It’s a known fact that men are stronger, but how much stronger are we really than women? Strength does vary by race as I have covered here extensively. However, I took another look at the only paper that I can find in the literature on black/white strength on the bench press and found one more data point that lends credence to my theory on racial differences in strength.
Strength and gender
Men are stronger than women. No one (sane) denies this. There are evolutionary reasons for this, main reason being, women selected us for higher levels of testosterone, along with differences in somatype. Now, what is not known by the general public is just how much stronger the average man is compared to the average woman.
Miller et al (2008) studied the fiber type and area and strength of the biceps brachii and vastus lateralis in 8 men and 8 women. They were told to do two voluntary tests of strength, using elbow flexion (think biceps curl) and knee extension. (Note: I am assuming they are exercises similar to biceps curls and knee extension, as the authors write that they had custom-made equipment from Global Gym.) They also measured motor unit size, number, and activation during both movements.
The women had 45 percent smaller muscle cross-section area (CSA) in the brachii, 41 percent in the total elbow flexor, 30 percent in the vastus laterus, and 25 percent smaller knee extensors. The last point makes sense, since women have stronger lower bodies compared to their upper bodies (as you can see).
Men were significantly stronger in both upper and lower body strength. In the knee extension, women was 62 and 59 percent of male 1RM and maximal voluntary isometric contraction (MVC) respectively. As for elbow strength, women were 52 percent as strong as men in both 1RM and MVC. Overall, women were 70 and 80 percent as strong as men in the arms and the legs. This is attributed to either men’s bigger fibers or men putting themselves into more physical situations to have bigger fibers to be stronger (…a biological explanation makes more sense). However, no statistical difference between muscle fibers was found between gender, lending credence to the hypothesis that men’s larger fibers are the cause for greater overall upper-body strength.
The cause for less upper-body strength in women is due the distribution of women’s lean tissue being smaller. Women, as can be seen in the study, are stronger in terms of lower limb strength and get substantially weaker when upper-body strength is looked at.
Other studies have shown this stark difference between male and female strength. Men have, on average, 61 percent more total muscle mass than women, 75 percent more arm muscle mass, which translates approximately into a 90 percent greater upper body strength in men. 99.9 percent of females fall below the male mean, meaning that sex accounts for 70 percent of human variation in muscle mass and upper-body strength in humans (Lassek and Gaulin, 2009). Women select men for increased muscular size, which means increased testosterone, but this is hard to maintain so it gets naturally selected against. There is, obviously, a limit to muscle size and how many kcal you can intake and partition enough kcal to your growing muscles. However, women are more attracted to a muscular, mesomorphic phenotype (Dixson et al, 2009) so selection will occur by women for men to have a larger body type due to higher levels of testosterone.
Strength and race
The only study I know of comparing blacks and whites on a big three lift (bench pressing) is by Boyce et al (2014). They followed a sample of 13 white female officers, 17 black female officers, 41 black male officers and 238 white male officers for 12.5 years, assessing bench pressing strength at the beginning and the end of the study. The average age of the sample was 25.1 for the 41 black males and 24.5 for the 237 white males. The average age for the black women was 24.9 and the average for white women was 23.9. This is a longitudinal study, and the methodology is alright, but I see a few holes.
An untrained eye looking at the tables in the study would automatically think that blacks are stronger than whites at the end of the study. At the initial recruitment, the black mean weight was 187 pounds and they benched 210 pounds. They benched 1.2 times their body weight. Whites weighed 180 pounds and benched 185 pounds. They benched 1.02 times their body weight. Black women weighed 130 pounds at initial recruitment and benched 85 pounds, benching .654 times their body weight. White women weighed 127 pounds at initial recruitment and bench 82 pounds, benching .646 times their body weight. Right off the bat, you can see that the difference between black and white women is not significant, but the difference between blacks and whites is.
At the follow-up, the black sample weighed 224 pounds and benched 240 pounds while the whites weighed 205 pounds benching 215 pounds. Looking at this in terms of strength relative to body weight, we see that black males benched 1.07 times their body weight while whites benched 1.04 times their body weight. A very slight difference favoring black males. However, there were more than 5 times the amount of whites in comparison to blacks (41 compared to 238), so I can’t help but wonder if the smaller black sample compared to the white sample may have anything to do with it.
Black women weighed 150 pounds at the follow-up, benching 99 pounds while white women weighed 140 pounds benching 90 pounds. So black women benched 6.6 times their body weight while white women benched .642 times their body weight.
Another thing we have to look at is black body weight compared to bench press decreased in the 12 years while white body weight compared to bench press was diverging with the black bench press compared to body weight.
Furthermore, this study is anomalous as the both cohorts gained strength into their late 30s (testosterone begins to decline at a rate of 1-2 percent per year at age 25). It is well known in the literature that strength begins to decrease at right around 25 years of age (Keller and Englehardt, 2014).
Another pitfall is that, as they rightly point out, they used skin caliper measuring on the black cohort. It has been argued in the literature that blacks should have a different BMI scale due to differing levels of fat-free body mass (Vickery et al, 1988). Remember that black American men with more African ancestry are less likely to be obese, which is due to levels of fat-free body mass. Since fat-free mass is most likely skewed, I shouldn’t even look at the study. I do believe that black Americans should have their own BMI scale; they’re physiologically different enough from whites—though the differences are small—they lead to important medical outcomes. This is why race most definitely should be implemented into medical research. The authors rightly state that when further research is pursued the DXA scan should be used to assess fat-free body mass.
Unfortunately, the authors did not have access to the heights of the cohort due to an ongoing court case on the department for discrimination based on height. So, unfortunately, this is the only anthropometric value that could not be assessed and is an extremely important variable. Height can be used to infer somatype. Somatype can then be used to infer limb length. Longer limbs increase the ROM, in turn, decreaseing strength. The missing variable of height is a key factor in this study.
