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Race, Obesity, Poverty, and IQ

2100 words

America has a current and ongoing obesity epidemic. Some ethnicities are more likely to be obese or overweight than others due to lower intelligence which means a lack of ability to delay gratification, lack of ability to think into the future, lower funds which translates to eating more refined carbohydrates which means more blood glucose spikes which then leads to obesity as I will show. Insulin has a causal relationship with obesity so those who lack funds to buy healthier food then turn to refined foods high in carbohydrates as they are cheaper and more abundant in low-income neighborhoods.

Adult obesity rate by State (top 5) is: 1) Louisiana (36.2 percent), 2) Alabama (35.6), West Virginia (35.6), and Mississippi (35.6), and 5) Kentucky (34.6) with the 5 least obese States being 51) Colorado (20.2), 49) Hawaii (20.7), 48) Montana (23.6), 47) California (23.2), and 46) Massachusetts (24.3). Notice how the States with higher rates of obesity are in the South and the States with the lower rates are in the North, give or take. The average IQ for these States as follows: Lousiana: 95.3, Alabama: 95.7, West Virginia 98.7, Mississippi 94.2 (lowest IQ State in the country, largest black population at 37 percent), and Kentucky at 99.4. The average IQ for those States is 96.66. The average IQs for the States with the lowest obesity rates are: Colorado 101.6, Hawaii 95.6, Montana 103.4, California 95.5, and Massachusets 104.3 (highest IQ State). The average for these States being 100.08. So there is a 4 point IQ difference between the top 5 States with the highest and lowest percentage of obese people, which goes with the North/South gradient of higher IQ people living in the North and lower IQ people living in the South. Back in 2014, a California real estate group took 500,000 Tweets using a computer algorithm and estimated intelligence based on spelling, grammar, and word choice and found a difference in State by State intelligence. Notice how the further North you go the higher the average intelligence is, which is then correlated with the obesity levels in that State.

With poverty rates by State, we can see how the States in the South have less intelligent people in them which then correlates to the amount of obesity in the State. Though, there are some anomalies. West Virginia and Kentucky have a super majority of whites. This is easily explained by the fact that less intelligent whites live in those States, and since both the poverty rates and obesity rates are high, it follows that the State will be less intelligent than States that have more intelligent people and less obesity.

It is known that intelligence is correlated with obesity at around -.25 (Kanazawa, 2014). The negative correlation between intelligence and obesity means that they are inversely related so, on average, one with higher intelligence has less of a chance of being obese than one with lower intelligence. The States with the lowest IQ people having those with the highest BMIs corroborates this. In America, obesity rates by ethnicity are as follows: 67.3% for whites, 75.6% for blacks, and 77.9% for ‘Hispanics’.

Now that we know the average intelligence rates by State, the percentage of obese by State and the demographics by State, we can get into why obesity rates correlate with intelligence and race.

Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake.  Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.

Drewnowski and Specter (2004) showed that 1) the highest rates of obesity are found in populations with the lowest incomes and education (correlated with IQ), 2) an inverse relationship between energy density and energy cost, 3) sweets and fats have higher energy density and are more palatable (food scientists work feverishly in labs to find out different combinations of foods to make them more palatable so we will eat more of them), and 4) poverty and food insecurity are associated with lower food expenditures, lower fruit and vegetable intake, and lower-quality diet. All of these data points show that those who are poor are more likely to be obese due to more energy-dense food being cheaper and fats and sugars being more palatable.

Now that I’ve shown the relationship between race and IQ by state, obesity rates by state, insulin sensitivity by race, and that those in poverty are more likely to be obese, I can now talk about the actual CAUSE of obesity: insulin.

The conventional wisdom is that if you consume more kcal than you expend, you will gain weight, whereas if you consume less than your daily needs you will lose weight. This has been unchallenged for 50 years. Also known as Calories In and Calories Out (CICO), this mantra “eat less and move more!!!” has been bleated over and over with horrendous results. The CICO model only concerns itself with calories and not insulin which is a causal factor in obesity

In this study, participants in the basal insulin group which received the lowest average insulin dose gained the least average amount of weight at 4.2 pounds. Those on prandial insulin gained the most weight at 12.5 pounds. The intermediate group gained 10.3 pounds. More insulin, more weight gain. Moderate insulin, moderate weight gain. Low insulin, low weight gain.

Researchers compared a standard dose of insulin to tightly control blood sugars in type 1 diabetic patients. At the end of the 6 years, the study proved that intensive control of blood sugars resulted in fewer complications for those patients.

Though, in the high dose group, they gained on average 9.8 pounds more than those in the standard group.

More than 30 percent experienced major weight gain! Prior to the study, both groups were equal in weight. But the only difference was the amount of insulin administered. Were the ones given high levels of insulin all of a sudden more lazy? Were those who gained weight suddenly lacking in willpower? Were they lazier before the study? We’re they more gluttonous? No, no, and no!!

delprato_24

(source)

Finally, Henry et al (1993) took Type II diabetics and started them off with no insulin. They went from 0 units of insulin a day to 100 units at 6 months. As higher rates of insulin were administered, weight rose in the subjects. Insulin was given, people gained weight. A direct causal relationship (see figure above). However, what’s interesting about this study is that the researchers measured the amount of kcal ingested, the number of kcal ingested was reduced to 300 per day. Even as they took in less kcal, they gained 20 pounds! What’s going on here? Well, insulin is being administered and if you know anything about insulin it’s one of the hormones in the body that tells the body to either store fat or not burn it for energy. So what is occurring is the body is ramping down its metabolism in order for the subject to store more fat due to the exogenous insulin administered. Their TDEE dropped to about 1400 kcal, while they should have been losing weight on 1700 kcal! The CICO model predicts they should have lost weight, however, adaptive thermogenesis, better known as metabolic slow down, occurred which dropped the TDEE in order for the body to gain fat, as insulin directly causes obesity by signaling the body to store fat, so the body drops its metabolism in an attempt to do so. 

Putting this all together, blacks and ‘Hispanics’ are more likely to be in poverty, have lower intelligence, and have higher rates of obesity and diabetes. Furthermore, blacks are more likely to have metabolic diseases (adaptive thermogenesis aka metabolic slowdown is a metabolic disease) which are related with obesity due to their muscle fiber typing which leads to lower maximal aerobic capacity (less blood and oxygen get around the body). Type II skeletal muscle fibers’ metabolic profile contributes to lower average aerobic capacity in blacks. It also is related to cardiometabolic diseases, in my opinion because they don’t have the muscle fiber typing to run long distances, thus increasing their aerobic capacity and VO2 max.

Due to the diets they consume, which, due to being in poverty and having lower intelligence, they consume more carbohydrates than whites, which jacks their blood glucose levels up and the body then releases insulin to drive the levels glucose in the body down. As insulin levels are spiked, the body becomes insulin resistant due to the low-quality diet. Over time, even a change in diet won’t fix the insulin resistance in the body. This is because since the body is insulin resistant it created more insulin which causes insulin resistance, a vicious cycle.

Poverty, intelligence and race both correlate with obesity, with the main factor being lower intelligence. Since those with lower IQs have a lack of foresight into the future, as well as a lower ability to delay gratification which also correlates with obesity, they cannot resist low-quality, high-carb food the same way one with a higher IQ can. This is seen with the Diaz et al study I linked, showing that whites have higher levels of fat intake, which means lower levels of carbohydrate intake in comparison to blacks and ‘Hispanics’. As I’ve shown, those in poverty (code word for low intelligence) ingest more refined carbohydrates, they have higher levels of obesity due to the constant spiking of their insulin, as I have shown with the 3 aforementioned studies. Since blacks and ‘Hispanics’ have lower levels of intelligence, they have lower levels of income which they then can only afford cheap, refined carbs. This leads to insulin being constantly spiked, and with how Americans eat nowadays (6 times a day, 3 meals and snacks in between), insulin is being spiked constantly with it only dipping down as the body goes into the fasted state while sleeping. This is why these populations are more likely to be obese, because they spike their insulin more. The main factor here, of course, is intelligence.

Another non-CICO cause for obesity is exposure to BPA in the womb. Researchers carried out BPA testing in three differing subjects: 375 babies invitro, (3rd trimester) children aged 3 (n=408) and aged 5 (n=518) (Hoepner, et al, 2016). They measured the children’s bodies as well as measuring body fat levels with bioelectrical impedance scales.Prenatal urinary BPA was positively associated with waist circumference as well as fat mass index, which was sex-specific. When analyzed separately, it was found that there were no associated outcomes in body fat for boys (however it does have an effect on testosterone), but there was for girls (this has to do with early onset puberty as well). They found that after controlling for SES and other environmental factors there was a positive correlation with fat mass index – a measure of body fat mass adjusted for height, body fat percentage and waist circumference. The researchers say that since there was no correlation between BPA and increased obesity, that prenatal exposure to BPA indicates greater vulnerability in that period. The sample was of blacks and Dominicans from New York City. Whites drink less bottled water, which has higher levels of BPA. Blacks and ‘Hispanics’ consume more, and thus have higher levels of obesity.

In conclusion, blacks and ‘Hispanics’ are more likely to be in poverty, have lower intelligence, higher rates of obesity and lower incomes. Due to lower incomes, cheap, refined carbohydrates is what they can afford in bulk as that’s mostly what’s around poor neighborhoods. Ingesting refined carbohydrates more often consistently jacks up blood glucose which the body then releases insulin to lower the levels. Over time, insulin resistance occurs, which then leads to obesity. As I’ve shown, there is a direct causal relationship between the amount of insulin administered and weight gain. With the aforementioned factors with these two populations, we can see how the hormonal theory of obesity fits in perfectly with what we know about these ethnic groups and the obesity rates within them. Since people in poverty gravitate more towards cheap and refined carbohydrates, they’re constantly spiking their insulin which, over time, leads to insulin resistance and obesity.

The ENA Theory: On Testosterone and Aggressive Behavior by Race/Ethnicity

3250 words

A commenter by the name of bbloggz alerted me to a new paper by Lee Ellis published this year titled Race/ethnicity and criminal behavior: Neurohormonal influences in which Ellis (2017) proposed his theory of ENA (evolutionary neuroandrogenic theory) and applied it to racial/ethnic differences in crime. On the face, his theory is solid and it has great explanatory power for the differences in crime rates between men and women, however, there are numerous holes in the application of the theory in regards to racial/ethnic differences in crime.

In part I, he talks about racial differences in crime. No one denies that, so on to part II.

In part II he talks about environmental causes for the racial discrepancies, that include economic racial disparities, racism and societal discrimination and subordination, a subculture of violence (I’ve been entertaining the honor culture hypothesis for a few months; Mazur (2016) drives a hard argument showing that similarly aged blacks with some college had lower levels of testosterone than blacks with less than high school education which fits the hypothesis of honor culture. Though Ellis’ ENA theory may account for this, I will address this below). However, if the environment that increases testosterone is ameliorated (i.e., honor culture environments), then there should be a subsequent decrease in testosterone and crime, although I do believe that testosterone has an extremely weak association with crime, nowhere near high enough to account for racial differences in crime, the culture of honor could explain a good amount of the crime gap between blacks and whites.

Ellis also speaks about the general stress/strain explanation, stating that blacks have higher rates of self-esteem and Asians the lowest, with that mirroring their crime rates. This could be seen as yet another case for the culture of honor in that blacks with a high self-esteem would feel the need to protect their ‘name’ or whatever the case may be and feel the need for physical altercation based on their culture.

In part III, Ellis then describes his ENA theory, which I don’t disagree with on its face as it’s a great theory with good explanatory power but there are some pretty large holes that he rightly addresses. He states that, as I have argued in the past, females selected men for higher rates of testosterone and that high rates of testosterone masculinize the brain, changing it from its ‘default feminine state’ and that the more androgens the brain is exposed to, the more likely it is for that individual to commit crime.

Strength

Ellis cites a study by Goodpaster et al (2006) in which he measured the races on the isokinetic dynamometry, pretty much a leg extension. However, one huge confound is that participants who did not return for follow-up were more likely to be black, obese and had more chronic disease (something that I have noted before in an article on racial grip strength). I really hate these study designs, but alas, it’s the best we have to go off of and there are a lot of holes in them that must be addressed. Though I applaud the researchers’ use of the DXA scan (regular readers may recall my criticisms on using calipers to assess body fat in the bench press study, which was highly flawed itself; Boyce et al, 2014) to assess body fat as it is the gold standard in the field.

