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Diet Or Socializing—What Caused Primate Brain Size To Increase?

1100 words

The social brain hypothesis argues that the human brain did not increase in size to solve increasingly complex problems, but as a means of surviving and reproducing in complex social groups (Dubar, 2009). The social brain hypothesis is one of the most largely held views when it comes to explaining primate encephalization. However, an analysis of new phylogeny and more primate samples shows that differences in human and non-human primate brain evolution come down to diet, not sociality.

Diet is one of the most important factors in regards to brain and body size. The more high-quality food an animal has, the bigger its brain and body will be. Using a larger sample (3 times as large, 140 primates), more recent phylogenies (which show inferred evolutionary relationships amongst species, not which species is ‘more evolved’ than another), and updated statistical techniques, Decasien, Williams, and Higham (2017) show that diet best predicts brain size in primates, not social factors after controlling for body size and phylogeny (humans were not used because we are an outlier).

The social scheme they used consisted of solitary, pair-living, harem polygyny (one or two males, “a number of females” and offspring), and polygynandry (males and females have multiple breeding partners during the mating season). The diet scheme they used consisted of folivore (leaf-eater), frugivore-folivore (fruit and leaf eater), frugivore (fruit-eater) and omnivore (meat- and plant-eaters).

None of the sociality measures used in the study showed a relative increase in primate brain size variation, whereas diet did. Omnivores have bigger brains than frugivores. Frugivores had bigger brains than folivores. This is because animal protein/fruit contains higher quality energy when compared to leaves. Bigger brains can only evolve if there is sufficient and high-quality energy being consumed. The predicted difference in neurons between frugivores and folivores as predicted by Herculano-Houzel’s neuronal scaling rules was 1.08 billion.

The authors conclude that frugivorous primates have larger brains due to the cognitive demands of “(1) necessity of spatial information storage and retrieval; (2) cognitive demands of ‘extractive foraging’ of fruits and seeds; and (3) higher energy turnover and enhanced diet quality for energy needed during fetal brain growth.” (Decasien, Williams, and Higham, 2017). Clearly, frugivory provided some selection pressures, and, of course, the energy needed to power a larger brain.

The key here is the ability to overcome metabolic constraints. Without that, as seen with the primates that consumed a lower-quality diet, brain size—and therefore neuronal count—was relatively smaller/lower in those primates. Overall brain size best predicts cognitive ability across non-human primates—not encephalization quotient (Deaner et al, 2007). Primate brains increase approximately isometrically as a function of neuron number and its overall size with no change in neuronal density or neuronal/glial cell ratio with increasing brain size (in contrast to rodent brains) (Herculano-Houzel, 2007). If brain size best predicts cognitive ability across human primates and primate brain size increases isometrically as a function of neuron number with no change in neuronal density with increasing brain size, then primates with larger brains would need to have a higher quality diet to afford more neurons.

The results from DeCasien, Williams, and Higham (2017) call into question the social brain hypothesis. The recent expansion of the cerebellum co-evolved with tool-use (Vandervert, 2016), suggesting that our ability to use technology (to crush and mash foods, for instance) was at least as important as sociality throughout our evolution.

The authors conclude that both human and non-human primate brain evolution was driven by increased foraging capability which then may have provided the “scaffolding” for the development of social skills. Increased caloric consumption can afford larger brains with more neurons and more efficient metabolisms. It’s no surprise that frugivorous primates had larger brains than folivorous primates. Just as Fonseca-Azevedo and Herculano-Houzel (2012) observed, primates that consumed a higher quality diet had larger brains.

In sum, this points in the opposite direction of the social brain hypothesis. This is evidence for differing cognitive demands placed on getting foods. Those who could easily get food (folivores) had smaller brains than those who had to work for it (frugivores, omnivores). However, to power a bigger brain the primate needs the energy from the food that takes the complex behavior—and thus larger brain—to obtain. This lends credence to Lieberman’s (2013) hypothesis that bipedalism arose after we came out of the trees and needed to forage for fruit to survive.

Brain size in non-human primates is predicted by diet, not social factors, after controlling for body size and phylogeny. Diet is the most important factor in the evolution of species. With a lower quality diet, larger brains with more neurons (in primates, 1 billion neurons takes 6 kcal per day to power) would not evolve. Brain size is predicated on a high-quality diet, and without it, primates—including us—would not be here today. Diet needs to be talked about a lot more when it comes to primate evolution. If we would have continued to eat leaves and not adopt cooking, we would still have smaller brains and many of the things that immediately came after cooking would not have occurred.

Since we are primates we have the right morphology to manipulate our environment and forage for higher quality foods. But those primates with access to foods with higher quality have larger brains and are thus more intelligent (however, there are instances where primate brain size increases and decreases and it comes back to, of course, diet). Sociality comes AFTER having larger brains driven by nutritional factors—and would not be possible without that. Social factors drove our evolution—no doubt about it. But the importance of diet throughout hominin evolution cannot be understated. Without our high-quality diet, we’d still be like our hominin ancestors such as Lucy and her predecessors. Higher quality diet—not sociality, drives primate brain size.


DeCasien, A. R., Williams, S. A. & Higham, J. P. Primate brain size is predicted by diet but not sociality. Nat. Ecol. Evol. 1, 0112 (2017).

Deaner, R. O., Isler, K., Burkart, J., & Schaik, C. V. (2007). Overall Brain Size, and Not Encephalization Quotient, Best Predicts Cognitive Ability across Non-Human Primates. Brain, Behavior and Evolution,70(2), 115-124. doi:10.1159/000102973

Dunbar, R. (2009). The social brain hypothesis and its implications for social evolution. Annals of Human Biology,36(5), 562-572.

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

Herculano-Houzel, S. (2007). Encephalization, neuronal excess, and neuronal index in rodents. Anat. Rec. 290, 1280–1287.

Lieberman, D. (2013). The story of the human body: evolution, health and disease. London: Penguin Books.

Vandervert, L. (2016). The prominent role of the cerebellum in the learning, origin and advancement of culture. Cerebellum & Ataxias,3(1). doi:10.1186/s40673-016-0049-z

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.


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.


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.


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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

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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

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Testosterone and Society

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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).

Genetic Changes from Cooking

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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.


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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 bipedalismProceedings of the National Academy of Sciences,104(30), 12265-12269. doi:10.1073/pnas.0703267104

An Evolutionary Look At Obesity

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Diet is the main driver of our evolution. Without adequate energy, we wouldn’t be able to able to have a brain as large as we do that has the number of neurons we have due to how calorically expensive each neuron is (6 kcal per billion neurons). However, as I’m sure everyone can see, our current diets and environment has caused the current obesity crisis in the world. What is the cause of this? Our genomes are adapted for a paleolithic diet and not our modern environment with processed foodstuffs along with an overabundance of energy. With an overabundance of novel food items and situations due to our obesogenic environments, it is easier for a higher IQ person to stay thinner than it is for a lower IQ person. Tonight I will talk about the causes for this, how and what we evolved to eat and, of course, how to reverse this phenomenon.

“Gourmet Sapiens” arose around 1-1.5 mya with the advent of cooking by Homo erectus. Even before then, when we became bipedal our hands were freed which then allowed us to make tools. With these tools, we could mash and cut food which was a sort of pre-digestion outside the body (exactly what cooking is). Over time, our guts shrank (Aiello, 1997) and we became adapted for a certain diet (Eaton, 2006). Over time, we evolved to eat a certain way—that is, we had times of feast and famine. Due to this, eating three meals a day is abnormal from an evolutionary perspective (Mattson et al, 2014). This sets the stage for the acquisition of diseases of civilization along with the explosion of obesity rates.

When looking for the causes—and not symptoms—of the rise of obesity rates, the first thing we should do is look at our current environment. How is it constructed? What type of foodstuffs are in it? What kinds of foods get advertised to us and how does this have an effect on our psyche and what we eventually buy? All three of these questions are extremely important to think of when talking about why we are so obese as a society. First-world environments are obesogenic (Galgani and Ravussin, 2008) due to being evolutionarily novel. Our genomes are adapted to a paleolithic diet, and so the introduction of the neolithic diet and agriculture reduced our quality of life, with a marked decrease in the quality of skeletal remains discovered after the advent of agriculture. However, agriculture is obviously responsible for the population boom that allowed us to become the apes the took over the world, cause being the population boom that followed the agricultural revolution (Richards, 2002).