Finally, and perhaps most importantly, they assessed the strength of the cohort on a Smith Machine Bench Press.
- The Smith Machine is set on a fixed range of motion; not all people have the same ROM, so assessing strength on a smith machine makes no sense.
- To get into position for the Smith Machine, since the bar path is the same, you need to get in pretty much the same position as everyone else. I don’t need to explain the anatomical reasons why this is a problem in regards to testing a 1RM.
- An Olympic bar weighs 45 pounds, but numerous Smith Machines decreases the weight by 10-20 pounds.
- Since the individual is not able to stabilize the bar due to the machine, the chest, triceps, and biceps are less activated during the Smith Machine lift (Saeterbakken et al, 2011)
Due to all of these things wrong with the study, especially the Smith Machine bench press, it’s hard to actually gauge the true strength of the cohort. Depending on the brand, Smith Machines can decrease the load by 10-30 pounds. Combined with the unnatural, straight-line bar path of the movement, it’s not ideal for a true strength test.
Gender differences in strength have a biological basis (obviously) and are why women shouldn’t be able to serve in the military and transgendered people shouldn’t be able to compete with ‘the gender they feel that they are’ (coming in the future).
The more interesting topic is the one on racial differences in strength. The untrained eye may read that paper and walk away assuming that the average black person is somehow stronger than the average white person. However, this study is anomalous since the cohort gained strength into their 30s when the literature shows otherwise. The biggest problem with the study is the Smith Machine bench press. It is not a natural movement and decreases muscle activation in key areas of the chest and triceps which aid in power while doing a regular bench press. Due to this, and the other problems I pointed out, I can’t accept this study.
Of course, height not being noted is not the fault of the researchers, but more questions would be answered if we knew the heights of the officers—which is an extremely critical variable. White males also gained more lean mass over the course of the study compared to blacks—47 percent and 44 percent respectively—which, as I pointed out, is anomalous.
There is more to HBD than IQ differences. I contend that somatype differences between the races are much more interesting. I will be writing about that more in the future.
Furthermore, for anyone with any basic physiology and anatomy knowledge, they’d know that different leverages affect strength. The races differ in somatype on average and thusly have different leverages. This is one out of many reasons why there are racial differences in strength and elite sports. Leverages and muscle fiber typing.
My points on racial differences in strength still hold; the anthropmetric data backs me up, elite sporting events back me up. My theory as a whole to racial differences in sports is sound, and this study does nothing to make me think twice about it. There are way too many confounds for me to even take it seriously when reevaluating my views on racial differences in strength. This study was garbage to assess absolutely strength due to the numerous things wrong with it. I await a more robust study with actual strength exercises, not one done on an assisted machine.
Boyce, R. W., Willett, T. K., Jones, G. R., & Boone, E. L. (2014). Racial Comparisons in Police Officer Bench Press Strength over 12.5 Years. Int J Exerc Sci 7 (2), 140-151.
Dixson, B. J., Dixson, A. F., Bishop, P. J., & Parish, A. (2009). Human Physique and Sexual Attractiveness in Men and Women: A New Zealand–U.S. Comparative Study. Archives of Sexual Behavior,39(3), 798-806. doi:10.1007/s10508-008-9441-y
Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. MLTJ. 2013;3(4):346–350.
Lassek, W. D., & Gaulin, S. J. (2009). Costs and benefits of fat-free muscle mass in men: relationship to mating success, dietary requirements, and native immunity. Evolution and Human Behavior,30(5), 322-328. doi:10.1016/j.evolhumbehav.2009.04.002
Miller, A. E., Macdougall, J. D., Tarnopolsky, M. A., & Sale, D. G. (1993). Gender differences in strength and muscle fiber characteristics. European Journal of Applied Physiology and Occupational Physiology,66(3), 254-262. doi:10.1007/bf00235103
Saeterbakken, A. H., Tillaar, R. V., & Fimland, M. S. (2011). A comparison of muscle activity and 1-RM strength of three chest-press exercises with different stability requirements. Journal of Sports Sciences,29(5), 533-538. doi:10.1080/02640414.2010.543916
Vickery SR, Cureton KJ, Collins MA. Prediction of body density from skinfolds in black and white young men. Hum Biol 1988;60:135–49.
One of the HBD’s supposed biggest findings is that IQ increases as a function of distance from the equator. The theory holds that those groups who experienced colder winters were selected for levels of higher g and they passed on their high IQ genes. Cold winter theory is supposed to explain why some races have higher levels of achievement and IQ than others. However, after a conversation with PumpkinPerson about cold winter theory and tool use, something clicked in my head: the real reason for the increase in brain size in peoples further from the equator wasn’t for IQ, but expertise capacity. I will go through the reasons how and why our brain size increased for the capacity for expertise and not IQ and hopefully put the cold winter theory to rest for good.
Tool complexity/use and brain size
PumpkinPerson is one of the biggest champions of the cold winter theory, writing: “I don’t even understand how one can believe in racially genetic differences in IQ without also believing that cold winters select for higher intelligence because of the survival challenges of keeping warm, building shelter, and hunting large game.” He wrongly assumes that climate theories are the only explanation for racial gaps in intelligence when other theories (such as differing types of sexual selection) could explain the gap just as well. However, since Rushton and Lynn have pushed this theory for 30+ years, it’s still engrained in the minds of some people. It is hard to change your views in the face of contrary data, but for those of my readers who are proponents of cold winters increasing IQ, I hope tonight I can sway you into believing that brain size increased as a function of climate and tool-making, not for IQ.
In his article he cites Richard Lynn (2006: 148), saying:
… hunter-gatherer peoples in tropical and subtropical latitudes such as the Amazon basin and New Guinea typically have between 10 and 20 different tools, whereas those in the colder northern latitudes of Siberia, Alaska, and Greenland have between 25 and 60 different tools. In addition, peoples in cold northern environments make more complex tools, involving the assembly of components, such as hafting a sharp piece of stone or bone onto the end of a spear and fixing a stone axe head onto a timber shaft.