Ellis (2017: 40) writes: “as brain exposure to testosterone surges at puberty, the prenatally-programmed motivation to strive for resources, status, and mating opportunities will begin to fully activate.” This is true on the face, however as I have noted the correlation between physical aggression and testosterone although positive is low at .14 (Archer, 1991; Book et al, 2001). Testosterone, as I have extensively documented, does cause social dominance and confidence which do not lead to aggression. However, when other factors are coupled with high testosterone (as noted by Mazur, 2016), high rates of crime may occur and this may explain why blacks commit crime; a mix of low IQ, high testosterone and low educational achievement making a life of crime ‘the smart way’ to live seeing as, as Ellis points out, and that intelligent individuals find legal ways to get resources while less intelligent individuals use illegal ways.

ENA theory may explain racial differences in crime

In part IV he attempts to show how his ENA theory may explain racial differences in crime—with testosterone sitting at the top of his pyramid. However, there are numerous erroneous assumptions and he does rightly point out that more research needs to be done on most of these variables and does not draw any conclusions that are not warranted based on the data he does cite. He cites one study in which testosterone levels were measured in the amniotic fluid of the fetus. The sample was 59 percent white and due to this, the researchers lumped blacks, ‘Hispanics’ and Native Americans together which showed no significant difference in prenatal testosterone levels (Martel and Roberts, 2014).

Umbilical cord and testosterone exposure

Ellis then talks about testosterone in the umbilical cord, and if the babe is exposed to higher levels of testosterone in vitro, then this should account for racial/ethnic differences in crime. However, the study he cited (Argus-Collins et al, 2012) showed no difference in testosterone in the umbilical cord while Rohrmann et al (2009) found no difference in testosterone between blacks and whites but found higher rates of SHBG (sex hormone-binding globulin) which binds to testosterone and makes it unable to leave the blood which largely makes testosterone unable to affect organ development. Thusly, if the finding of higher levels of SHBG in black babes is true, then they would be exposed to less androgenic hormones such as testosterone which, again, goes against the ENA theory.

He also cites two more studies showing that Asian babes have higher levels of umbilical cord testosterone than whites (Chinese babes were tested) (Lagiou et al, 2011; Troisi et al, 2008). This, again, goes against his theory as he rightly noted.

Circulating testosterone

Next he talks about circulating differences in testosterone between blacks and whites. He rightly notes that testosterone must be assayed in the morning within an hour after waking as that’s when levels will be highest, yet cites Ross et al (1986) where assay times were all over the place and thusly testosterone cannot be said to be higher in blacks and whites based on that study and should be discarded when talking about racial differences in testosterone due to assay time being between 10 am and 3 pm. He also cites his study on testosterone differences (Eliss and Nyborg, 1993), but, however, just as Ross et al (1986) did not have a control for WC (waist circumference) Ellis and Nyborg (1993) did not either, so just like the other study that gets cited to show that there is a racial difference in testosterone, they are pretty hugely flawed and should not be used in discussion when discussing racial differences in testosterone. Why do I not see these types of critiques for Ross et al (1986) in major papers? It troubles me…

He also seems to complain that Lopez et al (2013) controlled for physical activity (which increases testosterone) and percent body fat (which, at high levels, decreases testosterone). These variables, as I have noted, need to be controlled for. Testosterone varies and fluctuated by age; WC and BMI vary and fluctuate by age. So how does it make sense to control for one variable that has hormone levels fluctuate by age and not another? Ellis also cites studies showing that older East Asian men had higher levels of testosterone (Wu et al, 1995). Nevertheless, there is no consensus; some studies show Chinese babes have higher levels of testosterone than whites and some studies show that whites babes have higher levels of testosterone than Chinese babes. Indeed, this meta-analysis by Ethnicmuse shows that Asians have the highest levels, followed by Africans then Europeans, so this needs to be explained to save the theory that testosterone is the cause of black overrepresentation of violence (as well as what I showed that testosterone is important for vital functioning and is not the boogeyman the media makes it out to be).

Bone density and crime

Nevertheless, the next variable Ellis talks about is bone density and its relationship to crime. Some studies find that blacks are taller than whites while other show no difference. Whites are also substantially taller than Asian males. Blacks have greater bone density than the other three races, but according to Ellis, this measure has not been shown to have a relationship to crime as of yet.

Penis size, race and crime

Now on to penis size. In two articles, I have shown that there is no evidence for the assertion that blacks have larger penises than whites. However, states that penis length was associated with higher levels of testosterone in Egyptian babes. He states that self-reported penis size correlates with self-reports of violent delinquency (Ellis and Das, 2012). Ellis’ main citations for the claim that blacks have larger penises than other races comes from Nobile (1982), the Kinsey report, and Rushton and Boagert (1987) (see here for a critique of Rushton and Boagert, 1987), though he does cite a study stating that blacks had a longer penis than whites (blacks averaging 5.77 inches while whites averaged 5.53 inches). An HBDer may go “Ahah! Evidence for Rushton’s theory!”, yet they should note that the difference is not statistically significant; just because there is a small difference in one study also doesn’t mean anything for the totality of evidence on penis size and race—that there is no statistical difference!

He then cites Lynn’s (2013) paper which was based on an Internet survey and thus, self-reports are over-measured. He also cites Templer’s (2002) book Is Size Important?, which, of course, is on my list of books to read. Nevertheless, the ‘evidence’ that blacks average larger penises than whites is extremely dubious, it’s pretty conclusive that the races don’t differ in penis size. For further reading, read The Pseudoscience of Race Differences in Penis Sizeand read all of Ethnicmuses’ posts on penis size here. It’s conclusive that there is no statistical difference—if that—and any studies showing a difference are horribly flawed.

2d/4d ratio and race

Then he talks about 2d/4d ratio, which supposedly signifies higher levels of androgen exposure in vitro (Manning et al, 2008) however these results have been challenged and have not been replicated (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010). Even then, Ellis states that in a large analysis of 250,000 respondents, Asians had the lowest 2d/4d ratio, which if the hypothesis of in vitro hormones affecting digit length is to be believed, they have higher levels of testosterone than whites (the other samples had small ns, around 100).

Prostate-specific antigens, race, and prostate cancer

He then talks about PSA (prostate-specific antigen) rates between the races. Blacks are two times more likely to get prostate cancer, which has been blamed on testosterone. However, I’ve compiled good evidence that the difference comes down to the environment, i.e., diet. Even then, there is no evidence that testosterone causes prostate cancer as seen in two large meta-analyses (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Even then, rates of PCa (prostate cancer) are on the rise in East Asia (Kimura, 2012; Chen et al, 2015Zhu et al, 2015) which is due to the introduction of our Western diet. I will cover the increases in PCa rates in East Asia in a future article.

CAG repeats

He then reviews the evidence of CAG repeats. There is, however, no evidence that the number of CAG repeats influences sensitivity to testosterone. However, intra-racially, lower amounts of CAG repeats are associated with higher spermatozoa counts—but blacks don’t have higher levels of spermatozoa (Mendiola et al, 2011; Redmon et al, 2013). Blacks do have shorter CAG repeats, and this is consistent with the racial crime gap of blacks > whites > Asians. However, looking at the whole of the evidence, there is no good reason to assume that this has an effect on racial crime rates.

Intelligence and education

Next he talks about racial differences in intelligence and education, which have been well-established. Blacks did have higher rates of learning disabilities than whites who had higher levels of learning disabilities then Asians in a few studies, but other studies show whites and South Asians having different rates, for instance. He then talks about brain size and criminality, stating that the head size of males convicted for violent crimes did not differ from males who committed non-violent crimes (Ikaheimo et al, 2007). I won’t bore anyone with talking about what we know already: that the races differ in average brain size. However, a link between brain size and criminality—to the best of my knowledge—has yet to been discovered. IQ is implicated in crime, so I do assume that brain size is as well (no matter if the correlation is .24 or not; Pietschnig et al, 2015).

Prenatal androgen exposure

Now to wrap things up, the races don’t differ in prenatal androgen exposure, which is critical to the ENA theory; there is a small difference in the umbilical cord favoring blacks, and apparently, that predicts a high rate of crime. However, as noted, blacks have higher levels of SHBG at birth which inhibits the production of testosterone on the organs. Differences in post-pubertal testosterone are small/nonexistent and one should not talk about them when talking about differences in crime or disease acquisition such as PCa. DHT only shows a weak positive correlation with aggression—the same as testosterone (Christiansen and Winkler, 1992; however other studies show that DHT is negatively correlated with measures of physical aggression; Christiansen and Krussmann, 1987; further, DHT is not so evil after all).

Summing it all up

Blacks are not stronger than whites, indeed evidence from the races’ differing somatype, grip strength and leverages all have to do with muscular strength. Furthermore, the study that Ellis cites as ‘proof’ that blacks are stronger than whites is on one measure; an isokinetic dynamometry machine which is pretty much a leg extension. In true tests of strength, whites blow blacks away, which is seen in all major professional competitions all around the world. Blacks do have denser bones which is due to androgen production in vitro, but as of yet, there has been no research done into bone density and criminality.

The races don’t differ on penis size—and if they do it’s by tenths of an inch which is not statisitcally significant and I won’t waste my time addressing it. It seems that most HBDers will see a racial difference of .01 and say “SEE! Rushton’s Rule!” even when it’s just that, a small non-significant difference in said variable. That’s something I’ve encountered a lot in the past and it’s, frankly, a waste of time to converse about things that are not statistically significant. I’ve also rebutted the theory on 2d/4d ration as well. Finally, Asians had a similar level of androgen levels compared to blacks, with whites having the least amount. Along with a hole in the theory for racial differences in androgen causing crime, it’s yet another hole in the theory for racial differences in androgens causing racial differences in penis size and prostate cancer.

On intelligence scores, no one denies that blacks have scored about 1 SD lower than whites for 100 years, no one denies that blacks have a lower educational attainment. In regards to learning disabilities, blacks seem to have the highest rates, followed by Native Americans, than non-Hispanic whites, East Asians and the lowest rates found in South Asians. He states only one study links brain size to criminal behavior and it showed a significant inverse relationship with crime but not other types of offenses.

This is a really good article and I like the theory, but it’s full of huge holes. Most of the variables described by Ellis have been shown to not vary at all or much between the races (re: penis size, testosterone, strength [whites are stronger] prostate cancer caused mainly by diet, 2d/4d ratio [no evidence of it showing a digit ratio difference], and bone density not being studied). Nevertheless, a few of his statements do await testing so I await future studies on the matter. He says that androgen exposure ‘differs by race and ethnicity’, yet the totality of evidence shows ‘not really’ so that cannot be the cause of higher amounts of crime. Ellis talks about a lot of correlates with testosterone, but they do not pass the smell test. Most of it has been rebutted. In fact, one of the central tenets of the ENA theory is that the races should differ in 2d/4d ratio due to exposure of differing levels of the hormone in vitro. Alas, the evidence to date has not shown this—it has in fact shown the opposite.

ENA theory is good in thought, but it really leaves a lot to be desired in regards to explaining racial differences in crime. More research needs to be looked into in regards to intelligence and education and its effect on crime. We can say that low IQ people are more likely to drop out of school and that is why education is related to crime. However, in Mazur (2016) shows that blacks matched for age had lower levels of testosterone if they had some college under their belt. This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have the lowest rate of crime in the worle!

This seems to point in the direction of the ENA theory, however then all of the above problems with the theory still need to be explained away—and they can’t! Furthermore, one of the nails in the coffin should be this: East Asian males are found to have higher levels of testosterone than white males, often enough, and East Asian males actually have some of the lowest rate of crime in the world (Rushton, 1995)! So this is something that needs to be explained if it is to be shown that testosterone facilitates aggression and therefore, crime.

Conclusion

I’ve shown—extensively—that there is a low positive correlation between testosterone and physical aggression, why testosterone does not cause crime, and have definitively shown that, by showing how flawed the other studies are that purport to show blacks have higher testosterone levels than whites, along with citing large-scale meta-analyses, that whites and blacks either do not differ or the differences is small to explain any so-called differences in disease acquisition or crime. One final statement on the CAG repeats, they are effect by obesity, men who had shorter CAG repeats were more likely to be overweight, which would skew readings (Gustafsen, Wen, and Koppanati, 2003). So depending on the study—and in most of the studies I cite whites have a higher BMI than blacks—BMI and WC should be controlled for due to the depression of testosterone.