Evolutionary mismatches occur when the rate of cultural or technological change is far faster than the genome can change to adapt to the new pressure. These dietary mismatches occur when cultural and technological change which can vastly outstrip biological evolution. The two big events that occurred in human history that have vastly outstripped biological evolution are the agricultural and Industrial Revolution. Contrary to Ryan Faulk’s belief, East Asians are not ‘less sensitive to carbohydrates’ and he did not “solve Gary Taubes’ race problem” in regards to diabesity rates. The rate of cultural and technological change has had large deleterious effects on our quality of life, and our increasing obesity rates have a lot to do with it.

Cofnas (2016) showed that mice taken off of their ancestral diet lead to worse healthy outcomes. The results of Lamont et al (2016) show that we, as animals, are adapted for ancestral diets, not the diets of the environment we have currently made for ourselves. This is a big point to take home from this. All organisms are adapted/evolved for what occurred in the ancestral past, not any possible future events. Therefore, to be as healthy as possible, it stands to reason you should eat a diet that’s closer to the ones your ancestors ate, especially since it can reverse type II diabetes and reverse bad blood markers (Klonoff, 2009). Even a short-term switch to a paleo diet “improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles without weight loss in healthy sedentary humans.” (Frassetto et al, 2009) Since we evolved for a past environment and not any possible future ones, then eating a diet that’s as close as possible to our paleolithic ancestors looks like a smart way to beat the evolutionary mismatch in terms of our new, current obesogenic environment.

In one extremely interesting study, O’dea (1984) took ten middle-aged Australian Aborigines with type 2 diabetes and had them return to their ancestral hunter-gatherer lifestyle. With seven weeks of an ancestral diet and exercise, the diabetes had almost completely reversed! Clearly, when the Aborigines were taken off of our Western diet and put back in their ancestral environment with their ancestral diet, their diabetes disappeared. If we went back to a more ancestral eating pattern, the same would happen with us. This one small study lends credence to my claim that we need to eat a diet that’s more ancestral to us for us to ameliorate diseases of civilization (Eaton, 2006).

Further, looking at obesity from an evolutionary perspective can and will help us understand the disease of obesity (Ofei, 2005) better. Speakman (2009) reviewed three different explanations of the current obesity epidemic and assessed their usefulness in explaining the epidemic. The thrifty gene hypothesis states that obesity is an adaptive trait, that people who carry so-called ‘thrifty genes’ would be at an adaptive advantage. And since we have an explosion of obesity today from the 70s to today, this must explain a large part of the variance, right? There is evidence pointing in this direction, however (Southam et al, 2009). The second cause that Speakman looks at is the adaptive viewpoint—that obesity may have never been advantageous in our history, but genes that ultimately predispose us to obesity become “selected as a by-product of selection on some other trait that is advantageous.” (Speakman, 2009) The third and final perspective he proposes is that it’s due to random genetic drift, called ‘drifty genes’, predisposing some—and not others—to obesity. Whatever the case may be, there is some truth to their being genetic factors involved in the acquisition of fat storage. Though drifty genes and the adaptive viewpoint on obesity make more sense than any thrifty gene hypothesis.

For there to be any changes in the rate of obesity in the world, we need to begin to change our obesogenic environments to environments that are more like our ancestral one in terms of what foods are available. Once we alter our obesogenic environment into one that is more ancestrally ‘normal’ (since we are adapted for our past environments and not any possible future ones) then and only then will we see a reduction in obesity around the world. We are surrounded and bombarded with ads since we are children, which then effects our choices later in life; children consume 45 percent more when exposed to advertising (Harris et al, 2009). Clearly, advertisements can have one eat more, and the whole environmental mismatch in regards to being surrounded by foodstuffs not ancestral to us causes the rate of obesity to rise.

Finally, one thing we need to look at is the n-3 to n-6 ratio of our diets. As I covered last month, the n-6/n-3 is directly related to cognitive ability (Lassek and Gaulin, 2011). Our obesogenic environments cause our n-3/n-6 levels to be thrown out of whack. Our hunter-gatherer ancestors had a 1:1 level of n-3 and n-6 (Kris-Etherton, 2000). However, today, our diets contain 14 to 25 times more n-6 than n-3!! Still wondering why we are getting stupider and fatter? Further,  Western-like diets (high in linolic acid; an n-6 fatty acid) induces a general fat mass enhancement, which is in line with the observation of increasing obesity in humans (Massiera et al, 2010). There is extreme relevance to the n-3/n-6 ratio on human health (Griffin, 2008), so to curb obesity and illness rates, we need to construct environments that promote a healthy n-3/n-6 ratio, as that will at least curb the intergenerational transmission of obesity. Lands (2015) has good advice: “A useful concept for preventive nutrition is to NIX the 6 while you EAT the 3.” Here is a good list to help balance n-6 to n-3 levels.

In sum, obesity rates are a direct product of obesogenic environments. These environments cause obesity since we are surrounded by evolutionary novel situations and food. The two events in human history that contribute to this is the agricultural and Industrial Revolution. We have paleolithic genomes in a modern-day world, which causes a mismatch between our genomes and environment. This mismatch can be ameliorated if we construct differing environments—ones that are less obesogenic with less advertisement of garbage food—and we should see rates of obesity begin to decline as our environment becomes more and more similar to our ancestral one (Genné-Bacon, 2014).

The study on mice showed that for them to be healthy they need to eat a diet that is ancestral to them. We humans are no different.The evidence from the study on Australian Aborigines and the positive things that occur after going on a paleo diet for humans—even for sedentary people—shows that for us to be as healthy as possible in these obesogenic environments that we’ve made for ourselves, we need to eat a diet that matches with our paleolithic genome. This is how we can begin to fight these diseases of civilization and heighten our quality of life.

Note: Diet and exercise only under Doctor’s supervision, of course


Aiello, L. C. (1997). Brains and guts in human evolution: The Expensive Tissue Hypothesis. Brazilian Journal of Genetics,20(1). doi:10.1590/s0100-84551997000100023

Cofnas, N. (2016). Methodological problems with the test of the Paleo diet by Lamont et al. (2016). Nutrition & Diabetes,6(6). doi:10.1038/nutd.2016.22

Eaton, S. B. (2006). The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Proceedings of the Nutrition Society,65(01), 1-6. doi:10.1079/pns2005471

Frassetto, L. A., Schloetter, M., Mietus-Synder, M., Morris, R. C., & Sebastian, A. (2009). Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. European Journal of Clinical Nutrition,63(8), 947-955. doi:10.1038/ejcn.2009.4

Galgani, J., & Ravussin, E. (2008). Energy metabolism, fuel selection and body weight regulation. International Journal of Obesity,32. doi:10.1038/ijo.2008.246

Genné-Bacon EA, Thinking evolutionarily about obesity. Yale J Biol Med 87: 99112, 2014

Griffin, B. A. (2008). How relevant is the ratio of dietary n-6 to n-3 polyunsaturated fatty acids to cardiovascular disease risk? Evidence from the OPTILIP study. Current Opinion in Lipidology,19(1), 57-62. doi:10.1097/mol.0b013e3282f2e2a8

Harris, J. L., Bargh, J. A., & Brownell, K. D. (2009). Priming effects of television food advertising on eating behavior. Health Psychology,28(4), 404-413. doi:10.1037/a0014399

Klonoff, D. C. (2009). The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and other Risk Factors for Cardiovascular Disease. Journal of Diabetes Science and Technology,3(6), 1229-1232. doi:10.1177/193229680900300601

Kris-Etherton PM, Taylor DS,  Yu-Poth S, et al. Polyunsaturated fatty acids in the food chain in the United States.  Am J Clin Nutr, 2000, vol. 71 suppl(pg. 179S-88S)

Lamont, B. J., Waters, M. F., & Andrikopoulos, S. (2016). A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. Nutrition & Diabetes,6(2). doi:10.1038/nutd.2016.