I, of course, don’t doubt that peoples in cold northern environments need more (and complex) tools compared to those in tropical climes. But I look at it from a different point of view.
This is based on the research of Terrence (1983) and his study on time budgeting and hunter-gathering technology. The data does show that the number of tools correlates to latitude, but he leaves out that it also correlates with mobile and immobile and diet. That’s a pretty big factor. Of course, the type of animals around and what you need to do to kill/extract the meat involves a certain type of complex tool. In northern environments, a few more tools are needed to survive, so what? That doesn’t really mean anything. The whole brain-size/IQ latitude cold winter theory can be explained in another way.
Tool use increased our brain size throughout our evolutionary history, so with Arctic peoples living in cold climes where having a bigger brain is advantageous, they already had more neural columns for expertise capacity. The construction of complex tools increased brain size along with the colder climate. If tool use can explain part of the increase in our brain size over 3 million years, why can’t it partly explain why Arctic peoples—who use more (and complex) tools—larger brains over those further from the Arctic? Because brain size increased for expertise capacity, not IQ. Since they had bigger brains they were able to master the creation of complex tools, which further increased their brain size along with colder climates. Those who could make better tools could pass their genes, selecting for bigger brains.
Brain size increased for expertise capacity, not IQ
Table 3.1 in Torrence (1983) makes reference to technounits, a way to gauge the complexity of a particular item (Collard et al, 2011). Those in northerly climes do have tools with higher technounits, however, that’s showing that what is needed to construct the tools is a high capacity for expertise.
Skoyles (1999) posits that brain size increased for expertise capacity, not IQ. Bigger brains cause extreme complications during birth, calling for Caesarian sections (which is driving the evolution of bigger heads), so selection for bigger brains must have been advantageous in another way. Skoyles cites studies showing that microcephalics have brains in the average range of Erectus while having IQs in the normal/above average range. This implies that Erectus could have had IQs in our range, and that selection for bigger heads was caused by something else—the need for expertise.
Even then, the correlation between brain size and IQ cannot be invoked here. A .33-.4 correlation between brain size and IQ still leaves a lot of room for people to have brain sizes in the range of Erectus and still have above average IQs. Assuming a correlation of .51, that leaves 74 percent of the brain size/IQ correlation unexplained. This leaves a lot of room for other explanations for the remaining variance.
So if you think of the implications of Skoyles’ (1999) paper in regards to human races and the quote provided from Lynn (2006), you can look at it as Arctic peoples needed to be able to learn how to make complex tools which required a certain amount of expertise. Acquiring certain types of expertise does lead to certain local changes in the brain due to environmental demands, for instance in racecar drivers (Bernardi et al, 2013) and in taxi drivers in London who were “on The Knowledge” (Maguire et al, 2000). Tool use did cause increases in our brain size in our ancestral past, so the fact that Arctic peoples have bigger brains but lower IQs is explained by brain size being selected for expertise (their expertise to make their numerous tools) and cold climates but cold temperatures do NOT explain intelligence differences between the races.
Indeed, there is evidence that ‘chunks’ form in the brain due to certain types of expertise (Gobet and Simon, 1998). In their study, Gobet and Simon showed that Chess masters used significantly more chunks, extending the chunking theory ” to take account of the evidence for large retrieval structures (templates) in long-term memory.” This study is direct evidence for Skoyles’ contention on “informational chunks (Skoyles, 1999) lending credence to the claim that people who master something have more information stored in their ‘chunks’.
Furthermore, high and low skill employees organize their conceptual knowledge about a problem differently (Lamberti and Newsome, 1989). Low-skilled workers performed much faster on the tasks that needed concrete information organization whereas high-skilled workers were better on the more abstract concepts. Overall, both high- and low-skilled workers processed the same information differently. This study has nothing to do with IQ itself, just how high- and low-skilled workers process information differently (which may come down to ‘chunks’ in the brain).
Chase and Simon (1973) show that the amount of information extracted during a memory and perception task is directly related to the amount of time the individual has played chess. They state that chess skill is “reflected in the speed with which chunks are perceived in the perception task and the size of the chunks in the memory task.” Of course, you can’t just throw anyone into a chess game who has never played before—IQ be damned—and expect them to do well. You need to hone your strategy and skill over time by noticing all types of moves, thinking ahead and guessing what your opponent will do ahead of time. This all takes time playing the game, and since people who have played longer can more easily tap into the ‘chunks’, this shows that chess skill is largely a function of time spend playing (note: IQ is still important, of course. Just, practice makes perfect and one with practice and a low IQ will beat someone with no/little practice and a high IQ).
Expertise does, indeed, take deliberate practice. Practice DOES make perfect.
Our brains increased evolutionarily speaking as to acquire more expertise. Bigger brains (and therefore bigger heads) cause problems with childbirth and so natural selection must have selected bigger brains since they increase expertise capacity. The fact that there are numerous people in the world with Erectus-sized brains and IQs in the normal/above average range lends credence to the claim. Erectus could have possibly had intelligence level near our own. But what really needs to be thought about here is this: It just so happens that the brain size increase corresponds with the beginnings of our modern gait and pelvis (Lieberman et al, 2006). The beginnings of cultural acquisition and transference began around that time (Herculano-Houzel and Kaas, 2011) and so our brain size would have increased due to cooking allowing us to have the energy for a bigger brain with more neurons.
Of course Erectus would need to become an expert with the new-found technology he acquired. Over time, the more ‘expert’ Erectus would have passed their genes on, both for increased brain size and expertise, and the hominin brain size then increased.