It’s pretty conclusive that testosterone itself does not cause crime. Most of the examples cited by Ellis have been definitively refuted, and his other claims lack evidence at the moment. Even then, his theory rests on the 2d/4d ratio and how blacks may have a lower 2d/4d ratio than whites. However, I’ve shown that there is no significant relationship between 2d/4d ratio and traits mediated by testosterone (Kohler, Simmons, and Rhodes, 2004) so that should be enough to put the theory to bed for good.

Race, Testosterone, and Prostate Cancer

1900 words

I have explicitly shown how the ‘black men have more T’ canard is false. I have provided sufficient evidence for this claim. People claim to be unbiased—like PumpkinPerson—and say they’re only ‘looking for the truth’. However, it’s clear that in all of my conversations with him on the matter, he’s reaching for anything that affirms his worldview when he is shown evidence to the contrary of his beliefs (Nyhan and Reifler, 2012). It’s so very easy to notice this. I will provide yet more robust data on the black/white testosterone ‘gap’ while also critiquing some other studies that didn’t control for some pretty important variables. The gist is: after controlling for the most important variables, (waist circumference, BMI) the ‘testosterone difference’ all but disappears—and I don’t think people will argue for .0068 ng/ml higher testosterone cause things like prostate cancer and higher rates of crime.

Gapstur et al (2002) studied 5,115 individuals from aged 18-30 who completed baseline examinations at one of four locations from 1985-86: Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California. Then, 4 follow-ups were completed (Year 2: 1987-88; year 5: 1990-91; year 7: 1992-93; and year 10: 1995-96).

The number of blacks who completed the baseline information was 1157 whereas for whites it was 1171. They measured waist circumference (WC) at the minimal abdominal girth. Whether or not one took medication was self-reported, so Gapstur et al (2002) separated medications into two categories: regulation or interfering with binding likely, or interfering with binding unlikely/impossible.

Now, before I discuss the results of Gapstur et al (2002) I must talk about why they controlled for BMI (body mass index) and WC along with age. Since the obesity rate differs by race/ethnicity, along with obesity frequently changing with age, all three of the variables need to be controlled for to get a clearer picture of what circulating testosterone looks like—on average—between blacks and whites. White men are slightly more likely than black men to be obese/overweight in America (being African-American seems to be a protector against obesity; African American men with more African ancestry are less likely to be obese), however the sample used by Gapstur et al (2002) had blacks who had a higher WC and BMI than whites.

At year 2, there was no significant difference in total serum testosterone between the races with or without adjustment for age, BMI and WC. The only part in this analysis that blacks had higher testosterone levels than whites was at year ten, with black ‘enjoying’ .0063 ng/ml higher levels than whites. Furthermore, there was no significant difference in testosterone between blacks and whites after adjustment for age. Only adjusting for BMI, blacks had substantially higher levels of testosterone (.21 ng/ml) however after including WC and the changes in WC between blacks and whites (blacks had a greater change over the study) this difference all but disappeared. The age-associated changes in testosterone between blacks and whites were similar after adjusting for waist circumference and BMI. Also, after adjusting for the relevant confounds, free testosterone did not differ between blacks and whites.

Measures of body size (i.e., BMI and WC) must be controlled for when comparing race/ethny since levels of obesity vary amongst them as well as obesity constantly changing with age. Furthermore, testosterone increased for both groups between the ages of 20-21 to 22-23 (blacks had a higher T level by .7 ng/ml at age 20-21), with the two groups diverging at age 22-23 with blacks having higher levels of total testosterone by .1 ng/ml.

The average ages for the cohort were 28.4 and 28.8 for blacks and whites respectfully. Thus, blacks (theoretically) had a slight advantage due to the age confound, which had to be controlled for. The unadjusted mean total testosterone, SHGB, and free testosterone were not statistically significant at any point in the study except at year 10 where blacks had slightly higher levels at 5.8 ng/ml compared to whites’ 5.69 ng/ml. The difference in year 2 (when testosterone levels raised for both groups) was a difference of 5.8 and 5.75 for blacks and whites respectfully. Free testosterone did not differ at all from years 2, 7, and 10 (.17 compared to .17 in year 2; .16 to .15 in year 7; and .16 to .15 in year 10; blacks and whites respectfully).

Levels of testosterone were also found to be lower in 12-13-year-old blacks compared to whites (Lopez et al, 2013). In this study, Mexican Americans had higher T levels, while after adjustments for confounds, blacks and whites did not differ. They conclude that testosterone levels were not higher in black compared to white adolescents. Black men have higher levels of estradiol than white men, not testosterone (Roerrmann et al, 2007; Lopez et al, 2013). These studies are done to see the relationship between PCa (prostate cancer) and certain hormones. These and other studies have shown that the black-white difference isn’t large (Richard et al, 1992; Roerrmann et al, 2007; Lopez et al, 2013; Richard et al, 2014) and that prostate cancer is not caused by abnormally high testosterone levels (Stattin et al, 2003; Michaud, Billups, and Partins, 2015).

Ross et al (1986) did not have a measure of central adiposity (WC), thusly the results were confounded. Further, the other study Rushton cited in Race, Evolution, and Behavior is and Nyborg (1992) on discharged army veterans stating a difference of 3 percent, Ellis and Nyborg did not control for WC nor BMI. As seen in the Gapstur et al (2002) study, WC is an extremely important variable to control for as decreases in testosterone are high when central adiposity is high (Wang et al, 2011) so if we are trying to compare two ethnies on one variable such as testosterone, all of the above variables MUST be controlled for, and if they are not then they can be safely disregarded.

The non-inclusion of a measure of WC is the most likely cause of the different results found in Gapstur et al (2002). If you don’t control for WC, then you cannot get an actual and reliable testosterone reading since the results will be confounded. Anyone who says otherwise that the aforementioned variables do not need to be controlled for literally have no idea what they’re talking about.

Lastly, a few more things must be addressed. In PumpkinPerson’s most recent article “Racial differences in testosterone“, he seems to now disavow testosterone as a useful measure since it can fluctuate due to winning sports games, to marriage, to anticipating confrontation, to being in a relationship, to honor culture. Now his thing is exposure to androgens (testosterone) in the womb. Supposedly, blacks have the lowest digit ratio, and low digit ratios signify higher levels of testosterone in vitro (Manning et al, 2004). However, the relationship is far from proven (Koehler, Simmons, and Rhodes, 2004; Yan et al, 2008, Medland et al, 2010) with these results, leaning towards no. Koheler, Simmons, and Rhodes (2004) failed to find any significant correlation between 2d/4d ratio and traits mediated by testosterone. So this is another claim that’s been put to bed as well.

There is a lot of bullshit to sift through out there; some things may seem simple at face value, but if you dig into it, it’s much more likely to be more complex than what it looks to be on the surface. This one singular variable (testosterone) is one of them. It does not differ between the races; exposure to androgens in the womb doesn’t affect digit ratio; high testosterone does not cause prostate cancer, but low testosterone does (Morgentaler, Brunning, and DeWolf, 1996) ; you can literally inject exogenous testosterone into a man with PCa and not effect this malady (Eisenberg, 2015; Boyle et al, 2016)

I hope this is the last time I have to say this: testosterone does not differ between blacks and whites. Testosterone is not the cause of differences in mortality rate in regards to PCa. (Diet is the much more likely factor) People still regurgitate Rushton’s bullshit from REB; Ross et al (1986) still gets cited to this day, when there are much more robust studies and samples that controlled for the relevant confounds that Ross et al (1986) did not control for. This is why that study is garbage and should not be looked at when assessing testosterone differences between the races. Much larger and robust samples show that there is no testosterone difference when the WC is controlled for.

Testosterone is not higher in black Americans; the data shows either an extremely negligible difference or no difference, not the huge 13 and 21 percent difference in free and total testosterone in black Americans in Ross et al (1986).

For the last time, and say it with me: testosterone does NOT differ by race, 2d:4d ratio is NOT influenced by androgens in vitro, and testosterone does NOT influence PCa rates. Testosterone is an extremely important hormone for vital functioning, so whoever believes the myths of the high testosterone savage and LIKES having low testosterone, have fun with a slew of maladies later in life.

References

Boyle, P., Koechlin, A., Bota, M., Donofrio, A., Zaridze, D. G., Perrin, P., . . . Boniol, M. (2016). Endogenous and exogenous testosterone and the risk of prostate cancer and increased prostate-specific antigen (PSA) level: a meta-analysis. BJU International,118(5), 731-741. doi:10.1111/bju.13417

Dobs, A., & Morgentaler, A. (2008). Does Testosterone Therapy Increase the Risk of Prostate Cancer? Endocrine Practice,14(7), 904-911. doi:10.4158/ep.14.7.904

Eisenberg, M. L. (2015). Testosterone Replacement Therapy and Prostate Cancer Incidence. The World Journal of Men’s Health, 33(3), 125–129. http://doi.org/10.5534/wjmh.2015.33.3.125

Gapstur, S. M., Kopp, P., Gann, P. H., Chiu, B. C., Colangelo, L. A., & Liu, K. (2006). Changes in BMI modulate age-associated changes in sex hormone binding globulin and total testosterone, but not bioavailable testosterone in young adult men: the CARDIA Male Hormone Study. International Journal of Obesity. doi:10.1038/sj.ijo.0803465

Koehler, N., Simmons, L. W., & Rhodes, G. (2004). How well does second-to-fourth-digit ratio in hands correlate with other indications of masculinity in males? Proceedings of the Royal Society B: Biological Sciences,271(Suppl_5). doi:10.1098/rsbl.2004.0163

Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Medland, S. E., Zayats, T., Glaser, B., Nyholt, D. R., Gordon, S. D., Wright, M. J., . . . Evans, D. M. (2010). A Variant in LIN28B Is Associated with 2D:4D Finger-Length Ratio, a Putative Retrospective Biomarker of Prenatal Testosterone Exposure. The American Journal of Human Genetics,86(4), 519-525. doi:10.1016/j.ajhg.2010.02.017

Manning, J., Stewart, A., Bundred, P., & Trivers, R. (2004). Sex and ethnic differences in 2nd to 4th digit ratio of children. Early Human Development,80(2), 161-168. doi:10.1016/j.earlhumdev.2004.06.004

Morgentaler, A., Brunning, C. O., 3rd, & DeWolf, W. C. (1996). Occult Prostate Cancer in Men With Low Serum Testosterone Levels. JAMA: The Journal of the American Medical Association,276(23), 1904. doi:10.1001/jama.1996.03540230054035

Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions. Political Behavior,32(2), 303-330. doi:10.1007/s11109-010-9112-2

Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x

Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028

Wang, C., Jackson, G., Jones, T. H., Matsumoto, A. M., Nehra, A., Perelman, M. A., … Cunningham, G. (2011). Low Testosterone Associated With Obesity and the Metabolic Syndrome Contributes to Sexual Dysfunction and Cardiovascular Disease Risk in Men With Type 2 Diabetes. Diabetes Care, 34(7), 1669–1675. http://doi.org/10.2337/dc10-2339

Yan RHY, Malisch JL, Hannon RM, Hurd PL, Garland T Jr (2008) Selective Breeding for a Behavioral Trait Changes Digit Ratio. PLoS ONE 3(9): e3216. https://doi.org/10.1371/journal.pone.0003216

Race, Testosterone, and Honor Culture

2300 words

Misinformation about testosterone and strength in regards to race is rampant in the HBD-o-sphere. One of the most oft-repeated phrases is that “Blacks have higher levels of testosterone than whites”, even after controlling for numerous confounds. However, the people who believe this literally only cite one singular study with 50 blacks and 50 whites. Looking at more robust data with higher ns shows a completely different story. Tonight I will, again, go through the race/testosterone conundrum (again).

Type I fibers fire first when heavy lifting. Whites have more type I fibers. Powerlifters and Olympic lifters have a greater amount type IIa fibers, with fewer type IIx fibers (like whites). This explains why blacks are hardly represented in powerlifting and strongman competitions.

