Testosterone alone does not cause violence, but it does cause men to be socially dominant. Testosterone has been shown to increase in the aggressive phases of sports games and when shown artificial humans made to invoke physiologic responses, leading some researchers to argue that testosterone should be classified as a stress hormone. Testosterone does change based on watching one’s favorite soccer team winning or losing in a sample of 21 men (Bernhardt et al, 1998), lending some credence to the claim that testosterone is and should be classified as a stress hormone. Also of interest is that men who administered high levels of testosterone did not report higher levels of aggression (Batrinos, 2012).
I’ve heard some people literally say that having low testosterone is ‘a good thing’. People say this out of ignorance. There are a whole slew of problems associated with low testosterone, including but not limited to: insulin resistance in diabetic men (Grossmann et al, 2008); metabolic syndrome (Tsuijimura et al, 2013); muscle loss (Yuki et al, 2013); stroke and transient ischemic attack (a mini-stroke; Yeap et al, 2009); associated with elevated risk for dementia in older men (Carcaillon et al, 2014); myocardial infarction (heart attack) in diabetic men (Daka et al, 2015) etc. So it seems that the fear of testosterone from those in the anti-testosterone camp are largely blown out of proportion.
Testosterone is also a ‘food’ for the brain, with low levels being related to mental illness, sexual dysfunction, lower quality of life and cognitive impairment (Moffat et al, 2011) in both sexes (Ciocca et al, 2016). Noticed in both men in women with testosterone deficits were: cognitive impairment (reduction of working memory, episodic memory, processing speed, visual-spatial functioning and executive performance); a decrease in sexual activity; anxiety, schizophrenia, depression and stress; and alterations in cortical thickness in the brain. The fact that testosterone is so heavily important to the body’s central functioning is extremely clear. This is why it’s laughable that some people would be happy and brag about having low testosterone.
I recently came across a book called The Testosterone Hypothesis: How Hormones Regulate the Life Cycles of Civilization. Barzilai’s main premise is that the rise and fall of the West is mediated by the hormone testosterone, and due to lower testosterone levels this is one large reason for what is currently occurring in the West. The book has an extremely interesting premise. Barzilai’s hypothesis does line up with the declining levels of testosterone in America (Travison et al, 2007) though other research shows no decline in American testosterone levels from the years 88-91 to 99-04 (Nyante et al, 2007). Moreover, men who had higher level of n-6 in their blood then n-3 were far more likely to be infertile (Safarinejad et al, 2010) a marker of low testosterone (Sharpe, 2012). 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, 1992). The ratio of n-6 to n-3, on top of lowering sperm count (which is correlated with testosterone) also has negative effects on male and female cognitive ability (Lassek and Gaulin, 2011).
Barzilai’s research also corroborates Rushton’s (1986) theory of why there are lower birthrates for Europeans around the world. Rushton stated that this cycle has been noticed throughout history, with empires rising and falling due to differential birthrates between the ruling class and the ruled. Rushton also hypothesized that the cultures and gene pools associated with the Graeco-Roman empire were “evolutionary dead ends” (Rushton, 1986: 148). Knowing what we now know about the relationship between cognitive ability, testosterone, and fertility, we now have a plausible hypothesis for Rushton’s hypothesis and one of the (many) reasons why the Graeco-Roman empire collapsed. Rushton further hypothesized that the cause for lower fertility in European populations “may be partly mediated by a psychological process in which the desire to be in control of both oneself and one’s environment is taken to an extreme.” Of course there’s a good chance that this psychological process is mediated/influenced by testosterone.
Europe is the continent with the lowest fertility (ESHRE Capri Workshop Group, 2010). Testosterone has declined in Europe as a whole (Rivas et al, 2014), and this is a strong cause for the lower birthrates in Europe (along with genetic reasons) and in Finland (Perheentupa et al, 2013). The introduction of Westernized diets lowers testosterone, so this is no surprise that a reduction is seen in countries that begin to consume a Western diet. Another probable cause for lower testosterone/fertility in Europe at the moment is the large number of European men that died in WWI and WWII. Those that were more willing to fight died, meaning there was less of a chance he spread his genes. So, over time, this lead to the current cucking of Europe that we are now witnessing.