Looking at racial differences in brain size while thinking about how expertise capacity increases brain size and thinking about tool use/complexity of Arctic peoples is an alternate (and in my opinion) better theory of explaining racial differences in brain size. I obviously don’t believe that brain size differences cause IQ differences, the brain size differences are a function of climate and tool use/complexity. To make complex tools you need a sort of ‘expertness’, which, as Skoyles argues, causes brain size to increase. This explains the so-called anomalous Inuits with a brain size equal to that of East Asians but with an IQ in the low 90s.
Put simply, complex tools+cold winters+ cooked food=big brains. Cold climates DO NOT by themselves CAUSE higher levels of g. It’s just a correlation, it does not mean that it is causal. Big brains retain heat better in the cold whereas smaller heads cool better. That’s the reason for racial brain size differences, but climate and brain size in and of themselves do not CAUSE racial differences in IQ.
I now believe that sexual selection is a cause for racial differences in IQ, but that’s for another day.
Bernardi, G., Ricciardi, E., Sani, L., Gaglianese, A., Papasogli, A., Ceccarelli, R., . . . Pietrini, P. (2013). How Skill Expertise Shapes the Brain Functional Architecture: An fMRI Study of Visuo-Spatial and Motor Processing in Professional Racing-Car and Naïve Drivers. PLoS ONE,8(10). doi:10.1371/journal.pone.0077764
Chase, W. G., & Simon, H. A. (1973). Perception in chess. Cognitive Psychology,4(1), 55-81. doi:10.1016/0010-0285(73)90004-2
Collard, M., Buchanan, B., Morin, J., & Costopoulos, A. (2011). What Drives the Evolution of Hunter–Gatherer Subsistence Technology? A Reanalysis of the Risk Hypothesis with Data from the Pacific Northwest. Culture Evolves, 341-358. doi:10.1093/acprof:osobl/9780199608966.003.0020
Dr. John R. Skoyles (1999) HUMAN EVOLUTION EXPANDED BRAINS TO INCREASE EXPERTISE CAPACITY, NOT IQ. Psycoloquy: 10(002) brain expertise
Gobet, F., & Simon, H. A. (1998). Expert Chess Memory: Revisiting the Chunking Hypothesis. Memory,6(3), 225-255. doi:10.1080/741942359
Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.
Lamberti, D. M., & Newsome, S. L. (1989). Presenting abstract versus concrete information in expert systems: what is the impact on user performance? International Journal of Man-Machine Studies,31(1), 27-45. doi:10.1016/0020-7373(89)90031-x
Lieberman, D. E., Raichlen, D. A., Pontzer, H., Bramble, D. M., & Cutright-Smith, E. (2006). The human gluteus maximus and its role in running. Journal of Experimental Biology,209(11), 2143-2155. doi:10.1242/jeb.02255
Lynn, R. (2006). Race differences in intelligence: An evolutionary analysis. Augusta, Ga.: Washington Summit Publishers.
Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences,97(8), 4398-4403. doi:10.1073/pnas.070039597
Torrence, R. (1983). Time budgeting and hunter-gatherer technology. In G. Bailey (Ed.). Hunter-Gatherer Economy in Prehistory: A European Perspective. Cambridge, Cambridge University Press.
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).
Some people are scared of testosterone. This is no surprise, since a super-majority of people have no background in the human sciences. I’m sure plenty men know what it’s like to have low testosterone, just like some men know what it’s like to have higher T levels than average. What is the optimum level of testosterone? Why are some people scared of this hormone?
Rushton (1997) posited that r/K Selection Theory could be used to classify the races of Man on a spectrum, going from r-selection (having many children but showing little to no parental care) to K-selection (having fewer children but showing a lot of parental care). He stated that the traits of the races were also on the r/K spectrum, with the races having stark differences in morphology. Rushton’s application of r/K theory to humans isn’t completely wrong, though I do have some problems with some of his claims, such as his claims that the races differ in average penis size. He contends that testosterone is the cause for higher crime rates for black Americans and higher rates of prostate cancer in black Americans compared to white Americans.
However, in 2014, Richard et al showed that when controlling for age, blacks had 2.5 to 4.9 percent more testosterone than whites, on average. This cannot explain racial differences in prostate cancer. However, some people may emphatically claim that the races differ in average testosterone, with blacks having 13 percent higher free testosterone than whites on average. The citation that gets used the most to prove that blacks supposedly have higher testosterone than whites is Ross et al (1986), which is based on a sample of 100 people (50 black, 50 white). He claims that it’s when T levels are higher, so it’s a ‘better study’ even though the sample leaves a lot to be desired. A much more robust study showed that the difference was negligible, and not enough to account for the differential prostate cancer rates between the races.
Rohrmann et al (2007) show that there are no differences in circulating testosterone between blacks and whites in a nationally representative sample of American men. Mexicans had the highest levels. There were, however, B-W differences in estradiol production. They couldn’t confirm the other studies that stated that blacks had higher testosterone, possibly due to variations in age or using non-representative samples (that’s the culprit). Their nationally representative sample showed there was no difference in testosterone between blacks is whites, while the meta-analysis showed by Richard et al (2014) showed the difference was negligible at 2.5 to 4.9 percent higher rate of testosterone which doesn’t explain why blacks have a higher rate of acquiring prostate cancer.
The much more likely culprit for blacks having higher rates of prostate cancer, as I have written about before, are environmental factors. The two main factors are receiving less sunlight and diet. There is no evidence that higher levels of testosterone lead to prostate cancer (Michaud, Billups, and Partin, 2015). Contrary to those who say that higher levels of T cause prostate cancer, there is growing evidence that lower levels of T lead to prostate cancer (Park et al, 2015). Put simply, there is no evidence for testosterone’s supposed impact on the prostate (Stattin et al, 2013).