Somatype, too, also plays a role. Whites are more endo than blacks who are more meso. Endomorphic individuals are stronger, on average, than mesomorphic and ectomorphic individuals.

Blacks have narrower hips and pelves. This morphological trait further explains why blacks dominate sports. Some people may attempt to pick out one variable that I speak about (fiber type, morphology, somatype, fat mass, etc) and attempt to disprove it, thinking that disproving that variable will discredit my whole argument. However, fiber typing is set by the second trimester, with no change in fiber type from age 6 to adulthood (Bell et al, 1980).

It is commonly believed that blacks have higher levels of testosterone than whites. However, this claim is literally based off of one study (Ross et al, 1986) when other studies have shown low to no difference in T levels (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Richard et al 2014). People who still push the “blacks-have-higher-T-card” in the face of this evidence are, clearly, ideologues who want to cushion their beliefs when presented with contradictory evidence (Nyhan and Reifler, 2010).

‘Honor Culture’ and testosterone

In all of my articles on this subject, I have stated—extensively—that testosterone is mediated by the environment. That is, certain social situations can increase testosterone. This is a viewpoint that I’ve emphatically stated. I came across a paper while back that talks about a sociological perspective (I have huge problems with social ‘science’, [more on that soon] but this study was very well done) in regards to the testosterone difference between blacks and whites.

Some people when they read this, however, may go immediately to the part of the paper that says what they want it to say without fully assessing the paper. In this section, I will explain the paper and how it confirms my assertions/arguments.

Mazur (2016) begins the paper talking about ‘honor culture‘, which is a culture where people avoid intentionally offending others while also maintaining a status for not backing down from a confrontation. This theory was proposed by Richard Nisbett in 1993 to explain why the South had higher rates of violence—particularly the Scotch-Irish.

However parsimonious the theory may sound, despite its outstanding explanatory power, it doesn’t hold while analyzing white male homicides in the South. It also doesn’t hold analyzing within-county homicide rates either, since apparently poverty better explains higher homicide rates.

But let’s assume it’s true for blacks. Let’s assume the contention to be true that there is an ‘honor culture’ that people take part in.

Young black men with no education had higher levels of testosterone than educated whites and blacks. Looking at this at face value—literally going right to the section of the paper that says that poor blacks had higher testosterone, nearly 100 ng/ml higher than the mean testosterone of whites. As Mazur (2016) notes, this contradicts his earlier 2009 study in which he found no difference in testosterone between the races.

fsoc-01-00001-g001

Note the low testosterone for both races at age 20-29—ranging from about 515 to 425—why such low testosterone levels for young men? Anyway, the cause for the higher levels is due to the type of honor culture that blacks participate in, according to Mazur (which is consistent with the data showing that testosterone rises during conflict/aggressive situations).

Mazur cites Elijah Anderson, saying that most youths have a “code of the streets” they take part in, which have to do with interpersonal communication such as “gait and verbal expressions” to deter aggressive behavior.

Testosterone is not a causal variable in regards to violent behavior. But it does rise during conflicts with others, watching a favorite sports team, asserting dominance, and even how you carry yourself (especially your posture). Since low-class blacks participate in these types of behaviors, then they would have higher levels of testosterone due to needing to “keep their status.”

When testosterone rises in these situations, it increases the response threat in mens’ brains, most notably showing increased activity in the amygdala. Further, dominant behavior and posture also increase testosterone levels. Putting this all together, since blacks with only a high school education have higher testosterone levels and are more likely to participate in honor culture compared to whites and blacks with higher educational achievement, then they would have higher testosterone levels than whites and blacks with a high school education who do not participate in honor culture.

Further, as contrary to what I have written in the past (and have since rescinded), there is no indication of higher testosterone levels in black women with low education. It seems this ‘honor culture’ effect on testosterone only holds for black men with only a high school education.

Mazur’s (2016) most significant finding was that black men aged 20-29 with only a high school education had 91 ng/ml higher testosterone than whites. Among older and/or educated men, testosterone did not vary. This indicates that since they have attained higher levels of educational success, there is no need to participate in ‘honor culture’.

This is yet further evidence for my assertion that environmental variables such as posture, dominance, and aggressive behavior raise testosterone levels.

The honor culture hypothesis is found to hold in Brazil in a comparative study of 160 inmates and non-inmates (De Souza et al, 2016). As Mazur (2016) notes, the honor culture hypothesis could explain the high murder rate for black Americans—the need to ‘keep their status’. It’s important to note that this increase in testosterone was not noticed in teenage or female blacks (because they don’t participate in honor culture).

There is a perfectly good environmental—not genetic—reason for this increase in testosterone in young blacks with only a high school education. Now that we know this, back to race and strength.

Mazur (2009) found that black men in the age range of 20-69, they averaged .39 ng/ml higher testosterone than whites, which is partly explained by lower marriage rates and low adiposity. White men are more likely to be obese than black men, since black men with more African ancestry are less likely to be obese. When controlling for BMI, blacks are found to have 2.5-4.9 percent more testosterone than whites (Gapstur et al, 2002, Rohrmann et al, 2007, Richard et al, 2014). There is little evidence for the assertion that blacks have higher levels of testosterone without environmental triggers.

Blacks between the age of 12 and 15 average lower levels of testosterone than whites. However, after the age of 15, “testosterone levels increase rapidly” with blacks having higher peak levels than whites (seen in table 2 below). After adjusting for the usual confounds (BMI, smoking, age, physical activity, and waist circumference), blacks still had higher levels of testosterone—which is attributed to higher levels of lean mass.

testosterone

As seen above in table 2 from Hu et al (2014), the difference in total testosterone between blacks and whites aged 20-39 was 6.29 ng/ml and 5.04 ng/ml respectively, with free testosterone for whites being 11.50 and 13.56 for blacks and finally bioavailable testosterone for whites and blacks aged 20-39 was 281.23 and 327.18 ng/ml respectively. These small differences in testosterone cannot account for racial disparities in violence nor prostate cancer—since there is no relationship between prostate cancer and testosterone (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).

In regards to Africans, the best studies I can find comparing some African countries with the West study salivary testosterone. However, there is a direct correlation between salivary testosterone and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burrin, 1987). Of the studies I could find, Kenyan pastoralists called the Ariaal have lower levels of testosterone than Western men (Campbell, O’Rourke, and Lipson, 2003; Campbell, Gray, and Ellison, 2006) while men in Zimbabwe had levels “much lower” compared to Western populations (Lukas, Campbell, and Ellison, 2004). Lastly, among men aged 15 to 30, salivary testosterone levels in an American sample was 335 pmol//l compared to 286 pmol/l in men from the Congo (Elisson et al, 2002). Even certain African populations don’t have higher testosterone levels than Western peoples.

Conclusion

The meme that blacks have higher rates of testosterone in comparison to whites needs to be put to rest. This is only seen in blacks who participate in ‘honor culture’, which is an environmental variable. This is in contrast to people who believe that it is genetic in nature—environmental variables can and do drive hormones. Mazur (2016) is proof of that. Mazur (2016) also shows that the honor culture hypothesis doesn’t hold for teens or black males—so they don’t have elevated levels of testosterone. Certain studies of African populations, however, do not show higher levels of testosterone than Western populations.

Looking at the complete literature—rather than a select few studies— we can see that testosterone levels between white and black Americans are not as high as is commonly stated (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Further, even if blacks did have higher levels of testosterone than whites—across the board (sans honor culture), it still wouldn’t explain higher rates of black violence when compared to whites, nor would it explain higher prostate cancer rates (Stattin et al, 2003; Michaud, Billups, and Partin, 2015).

Only blacks with low educational achievement have higher levels of testosterone—which, even then is not enough to explain higher rates of violence or prostate cancer acquisition. Other factors explain the higher murder rate (i.e., honor culture, which increases testosterone, the environmental trigger matters first and foremost) and violent crime that blacks commit. But attempting to explain it with 30-year-old studies (Ross et al, 1986) and studies that show that environmental factors increase testosterone (Mazur, 2016) don’t lend credence to that hypothesis.

References

Bell, R. D., Macdougall, J. D., Billeter, R., & Howald, H. (1980). Muscle fiber types and morphometric analysis of skeletal muscle in six-year-old children. Medicine & Science in Sports & Exercise,12(1). doi:10.1249/00005768-198021000-00007

Campbell, B., O’rourke, M. T., & Lipson, S. F. (2003). Salivary testosterone and body composition among Ariaal males. American Journal of Human Biology,15(5), 697-708. doi:10.1002/ajhb.10203

Campbell, B. C., Gray, P. B., & Ellison, P. T. (2006). Age-related patterns of body composition and salivary testosterone among Ariaal men of Northern Kenya. Aging Clinical and Experimental Research,18(6), 470-476. doi:10.1007/bf03324846

De Souza, Souza, B. C., Bilsky, W., & Roazzi, A. (2016). The culture of honor as the best explanation for the high rates of criminal homicide in Pernambuco: A comparative study with 160 convicts and non-convicts. Anuario de Psicología Jurídica,26(1), 114-121. doi:10.1016/j.apj.2015.03.001

Ellison, P. T., Bribiescas, R. G., Bentley, G. R., Campbell, B. C., Lipson, S. F., Panter-Brick, C., & Hill, K. (2002). Population variation in age-related decline in male salivary testosterone. Human Reproduction,17(12), 3251-3253. doi:10.1093/humrep/17.12.3251

Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 10417

Hu, H., Odedina, F. T., Reams, R. R., Lissaker, C. T., & Xu, X. (2014). Racial Differences in Age-Related Variations of Testosterone Levels Among US Males: Potential Implications for Prostate Cancer and Personalized Medication. Journal of Racial and Ethnic Health Disparities,2(1), 69-76. doi:10.1007/s40615-014-0049-8

Johnson, S. G., Joplin, G. F., & Burrin, J. M. (1987). Direct assay for testosterone in saliva: Relationship with a direct serum free testosterone assay. Clinica Chimica Acta,163(3), 309-318. doi:10.1016/0009-8981(87)90249-x

Lopez, D. S., Peskoe, S. B., Joshu, C. E., Dobs, A., Feinleib, M., Kanarek, N., . . . Platz, E. A. (2013). Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males. Cancer Causes & Control,24(4), 817-826. doi:10.1007/s10552-013-0154-8

Lukas, W. D., Campbell, B. C., & Ellison, P. T. (2004). Testosterone, aging, and body composition in men from Harare, Zimbabwe. American Journal of Human Biology,16(6), 704-712. doi:10.1002/ajhb.20083

Mazur, A. (2009). The age-testosterone relationship in black, white, and Mexican-American men, and reasons for ethnic differences. The Aging Male,12(2-3), 66-76. doi:10.1080/13685530903071802

Mazur, A. (2016). Testosterone Is High among Young Black Men with Little Education. Frontiers in Sociology,1. doi:10.3389/fsoc.2016.00001

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Nyhan, B., & Reifler, J. (2010). When Corrections Fail: The Persistence of Political Misperceptions. Political Behavior,32(2), 303-330. doi:10.1007/s11109-010-9112-2

Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x

Richards, R. J., Svec, F., Bao, W., Srinivasan, S. R., & Berenson, G. S. (1992). Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol–the Bogalusa Heart Study. The Journal of Clinical Endocrinology & Metabolism,75(2), 624-631. doi:10.1210/jcem.75.2.1639961

Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028

Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48

Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572

Wang, C., Plymate, S., Nieschlag, E., & Paulsen, C. A. (1981). Salivary Testosterone in Men: Further Evidence of a Direct Correlation with Free Serum Testosterone. The Journal of Clinical Endocrinology & Metabolism,53(5), 1021-1024. doi:10.1210/jcem-53-5-1021

Black-White Differences in Muscle Fiber and Its Role In Disease and Obesity

1700 words

How do whites and blacks differ by muscle fiber and what does it mean for certain health outcomes? This is something I’ve touched on in the past, albeit briefly, and decided to go in depth on it today. The characteristics of skeletal muscle fibers dictate whether one has a higher or lower chance of being affected by cardiometabolic disease/cancer. Those with more type I fibers have less of a chance of acquiring diabetes while those with type II fibers have a higher chance of acquiring debilitating diseases. This has direct implications for health disparities between the two races.