Lands, B. (2015). Choosing foods to balance competing n-3 and n-6 HUFA and their actions. Ocl,23(1). doi:10.1051/ocl/2015017

Lassek, W. D., & Gaulin, S. J. (2011). Sex Differences in the Relationship of Dietary Fatty Acids to Cognitive Measures in American Children. Frontiers in Evolutionary Neuroscience,3. doi:10.3389/fnevo.2011.00005

Massiera, F., Barbry, P., Guesnet, P., Joly, A., Luquet, S., Moreilhon-Brest, C., . . . Ailhaud, G. (2010). A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations. The Journal of Lipid Research,51(8), 2352-2361. doi:10.1194/jlr.m006866

Mattson, M. P., Allison, D. B., Fontana, L., Harvie, M., Longo, V. D., Malaisse, W. J., . . . Panda, S. (2014). Meal frequency and timing in health and disease. Proceedings of the National Academy of Sciences,111(47), 16647-16653. doi:10.1073/pnas.1413965111

O’dea, K. (1984). Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes,33(6), 596-603. doi:10.2337/diabetes.33.6.596

Ofei F. Obesity- a preventable disease. Ghana Med J 2005;39: 98-101

Richards, M. P. (2002). A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence. European Journal of Clinical Nutrition,56(12), 1270-1278. doi:10.1038/sj.ejcn.1601646

Southam, L., Soranzo, N., Montgomery, S. B., Frayling, T. M., Mccarthy, M. I., Barroso, I., & Zeggini, E. (2009). Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants? Diabetologia,52(9), 1846-1851. doi:10.1007/s00125-009-1419-3

Speakman, J. R. (2013). Evolutionary Perspectives on the Obesity Epidemic: Adaptive, Maladaptive, and Neutral Viewpoints. Annual Review of Nutrition,33(1), 289-317. doi:10.1146/annurev-nutr-071811-150711

Out of FACTfrica

1650 words

Ever since Chris Stringer and Peter Andrews (1988) discovered that the genetic and archaeological evidence confirms OoA, there has been uproar in some of the less intellectually inclined and ideological sects of the Internet. These people emphatically deny—without evidence (using their emotions like a leftist, ironic…)—that the OoA hypothesis is wrong, because ‘I can’t be related to Africans, my skin is white and theirs is black—black skin cannot turn white!’ (one of the more ridiculous statements I’ve come across in my time). The fact of the matter is, people who deny OoA have ideological reasons to do so, which are not backed by science. I will provide the best (and most recent) data pointing to the OoA hypothesis, as well as go through the main paper that OoA-deniers may bring up.

OoA was first proposed by archaeologist Christ Stringer in the late 1980s (Stringer and Andrews, 1988). The totality of genetic and archaeological evidence points to Africa as the home for Anatomically Modern Humans (AMH). One of the best points of evidence is that Africans have the highest level of genetic diversity amongst humans on the planet (Campbell and Tishkoff, 2008; Gomez, Hirbo and Tishkoff, 2014;  Ashraf and Galor, 2014). Furthermore, Tattersall (2009) showed that a “radical reorganization of gene expression that underwrote the distinctive physical appearance of H. sapiens was probably also responsible for the neural substrate that permits symbolic cognition.” Here are the first signs of behavioral modernity that PumpkinPerson speaks about. What people do not understand (nor grasp), is that most of our modern-day behaviors originated in Africa (see comments by Jm8 here).

Proving OoA, nowadays, is pretty ‘easy’. I say ‘easy’, because nothing ever really gets ‘proven’ in science; as any theory can be uprooted when new evidence is available. However, there are a few key data points that point to OoA being a fact:

  1. Melanesians and Australoids share genetic affinities linked to the OoA exodus 50kya.
  2. OoA was only really in dispute due to the lack of AMH fossil evidence in Melanesia/Australia (at the time of the exodus they were a conjoined landmass (the landbridge becoming submerged underwater around 8kya).
  3. Minor secondary gene flow into the area, but after the disappearance of the land bridge, they became more homogeneous. So any differences in the archaeological record are due to isolation from the landbridge disappearing. Hudjasov et al (2007)

Further, genetic evidence also attests to the appearance of AMH in Africa. Nei (1995) provides evidence that AMH arose 100-200 kya with all humans alive today being descendants of migrations that began ~100 kya (around 70 kya). Further, since genetic diversity decreases as the distance from Africa increases shows the OoA hypothesis to be true. Bottlenecks and founder effects reduce genetic diversity. There is also recent data that suggests that the population bottleneck coming OoA along with deleterious alleles that introgressed from Neanderthal to Eurasians caused a 1 percent decrease in historic fitness respectively (Harris and Nielson, 2016). This is further evidence that AMH began in Africa: the main piece of evidence is the population bottleneck. Since population bottlenecks and founder effects reduce genetic diversity, and the further you go from Africa, more and more populations show less and less genetic diversity from Africans, this is one major clue.

Furthermore, a human skull discovered in South Africa further attests to the truth of OoA. This skull shows similarities with skulls found in Europe at that same time period; predicting that AMH would have been found in Europe about 40 kya. This is true, and yet another piece of evidence for the OoA hypothesis. Why would two skulls separated by tens of thousands of miles be similar? Because they have the same origins, obviously.

For a solid review of the OoA hypothesis vs. the multiregional hypothesis see Edwards (2012). The preponderance of evidence points to Africa as the origin for AMH. (This article will be frequently updated with new information).

OoA Denial

Referring back to what I stated at the beginning of this piece, many people will deny OoA due to ideological reasons. When they hear of people pushing (what is currently archaeologically/genetically true) OoA, they get upset. “How could I be descended from people with dark skin, I am white!” Clearly, people don’t understand the mechanisms of evolution, nor how people adapt to climate through natural selection (obviously drift, migration and mutation plays a role here as well). I will present and go through two pieces of ‘evidence’ that OoA deniers cite when attempting to show the OoA hypothesis wrong.

No, Not Africa, RUSSIA!

This one is ridiculous. It is also the most cited study from OoA deniers. In 2012, researchers Klyosov and Rozhanskii reportedly ‘debunked’ the OoA hypothesis. Their most major claims are: AMH arose on the ‘Russian plain’ which extends from Russia to Germany and France (WOW what a huge ground for them! Seems like he ‘posited’ this large area so he ‘may be right by chance—a fat chance); that the AMH spoke a proto-Slavic language (….); Indo-Europeans being synonomous with Slavs etc. It’s ridiculous. A comment from the abstract of the article:

The earliest anatomically modern humans outside Africa and the Middle East very close to Africa, (there are some 100,000 year old specimens in Israel), are 60,000 years old-and they didn’t come near Russia. The next oldest anatomically modern humans in Europe and most of Asia are 46,000 years old. So the very concept of the first anatomically modern humans first coming into being in Russia is hilarious.

And now we have this article: Jewish-Academic subversive, malicious ‘Out of Africa Hypothesis’ annihilated which uses the Kysolov study, as well as misrepresenting another in order to ‘prove’ that the OoA hypothesis is false.

One of the largest claims he makes is that Kysolov’s paper proves there is no link to Australia from Africa. However, Hudjasov (2007) showed that Melanesians and Australoids do show affinities to Africans.

His main point is that it’s not Out of Africa—it’s Out of Australia. “Humans weren’t one coherent group”, except Homo Sapiens dispersed OoA, spreading maternal haplotype L3 all around the world between 50,000-100,000 ya (Moreno, 2011; Pagani et al, 2015; Stock, 2008; Klein, 2009). The dispersal of the L3 haplogroup confirms OoA (Rito et al, 2013).

Finally, we have the evolution of white skin. The allele that codes for white skin, SLC24A5, evolved around 7500 ya (Malick et al, 2013). This allele has the greatest effect on skin color in Europeans and neighboring populations (Cochran and Harpending, 2009). This throws a wrench into that theory; the phenotypes we racially code are recent (Mathieson et al, 2015). This is why peoples can ‘look similar’ despite being geographically separated: because the races we see today are new. Europeans are an amalgamation of three populations: the Yamna, West-European hunter-gatherers and Anatolian Farmers. I’m not saying that racial categories aren’t meaningful; just saying that they’re recent (which attests to the recent how fast racial differences have been occurring). Furthermore, faster evolution means more racial differences due to genetic isolation.