Differences in androgen/androgen receptors have been explained as a cause for racial differences in prostate cancer (Pettaway, 1999), however, these results haven’t been consistent (Stattin et al, 2003) and these differences in circulating androgen may possibly be explained by differences in obesity between the two populations (Gapstur et al, 2002; also see my posts on obesity and race).
Due to the ‘testosterone scare’, some people may believe that having low T is a ‘good thing’, something that’s preferred over being a high T savage. However, testosterone and the androgen receptor gene polymorphism are both associated with competitiveness and confidence in men (Eisenegger et al, 2016) and a reduced risk of cardiovascular disease in elderly men (Ohlsson et al, 2011). Obviously, lower testosterone is related to less overall confidence. People who have the thought in their head that testosterone is a ‘bad hormone’ will believe the negativity about it in the media and popular headlines.
Testosterone alone does not cause violence, but it does cause men to be socially dominant. Testosterone has been shown to increase in the aggressive phases of sports games and when shown artificial humans made to invoke physiologic responses, leading some researchers to argue that testosterone should be classified as a stress hormone. Testosterone does change based on watching one’s favorite soccer team winning or losing in a sample of 21 men (Bernhardt et al, 1998), lending some credence to the claim that testosterone is and should be classified as a stress hormone. Also of interest is that men who administered high levels of testosterone did not report higher levels of aggression (Batrinos, 2012).
I’ve heard some people literally say that having low testosterone is ‘a good thing’. People say this out of ignorance. There are a whole slew of problems associated with low testosterone, including but not limited to: insulin resistance in diabetic men (Grossmann et al, 2008); metabolic syndrome (Tsuijimura et al, 2013); muscle loss (Yuki et al, 2013); stroke and transient ischemic attack (a mini-stroke; Yeap et al, 2009); associated with elevated risk for dementia in older men (Carcaillon et al, 2014); myocardial infarction (heart attack) in diabetic men (Daka et al, 2015) etc. So it seems that the fear of testosterone from those in the anti-testosterone camp are largely blown out of proportion.
Testosterone is also a ‘food’ for the brain, with low levels being related to mental illness, sexual dysfunction, lower quality of life and cognitive impairment (Moffat et al, 2011) in both sexes (Ciocca et al, 2016). Noticed in both men in women with testosterone deficits were: cognitive impairment (reduction of working memory, episodic memory, processing speed, visual-spatial functioning and executive performance); a decrease in sexual activity; anxiety, schizophrenia, depression and stress; and alterations in cortical thickness in the brain. The fact that testosterone is so heavily important to the body’s central functioning is extremely clear. This is why it’s laughable that some people would be happy and brag about having low testosterone.
I recently came across a book called The Testosterone Hypothesis: How Hormones Regulate the Life Cycles of Civilization. Barzilai’s main premise is that the rise and fall of the West is mediated by the hormone testosterone, and due to lower testosterone levels this is one large reason for what is currently occurring in the West. The book has an extremely interesting premise. Barzilai’s hypothesis does line up with the declining levels of testosterone in America (Travison et al, 2007) though other research shows no decline in American testosterone levels from the years 88-91 to 99-04 (Nyante et al, 2007). Moreover, men who had higher level of n-6 in their blood then n-3 were far more likely to be infertile (Safarinejad et al, 2010) a marker of low testosterone (Sharpe, 2012). The ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 1992). The ratio of n-6 to n-3, on top of lowering sperm count (which is correlated with testosterone) also has negative effects on male and female cognitive ability (Lassek and Gaulin, 2011).
Barzilai’s research also corroborates Rushton’s (1986) theory of why there are lower birthrates for Europeans around the world. Rushton stated that this cycle has been noticed throughout history, with empires rising and falling due to differential birthrates between the ruling class and the ruled. Rushton also hypothesized that the cultures and gene pools associated with the Graeco-Roman empire were “evolutionary dead ends” (Rushton, 1986: 148). Knowing what we now know about the relationship between cognitive ability, testosterone, and fertility, we now have a plausible hypothesis for Rushton’s hypothesis and one of the (many) reasons why the Graeco-Roman empire collapsed. Rushton further hypothesized that the cause for lower fertility in European populations “may be partly mediated by a psychological process in which the desire to be in control of both oneself and one’s environment is taken to an extreme.” Of course there’s a good chance that this psychological process is mediated/influenced by testosterone.
Europe is the continent with the lowest fertility (ESHRE Capri Workshop Group, 2010). Testosterone has declined in Europe as a whole (Rivas et al, 2014), and this is a strong cause for the lower birthrates in Europe (along with genetic reasons) and in Finland (Perheentupa et al, 2013). The introduction of Westernized diets lowers testosterone, so this is no surprise that a reduction is seen in countries that begin to consume a Western diet. Another probable cause for lower testosterone/fertility in Europe at the moment is the large number of European men that died in WWI and WWII. Those that were more willing to fight died, meaning there was less of a chance he spread his genes. So, over time, this lead to the current cucking of Europe that we are now witnessing.
Testosterone is also hypothesized to have driven evolution (Howard, 2001). Testosterone is such an important part of human evolution and development, so much so that if we had a lower level of the hormone all throughout our evolution that we would be a different species today. Testosterone is needed for sexual functioning, good mental and brain health, fertility, cognitive ability, muscle mass retention in both young and old men, etc. Testosterone is one of the most important hormones for both men and women, and low levels for both sexes are detrimental to a high quality of life. The current data on testosterone and prostate cancer shows that higher levels of testosterone don’t contribute to prostate cancer. Testosterone, then, also isn’t a cause for the racial gap in prostate cancer because other environmental factors better explain it. If people really are happy about having lower testosterone, then I hope they have fun living a life with a low sex drive, lower cognition in old age, lower muscle mass and a higher chance of stroke and metabolic syndrome.