Muscle fiber typing by race

Racial differences in muscle fiber typing explain differences in strength and mortality. I have, without a shadow of a doubt, proven this. So since blacks have higher rates of type II fibers while whites have higher rates of type I fibers (41 percent type I for white Americans, 33 percent type I for black Americans, Ama et al, 1985) while West Africans have 75 percent fast twitch and East Africans have 25 percent fast twitch (Hobchachka, 1988). Further, East and West Africans differ in typing composition, 75 percent fast for WAs and 25 percent fast for EAs, which has to do with what type of environment they evolved in (Hochhachka, 1998). What Hochhachka (1998) also shows is that high latitude populations (Quechua, Aymara, Sherpa, Tibetan and Kenyan) “show numerous similarities in physiological hypoxia defence mechanisms.” Clearly, slow-twitch fibers co-evolved here.

Clearly, slow-twitch fibers co-evolved with hypoxia. Since hypoxia is the deficiency in the amount of oxygen that reaches the tissues, populations in higher elevations will evolve hypoxia defense mechanisms, and with it, the ability to use the oxygen they do get more efficiently. This plays a critical role in the fiber typing of these populations. Since they can use oxygen more efficiently, they then can become more efficient runners. Of course, these populations have evolved to be great distance runners and their morphology followed suit.

Caesar and Henry (2015) also show that whites have more type I fibers than blacks who have more type II fibers. When coupled with physical inactivity, this causes higher rates of cancer and cardiometabolic disease. Indeed, blacks have higher rates of cancer and mortality than whites (American Cancer Society, 2016), both of which are due, in part, to muscle fiber typing. This could explain a lot of the variation in disease acquisition in America between blacks and whites. Physiologic differences between the races clearly need to be better studied. But we first must acknowledge physical differences between the races.

Disease and muscle fiber typing

Now that we know the distribution of fiber types by race, we need to see what type of evidence there is that differing muscle fiber typing causes differences in disease acquisition.

Those with fast twitch fibers are more likely to acquire type II diabetes and COPD (Hagiwara, 2013); cardiometabolic disease and cancer (Caesar and Henry, 2015); a higher risk of cardiovascular events (Andersen et al, 2015, Hernelahti et al, 2006); high blood pressure, high heart rate, and unfavorable left ventricle geometry leading to higher heart disease rates and obesity (Karjalainen et al, 2006) etc. Knowing what we know about muscle fiber typing and its role in disease, it makes sense that we should take this knowledge and acknowledge physical racial differences. However, once that is done then we would need to acknowledge more uncomfortable truths, such as the black-white IQ gap.

One hypothesis for why fast twitch fibers are correlated with higher disease acquisition is as follows: fast twitch fibers fire faster, so due to mechanical stress from rapid and forceful contraction, this leads the fibers to be more susceptible to damage and thus the individual will have higher rates of disease. Once this simple physiologic fact is acknowledged by the general public, better measures can be taken for disease prevention.

Due to differences in fiber typing, both whites and blacks must do differing types of cardio to stay healthy. Due to whites’ abundance of slow twitch fibers, aerobic training is best (not too intense). However, on the other hand, due to blacks’ abundance of fast twitch fibers, they should do more anaerobic type exercises to attempt to mitigate the diseases that they are more susceptible due to their fiber typing.

Black men with more type II fibers and less type I fibers are more likely to be obese than ‘Caucasian‘ men are to be obese (Tanner et al, 2001). More amazingly, Tanner et al showed that there was a positive correlation (.72) between weight loss and percentage of type I fibers in obese patients. This has important implications for African-American obesity rates, as they are the most obese ethny in America (Ogden et al, 2016) and have higher rates of metabolic syndrome (a lot of the variation in obesity does come down food insecurity, however). Leaner subjects had higher proportions of type I fibers compared to type II. Blacks have a lower amount of type I fibers compared to whites without adiposity even being taken into account. Not surprisingly, when the amount of type I fibers was compared by ethnicity, there was a “significant interaction” with ethnicity and obesity status when type I fibers were compared (Tanner et al, 2001). Since we know that blacks have a lower amount of type I fibers, they are more likely to be obese.

In Tanner et al’s sample, both lean blacks and whites had a similar amount of type I fibers, whereas the lean blacks possessed more type I fibers than the obese black sample. Just like there was a “significant interaction” between ethnicity, obesity, and type I fibers, the same was found for type IIb fibers (which, as I’ve covered, black Americans have more of these fibers). There was, again, no difference between lean black and whites in terms of type I fibers. However, there was a difference in type IIb fibers when obese blacks and lean blacks were compared, with obese blacks having more IIb fibers. Obese whites also had more type IIb fibers than lean whites. Put simply (and I know people here don’t want to hear this), it is easier for people with type I fibers to lose weight than those with type II fibers. This data is some of the best out there showing the relationship between muscle fiber typing and obesity—and it also has great explanatory power for black American obesity rates.

Conclusion

Muscle fiber differences between blacks and whites explain disease acquisition rates, mortality rates (Araujo et al, 2010), and differences in elite sporting competition between the races. I’ve proven that whites are stronger than blacks based on the available scientific data/strength competitions (click here for an in-depth discussion). One of the most surprising things that muscle fibers dictate is weight loss/obesity acquisition. Clearly, we need to acknowledge these differences and have differing physical activity protocols for each racial group based on their muscle fiber typing. However, I can’t help but think about the correlation between strength and mortality now. This obesity/fiber type study puts it into a whole new perspective. Those with type I fibers are more likely to be physically stronger, which is a cardioprotectant, which then protects against all-cause mortality in men (Ruiz et al, 2008; Volaklis, Halle, and Meisenger, 2015). So the fact that black Americans have a lower life expectancy as well as lower physical strength and more tpe II fibers than type I fibers shows why blacks are more obese, why blacks are not represented in strength competitions, and why blacks have higher rates of disease than other populations.The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.

The study by Tanner et al (2001) shows that there obese people are more likely to have type II fibers, no matter the race. Since we know that blacks have more type II fibers on average, this explains a part of the variance in the black American obesity rates and further disease acquisition/mortality.

Differences in muscle fiber typing do not explain all of the variance in disease acquisition/strength differences, however, understanding what the differing fiber typings do, metabolically speaking, along with how they affect disease acquisition will only lead to higher qualities of life for everyone involved.

References

Araujo, A. B., Chiu, G. R., Kupelian, V., Hall, S. A., Williams, R. E., Clark, R. V., & Mckinlay, J. B. (2010). Lean mass, muscle strength, and physical function in a diverse population of men: a population-based cross-sectional study. BMC Public Health,10(1). doi:10.1186/1471-2458-10-508

Andersen K, Lind L, Ingelsson E, Amlov J, Byberg L, Miachelsson K, Sundstrom J. Skeletal muscle morphology and risk of cardiovascular disease in elderly men. Eur J Prev Cardiol 2013.

Ama PFM, Simoneau JA, Boulay MR, Serresse Q Thériault G, Bouchard C. Skeletal muscle characteristics in sedentary Black and Caucasian males. J Appl Physiol 1986: 6l:1758-1761.

American Cancer Society. Cancer Facts & Figures for African Americans 2016-2018. Atlanta: American Cancer Society, 2016.

Ceaser, T., & Hunter, G. (2015). Black and White Race Differences in Aerobic Capacity, Muscle Fiber Type, and Their Influence on Metabolic Processes. Sports Medicine,45(5), 615-623. doi:10.1007/s40279-015-0318-7

Hagiwara N. Muscle fibre types: their role in health, disease and as therapeutic targets. OA Biology 2013 Nov 01;1(1):2.

Hernelahti, M., Tikkanen, H. O., Karjalainen, J., & Kujala, U. M. (2005). Muscle Fiber-Type Distribution as a Predictor of Blood Pressure: A 19-Year Follow-Up Study. Hypertension,45(5), 1019-1023. doi:10.1161/01.hyp.0000165023.09921.34

Hochachka, P.W. (1998) Mechanism and evolution of hypoxia-tolerance in humans. J. Exp. Biol. 201, 1243–1254

Karjalainen, J., Tikkanen, H., Hernelahti, M., & Kujala, U. M. (2006). Muscle fiber-type distribution predicts weight gain and unfavorable left ventricular geometry: a 19 year follow-up study. BMC Cardiovascular Disorders,6(1). doi:10.1186/1471-2261-6-2

Ogden C. L., Carroll, M. D., Lawman, H. G., Fryar, C. D., Kruszon-Moran, D., Kit, B.K., & Flegal K. M. (2016). Trends in obesity prevalence among children and adolescents in the United States, 1988-1994 through 2013-2014. JAMA, 315(21), 2292-2299.

Ruiz, J. R., Sui, X., Lobelo, F., Morrow, J. R., Jackson, A. W., Sjostrom, M., & Blair, S. N. (2008). Association between muscular strength and mortality in men: prospective cohort study. Bmj,337(Jul01 2). doi:10.1136/bmj.a439

Tanner, C. J., Barakat, H. A., Dohm, G. L., Pories, W. J., Macdonald, K. G., Cunningham, P. R., . . . Houmard, J. A. (2001). Muscle fiber type is associated with obesity and weight loss. American Journal of Physiology – Endocrinology And Metabolism,282(6). doi:10.1152/ajpendo.00416.2001

Volaklis, K. A., Halle, M., & Meisinger, C. (2015). Muscular strength as a strong predictor of mortality: A narrative review. European Journal of Internal Medicine,26(5), 303-310. doi:10.1016/j.ejim.2015.04.013

The Testosterone and Fertility Conundrum: A Western Perspective

2750 words

Some people are scared of testosterone. This is no surprise, since a super-majority of people have no background in the human sciences. I’m sure plenty men know what it’s like to have low testosterone, just like some men know what it’s like to have higher T levels than average. What is the optimum level of testosterone? Why are some people scared of this hormone?

Rushton (1997) posited that r/K Selection Theory could be used to classify the races of Man on a spectrum, going from r-selection (having many children but showing little to no parental care) to K-selection (having fewer children but showing a lot of parental care). He stated that the traits of the races were also on the r/K spectrum, with the races having stark differences in morphology. Rushton’s application of r/K theory to humans isn’t completely wrong, though I do have some problems with some of his claims, such as his claims that the races differ in average penis size. He contends that testosterone is the cause for higher crime rates for black Americans and higher rates of prostate cancer in black Americans compared to white Americans.

However, in 2014, Richard et al showed that when controlling for age, blacks had 2.5 to 4.9 percent more testosterone than whites, on average. This cannot explain racial differences in prostate cancer. However, some people may emphatically claim that the races differ in average testosterone, with blacks having 13 percent higher free testosterone than whites on average. The citation that gets used the most to prove that blacks supposedly have higher testosterone than whites is Ross et al (1986), which is based on a sample of 100 people (50 black, 50 white). He claims that it’s when T levels are higher, so it’s a ‘better study’ even though the sample leaves a lot to be desired. A much more robust study showed that the difference was negligible, and not enough to account for the differential prostate cancer rates between the races.

Rohrmann et al (2007) show that there are no differences in circulating testosterone between blacks and whites in a nationally representative sample of American men. Mexicans had the highest levels. There were, however, B-W differences in estradiol production. They couldn’t confirm the other studies that stated that blacks had higher testosterone, possibly due to variations in age or using non-representative samples (that’s the culprit). Their nationally representative sample showed there was no difference in testosterone between blacks is whites, while the meta-analysis showed by Richard et al (2014) showed the difference was negligible at 2.5 to 4.9 percent higher rate of testosterone which doesn’t explain why blacks have a higher rate of acquiring prostate cancer.

The much more likely culprit for blacks having higher rates of prostate cancer, as I have written about before, are environmental factors. The two main factors are receiving less sunlight and diet. There is no evidence that higher levels of testosterone lead to prostate cancer (Michaud, Billups, and Partin, 2015). Contrary to those who say that higher levels of T cause prostate cancer, there is growing evidence that lower levels of T lead to prostate cancer (Park et al, 2015). Put simply, there is no evidence for testosterone’s supposed impact on the prostate (Stattin et al, 2013).

Differences in androgen/androgen receptors have been explained as a cause for racial differences in prostate cancer (Pettaway, 1999), however, these results haven’t been consistent (Stattin et al, 2003) and these differences in circulating androgen may possibly be explained by differences in obesity between the two populations (Gapstur et al, 2002; also see my posts on obesity and race).