In sum, the preponderance of evidence points to Africa as being the birthplace of AMH. People can deny it for ideological reasons due to ignorance of how the evolutionary process works, but just because people don’t believe something doesn’t mean it’s not true. In my opinion, one of the best pieces of evidence for the dispersal of Man out of Africa is, as Darwin first noticed, apes and gorillas evolved in Africa. It’s only logical to posit that Man also evolved in Africa, from a primate with a common ancestor. Multiregional hypotheses don’t make sense with the genetic data.


Ashraf, Q., & Galor, O. (2011). The “Out of Africa” Hypothesis, Human Genetic Diversity, and Comparative Economic Development. doi:10.3386/w17216

Campbell, M. C., & Tishkoff, S. A. (2008). African Genetic Diversity: Implications for Human Demographic History, Modern Human Origins, and Complex Disease Mapping. Annual Review of Genomics and Human Genetics,9(1), 403-433. doi:10.1146/annurev.genom.9.081307.164258

Cochran, G., & Harpending, H. (2009). The 10,000 year explosion: how civilization accelerated human evolution. New York: Basic Books.

Edwards, S. (n.d.). (2012) ANTHROJOURNAL Analysis of Two Competing Theories on the Origin of Homo sapiens sapiens: Multiregional Theory vs. the Out of Africa 2 Model. Retrieved February 08, 2017, from

Gomez, F., Hirbo, J., & Tishkoff, S. A. (2014). Genetic Variation and Adaptation in Africa: Implications for Human Evolution and Disease. Cold Spring Hanrbor Perspectives in Biology,6(7). doi:10.1101/cshperspect.a008524

Harris, K., & Nielsen, R. (2015). The Genetic Cost of Neanderthal Introgression. Genetics, 2016 doi:10.1101/030387

Hudjashov, G., Kivisild, T., Underhill, P. A., Endicott, P., Sanchez, J. J., Lin, A. A., . . . Forster, P. (2007). Revealing the prehistoric settlement of Australia by Y chromosome and mtDNA analysis. Proceedings of the National Academy of Sciences,104(21), 8726-8730. doi:10.1073/pnas.0702928104

Klein, R. G. (2009). Darwin and the recent African origin of modern humans. Proceedings of the National Academy of Sciences,106(38), 16007-16009. doi:10.1073/pnas.0908719106

Klyosov, A. A., & Rozhanskii, I. L. (2012). Re-Examining the “Out of Africa” Theory and the Origin of Europeoids (Caucasoids) in Light of DNA Genealogy. Advances in Anthropology,02(02), 80-86. doi:10.4236/aa.2012.22009

Mathieson, I., Lazaridis, I., Rohland, N., Mallick, S., Patterson, N., Roodenberg, S. A., . . . Reich, D. (2015). Genome-wide patterns of selection in 230 ancient Eurasians. Nature,528(7583), 499-503. doi:10.1038/nature16152

Nei, M. (1995). Genetic support for the out-of-Africa theory of human evolution. Proceedings of the National Academy of Sciences,92(15), 6720-6722. doi:10.1073/pnas.92.15.6720

Mallick, C. B., Iliescu, F. M., Mã¶Ls, M., Hill, S., Tamang, R., Chaubey, G., . . . Kivisild, T. (2013). The Light Skin Allele of SLC24A5 in South Asians and Europeans Shares Identity by Descent. PLoS Genetics,9(11). doi:10.1371/journal.pgen.1003912

Moreno, E. 2011. The society of our ‘out of Africa’ ancestors (1). Communicative & Integrative Biology, 4, 163e170

Pagani, L., Schiffels, S., Gurdasani, D., Danecek, P., Scally, A., Chen, Y., . . . Tyler-Smith, C. (2015). Tracing the Route of Modern Humans out of Africa by Using 225 Human Genome Sequences from Ethiopians and Egyptians. The American Journal of Human Genetics,96(6), 986-991. doi:10.1016/j.ajhg.2015.04.019

Rito, T., Richards, M. B., Fernandes, V., Alshamali, F., Cerny, V., Pereira, L., & Soares, P. (2013). The First Modern Human Dispersals across Africa. PLoS ONE,8(11). doi:10.1371/journal.pone.0080031

Stock, J. T. (2008). Are humans still evolving? Technological advances and unique biological characteristics allow us to adapt to environmental stress. Has this stopped genetic evolution? EMBO reports,9. doi:10.1038/embor.2008.63

Stringer, C., & Andrews, P. (1988). Genetic and fossil evidence for the origin of modern humans. Science,239(4845), 1263-1268. doi:10.1126/science.3125610

Tattersall, I. (2009). Human origins: Out of Africa. Proceedings of the National Academy of Sciences,106(38), 16018-16021. doi:10.1073/pnas.0903207106

Human Mating and Aggression—An Evolutionary Perspective

1650 words

One of the many oft-repeated statements from feminists is “Who commits over 80 percent of all violent crime?! MEN!!!!” This is true. No one denies this. Is this stark disparity due to biology or culture? Anyone who reads this blog knows the answer to that question, however, a lot of people (mostly feminists and other radical leftists) disagree and, of course, believe that all differences within and between people are explainable by environmental factors.

Men commit 80 percent of all crimes. Feminists may point to this stat and say that men are more dangerous than men, and, for instance, use the crime argument for separation from men the way some people use the black crime argument as a point to argue for separation. It’s clear that people who say these things don’t understand biology, because things such as this are easily explainable.

Men average 270-1,070 ng/dl on average compared to women’s 15-70 ng/dl.This large variation in testosterone between men and women is an indication that the testosterone ‘gap’ (which should be there, biologically speaking) is the main factor in explaining the crime disparities between males and females (Dabbs et al, 1995; Batrinos, 2012).

Testosterone regulates morphological traits which are then sexually selected for (Hillgarth, Ramenofsky and Wingfield, 1997). So, in a way, testosterone itself was being selected for, as it is the mediator of all of the morphological characteristics that make Men men.

These same differences in testosterone between men and women also explain the huge variation in muscle mass and strength between men and women. Muscle mass was, potentially, a way to attract mates. Though muscle mass itself is a sexually selected trait, in terms of natural selection it is a negative. This is because the more muscle mass you have, the more calories you need to consume. Men have 61 percent more upper body strength than women and 75 percent more arm mass, which translates to 90 percent greater upper body strength in men. 99.9 percent of females fall below the male mean here, which is to be expected with what we know about anatomy and physiology in regards to the human sexes. The effect was almost as large when it came to lower body mass, with men having 50 percent more muscle mass while being 65 percent stronger than women (Lassek and Gaulin, 2009). Muscle mass is also a feature in men that gets sexually selected for (Puts, 2016)

When women are ovulating, they “show a weakness” for men with “good genes” when they are at their most fertile. This shows a causal mechanism through sexual selection for high levels of testosterone to be selected for in men, which then causes the differences in fat-free mass and aggression rates, among other variables. Indeed, we do know that, on average, women want a mate that is successful, good looking, has money, has a desire for home and children, and being a loving partner. Women, obviously, secure a man’s genes when she bears his child. So a woman would always attempt to secure the best combination of these traits in the same man (Buss and Shackelford, 2008). Sexual selection explains sex differences in aggression (Archer, 2009). So, as you can see (evolutionarily speaking), it’s women that are the cause for the so-called aggression that feminists complain about—they sexually selected us for higher levels of aggression and testosterone, then complain about it in the modern world. 

Sexual and natural selection are the causes for increased aggression/testosterone rates in men when compared to women. These traits were clearly advantageous during in our ancestral habitat, as a more aggressive mate would provide better protection and food acquisition. When organisms compete for scarce, nutritious food, mates, and space, competition increases between organisms. This can lead to injury or death (the less-able being naturally selected out of the gene pool); chronically elevated levels of testosterone associated with aggressive competition may suppress the immune system and have negative effects for health and fitness (elevated cortisol levels, which triggers fight or flight is also a negative); it may increase risk of predation since a high testosterone organism won’t notice predators around them; aggressive contests tend to be physically demanding, sapping energy; and it may damage social relationships, for instance if a male is aggressive to a female that male won’t mate and thus get selected out of the gene pool (Georgiev et al, 2013).