Testosterone is also hypothesized to have driven evolution (Howard, 2001). Testosterone is such an important part of human evolution and development, so much so that if we had a lower level of the hormone all throughout our evolution that we would be a different species today. Testosterone is needed for sexual functioning, good mental and brain health, fertility, cognitive ability, muscle mass retention in both young and old men, etc. Testosterone is one of the most important hormones for both men and women, and low levels for both sexes are detrimental to a high quality of life. The current data on testosterone and prostate cancer shows that higher levels of testosterone don’t contribute to prostate cancer. Testosterone, then, also isn’t a cause for the racial gap in prostate cancer because other environmental factors better explain it. If people really are happy about having lower testosterone, then I hope they have fun living a life with a low sex drive, lower cognition in old age, lower muscle mass and a higher chance of stroke and metabolic syndrome.
One of the most interesting things about testosterone is the possibility that it explains why civilizations rise and fall. There is anecdotal evidence from Rushton, as well as his theorizing that the higher classes in Rome didn’t breed which led to their downfall. We now know that lower fertility rates for men are associated with lower testosterone, so along with Barzilai’s thesis of testosterone causing the rise and fall of civilizations, Rushton’s theorizing of the cause of lower European fertility and the cause of the fall of the Graeco-Roman empire.
Testosterone is an extremely important hormone, one that drives human evolution and society formation since it’s associated with dominance and confidence. Low testosterone is looked at as ‘good’ because those with higher intelligence have lower levels of the hormone (indicated by lower confidence and having sex at a later age). I showed that the higher IQ East Asian men have a problem finding dates and being looked at as sexually attractive (even though they rated themselves as average). Along with lower East Asian fertility, specifically in Japan, does it seem to you like the high IQ people are more desired if they are having problems keeping their birthrates up? The fact of the matter is, lower levels of testosterone are correlated with lower levels of fertility. If men don’t have as much testosterone pumping through their veins, they will be less likely to have sex and thusly reproduce.
References
Batrinos, M. L. (2012). Testosterone and aggressive behavior in man. International Journal of Endocrinology & Metabolism,10(3), 563-568. doi:10.5812/ijem.3661
Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4
Carcaillon, L., Brailly-Tabard, S., Ancelin, M., Tzourio, C., Foubert-Samier, A., Dartigues, J., . . . Scarabin, P. (2014). Low testosterone and the risk of dementia in elderly men: Impact of age and education. Alzheimer’s & Dementia,10(5). doi:10.1016/j.jalz.2013.06.006
Ciocca G, Limoncin E, Gravina GL, et al. Is testosterone a food for brain? Sex Med Rev 2016;4:15-25.
Daka, B., Langer, R. D., Larsson, C. A., Rosén, T., Jansson, P. A., Råstam, L., & Lindblad, U. (2015). Low concentrations of serum testosterone predict acute myocardial infarction in men with type 2 diabetes mellitus. BMC Endocrine Disorders,15(1). doi:10.1186/s12902-015-0034-1
Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011
, , , , , . Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 1041–7
Grossmann, M., Thomas, M. C., Panagiotopoulos, S., Sharpe, K., Macisaac, R. J., Clarke, S., . . . Jerums, G. (2008). Low Testosterone Levels Are Common and Associated with Insulin Resistance in Men with Diabetes. The Journal of Clinical Endocrinology & Metabolism,93(5), 1834-1840. doi:10.1210/jc.2007-2177
Howard JM (2001): Androgens in human evolution. A new explanation of human evolution.
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
Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633
Moffat, S. D., Zonderman, A. B., Metter, E. J., Blackman, M. R., Harman, S. M., & Resnick, S. M. (2002). Longitudinal Assessment of Serum Free Testosterone Concentration Predicts Memory Performance and Cognitive Status in Elderly Men. The Journal of Clinical Endocrinology & Metabolism,87(11), 5001-5007. doi:10.1210/jc.2002-020419
Nyante, S. J., Graubard, B. I., Li, Y., Mcquillan, G. M., Platz, E. A., Rohrmann, S., . . . Mcglynn, K. A. (2011). Trends in sex hormone concentrations in US males: 1988-1991 to 1999-2004. International Journal of Andrology,35(3), 456-466. doi:10.1111/j.1365-2605.2011.01230.x
Ohlsson C, Barrett-Connor E, Bhasin S, et al. High serum testosterone is associated with reduced risk of cardiovascular events in elderly men: the MrOS (Osteoporotic Fractures in Men) study in Sweden. J Am Coll Cardiol. 2011; 58(16):1674-1681.