One of the most interesting things about testosterone is the possibility that it explains why civilizations rise and fall. There is anecdotal evidence from Rushton, as well as his theorizing that the higher classes in Rome didn’t breed which led to their downfall. We now know that lower fertility rates for men are associated with lower testosterone, so along with Barzilai’s thesis of testosterone causing the rise and fall of civilizations, Rushton’s theorizing of the cause of lower European fertility and the cause of the fall of the Graeco-Roman empire.
Testosterone is an extremely important hormone, one that drives human evolution and society formation since it’s associated with dominance and confidence. Low testosterone is looked at as ‘good’ because those with higher intelligence have lower levels of the hormone (indicated by lower confidence and having sex at a later age). I showed that the higher IQ East Asian men have a problem finding dates and being looked at as sexually attractive (even though they rated themselves as average). Along with lower East Asian fertility, specifically in Japan, does it seem to you like the high IQ people are more desired if they are having problems keeping their birthrates up? The fact of the matter is, lower levels of testosterone are correlated with lower levels of fertility. If men don’t have as much testosterone pumping through their veins, they will be less likely to have sex and thusly reproduce.
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Daka, B., Langer, R. D., Larsson, C. A., Rosén, T., Jansson, P. A., Råstam, L., & Lindblad, U. (2015). Low concentrations of serum testosterone predict acute myocardial infarction in men with type 2 diabetes mellitus. BMC Endocrine Disorders,15(1). doi:10.1186/s12902-015-0034-1
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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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When critics of the mainstream approach towards modern African-American grievance questions the agency of the population to improve their standards of living, they often cite either how minorities such as poor European immigrants of the Early 20th century assimilated better despite discrimination, or how Black immigrants from Africa occupy a higher mode of living.
While multiple factors contribute to the discrepancy, one caught my attention which struck me a paradoxical but soon started to make sense as I dug deeper. That trait being the lack of effective widespread “unity” among not just Black Americans but many other populations, especially those in Africa.
– The Situation
As for my titular use of “chaos” to describe it, I owe it to an Unz commenter who contrasted it from individualism or collectivism. For an intra-regional example, you have riots or protests regarding threats seen as pertaining to the racial mass, yet you have commonly cited the lack of the same regard for those killed by perpetrators of the same race.
From an inter-regional example I refer to the words of my father that, despite the beliefs of some, there is no “Black America” in which the interests or beliefs of blacks due to having comparatively looser connections than others based on a national level. This is noted by regional variance in ideology between blacks during the Progressive Era or better yet modern African conflicts, many of which can be classified as Christians versus Muslims on the larger scale yet can even be observed on a finer, pre-colonial level of identities (Osaghae and Suberu 2005).
“There are numerous examples of pre-colonial migration, usually stimulated by wars or natural disasters, which have continued to generate bitter conflicts today owing to continuing discrimination against the immigrants by the original settlers. These include the eighteenth century mass migration of Oyo Modakeke into Ife in search of a safe haven from the internecine wars of the Oyo empire; the movement of Urhobo and Ijaw into Warri, where the Itsekiri claim to have been the original settlers; the migration of the Jukun-Chamba from Cameroon to parts of the present Taraba state, originally settled by the Kuteb; and the sixteenth century settlement of Hausa merchants in Zangon Kataf within a territory occupied by the Kataf (Isumonah 2003; Mustapha 2000). “
I attribute three reasons why this would be.
One being geography, as these behaviors are most notable with African nations that often overlap in cultural spheres despite living on a huge continent, and also how Black Americans probably covering the largest area relative to other New World African descent populations thus making diversification more enabled.
The second being the process of slavery in New World populations giving various forms of cultural transmission amongst black slaves by region who as well came through different tribes, either producing the typical “Scot-Irish” Black culture or a “Creole” culture, like the Gullah people of the South East. The Third, the Basal reason, being the effects of Genetic interests at hand as put by RR and how African Diversity works.
Here Razib Khan explains that when Foreign Admixture is removed, African diversity is higher among individuals than for major geographical groups.In other words, while geographically diverse, the actual organization of the diversity in the context of cultural boundaries is more stratified due to the lack of breeding, be it outbreeding or replacement involved in nations.
This suggestion is strengthened by famous blogger Jayman attributing this to the lack of large states in Africa to the lack of especially large states in Africa. Granted, you did have relatively large ones in the Sahel but the didn’t last as long as those in Eurasia, falling mainly due to internal struggles.
In the presence of cultural homogeneity, reflecting of a shared lineage, you see improvements in places such as Botswana (Tswana-Sotho) or Ghana (Akan people) partially due to better cultural, and thus likely genetic, unity due to past nationhoods. Apparently, though for short duration, the Tswana formed a political body as large as France,
This is also consistent with the observations made by Sir Harry Hamilton Johnston, a famous colonialist researcher on African and US blacks, on African born blacks on the sea Islands of the South East, which he describes as of “Yoruba Stock” in semblance.
“Also they are when away from white influence inclined to sparsity of clothing-not nowadays a common trait in the United States negro. They are also pure negroes entirely without any infusion of white blood. Crime is very rare among them.” The Negro in the New World by Harry Hamilton Johnston p. 470
A good modern example would be the demographics of West Africa Immigrants, being principally Akan of Ghana and the Yoruba or Igbo of Nigeria, who each come from relatively well constructed precolonial formations. What is also of note is how their prominence seems to be correlated to the extent in which Cousin Marriage is practiced, possibly reflective of the precolonial patterns of cousin marriage
Application for the U.S population in kin networks, where it does not work.
PP, in which he discussed the ethnocentrism of different groups, said this regarding blacks and kin altruism.
“And yet eventually these extremely different tribes mixed, and so you would have parents raising kids who have genetic variants very alien to their own, and this probably contributed to the breakdown of the black family: it’s harder for kin altruism to get selected when the kids you are altruistic to, don’t resemble you that much genetically because their other parent is so unlike you that they don’t inherit your high degree of kin altruism or inherit it as a recessive unexpressed trait. And when kin altruism gets only weakly selected for, racial loyalty (which is probably just an outgrowth of kin loyalty) is probably weakly selected for too.”