A study in Sweden looked at the frequency and how often men committed acts of violent crime compared to women (Trägårdh et al, 2016). They discovered that in the two decades from 1990 to 2010, there were 1,570 cases of deadly violence with men accounting for 1,420 of the cases (90.4 percent) while 150 women committed violent crime (9.6 percent). Women accounted for one-third of crimes committed against children, however, which has its basis in evolutionary psychology as well.

The risk of being killed is highest in your first year of life (Friedman and Resnick, 2007). Why? Infanticide. The mean age that mothers commit filicide at is 29.5 while the mean age of the babe is 3.5 years (Rouge-Maillart et al, 2005). The evolutionary explanation for this is that the mother still has time to conceive more children, so the fitness hit is not too large. Further, women are more likely to commit filicide if they have a second child under the age of 20 (Bourget, Grace, and Whitehurts, 2007). So obviously, the older a woman is the less of a chance there is that filicide will be committed since it would be a fitness hit since older women have less of a chance to conceive children, along with a higher chance for the child to have birth defects (Stein and Susser, 2000; Lampinen, Vehviläinen-Julkunen and Kankkunen, 2009; Jolly et al, 2000). So from an evolutionary perspective, it doesn’t make sense for a woman to kill her child if she’s about to hit the age-40 wall (Reproductive Endocrinology Infertility Committee et al, 2011; O’Reilly-Green and Cohen, 1993; van Katwjk and Peeters, 1998; Yaniv et al, 2010).

Male infanticide is associated with social monogamy in primates; male infanticide may be what causes females to stay and mate with one male (Opie et al, 2013). This is caused by females choosing to stay faithful to mates, which then drives monogamous relationships. Serial and social monogamy is the norm for humans (Brandon, 2016). This, then, goes back to what a woman looks for in a man, and has her want to stay with that one man who has all of the qualities necessary to be a good mate and father.

In sum, when feminists complain about male aggression and crime, there are substantial evolutionary underpinnings behind them. They do not even realize that even when they are fighting for ‘equality’ between the sexes, that they are directly helping our arguments that there are inherent biological, physiological and morphological differences between the sexes—driven by sexual selection—which is then a cause for a large amount of the variation in crime (and other variables) between men and women. These intrinsic differences between men and women are why we are so different from each other.The sexes also differ in the brain. There are numerous biological explanations between differences in aggression between men and women, and they come down to sexual selection and what propagated our species in during our ancestral evolution. A large cause for these differences is mate selection—which would, technically, make women the culprits, as they  selected us for these traits. The fact that these differences are still so profound in modern-day society is not at all surprising.


Archer, J. (2009). Does sexual selection explain human sex differences in aggression? Behavioral and Brain Sciences,32(3-4), 249. doi:10.1017/s0140525x09990951

Batrinos, M. L. (2012). Testosterone and aggressive behavior in man. International Journal of Endocrinology & Metabolism, 10(3), 563-568. doi:10.5812/ijem.3661

Bourget D, Grace J, Whitehurst L. A review of maternal and paternal filicide. J Am Acad Psychiatry Law, 2007, vol. 35 (pg. 74-82)

Buss, D. M., & Shackelford, T. K. (2008). Attractive Women Want it All: Good Genes, Economic Investment, Parenting Proclivities, and Emotional Commitment. Evolutionary Psychology,6(1), 147470490800600. doi:10.1177/147470490800600116

Dabbs, J. M., Carr, T. S., Frady, R. L., & Riad, J. K. (1995). Testosterone, crime, and misbehavior among 692 male prison inmates. Personality and Individual Differences, 18(5), 627-633. doi:10.1016/0191-8869(94)00177-t

Friedman SH, Resnick PJ. Child murder by mothers: patterns and prevention. World Psychiatry 2007;6:137-41.

Georgiev, A. V., Klimczuk, A. C., Traficonte, D. M., & Maestripieri, D. (2013). When Violence Pays: A Cost-Benefit Analysis of Aggressive Behavior in Animals and Humans. Evolutionary Psychology,11(3), 147470491301100. doi:10.1177/147470491301100313

Hillgarth, N., Ramenofsky, M., & Winfield, J. (1997). Testosterone and sexual selection. Behavioral Ecology,8(1), 108-109. doi:10.1093/beheco/8.1.108

Jolly, M. (2000). The risks associated with pregnancy in women aged 35 years or older. Human Reproduction,15(11), 2433-2437. doi:10.1093/humrep/15.11.2433

Lampinen, R., Vehviläinen-Julkunen, K., & Kankkunen, P. (2009). A Review of Pregnancy in Women Over 35 Years of Age. The Open Nursing Journal,3, 33-38. doi:10.2174/1874434600903010033

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

Opie, C., Atkinson, Q. D., Dunbar, R. I., & Shultz, S. (2013). Male infanticide leads to social monogamy in primates. Proceedings of the National Academy of Sciences,110(33), 13328-13332. doi:10.1073/pnas.1307903110

O’Reilly-Green C, Cohen W R. Pregnancy in women aged 40 and older.  Obstet Gynecol Clin North Am. 1993;  20 313-331

Puts, D. (2016). Human sexual selection. Current Opinion in Psychology, 7, 28–32. doi:10.1016/j.copsyc.2015.07.011

Reproductive E, Infertility C. Family physicians advisory C, maternal-fetal medicine C, executive, council of the society of O et al. Advanced reproductive age and fertility. Journal of obstetrics and gynaecology, Canada : JOGC. Journal d’obstetrique et gynecologie du Canada : JOGC. 2011;33(11):1165–75.

Rouge-Maillart, C., Jousset, N., Gaudin, A., Bouju, B., & Penneau, M. (2005). Women Who Kill Their Children. The American Journal of Forensic Medicine and Pathology,26(4), 320-326. doi:10.1097/01.paf.0000188085.11961.b2

Stein, Z., & Susser, M. (2000). The risks of having children in later life. Western Journal of Medicine,173(5), 295-296. doi:10.1136/ewjm.173.5.295

Trägårdh, K., Nilsson, T., Granath, S., & Sturup, J. (2016). A Time Trend Study of Swedish Male and Female Homicide Offenders from 1990 to 2010. International Journal of Forensic Mental Health,15(2), 125-135. doi:10.1080/14999013.2016.1152615

van Katwijk, C., & Peeters, LLH. (1998). Clinical aspects of pregnancy after the age of 35 years: a review of the literature. Human Reproduction Update 4(2):185–94.

Yaniv, S. S., Levy, A., Wiznitzer, A., Holcberg, G., Mazor, M., & Sheiner, E. (2010). A significant linear association exists between advanced maternal age and adverse perinatal outcome. Archives of Gynecology and Obstetrics,283(4), 755-759. doi:10.1007/s00404-010-1459-4

The Ape That Took Over the World

1600 words

What gave us the ability to become the apes that took over the world comes down to three things: bipedalism, tool-making, and fire use and acquisition. Those three things catapulted our evolution and brain size (number of neurons) and made it possible for us to be human. The cause of our extraordinary cognitive abilities is the number of neurons in our brain in total—16 billion in all. The only thing that could power a brain so energy-demanding is a diet of cooked meat and other foods. This acts as a predigestion outside of the body so more nutrients can get extracted more efficiently, to power a growing brain due to other selective pressures. Clearly, without cooking, our brains we wouldn’t have the cognitive capacity to take over the world.

In 2001 a huge finding was made in Africa, that of an ape with the beginnings of a bipedal pelvis. Soon after, footprints were discovered where the skeleton was found. A huge debate broke out, with researchers wondering how this new finding fit in with our evolution. Since Lucy had the beginnings of a bipedal pelvis, this conserved about 75 percent more energy than walking on all fours did (Sockol, Raichlen, and Pontzer, 2007). Since the human brain is our most costly organ, the advent of bipedalism freed up an immense amount of energy to power our soon to be big brains.

After the advent of bipedalism, we could then manipulate our environment which called for the need for tools. To have the ability to make tools—and make them efficiently—our ancestors needed to have hands and opposable thumbs. Since we are primates just like them, we just happen to have this evolutionary trait. To create a usable stone tool for the right situation, one needed a certain expertise in making that tool. There is evidence that our brain size increased since we needed the expertise to survive in our ancestral past (Skoyles, 2007).