Park, J., Cho, S. Y., Jeong, S., Lee, S. B., Son, H., & Jeong, H. (2015). Low testosterone level is an independent risk factor for high-grade prostate cancer detection at biopsy. BJU International,118(2), 230-235. doi:10.1111/bju.13206
Perheentupa, A., Makinen, J., Laatikainen, T., Vierula, M., Skakkebaek, N. E., Andersson, A., & Toppari, J. (2012). A cohort effect on serum testosterone levels in Finnish men. European Journal of Endocrinology,168(2), 227-233. doi:10.1530/eje-12-0288
Pettaway CA. Racial differences in the androgen/androgen receptor pathway in prostate cancer. J Natl Med Assoc 1999, 91: 653:650
Raper, N. R., Cronin, F. J., & Exler, J. (1992). Omega-3 fatty acid content of the US food supply. Journal of the American College of Nutrition,11(3), 304-308. doi:10.1080/07315724.1992.10718231
Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x
Rivas AM, Mulkey Z, Lado-Abeal J, Yarbrough S. Diagnosing and managing low serum testosterone. Proc (Bayl Univ Med Cent) 2014;27:321-324
Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028
Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48
Rushton, J. P. (1986). Gene-Culture Coevolution and Genetic Similarity Theory: Implications for Ideology, Ethnic Nepotism, and Geopolitics. Politics and the Life Sciences,4(02), 144-148. doi:10.1017/s0730938400004706
Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).
Safarinejad, M. R., Hosseini, S. Y., Dadkhah, F., & Asgari, M. A. (2010). Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: A comparison between fertile and infertile men. Clinical Nutrition,29(1), 100-105. doi:10.1016/j.clnu.2009.07.008
Sharpe, R. M. (2012). Sperm counts and fertility in men: a rocky road ahead. EMBO reports,13(5), 398-403. doi:10.1038/embor.2012.50
Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572
Travison, T. G., Araujo, A. B., O’Donnell, A. B., Kupelian, V., & Mckinlay, J. B. (2007). A Population-Level Decline in Serum Testosterone Levels in American Men. The Journal of Clinical Endocrinology & Metabolism,92(1), 196-202. doi:10.1210/jc.2006-1375
Tsujimura, A., Miyagawa, Y., Takezawa, K., Okuda, H., Fukuhara, S., Kiuchi, H., . . . Nonomura, N. (2013). Is Low Testosterone Concentration a Risk Factor for Metabolic Syndrome in Healthy Middle-aged Men? Urology,82(4), 814-819. doi:10.1016/j.urology.2013.06.023
Yeap, B. B., Hyde, Z., Almeida, O. P., Norman, P. E., Chubb, S. A., Jamrozik, K., . . . Hankey, G. J. (2009). Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men. Endocrine Reviews,30(4), 411-411. doi:10.1210/edrv.30.4.9994
Yuki, A., Otsuka, R., Kozakai, R., Kitamura, I., Okura, T., Ando, F., & Shimokata, H. (2013). Relationship between Low Free Testosterone Levels and Loss of Muscle Mass. Scientific Reports,3. doi:10.1038/srep01818
Heritability, the Grandeur of Life, and My First Linkfest on Human Evolution and IQ
1100 words
Benjamin Steele finally replied to my critique of his ‘strong evidence and argument’ on race, IQ and adoption. He goes on to throw baseless ad hominem attacks as well as appealing to motive (assuming my motivation for being a race realist; assuming that I’m a ‘racist’, whatever that means). When I do address his ‘criticisms’ of my response to him, I will not address his idiotic attacks as they are a waste of time. He does, however, say that I do not understand heritability. I understand that the term ‘heritable’ doesn’t mean ‘genetic’. I understand that heritability is the proportion of phenotypic variance attributed to genetic variance. I do not believe that heritability means a trait is X percent genetic. 80 percent of the variation in the B-W IQ gap is genetic, with 20 percent explained by environmental effects. Note that I’m not claiming that heritable means genetic. All that aside, half of his reply to me is full of idiotic, baseless and untrue accusations which I will not respond to. So, Mr. Steele, if you do decide to reply to my response to you this weekend, please leave the idiocy at the door. Anyway, I will tackle that this weekend. Quick note for Mr. Steele (in case he reads this): if you don’t believe me about the National Crime and Victimization Survey showing that police arrest FEWER blacks than are reported by the NCVS, you can look it up yourself, ya know.