Which would be incorrect. Yes, while crossing over does occur, a child would be overall close to their parent’s overall genetic background on the level of relatedness. Leaping from that neglected detail, he assumes from his evidence of “lack of racial loyalty” would that blacks have less ethnic nepotism and thus weaker kin altruism despite not taking into account of selection occurring within subgroups of various constructs like you see in Africa which would apply to families inside them.
If this theory was even supportable, one would expect the opposite that actually occurs with the percentage of Black children to return to relatives compared to White children.
“Of the 94,483 black children discharged from foster care, 12,860, or 13%, were discharged to a relative guardian. Of the 182,941 white children discharged from foster care in 2004, 20,453, or 11%, were discharged to a relative guardian.Of the 15,087 black children adopted from foster care, 4077, or 27%, were adopted by a relative. Of the 29,244 white children adopted from foster care, 5861, or 20%, were adopted by a relative. Of the 279,421 black kids living in foster care for some portion of the year, 69,888 or 25% were living with relatives. Of the 474,734 white children living in foster care for some portion of the year, 101,300, or 21%, were living with relatives.
So black children getting adopted from foster care are somewhat more likely to be adopted by relatives than white kids (27% vs. 20%), black kids exiting foster care are slightly more likely to be discharged to a relative guardian than white kids (13% to 11%), and black kids in foster care are slightly more likely to be living with relatives than white kids (25% vs. 21%). The differences support the hypothesis that blacks are more likely to utilize kinship care networks, but not by a lot, at least in regard to the foster care system.”
From Audacious Epigone, who also notes that despite the higher likelihood of such networks that doesn’t explain disproportion in foster care. Though evidence for IQ is at best moderate, interpersonal indicators were stronger (Azar, Stevenson, and Johnson 2012)).
“SIP problems were associated with direct measures of neglect (e.g., cognitive stimulation provided children, home hygiene, belief regarding causes of child injuries). Further, for the direct measures that were most closely linked to CPS Neglect Status, IQ did not add significant predictive capacity beyond SIP factors in preliminary model testing. Implications for intervention with PID discussed.”
This is possibly linked to EI scores found to differ between Whites and Blacks (Whitman, Kraus, and Rooy 2014)
“The present work examines applicant reactions to a test of emotional intelligence (EI) using an organizational sample of 334 job applicants. Results indicated that Blacks had higher face validity and opportunity to perform perceptions of EI than Whites, but that Whites performed significantly better than Blacks on the EI test. Although exploratory analyses revealed that test performance was positively related to test reactions, we also found that the magnitude of this relationship differed between Blacks and Whites for the opportunity to perform perceptions. We discuss our findings by offering practical advice for organizations considering or using a measure of EI for selection and assessment.”
Evidence for Kin networks is also supported by more data (Taylor 2013).
“Turning first to findings for family support networks, four significant differences were observed in this analysis. African Americans gave assistance to their family members more often than non-Hispanic Whites, were more likely to have daily contact with their extended family members than both non-Hispanic Whites and Black Caribbeans, and had more frequent interactions with their family than Black Caribbeans. Three general conclusions can be drawn from these findings for family assistance and interaction. First, these findings are consistent with prior work indicating that African Americans have similar or higher levels of involvement with kin than non-Hispanic Whites, but are inconsistent with reports that African Americans have lower levels of family support than Whites (e.g., Hogan et al., 1993). As noted in previous reviews of this literature (Sarkisian & Gertsel, 2004), comparisons across studies are problematic given important differences in the dependent variables used. The present study’s investigation of several dimensions of family support relationships (e.g., enacted support, emotional support, contact, negative interaction) in diverse groups of the population and using a common set of sociodemographic correlates clarifies the nature of race/ethnic differences in these relationships.”
It also found, however, weaker ties outside the family, which strengthen my suggestion of finer stratification of kin ties than just simply less selection.
“Several significant differences in friendship networks were observed in this analysis. Non-Hispanic Whites interacted with their friends and gave support to their friends more frequently than African Americans. Additionally, non-Hispanic Whites received support from friends more frequently than both African Americans and Black Caribbeans. Many of the differences between African Americans and non-Hispanic Whites could reflect basic differences in their levels of involvement in friendship networks. For instance, 16.7% of African-Americans, 16.1 % of Black Caribbeans and 9.7% of non-Hispanic Whites report that they never receive help from friends. Similarly, African Americans (11%) were twice as likely as non-Hispanic Whites (4.7%) to indicate that they hardly ever or never interact with friends. Lower levels of involvement with friends among African Americans could be due to estrangement from friends, isolation from friends or exclusive involvement with kinship networks (Ajrouch et al., 2001). Collectively, these results, and previous research (Griffin et al., 2006; Waite & Harrison, 1992), indicate that non-Hispanic Whites are more likely than African Americans to interact with friendship networks and to identify friends as an important source of support.”
This lack of support was not seen, however, with fictive kin or congregational members. So perhaps wither the perception of relationship or differences in genetic similarity may answer some of these questions.
By Scott Jameson
I’ve been active in the blogosphere for around 24 hours now and I’ve already gotten a negative response from someone who happens to be wrong. That’s a win in my book.
The argument we’re having is, as best I can tell, why some populations out there just don’t have obesity as an observed phenotype amongst their members. TL;DR: Pumpkin Person and Robert Lindsay believe that genetics explain why there are no obese New Guineans. But it ain’t so.
The original context is an old Pumpkin Person post. Much of what he’s saying here doesn’t seem too off-base; for example he says that behavioral genetics may explain much of the differences in BMI between individuals within the same population. True. It is possible that some people are genetically inclined to eat more or unhealthier foods, rather than simply being genetically inclined to putting on weight regardless of what they do.