Soon after, our ancestor Homo erectus appeared on the scene. The fossil record shows that our brain size really began to increase around 2 million years ago, (Herculano-Houzel, 2016). What could have driven such a rapid increase in brain size? The advent of cooking. Herculano-Houzel (2016) defines cooking as things cooked with fire, as well as foodstuffs mashed with the stone tools we could now create with our newly freed hands. After these two discoveries, brain size then nearly doubled in size. However, when the neuronal composition of the brain is looked at, it has the number of neurons expected for a brain its size (Herculano-Houzel, 2009). The human brain is not special in its neuronal composition.

Erectus began controlling fire between 1-1.5 mya (Berna et al, 2012). The use of fire softened food, making it easier to chew, decreasing our jaw muscles and size of our teeth which also allowed for our big brains with large amount of cerebral neurons—16 billion in all, the most out of any animal in the animal kingdom, and is the cause of our superior cognitive abilities (Herculano-Houzel, 2016).

Since the human brain is a primate brain, it has some key features that aren’t available in other brains. The most important being that we have the most neurons crowded into our cerebral cortex than other animals. That is the cause for our cognitive superiority over other animals, but not Neanderthals (Villa and Roebroeks, 2014). There is anthropological evidence that our so-called cognitive superiority over the Neanderthals may be a myth, since they discovered no data inferring that we had any ‘superiority’ over Neanderthals in terms of technology, social structure or cognitively.

Without our ability to control and create fire, starting with erectus (Berna et al, 2012), our brains wouldn’t have had the ability to power such a large brain, and thus our brains would have stayed erectus-sized. We can look at the evolution of great apes’ brains (Herculano-Houzel and Kaas, 2011) and say, with confidence, that if our hominin ancestors never would have controlled fire and passed down the useful skill down through the generations then we would not be here today. Looking at it in this way, we can thank the beginnings of cultural transference and acquisition for a large part of the reason why we are here today (mass extinctions and decimations aside). If we would have continued to eat our plant-based diet than our brains would have stayed around 600-800 cc, a size with nowhere near enough neurons for our outstanding cognitive abilities. So, Stephen Jay Gould may be on his way to vindication, as he wrote in his book Full House (1996): “We have no evidence that the modal form of human bodies or brains has changed at all in the past 100,000 years—a standard phenomenon of stasis for successful and widespread species, and not (as popularly misconceived) an odd exception to an expectation of continuous and progressive change.” There is now some evidence to corroborate his theorizing.

When talking about how we evolved to become the ape that took over the world, three things cannot be overlooked: 1) Bipedalism. We know that Lucy was the first hominin to have a pelvis close to our modern one (Harcourt-Smith and Aiello, 2004); 2) we could now stand upright, acquiring kcal was easier and more efficient (Lieberman, 2013); and 3) walking bipedally conserves 75 percent more energy compared to knuckle-walking (Sockol, Raichlen, and Pontzer, 2007). Bipedalism then freed our hands so we could use tools (Marzke, 2011). Furthermore, there are biomechanical reasons for the acquisition of bipedalism: one main factor being that every development of typical human morphology can be explained as adaptations to conserve energy walking long distances (Preuschoft, 2004). Bipedal walking may be one of the most important events in our evolution—for without that, every other great thing you see around you today would not be here since we then would not have the ability to manipulate the environment in which we live.

Just like our capacity for expertise may have increased our brain size, there is evidence that tool making increased our brain size as well (Stout et al, 2015). So this further increased our brain size, and when our brains reached around 800 cc with erectus, the ‘discovery’ of fire was able to occur due to the ability expertise capacity gained from becoming experts with creating tools and learning how to survive. This crude form of cooking (mashing/smashing foodstuffs to extract nutrients) allowed our brains to be fueled by the coming wave of nutrients. Furthermore, since the food was already ‘predigested’, so to speak, it was easier to chew. The softened foods then weakened our jaw muscles (Organ et al, 2011). So, in a way, you can say that human evolution is driven by dietary changes (Luca, Perry and Di Rienzo, 2010).


The advent of bipedalism allowed for the ability to make stone tools, which was one of the first cases of cultural transference. To see how important the use of fire was, one only needs to look at gorillas. Metabolic limitations resulting from the number of hours available to feed along with the low caloric yield of raw foods imposed a limitation on brain size for great apes and gorillas—imposing a tradeoff between the total neuronal amount and body size, making them the outlier in terms of body size (Fonseca-Azevedo and Herculano-Houzel, 2012). Thus, you can see the benefits of cultural transference and acquisition, which gave us the ability to have us become the ape that took over the world with our superior cognitive abilities primarily caused by the advent of cultural transference and acquisition beginning with the advent of bipedalism which allowed us to increase our foraging range, allowing us to consume higher-quality kcal to power our soon-to-be big brains, tool-making, and fire-use.


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 AfricaProceedings of the National Academy of Sciences,109(20). doi:10.1073/pnas.1117620109

Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise

Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolutionProceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109

Gould, S. J. (1996). Full house: The Spread of Excellence from Plato to Darwin. New York: Harmony Books.

Harcourt-Smith, W. E., & Aiello, L. C. (2004). Fossils, feet and the evolution of human bipedal locomotionJournal of Anatomy,204(5), 403-416. doi:10.1111/j.0021-8782.2004.00296.x

Herculano-Houzel, S. (2013). The Remarkable, Yet Not Extraordinary, Human Brain as a Scaled-Up Primate Brain and Its Associated Cost.

Herculano-Houzel, S. (2009). The human brain in numbers: a linearly scaled-up primate brainFrontiers in Human Neuroscience,3. doi:10.3389/neuro.09.031.2009

Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.

Herculano-Houzel, S. (2016). The Human Advantage: A New Understanding of How Our Brains Became Remarkable. doi:10.7551/mitpress/9780262034258.001.0001

Lieberman, D. (2013). The Story of the Human Body: Evolution, Health, and Disease. New York: Pantheon Books.

Luca, F., Perry, G., & Rienzo, A. D. (2010). Evolutionary Adaptations to Dietary ChangesAnnual Review of Nutrition,30(1), 291-314. doi:10.1146/annurev-nutr-080508-141048

Marzke, M. W. (2013). Tool making, hand morphology and fossil homininsPhilosophical Transactions of the Royal Society B: Biological Sciences,368(1630), 20120414-20120414. doi:10.1098/rstb.2012.0414

Organ, C., Nunn, C. L., Machanda, Z., & Wrangham, R. W. (2011). Phylogenetic rate shifts in feeding time during the evolution of HomoProceedings of the National Academy of Sciences,108(35), 14555-14559. doi:10.1073/pnas.1107806108

Preuschoft, H. (2004). Mechanisms for the acquisition of habitual bipedality: are there biomechanical reasons for the acquisition of upright bipedal posture? Journal of Anatomy,204(5), 363-384. doi:10.1111/j.0021-8782.2004.00303.x

Sockol, M. D., Raichlen, D. A., & Pontzer, H. (2007). Chimpanzee locomotor energetics and the origin of human bipedalismProceedings of the National Academy of Sciences,104(30), 12265-12269. doi:10.1073/pnas.0703267104

Stout, D., Hecht, E., Khreisheh, N., Bradley, B., & Chaminade, T. (2015). Cognitive Demands of Lower Paleolithic ToolmakingPlos One,10(4). doi:10.1371/journal.pone.0121804

Villa, P., & Roebroeks, W. (2014). Neandertal Demise: An Archaeological Analysis of the Modern Human Superiority ComplexPLoS ONE,9(4). doi:10.1371/journal.pone.0096424

Is General Intelligence Domain-Specific?

1600 words

Is the human brain ‘special’? Not according to Herculano-Houzel; our brains are just linearly scaled-up primate brains. We have the number of neurons predicted for a primate of our body size. But what does this have to do with general intelligence? Evolutionary psychologists also contend that the human brain is not ‘special’; that it is an evolved organ just like the rest of our body. Satoshi Kanazawa (2003) proposed the ‘Savanna Hypothesis‘ which states that more intelligent people are better able to deal with ‘evolutionary novel’ situations (situations that we didn’t have to deal with in our ancestral African environment, for example) whereas he purports that general intelligence does not affect an individuals’ ability to deal with evolutionarily familiar entities and situations. I don’t really have a stance on it yet, though I do find it extremely interesting, with it making (intuitive) sense.