Due to the ‘testosterone scare’, some people may believe that having low T is a ‘good thing’, something that’s preferred over being a high T savage. However, testosterone and the androgen receptor gene polymorphism are both associated with competitiveness and confidence in men (Eisenegger et al, 2016) and a reduced risk of cardiovascular disease in elderly men (Ohlsson et al, 2011). Obviously, lower testosterone is related to less overall confidence. People who have the thought in their head that testosterone is a ‘bad hormone’ will believe the negativity about it in the media and popular headlines.

Testosterone alone does not cause violence, but it does cause men to be socially dominant. Testosterone has been shown to increase in the aggressive phases of sports games and when shown artificial humans made to invoke physiologic responses, leading some researchers to argue that testosterone should be classified as a stress hormone. Testosterone does change based on watching one’s favorite soccer team winning or losing in a sample of 21 men (Bernhardt et al, 1998), lending some credence to the claim that testosterone is and should be classified as a stress hormone. Also of interest is that men who administered high levels of testosterone did not report higher levels of aggression (Batrinos, 2012).

I’ve heard some people literally say that having low testosterone is ‘a good thing’. People say this out of ignorance. There are a whole slew of problems associated with low testosterone, including but not limited to: insulin resistance in diabetic men (Grossmann et al, 2008); metabolic syndrome (Tsuijimura et al, 2013); muscle loss (Yuki et al, 2013); stroke and transient ischemic attack (a mini-stroke; Yeap et al, 2009); associated with elevated risk for dementia in older men (Carcaillon et al, 2014); myocardial infarction (heart attack) in diabetic men (Daka et al, 2015) etc. So it seems that the fear of testosterone from those in the anti-testosterone camp are largely blown out of proportion.

Testosterone is also a ‘food’ for the brain, with low levels being related to mental illness, sexual dysfunction, lower quality of life and cognitive impairment (Moffat et al, 2011) in both sexes (Ciocca et al, 2016). Noticed in both men in women with testosterone deficits were: cognitive impairment (reduction of working memory, episodic memory, processing speed, visual-spatial functioning and executive performance); a decrease in sexual activity; anxiety, schizophrenia, depression and stress; and alterations in cortical thickness in the brain. The fact that testosterone is so heavily important to the body’s central functioning is extremely clear. This is why it’s laughable that some people would be happy and brag about having low testosterone.

I recently came across a book called The Testosterone Hypothesis: How Hormones Regulate the Life Cycles of Civilization. Barzilai’s main premise is that the rise and fall of the West is mediated by the hormone testosterone, and due to lower testosterone levels this is one large reason for what is currently occurring in the West. The book has an extremely interesting premise. Barzilai’s hypothesis does line up with the declining levels of testosterone in America (Travison et al, 2007) though other research shows no decline in American testosterone levels from the years 88-91 to 99-04 (Nyante et al, 2007). Moreover, men who had higher level of n-6 in their blood then n-3 were far more likely to be infertile (Safarinejad et al, 2010) a marker of low testosterone (Sharpe, 2012). The ratio of n-6 to n-3 from the years 1935 to 1939 were 8.4 to 1, whereas from the years 1935 to 1985, the ratio increased to about 10 percent (Raper et al, 1992). The ratio of n-6 to n-3, on top of lowering sperm count (which is correlated with testosterone) also has negative effects on male and female cognitive ability (Lassek and Gaulin, 2011).

Barzilai’s research also corroborates Rushton’s (1986) theory of why there are lower birthrates for Europeans around the world. Rushton stated that this cycle has been noticed throughout history, with empires rising and falling due to differential birthrates between the ruling class and the ruled. Rushton also hypothesized that the cultures and gene pools associated with the Graeco-Roman empire were “evolutionary dead ends” (Rushton, 1986: 148). Knowing what we now know about the relationship between cognitive ability, testosterone, and fertility, we now have a plausible hypothesis for Rushton’s hypothesis and one of the (many) reasons why the Graeco-Roman empire collapsed. Rushton further hypothesized that the cause for lower fertility in European populations “may be partly mediated by a psychological process in which the desire to be in control of both oneself and one’s environment is taken to an extreme.” Of course there’s a good chance that this psychological process is mediated/influenced by testosterone.

Europe is the continent with the lowest fertility (ESHRE Capri Workshop Group, 2010). Testosterone has declined in Europe as a whole (Rivas et al, 2014), and this is a strong cause for the lower birthrates in Europe (along with genetic reasons) and in Finland (Perheentupa et al, 2013). The introduction of Westernized diets lowers testosterone, so this is no surprise that a reduction is seen in countries that begin to consume a Western diet. Another probable cause for lower testosterone/fertility in Europe at the moment is the large number of European men that died in WWI and WWII. Those that were more willing to fight died, meaning there was less of a chance he spread his genes. So, over time, this lead to the current cucking of Europe that we are now witnessing.

Testosterone is also hypothesized to have driven evolution (Howard, 2001). Testosterone is such an important part of human evolution and development, so much so that if we had a lower level of the hormone all throughout our evolution that we would be a different species today. Testosterone is needed for sexual functioning, good mental and brain health, fertility, cognitive ability, muscle mass retention in both young and old men, etc. Testosterone is one of the most important hormones for both men and women, and low levels for both sexes are detrimental to a high quality of life. The current data on testosterone and prostate cancer shows that higher levels of testosterone don’t contribute to prostate cancer. Testosterone, then, also isn’t a cause for the racial gap in prostate cancer because other environmental factors better explain it. If people really are happy about having lower testosterone, then I hope they have fun living a life with a low sex drive, lower cognition in old age, lower muscle mass and a higher chance of stroke and metabolic syndrome.

One of the most interesting things about testosterone is the possibility that it explains why civilizations rise and fall. There is anecdotal evidence from Rushton, as well as his theorizing that the higher classes in Rome didn’t breed which led to their downfall. We now know that lower fertility rates for men are associated with lower testosterone, so along with Barzilai’s thesis of testosterone causing the rise and fall of civilizations, Rushton’s theorizing of the cause of lower European fertility and the cause of the fall of the Graeco-Roman empire.

Testosterone is an extremely important hormone, one that drives human evolution and society formation since it’s associated with dominance and confidence. Low testosterone is looked at as ‘good’ because those with higher intelligence have lower levels of the hormone (indicated by lower confidence and having sex at a later age). I showed that the higher IQ East Asian men have a problem finding dates and being looked at as sexually attractive (even though they rated themselves as average). Along with lower East Asian fertility, specifically in Japan, does it seem to you like the high IQ people are more desired if they are having problems keeping their birthrates up? The fact of the matter is, lower levels of testosterone are correlated with lower levels of fertility. If men don’t have as much testosterone pumping through their veins, they will be less likely to have sex and thusly reproduce.

References

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

Bernhardt, P. C., Jr, J. M., Fielden, J. A., & Lutter, C. D. (1998). Testosterone changes during vicarious experiences of winning and losing among fans at sporting events. Physiology & Behavior,65(1), 59-62. doi:10.1016/s0031-9384(98)00147-4

Carcaillon, L., Brailly-Tabard, S., Ancelin, M., Tzourio, C., Foubert-Samier, A., Dartigues, J., . . . Scarabin, P. (2014). Low testosterone and the risk of dementia in elderly men: Impact of age and education. Alzheimer’s & Dementia,10(5). doi:10.1016/j.jalz.2013.06.006

Ciocca G, Limoncin E, Gravina GL, et al. Is testosterone a food for brain? Sex Med Rev 2016;4:15-25.

Daka, B., Langer, R. D., Larsson, C. A., Rosén, T., Jansson, P. A., Råstam, L., & Lindblad, U. (2015). Low concentrations of serum testosterone predict acute myocardial infarction in men with type 2 diabetes mellitus. BMC Endocrine Disorders,15(1). doi:10.1186/s12902-015-0034-1

ESHRE Capri Workshop Group. Europe the continent with the lowest fertilityHum Reprod Update 2010; 16: 590–602.

Eisenegger, C., Kumsta, R., Naef, M., Gromoll, J., & Heinrichs, M. (2016). Testosterone and androgen receptor gene polymorphism are associated with confidence and competitiveness in men. Hormones and Behavior. doi:10.1016/j.yhbeh.2016.09.011

Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race—the CARDIA male hormone study. Cancer Epidemiol Biomarkers Prev 2002; 11: 10417

Grossmann, M., Thomas, M. C., Panagiotopoulos, S., Sharpe, K., Macisaac, R. J., Clarke, S., . . . Jerums, G. (2008). Low Testosterone Levels Are Common and Associated with Insulin Resistance in Men with Diabetes. The Journal of Clinical Endocrinology & Metabolism,93(5), 1834-1840. doi:10.1210/jc.2007-2177

Howard JM (2001): Androgens in human evolution. A new explanation of human evolution.

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

Michaud, J. E., Billups, K. L., & Partin, A. W. (2015). Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Therapeutic Advances in Urology,7(6), 378-387. doi:10.1177/1756287215597633

Moffat, S. D., Zonderman, A. B., Metter, E. J., Blackman, M. R., Harman, S. M., & Resnick, S. M. (2002). Longitudinal Assessment of Serum Free Testosterone Concentration Predicts Memory Performance and Cognitive Status in Elderly Men. The Journal of Clinical Endocrinology & Metabolism,87(11), 5001-5007. doi:10.1210/jc.2002-020419

Nyante, S. J., Graubard, B. I., Li, Y., Mcquillan, G. M., Platz, E. A., Rohrmann, S., . . . Mcglynn, K. A. (2011). Trends in sex hormone concentrations in US males: 1988-1991 to 1999-2004. International Journal of Andrology,35(3), 456-466. doi:10.1111/j.1365-2605.2011.01230.x

Ohlsson C, Barrett-Connor E, Bhasin S, et al. High serum testosterone is associated with reduced risk of cardiovascular events in elderly men: the MrOS (Osteoporotic Fractures in Men) study in Sweden. J Am Coll Cardiol. 2011; 58(16):1674-1681.

Park, J., Cho, S. Y., Jeong, S., Lee, S. B., Son, H., & Jeong, H. (2015). Low testosterone level is an independent risk factor for high-grade prostate cancer detection at biopsy. BJU International,118(2), 230-235. doi:10.1111/bju.13206

Perheentupa, A., Makinen, J., Laatikainen, T., Vierula, M., Skakkebaek, N. E., Andersson, A., & Toppari, J. (2012). A cohort effect on serum testosterone levels in Finnish men. European Journal of Endocrinology,168(2), 227-233. doi:10.1530/eje-12-0288

Pettaway CA. Racial differences in the androgen/androgen receptor pathway in prostate cancer. J Natl Med Assoc 1999, 91: 653:650

Raper, N. R., Cronin, F. J., & Exler, J. (1992). Omega-3 fatty acid content of the US food supply. Journal of the American College of Nutrition,11(3), 304-308. doi:10.1080/07315724.1992.10718231

Richard, A., Rohrmann, S., Zhang, L., Eichholzer, M., Basaria, S., Selvin, E., . . . Platz, E. A. (2014). Racial variation in sex steroid hormone concentration in black and white men: a meta-analysis. Andrology,2(3), 428-435. doi:10.1111/j.2047-2927.2014.00206.x

Rivas AM, Mulkey Z, Lado-Abeal J, Yarbrough S. Diagnosing and managing low serum testosteroneProc (Bayl Univ Med Cent) 2014;27:321-324

Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., . . . Platz, E. A. (2007). Serum Estrogen, But Not Testosterone, Levels Differ between Black and White Men in a Nationally Representative Sample of Americans. The Journal of Clinical Endocrinology & Metabolism,92(7), 2519-2525. doi:10.1210/jc.2007-0028

Ross R, Bernstein L, Judd H, Hanisch R, Pike M, Henderson B. Serum testosterone levels in healthy young black and white men. J Natl Cancer Inst. 1986 Jan;76(1):45–48

Rushton, J. P. (1986). Gene-Culture Coevolution and Genetic Similarity Theory: Implications for Ideology, Ethnic Nepotism, and Geopolitics. Politics and the Life Sciences,4(02), 144-148. doi:10.1017/s0730938400004706

Rushton J P (1997). Race, Evolution, and Behavior. A Life History Perspective (Transaction, New Brunswick, London).