As an aside, genotypes that affect how you digest things also probably explain part of the BMI gap between skinny folks and fat folks within the first world. The APOA2 gene for example has a recessive allele that is associated with higher BMI in people who eat more saturated fats. The interactions between genes and environment which determine BMI are complicated and not yet fully understood, but I’m willing to bet that being genetically worse at processing certain nutrients is a part of the problem, and that being genetically inclined to stuff your face is a part of the problem as well. PP is probably right about that issue.
Where he and Lindsay get it wrong is using examples of people from Podunk, New Guinea as evidence for obesity “being genetic” (relative term). Obesity is a gene-environment interaction such that, without certain environmental inputs, you simply won’t get the phenotype. History tells us that that input is processed carbohydrates.
There was a time when people could have used Australian Aboriginals or Inuit or Pima Indians as examples of groups of people who just don’t have obese folks amongst their numbers, just as Lindsay did with a few populations. Homo sans lardicus. Then the White Devils showed up with their refined Einkorn wheat products and their firewater and so on. Now those populations have fat people in them.
There’s an ongoing debate as to whether some populations are more resistant to the fattening effects of processed carbs or not. My guess is, the answer’s yes (and you’d look at Europeans and East Asians to see the more carb-resistant people, in theory) but that topic would merit its own post. That being said, every population in the world will almost assuredly have obese people in it after you introduce processed carbs. All of the populations that were introduced to this diet, now have fat people in them.
Heritability of BMI is high within the first world because the relevant environmental input is pretty uniform: everybody has access to potatoes, everybody has access to broccoli. As PP points out, which you’re likely to eat and how much you’re likely to eat likely depends on your genetics. As I point out, how your body processes the nutrients also has a likely genetic component. But the environmental contribution to our within-population differences in BMI is low (~20%) because we all have access to roughly the same stuff.
Rural New Guineans, lacking a bunch of processed carbs, could hardly get fat if they tried their best to. That’s a big between-population, nonheritable cause for a phenotypic difference; this means that environment probably explains most of the BMI gap between them and us. If I wanted evidence to refute Lindsay’s assertion that New Guineans are skinnier thanks to genetics, I’d find a population of urbanized New Guineans somewhere with higher average BMI. Such a group would have New Guinean genetics but a “developed” environment vaguely similar to ours; if they were fatter than their rural ken, then Lindsay’s hypothesis that New Guineans are just genetically obesity-free would be falsified.
by Scott Jameson
For my first post on this blog, I thought I’d talk about something relevant to the mission of the blog: Political Correctness. I’m very grateful to RaceRealist for inviting me to hop on board here (although I should put out the categorical disclaimer that me posting here is not in and of itself an endorsement of any given thing he’s said over the years).
This is going to be something of an opinion essay about why denying reality is silly: because you still have to live in it. Most of my content is going to be more empirically driven, as you’re used to on this blog. Bear with me.
The SAT’s name change story is a classic case of “Political Correctness,” and is mirrored by KFC’s story of adapting to new nutritional standards. For those out of the loop: after the public realized how unhealthy fried foods are, Kentucky Fried Chicken changed its name to KFC. The point was to make the unhealthy nature of the food one conceptual extrapolation away from the name itself, in hopes that the public would not bother to recall what the “F” stood for.
SAT originally stood for “Scholastic Aptitude Test.” It was (and is) a test to determine how apt you are for scholarly endeavors. Put bluntly, it’s a somewhat sloppy IQ test oriented towards scholarly settings in particular. Of course, that name was too accurate, so it fell out of favor. The public does not want to live in a world wherein poor students are less apt than rich students and Black students are less apt than White students, and so the Scholastic Aptitude Test became the Scholastic Assessment Test. In order to be offended by that, you have to remember that what’s being assessed is aptitude and that nothing has changed. Like “KFC,” it was one conceptual extrapolation away from the reality at hand. Most people were probably too harebrained to see through that.
For some reason, they kept rolling with it. It became an alleged Reasoning Test, and then simply a series of letters that used to be an abbreviation: “the SAT,” no doubt an homage to The Colonel and the chicken he hawks. They’re both just a series of letters now – the unpleasant realities contained therein have been conceptually sterilized. Like the SAT, the nutritional content of the chicken hasn’t changed as much as the name has.
You may suspect that I’m simply flinging excrement in the general direction of The College Board, but there’s a point to what I’m saying here. What we call “Political Correctness” is a pervasive scrubbing of reality out of the consciousness of the public at large, especially the young. There was a time when people were allowed to say things like “I do not enjoy living around Blacks/Whites/Hispanics/whomever.” “Political Correctness” entered from stage left, and then Boomers had to say “bad schools” and “bad neighborhood” instead. Odds are, the Boomers understood the connotative meanings, at least at first. But if you asked millennials what those terms are, I’d bet on most of them actually being ignorant enough to think that the schools are themselves the problem. Nobody ever pointed out to these kids that almost all of the “bad schools” – the schools with low average test scores – are simply full of Hispanics (Mestizos) and African Americans who have low average test scores regardless of what school they’re in, and that the supermajority of all of the “good schools” aren’t. Anyone who doesn’t know this has been deliberately rendered ignorant of a reality that is important to their lives.
What we call “Political Correctness” is in fact the successful, systematic obfuscation of reality, and having reality perpetually hidden from you is dangerous. That is why we at this blog are NotPoliticallyCorrect. As long as I’m here, I can promise you my best attempt at discovering and conveying the truth in the NotPoliticallyCorrect fashion exemplified thus far by RaceRealist: bringing you interesting truths, obscure truths, and of course, controversial truths.
I’m not the first to make the SAT-KFC comparison, by the way. After I wrote this article, I looked around for sources only to dredge this up.