Kanazawa (2010) suggests that general intelligence may both be an evolved adaptation and an ‘individual-difference variable’. Evolutionary psychologists contend that evolved psychological adaptations are for the ancestral environment which was evolved in, not in any modern-day environment. Kanazawa (2010) writes:

The human brain has difficulty comprehending and dealing with entities and situations that did not exist in the ancestral environment. Burnham and Johnson (2005, pp. 130–131) referred to the same observation as the evolutionary legacy hypothesis, whereas Hagen and Hammerstein (2006, pp. 341–343) called it the mismatch hypothesis.

From an evolutionary perspective, this does make sense. A perfect example is Eurasian societies vs. African ones. you can see the evolutionary novelty in Eurasian civilizations, while African societies are much closer (though obviously not fully) to our ancestral environment. Thusly, since the situations found in Africa are not evolutionarily novel, it does not take high levels of to survive in, while Eurasian societies (which are evolutionarily novel) take much higher levels of to live and survive in.

Kanazawa rightly states that most evolutionary psychologists and biologists contend that there have been no changes to the human brain in the last 10,000 years, in line with his Savanna Hypothesis. However, as I’m sure all readers of my blog know, there were sweeping changes in the last 10,000 years in the human genome due to the advent of agriculture, and, obviously, new alleles have appeared in our genome, however “it is not clear whether these new alleles have led to the emergence of new evolved psychological mechanisms in the last 10,000 years.”

General intelligence poses a problem for evo psych since evolutionary psychologists contend that “the human brain consists of domain-specific evolved psychological mechanisms” which evolved specifically to solve adaptive problems such as survival and fitness. Thusly, Kanazawa proposes in contrast to other evolutionary psychologists that general intelligence evolved as a domain-specific adaptation to deal with evolutionary novel problems. So, Kanazawa says, our ancestors didn’t really need to think inorder to solve recurring problems. However, he talks about three major evolutionarily novel situations that needed reasoning and higher intelligence to solve:

1. Lightning has struck a tree near the camp and set it on fire. The fire is now spreading to the dry underbrush. What should I do? How can I stop the spread of the fire? How can I and my family escape it? (Since lightning never strikes the same place twice, this is guaranteed to be a nonrecurrent problem.)

2. We are in the middle of the severest drought in a hundred years. Nuts and berries at our normal places of gathering, which are usually plentiful, are not growing at all, and animals are scarce as well. We are running out of food because none of our normal sources of food are working. What else can we eat? What else is safe to eat? How else can we procure food?

3. A flash flood has caused the river to swell to several times its normal width, and I am trapped on one side of it while my entire band is on the other side. It is imperative that I rejoin them soon. How can I cross the rapid river? Should I walk across it? Or should I construct some sort of buoyant vehicle to use to get across it? If so, what kind of material should I use? Wood? Stones?

These are great examples of ‘novel’ situations that may have arisen, in which our ancestors needed to ‘think outside of the box’ in order to survive. Situations such as this may be why general intelligence evolved as a domain-specific adaptation for ‘evolutionarily novel’ situations. Clearly, when such situations arose, our ancestors who could reason better at the time these unfamiliar events happened would survive and pass on their genes while the ones who could not die and got selected out of the gene pool. So general intelligence may have evolved to solve these new and unfamiliar problems that plagued out ancestors. What this suggests is that intelligent people are better than less intelligent people at solving problems only if they are evolutionarily novel. On the other hand, situations that are evolutionarily familiar to us do not take higher levels of to solve.

For example, more intelligent individuals are no better than less intelligent individuals in finding and keeping mates, but they may be better at using computer dating services. Three recent studies, employing widely varied methods, have all shown that the average intelligence of a population appears to be a strong function of the evolutionary novelty of its environment (Ash & Gallup, 2007; D. H. Bailey & Geary, 2009; Kanazawa, 2008).

Who is more successful, on average, over another in modern society? I don’t even need to say it, the more intelligent person. However, if there was an evolutionarily familiar problem there would be no difference in figuring out how to solve the problem, because evolution has already ‘outfitted’ a way to deal with them, without logical reasoning.

Kanazawa then talks about evolutionary adaptations such as bipedalism (we all walk, but some of us are better runners than others); vision (we can all see, but some have better vision than others); and language (we all speak, but some people are more proficient in their language and learn it earlier than others). These are all adaptations, but there is extensive individual variation between them. Furthermore, the first evolved psychological mechanism to be discovered was cheater detection, to know if you got cheated while in a ‘social contract’ with another individual. Another evolved adaptation is theory of mind. People with Asperger’s syndrome, for instance, differ in the capacity of their theory of mind. Kanazawa asks:

If so, can such individual differences in the evolved psychological mechanism of theory of mind be heritable, since we already know that autism and Asperger’s syndrome may be heritable (A. Bailey et al., 1995; Folstein & Rutter, 1988)?

A very interesting question. Of course, since it’s #2017, we have made great strides in these fields and we know these two conditions to be highly heritable. Can the same be said for theory of mind? That is a question that I will return to in the future.

Kanazawa’s hypothesis does make a lot of sense, and there is empirical evidence to back his assertions. His hypothesis proposes that evolutionarily familair situations do noot take any higher levels of general intelligence to solve, whereas novel situations do. Think about that. Society is the ultimate evolutionary novelty. Who succeeds the most, on average, in society? The more intelligent.

Go outside. Look around you. Can you tell me which things were in our ancestral environment? Trees? Grass? Not really, as they aren’t the same exact kinds as we know from the savanna. The only thing that is constant is: men, women, boys and girls.

This can, however, be said in another way. Our current environment is an evolutionary mismatch. We are evolved for our past environments, and as we all know, evolution is non-teleological—meaning there is no direction. So we are not selected for possible future environments, as there is no knowledge for what the future holds due to contingencies of ‘just history’. Anything can happen in the future, we don’t have any knowledge of any future occurences. These can be said to be mismatches, or novelties, and those who are more intelligent reason more logically due to the fact that they are more adept at surviving evolutionary novel situations. Kanazawa’s theory provides a wealth of information and evidence to back his assertion that general intelligence is domain-specific.

This is yet another piece of evidence that our brain is not special. Why continue believing that our brain is special, even when there is evidence mounting against it? Our brains evolved and were selected for just like any other organ in our body, just like it was for every single organism on earth. Race-realists like to say “How can egalitarians believe that we stopped evolving at the neck for 50,000 years?” Well to those race-realists who contend that our brains are ‘special’, I say to them: “How can our brain be ‘special’ when it’s an evolved organ just like any other in our body and was subject to the same (or similar) evolutionary selective pressures?”

In sum, the brain has problems dealing with things that were not in its ancestral environment. However, those who are more intelligent will have an easier time dealing with evolutionarily novel situations in comparison to people with lower intelligence. Look at places in Africa where development is still low. They clearly don’t need high levels of to survive, as it’s pretty close to the ancestral environment. Conversely, Eurasian societies are much more complex and thus, evolutionarily novel. This may be one reason that explains societal differences between these populations. It is an interesting question to consider, which I will return to in the future.

Fatty Acids and PISA Math Performance

1800 words

There are much more interesting theories of the evolution of hominin intelligence other than the tiring (yawn) cold winter theory. Since I’m so interested in ancient hominin evolution and nutrition, theories of the nutritional effects of our ancient ancestors’ diets are of particular interest to me. Last month I wrote on why men are attracted to a low waist-to-hip ratio in women. However, the relationship between gluteofemoral fat (fat in the thighs and buttocks) is only part of the story on how DHA and fatty acids (FAs) drove our brain growth and our evolution as a whole. Tonight I will talk about how fatty acids predict ‘cognitive performance’ (it’s PISA, ugh) in a sample of 28 countries, particularly the positive relationship between n-3 (Omega-3s) and intelligence and the negative relationship between n-6 and intelligence. I will then talk about the traditional Standard American Diet (the SAD diet [apt name]) and how it affects American intelligence on a nation-wide level. Finally, I will talk about the best diet to maximize cognition in growing babes and women.