Safarinejad, M. R., Hosseini, S. Y., Dadkhah, F., & Asgari, M. A. (2010). Relationship of omega-3 and omega-6 fatty acids with semen characteristics, and anti-oxidant status of seminal plasma: A comparison between fertile and infertile men. Clinical Nutrition,29(1), 100-105. doi:10.1016/j.clnu.2009.07.008

Sharpe, R. M. (2012). Sperm counts and fertility in men: a rocky road ahead. EMBO reports,13(5), 398-403. doi:10.1038/embor.2012.50

Stattin, P., Lumme, S., Tenkanen, L., Alfthan, H., Jellum, E., Hallmans, G., . . . Hakama, M. (2003). High levels of circulating testosterone are not associated with increased prostate cancer risk: A pooled prospective study. International Journal of Cancer,108(3), 418-424. doi:10.1002/ijc.11572

Travison, T. G., Araujo, A. B., O’Donnell, A. B., Kupelian, V., & Mckinlay, J. B. (2007). A Population-Level Decline in Serum Testosterone Levels in American Men. The Journal of Clinical Endocrinology & Metabolism,92(1), 196-202. doi:10.1210/jc.2006-1375

Tsujimura, A., Miyagawa, Y., Takezawa, K., Okuda, H., Fukuhara, S., Kiuchi, H., . . . Nonomura, N. (2013). Is Low Testosterone Concentration a Risk Factor for Metabolic Syndrome in Healthy Middle-aged Men? Urology,82(4), 814-819. doi:10.1016/j.urology.2013.06.023

Yeap, B. B., Hyde, Z., Almeida, O. P., Norman, P. E., Chubb, S. A., Jamrozik, K., . . . Hankey, G. J. (2009). Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men. Endocrine Reviews,30(4), 411-411. doi:10.1210/edrv.30.4.9994

Yuki, A., Otsuka, R., Kozakai, R., Kitamura, I., Okura, T., Ando, F., & Shimokata, H. (2013). Relationship between Low Free Testosterone Levels and Loss of Muscle Mass. Scientific Reports,3. doi:10.1038/srep01818

Heritability, the Grandeur of Life, and My First Linkfest on Human Evolution and IQ

1100 words

Benjamin Steele finally replied to my critique of his ‘strong evidence and argument’ on race, IQ and adoption. He goes on to throw baseless ad hominem attacks as well as appealing to motive (assuming my motivation for being a race realist; assuming that I’m a ‘racist’, whatever that means). When I do address his ‘criticisms’ of my response to him, I will not address his idiotic attacks as they are a waste of time. He does, however, say that I do not understand heritability. I understand that the term ‘heritable’ doesn’t mean ‘genetic’. I understand that heritability is the proportion of phenotypic variance attributed to genetic variance. do not believe that heritability means a trait is X percent genetic. 80 percent of the variation in the B-W IQ gap is genetic, with 20 percent explained by environmental effects. Note that I’m not claiming that heritable means genetic. All that aside, half of his reply to me is full of idiotic, baseless and untrue accusations which I will not respond to. So, Mr. Steele, if you do decide to reply to my response to you this weekend, please leave the idiocy at the door. Anyway, I will tackle that this weekend. Quick note for Mr. Steele (in case he reads this): if you don’t believe me about the National Crime and Victimization Survey showing that police arrest FEWER blacks than are reported by the NCVS, you can look it up yourself, ya know.

I’m beginning to understand why people become environmentalists. I’ve recently become obsessed with evolution. Not only of Man, but of all of the species in the world. Really thinking about the grandeur of life and evolution and what leads to the grand diversity of life really had me thinking one day. It took billions of years for us to get to the point we did today. So, why should we continue to destroy environments, displacing species and eventually leading them to extinction? I’m not saying that I fully hold this view yet, it’s just been on my mind lately. Once a species is extinct, that’s it, it’s gone forever. So shouldn’t we do all we possibly can to preserve the wonder of life that took so long to get to the point that we did today?

Some interesting articles to read:

Study: IQ of firstborns differ from siblings (This is some nice evidence for Lassek and Gaulin’s theory stating why first-born children have higher IQs than their siblings: they get first dibs on the gluteofemoral fat deposits that are loaded with n-3 fatty acids, aiding in brain size and IQ.)

Why attitude is more important than IQ (Psychologist Carol Dweck states that attitude is more important than IQ and that attitudes come in one of two types: a fixed mindset or a growth mindset. Those with a fixed mindset believe ‘you are who you are’ and nothing can change it while those with a growth mindset believe they can improve with effort. Interesting article, I will find the paper and comment on it when I read it.)

Positively Arguing IQ Determinism And Effect Of Education (Intelligent people search for intellectually stimulating things whereas less intelligent people do not. This, eventually, will lead to the construction of environments based on that genotype.)

A scientist’s new theory: Religion was key to humans’ social evolution (Nicholas Wade pretty much argues the same in his book The Faith Instinct: How Religion Evolved and Why It EnduresIt is interesting to note that archaeologists have discovered what looks to be the beginnings of religiousity around 10kya, coinciding with the agrigultural revolution. I will look into this in the future.)

Galápagos giant tortoises show that in evolution, slow and steady gets you places (Interesting read, on tortoise migration)

Will Mars Colonists Evolve Into This New Kind of Human? (Very interesting and I hope to see more articles like this in the future. Of course, due to being a smaller population, evolution will occur faster due to differing selection pressures. Smaller populations incur more mutations at a faster rate than larger populatons. Will our skin turn a reddish tint? Bone density will decline leading to heavier bones. The need for C-sections due to heavier bones will lead to futher brain size increases. This is also going on on Earth at the moment, as I have previously discussed. Of course differences in culture and technology will lead the colonizers down different paths. I hope I am alive to see the first colonies on Mars and the types of long-term effects of the evolution of Man on the Red Planet.)

martians_bigheadstktkt_9f6199eb2f00598637272f5352daa1ce-nbcnews-ux-2880-1000

Evolution debate: Are humans continuing to evolve? (Of course we are)

Did seaweed make us who we are today? (Seaweed has many important vitamins and minerals that are imperative for brain development and growth—most importantly, it has poly-unsaturated fatty acids (PUFAs) and B12. We are only able to acquire these fatty acids through our diet—our body cannot synthesize the fatty acid on its own. This is just growing evidence for how important it is to have a good ratio of n-3 to n-6.)

Desert people evolve to drink water poisoned with deadly arsenic (More evidence for rapid evolution in human populations. AS3MT is known to improve arsonic metabolism in Chile and Argentina. Clearly, those who can handle the water breed/don’t die while those who cannot succumb to the effects of arsenic poisoning. Obviously, over time, this SNP will be selected for more and more while those who cannot metabolize the arsonic do not pass on their genes. This is a great article to show to anti-human-evolution deniers.)

Here Are the Weird Ways Humans Are Evolving Right Now (CRISPR and gene editing, promotion of obesity through environmental factors (our animals have also gotten fatter, probably due to the feed we give them…), autism as an adaptation (though our definition for autism has relaxed in the past decade). Human evolution is ongoing and never stops, even for Africans. I’ve seen some people claim that since they never left the continent that they are ‘behind in evolution’, yet evolution is an ongoing process and never stops, cultural ‘evolution’ (change) leading to more differences.)

‘Goldilocks’ genes that tell the tale of human evolution hold clues to variety of diseases (We really need to start looking at modern-day diseases through an evolutionary perspective, such as obesity, to better understand why these ailments inflict us and how to better treat our diseases of civilization.)

Understanding Human Evolution: Common Misconceptions About The Scientific Theory (Don’t make these misconceptions about evolution. Always keep up to date on the newest findings.)

Restore Western Civilization ( Enough said. As usual, gold from Brett Stevens. Amerika.org should be one of the first sites you check every day.)

I guess this was my first linkfest (ala hbd chick). I will post one a week.

 

An Evolutionary Look At Obesity

2050 words

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

Agriculture and Diseases of Civilization

2350 words

It is assumed that since the advent of agriculture that we’ve been better nourished than our hunter-gatherer ancestors. This assumption stems from the past 130 years since the advent of the Industrial Revolution and the increase in the quality of life of those who had the benefit of the Revolution. However, over a longer period of time, the advent of agriculture is linked to poorer health, vectors of disease and lower quality of life (in terms of intractable disease). Despite what I have claimed in the past about hunter-gatherer societies, they do have lower or nonexistent rates of the diseases that currently plague our first-world societies. Why do we have such extremely high rates of disease that they don’t?

Contrary to popular belief, agriculture has caused decreases in many facets of our lives. These diseases, more aptly termed ‘diseases of civilization‘ are directly caused by agricultural and societal ways of living. This increases disease rates as it’s easier for diseases to spread faster through bigger populations. Moreover, we haven’t had time to evolve to the current diet we now eat in first-world countries which has lead to what is termed an ‘evolutionary mismatch‘ between genes and environment. We evolved to eat a certain diet and the introduction of easily digestible carbohydrates which spike insulin the highest. Since insulin causes weight gain, and carbohydrate intake has dramatically increased since the 70s, obesity has increased as a result as countries begin to industrialize and more processed foods are available to the populace.

However, since the Industrial Revolution, height has increased along with IQ. Researchers argue that in first-world countries, high rates of obesity are not preventable due to the excess amounts of highly refined and processed foods. There is data for this theory. In first-world countries, the heritability of BMI is between .76 and .85. Since first-world countries are industrialized, we would expect them to hit their ‘genetic height and weight’ along with having the ability to reach their IQ potential. However, with the excess amount of highly processed and refined foods, this would also, in theory, have the population hit their ‘genetic weights’. This is what we see in first-world countries.

To see how first-world, industrialized societies cause these gene-environment mismatches, we can compare the disease acquisition rate—or lack thereof—to that of Europeans eating an industrialized, first-world diet (high in carbohydrates).

In his 2013 book The Story of the Human Body: Evolution, Health, and DiseasePaleoanthropologist Daniel Lieberman talks at length about evolutionary mismatches. The easiest way to think about this is to think about how one evolved to their environment and think how the processes that alter the environment. A perfect example is African farmers. They may dig a trench to divert water to better irrigate their crops, but this then would cause a higher rate of mosquitoes due to the increase in still water and then selection for genes that protect against malaria would be selected for. This is one example of an evolutionary mismatch turning into an advantage for a population. Most mismatch diseases are caused by changes in the environment which change how the body functions. In other words, the current first-world diet is correlated very highly with diseases of civilization and drive most of the mismatch diseases. Most likely, you will die from one of these mismatch diseases.

If you’re born in a hotter environment, you will have more sweat glands than if you were born in a cooler environment. If you grow up eating soft, processed food, your face will be smaller than if you ate harder foods. These are two ways in which ‘cultural evolution’ (cultural change) have an effect on how the human body grows and adapts to certain stimuli based on the environment around it.

The largest cause of the higher disease rate between industrialized peoples and those in hunter-gatherer societies is shifts in life history. As our life spans increased through modernization, so to did our chance of acquiring more diseases. Of course living longer affects how many children you have but it also raises your chances of acquiring an evolutionary mismatch and your chances of dying from one.

Daniel Lieberman writes on page 190 of his book The Story of the Human Body:

A typical hunter-gatherer adult female will manage to collect 2,000 calories a day and a male can hunt between 3,000 and 6,000 calories a day. (24) A hunter-gatherer groups combined efforts yield just enough food to feed small families. In contrast, a household of early Neolithic farmers from Europe using solely manual labor before the invention of the plow could produce an average if 12,800 calories per day over the course of a year, enough to feed families of six. (25) In other words, the first farmers could double their family size.

Thusly, you can see how evolutionary mismatches would occur with the advent of an agricultural diet that we didn’t evolve to be accustomed to. This is one of the biggest examples of the negative effects of agriculture, our inability to adapt quickly to our new diets which then accelerated after the Industrial Revolution. Further, hunter-gatherers will eat anything edible while agricultural societies will largely eat only what they grow. This would have huge implications for farmers if a few pests ruined their crops since they relied on a few crops to survive.