I’m beginning to understand why people become environmentalists. I’ve recently become obsessed with evolution. Not only of Man, but of all of the species in the world. Really thinking about the grandeur of life and evolution and what leads to the grand diversity of life really had me thinking one day. It took billions of years for us to get to the point we did today. So, why should we continue to destroy environments, displacing species and eventually leading them to extinction? I’m not saying that I fully hold this view yet, it’s just been on my mind lately. Once a species is extinct, that’s it, it’s gone forever. So shouldn’t we do all we possibly can to preserve the wonder of life that took so long to get to the point that we did today?
Some interesting articles to read:
Study: IQ of firstborns differ from siblings (This is some nice evidence for Lassek and Gaulin’s theory stating why first-born children have higher IQs than their siblings: they get first dibs on the gluteofemoral fat deposits that are loaded with n-3 fatty acids, aiding in brain size and IQ.)
Why attitude is more important than IQ (Psychologist Carol Dweck states that attitude is more important than IQ and that attitudes come in one of two types: a fixed mindset or a growth mindset. Those with a fixed mindset believe ‘you are who you are’ and nothing can change it while those with a growth mindset believe they can improve with effort. Interesting article, I will find the paper and comment on it when I read it.)
Positively Arguing IQ Determinism And Effect Of Education (Intelligent people search for intellectually stimulating things whereas less intelligent people do not. This, eventually, will lead to the construction of environments based on that genotype.)
A scientist’s new theory: Religion was key to humans’ social evolution (Nicholas Wade pretty much argues the same in his book The Faith Instinct: How Religion Evolved and Why It Endures. It is interesting to note that archaeologists have discovered what looks to be the beginnings of religiousity around 10kya, coinciding with the agrigultural revolution. I will look into this in the future.)
Galápagos giant tortoises show that in evolution, slow and steady gets you places (Interesting read, on tortoise migration)
Will Mars Colonists Evolve Into This New Kind of Human? (Very interesting and I hope to see more articles like this in the future. Of course, due to being a smaller population, evolution will occur faster due to differing selection pressures. Smaller populations incur more mutations at a faster rate than larger populatons. Will our skin turn a reddish tint? Bone density will decline leading to heavier bones. The need for C-sections due to heavier bones will lead to futher brain size increases. This is also going on on Earth at the moment, as I have previously discussed. Of course differences in culture and technology will lead the colonizers down different paths. I hope I am alive to see the first colonies on Mars and the types of long-term effects of the evolution of Man on the Red Planet.)

Evolution debate: Are humans continuing to evolve? (Of course we are)
Did seaweed make us who we are today? (Seaweed has many important vitamins and minerals that are imperative for brain development and growth—most importantly, it has poly-unsaturated fatty acids (PUFAs) and B12. We are only able to acquire these fatty acids through our diet—our body cannot synthesize the fatty acid on its own. This is just growing evidence for how important it is to have a good ratio of n-3 to n-6.)
Desert people evolve to drink water poisoned with deadly arsenic (More evidence for rapid evolution in human populations. AS3MT is known to improve arsonic metabolism in Chile and Argentina. Clearly, those who can handle the water breed/don’t die while those who cannot succumb to the effects of arsenic poisoning. Obviously, over time, this SNP will be selected for more and more while those who cannot metabolize the arsonic do not pass on their genes. This is a great article to show to anti-human-evolution deniers.)
Here Are the Weird Ways Humans Are Evolving Right Now (CRISPR and gene editing, promotion of obesity through environmental factors (our animals have also gotten fatter, probably due to the feed we give them…), autism as an adaptation (though our definition for autism has relaxed in the past decade). Human evolution is ongoing and never stops, even for Africans. I’ve seen some people claim that since they never left the continent that they are ‘behind in evolution’, yet evolution is an ongoing process and never stops, cultural ‘evolution’ (change) leading to more differences.)
‘Goldilocks’ genes that tell the tale of human evolution hold clues to variety of diseases (We really need to start looking at modern-day diseases through an evolutionary perspective, such as obesity, to better understand why these ailments inflict us and how to better treat our diseases of civilization.)
Understanding Human Evolution: Common Misconceptions About The Scientific Theory (Don’t make these misconceptions about evolution. Always keep up to date on the newest findings.)
Restore Western Civilization ( Enough said. As usual, gold from Brett Stevens. Amerika.org should be one of the first sites you check every day.)
I guess this was my first linkfest (ala hbd chick). I will post one a week.
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