Lassek and Gaulin (2013) used the 2009 PISA data to infer cognitive abilities for 28 countries (ugh, I’d like to see a study like this done with actual IQ tests). They also searched for studies that showed data providing “maternal milk DHA DHA values as percentages of total fatty acids in 50 countries”. Further, to control for SES influences on cognitive performance, they controlled for GDP/PC (gross domestic product per country) and “educational expenditures per pupil.” They further controlled for the possible effect of macronutrients on maternal milk DHA levels, they included estimates for each country of the average amount of kcal consumed from protein, fat, and carbohydrates. To explore the relationship between DHA and cognitive ability, they included foodstuffs high in n-3—fish, eggs, poultry, red meat, and milk which also contain DPA depending on the type of feed the animal is given. There is also a ‘metabolic competition’ between n-3 and n-6 fatty acids, so they also included total animal and vegetable fat as well as vegetable oils.

Lassek and Gaulin (2013) found that GDP/PC, expenditures per student and DHA were significant predictors of (PISA) math scores, whereas macronutrient content showed no correlation.

The predictive value of milk DHA on cognitive ability is only weak when either two of the SES variables are added in the multiple regression. When milk arachidonic (a type of Omega-6 fatty acid) is added to the regression, it is negatively correlated with math scores but not significantly (so it wasn’t added to the table below).


So countries with lower maternal milk levels of DHA score lower on the maths section of the PISA exam (not an IQ test, but it’s ‘good enough’). Knowing what is known about the effects of DHA on cognitive abilities, countries who have higher maternal milk levels of DPA do score higher on the maths section of the PISA exam.


Table 2 shows the correlations between grams per capita per day of food consumption in the data set they used and maternal milk DHA. As you can see, total fish and seafood consumption are substantially correlated with total milk DHA, while foods that are high in n-6 show medium negative correlations with maternal milk DHA. The combination of foods that explain the most of the variance in maternal milk DHA is total fat consumed and total fish consumed. This explained 61 percent of the variance in maternal milk DHA across countries.

Not surprisingly, foodstuffs high in n-6 showed significant negative correlations on maternal milk DHA. “Any regression including total fish or seafood, and vegetable oils, animal fat or milk consistently explains at least half of the variance in milk DHA, with fish or seafood having positive beta coefficients and the remainder having negative beta coefficients.”

The study showed that a country’s balance of n-3 and n-6 was strongly related to the students’ math performance on the PISA. This relationship between milk DHA and cognitive performance remains sufficient even after controlling for national wealth, macro intake and investment in education. The availability of DHA in populations is a better predictor of test scores than are SES factors (which I’ve covered here on Italian IQ), though SES explains a considerable portion of the variance, it’s not as much as the overall DHA levels by country. Furthermore, maternal DHA levels are strongly correlated to per capita fish and seafood consumption while a negative correlation was noticed with the intake of more vegetable oils, fat, and beef, which suggests ‘metabolic competition’ between the n-3 and n-6 fatty acids.

There are, of course, many possible errors with the study such as maternal milk DHA values not reflecting the total DHA in that population as a whole; measures of extracting milk fatty acids differed between studies; test results being due to sampling error; and finally the per capita consumption of foods is based on food disappearance, not amount of food consumed. However, even with the faults of the study, it’s still very interesting and I hope they do further work with actual measures of cognitive ability. Despite the pitfalls of the study (the main one being the use of PISA to test ‘cognitive abilities’), this is a very interesting study. I eventually hope that a study similar to this one is undertaken with actual measures of cognitive ability and not PISA scores.

We now know that n-6 is negatively linked with brain performance, and that n-3 is positively linked. What does this say about America?

As I’m sure all of you are aware of, America is one of the fattest nations in the world. Not surprisingly, Americans consume extremely low levels of seafood (very high in DPA) and more foods high in n-6 (Papanikolaou et al, 2014). High levels of n-3 (which we do not get enough of in America) and n-6 are correlated with obesity (Simopoulos, 2016). So not only do we have a current dysgenic effect in America due to decreased fertility of the more intelligent (which is also part of the reason why we have the effect of dysgenic fertility in America), obesity is also driven by high levels of n-6 in the Western diet, which then causes obesity down the generations (Massiera et al, 2010).

I also previously wrote on agriculture and diseases of civilization. Our hunter-gatherer ancestors were all around healthier than we were. This, clearly, is due to the fact that they ate a more natural diet and not one full of processed, insulin-spiking carbohydrates, among other things. Our hunter-gatherer ancestors consumed n-3 and n-6 at equal amounts (1:1) (Kris-Etherson, et al 2000). As I documented in my article on agriculture and disease, HGs had low to nonexistent rates of the diseases that plague us in our modern societies today. However, around 140 years ago, we entered the Industrial Revolution. The paradigm shift that this caused was huge. We began consuming less n-3 (fish and other assorted seafood and nuts among other foods) while n-6 intake increased (beef, grains, carbohydrates) (Kris-Etherson, et al 2000). Moreover, the ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 2013). We Americans also consume 20 percent of our daily kcal from one ‘food’ source—soybean oil—with almost 9 percent of the total kcal coming from n-6 linoleic acids (United States Department of Agriculture, 2007). The typical American diet contains about 26 percent more n-6 than n-3, and people wonder why we are slowly getting dumber (which is, obviously, a side effect of civilization). So our n-6 consumption is about 26 percent higher than it was when we were still hunter-gatherers. Does anyone still wonder why diseases of civilization exist and why hunter-gatherers have low to nonexistent rates of the diseases that plague us?

The bioavailability of n-6 is dependent on the amount of n-3 in fatty tissue (Hibbeln et al, 2006). This goes back to the ‘metabolic competition’ mentioned earlier. N-3 also makes up 10 percent of the overall brain weight since the first neurons evolved in an environment high in n-3. N-3 fatty acids were positively related to test scores in both men and women, while n-6 showed the reverse relationship (with a stronger effect in females). Furthermore, in female children, the effect of n-3 intake were twice as strong in comparison to male children, which also exceeded the negative effects of lead exposure, suggesting that higher consumption of foods rich in n-3 while consuming fewer foods rich in n-6 will improve cognitive abilities (Lassek and Gaulin, 2011).

The preponderance of evidence suggests that if parents want to have the healthiest and smartest babes that a pregnant woman should consume a lot of seafood while avoiding vegetable oils, total fat and milk (fat, milk and beef moreso from animals that are grain-fed) Grassfed beef has higher levels of n-3, which will balance out the levels of n-6 in the beef. So if you want your family to have the highest cognition possible, eat more fish and less grain-fed beef and animal products.

In sum, if you want the healthiest, most intelligent family you can possibly have, the most important factor is…diet. Diets high in n-3 and low in n-6 are extremely solid predictors of cognitive performance. Due to the ‘meatbolic competition’ between the two fatty acids. This is because n-6 accumulates in the blood and tissue lipids exacerbating the competiiton between linolic acid (the most common form of n-6) and n-3 for metabolism and acylation into tissue lipds (Innis, 2014). Our HG ancestors had lower rates of n-6 in their diets than we do today, along with low to nonexistent disease rates. This is due to the availability of n-6 in the modern diet, which was unknown to our ancestors. Yes, seafood intake had the biggest effect on the PISA math scores, which, in my opinion (I need to look at the data), is due in part to poverty. I’m very critical of PISA, especially as a measure of cognitive abilities, but this study is solid, even though it has pitfalls. I hope a study using an actual IQ test is done (and not Richard Lynn IQ tests that use children, a robust adult sample is the only thing that will satisfy me) to see if the results will be replicated.

I also think it’d be extremely interesting to get a representative sample from each country studied and somehow make it so that all maternal DHA levels are the same and then administer the tests. This way, we can see how all groups perform with the same amounts of DHA (and to see how much of an effect that DHA really does have). Furthermore, nutritonally impoverished countries will not have access to the high-quality foods with more DHA and healthy fatty acids that lead to higher cognitive function.

It’s clear: if you want the healthiest family you could possibly have, consume more seafood.