The thing about farming is that as the Agricultural Revolution began, this increased the population size as well as making that population pretty much stable in terms of migrating. This, then, led to higher rates of disease as larger populations foster new kinds of infectious diseases. Large populations didn’t happen until the advent of farming, and with it came the first plagues. The first farming villages were small, but “as the Reverend Malthus pointed out in 1798, even modest increases in a population’s birthrate will cause rapid increases in overall population size in just a few generations.” (Lieberman, 2013: 197) So as even small increases in population size would cause a boom in future generations, which along with it would drive disease acquisition and plagues in that new and stationary society.

Lieberman further writes on pages 199-200:

Not surprisingly, farming ushered in an era of epidemics, including tuberculosis, leprosy, syphilis, plague, smallpox and influenza. (44) This is not to say that hunter-gatherers did not get sick, but before farming, human societies primarily suffered from parasites such as lice, pinworms they acquired from contaminated food, and viruses or bacteria, such as herpes simplex, which they got from contact with mammals. (45) Diseases such as malaria and yaws (the nonvenereal precursor of syphilis) were probably also present among hunter-gatherers, but at much lower rates than in farmers. In fact, epidemics could not exist prior to the Neolithic because hunter-gatherer populations are below one person per square kilometer, which is below the threshold necessary for virulent diseases to spread. Smallpox, for example, is an ancient viral disease that humans apparently acquired from monkeys or rodents (the disease’s origins are unresolved) that was able to spread appreciably until the growth of large, dense settlements. (46)

Moreover, another evolutionary mismatch is the lack of sanitation that comes with stationary societies. Hunter-gatherers could just go and defecate in a bush, whereas with the advent of civilization, waste and refuse began to pile up in the area. As noted above, when farmers clear space for irrigation to plant crops, this introduces mosquitoes into the area which then causes more disease. Furthermore, we have also acquired about 50 diseases from living near animals (Lieberman, 2013: 201). There are more than 100 evolutionary mismatch diseases that agriculture has brought to humanity.

We can compare disease rates of people in industrialized societies and people in modern-day hunter-gatherer societies. In his 2008 book Good Calories, Bad CaloriesGary Taubes documents numerous instances of hunter-gatherer societies that have no to low rates of the same modern diseases that we have:

In 1914, Hoffman himself had surveyed physicians working for the Bureau of Indian Affairs. “Among some 63,000 Indians of all tribes,” he reported, “there occurred only 2 deaths from cancer as medically observed from the year 1914.” (Taubes, 2008: 92)

“There are no known reasons why cancer should not occasionally occur among any race of people, even though it be below the lowest degree of savagery and barbarism,” Hoffman wrote. (Taubes, 2008: 92)

“Granting the practical difficulties of determining with accuracy the causes of death among the non-civilized races, it is nevertheless a safe assumption that the large number of medical missionaries and other trained medical observers, living for years among native races throughout the world, would long ago have provided a substantial basis of fact regarding the frequency of malignant disease among the so-called “uncivilized” races, if cancer were met with among them to anything like the degree common to practically all civilized countries. Quite the contrary, the negative evidence is convincing that in the opinion of qualified medical observers cancer is exceptionally rare among the primitive peoples.” (Taubes, 2008: 92)

These reports, often published in the British Medical Journal, The Lancet or local journals like the East African Medical Journal, would typically include the length of service the author had undergone among the natives, the size of the local native population served by the hospital in question, the size of the local European population, and the number of cancers involved in both. F.P. Fouch, for instance, district surgeon of the Orange Free State in South Africa, reported to the BMJ in 1923 that he had spent six years at a hospital that served fourteen thousand natives. “I never saw a single case of gastric or duodenal ulcer, colitis, appendicitis, or cancer in any form in a native, although these diseases were frequently seen among the white or European population.” (Taubes, 2008: 92)

As a result of these modern processed foods, noted Hoffman, “far-reaching changes in bodily functioning and metabolism are introduced which, extending over many years, are the causes or conditions predisposing to the development of malignant new growths, and in part at least explain the observed increase in cancer death rate of practically all civilized and highly urbanized countries.” (Taubes, 2008: 96)

The preponderance of evidence shows that these people have low rates of disease that are endemic to our societies due to the advent of agriculture. There is one large difference between hunter-gatherer societies and industrialized ones: the type and amount of food we eat.

Along with the boom of agriculture, we see a slight decrease in height the longer people live in these types of societies. As the Neolithic began 11,500 years ago, height increased about 1.5 inches for males and slightly less for females. But around 7,500 years ago, stature began to decrease and we began noticing evidence of nutritional stress and skeletal markers of disease. There is evidence that as maize was introduced into eastern Tennessee about 1,000 years ago, a decrease of .87 inches in men and 2.4 inches in women were seen. Further, the height of early farmers in China and Japan decreased by 3.1 inches as rice farming progressed, with similar height decreases being seen in Mesoamerica in men (2.2 inches) and women (3.1 inches).

Anti-hereditarian Jared Diamond asks the question “Was farming worth it?” in which he writes:

With agriculture came the gross social and sexual inequality, the disease and despotism, that curse our existence.

The first two things he brings up are pretty Marxist in nature, though they are true. He implies that agriculture causes so-called ‘sexual inequalities’ in which women are made ‘beasts of burden’, made to do the work while men walk by ’empty handed’. This seems to be one negative to a society that is, supposedly, smarter than Europeans.

Regular readers may remember me criticizing Andrew Anglin and his stance on the paleo diet—with how it’s ‘how European man evolved to eat’. However, I am a data-driven person and I try to not let any bias get involved in my thought processes. I know do believe that we should eat a diet that closely mimics our hunter-gatherer ancestors, though we shouldn’t go overboard like certain people in the paleo community, we should be mindful of the quality of food we do it as we will greatly increase our life expectancy along with our quality of life. Indeed, researchers have proposed that we should adopt diets that are close in composition to what our hunter-gatherer ancestors ate in order to battle diseases of civilization. Based on what I’ve read over the past few months, I am inclined to agree. Indeed, evidence for this is seen in a sample of ten Australian Aborigines who were introduced back to their traditional lifestyle (O’Dea, 1984). In a 7 week period, they showed improvement in carbohydrate and lipid metabolism, effectively becoming diabetes-free in almost 2 months.

In sum, there were obviously both positive and negative effects on human life due to the advent of agriculture (leaning more towards negative). These range from diseases to increased population size, to ‘social inequalities’ to higher rates of obesity (this evolutionary mismatch will be extensively covered in the future) to a whole myriad of other diseases. These then lower the quality of life of the individual inflicted. However, the rates of these diseases are low to non-existent in hunter-gatherer societies due to them being nomadic and eating more plentiful foods. Agricultural societies become dependent on a few staple crops so when an endemic occurs, there is mass death since they do not know how to subsist on anything but what they have become accustomed to. The advent of agriculture leads to a decrease in stature as well as brain size. Further, agriculture and the processed foods that came with it caused us to become more susceptible to obesity, which was further exacerbated by the industrial revolutions and the ‘nutritional guidelines’ of the 60s and 70s that led to higher rates of coronary heart disease. It is the lifestyle change from agriculture that we have not adapted to yet that causes disease these diseases of civilization that shorten our life expectancies. I do now believe that all people should eat a diet as close to hunter-gatherer diet as possible, as that’s what the preponderance of evidence shows.

By the way, to my knowledge, contrary to what The Alternative Hypothesis says, there are no differences in carbohydrate metabolism between races (save for a few populations such as the Pima).

Agriculture and Evolution: A Reply to The Alternative Hypothesis

2050 words

I love nutrition science. So much so that I read a new book on it every week. The Alternative Hypothesis has a pretty old video on agriculture and evolution. I strongly disagree with his main thesis. I strongly disagree with his denigration of Gary Taubes. Most of all, I strongly disagree with what he says about the East Asian rice eaters because since that video has been made, the carbohydrate/insulin hypothesis of obesity has changed to the insulin hypothesis of obesity.

In the very beginning of the video he brings up Gary Taubes’s research on low-carb diets and how people tend to be healthier than those who eat higher carb diets. He brings up the East Asians who eat a lot of rice. However, it’s clear he doesn’t know that the percent of carbohydrate intake is nowhere near as important as the absolute amount of carbohydrate consumed:

  1. They consume a fraction of the sugar we do.  More sugar consumption leads to greater insulin resistance, more fat creation, less fat breakdown, and more fat accumulation.
  2. They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
  3. They consume a ratio of omega-6 to omega-3 PUFA that is much lower than we do.  This mayfurther reduce any insulin resistance brought on by the glucose they do consume (in smaller doses and with less sugar).

The fact that East Asians didn’t have high rates of diabesity (diabetes and obesity) was a big blow to the carbohydrate insulin hypothesis. However, the East Asian rice paradox is simply explained by low, if non-existent, consumption of refined carbohydrates. Those populations actually consume fewer total carbohydrates than Western diets, and have lower levels of glycemic load as a result. To quote Mark Sisson:

Before recently, Asians ate less refined sugar and used animal fats for cooking. Sugar intake is rising now, of course, and cooking oils made from corn and soybean have largely replaced lard and tallow, but rice in the context of a low-sugar, no-HFCS (remember, the oft-cited 55/45 fructose/glucose breakdown for HFCS is highly misleading and actually quite often incorrect), low-vegetable oil, nose-to-tail nutrient-dense diet is (or was) acceptable. You can’t reduce a food down to its constituent parts and focus on, say, the bit of fructose in a blueberry and then condemn the entire berry because of it. Similarly, you can’t reduce a diet down to a single constituent food and condemn – or praise – it based on that single food. You have to look at the entire picture, and the Asian diet is largely a nutritious one.

These paradoxes where one population seems to disprove a certain hypothesis are pretty easily explainable with the existing data. There are numerous reasons why East Asian rice eaters have lower rates of diabesity. Dr. Jason Fung also explains why:

Wheat, particularly in the modern iteration may be particularly fattening for numerous reasons.  The high level of amylopectin means that most of the starch contained in flour is efficiently converted to glucose.  This deadly combination of wheat and sugar has been introduced into the Chinese diet.  The result is a Chinese diabetes catastrophe.  The prevalence of diabetes in China has now even outstripped the USA.

This is the answer to the paradox of the Asian Rice eater puzzle.  Why didn’t the Chinese have a diabetes epidemic in 1990 with all their white rice?  Well, because they didn’t eat any sugar (fructose), they were not developing insulin resistance.  Because they were not snacking all the time, they had periods of low insulin level that helped prevent the development of insulin resistance.  So the high rice intake by itself was not enough to cause either of diabetes or obesity.

Then he says that whites intake more total carbs in comparison to blacks and ‘Hispanics’ (1:32 in the video). This is wrong.

Diaz et al (2005) showed that minority populations are more likely to be affected by diabetes mellitus which may be due to less healthy diets and/or genetic factors. Using the National Health and Nutrition Survey for 1999-2000, they analyzed overweight, healthy adults, calculating dietary intake variables and insulin sensitivity by ethnicity. They characterized insulin resistance with fasted insulin, as those who are more likely to become insulin resistant have higher fasted insulin levels (levels taken after waking, with the subject being told not to eat the night before as to get a better reading of fasted insulin levels). Non-‘Hispanic’ whites had higher energy and fat intake while ‘Hispanics’ had higher carb intake with blacks having lower fiber intake.  Blacks and ‘Hispanics’ were more likely to have lower insulin sensitivity. However, ‘Hispanics’ were more likely to have lower insulin sensitivity even after controlling for diet, showing that metabolic differences exist between ethnicities that affect carbohydrate metabolism which leads to higher rates of diabetes in those populations.

Diaz et al state in the results of the study:

Dietary differences are seen by ethnicity, with non-Hispanic whites having higher
energy, saturated fat and total fat intake, while Hispanics had higher carbohydrate intake and African-Americans had lower fibre intake.Both African-Americans and Hispanics had higher levels of fasting insulin, demonstrating lower insulin sensitivity in comparison with non-Hispanic whites.
Non-‘Hispanic’ whites have higher overall energy and fat intake. This means that carbohydrates are less of a percent of the overall diet. In comparison, blacks had lower fiber intake. This means that they eat more processed foods. The same with ‘Hispanics’. Since they constantly spike their insulin with refined carbs, they have higher rates of fasted insulin and thus, have lower insulin sensitivity which is a risk factor for pre-diabetes.
Moreover, from my own personal work with people’s diets, whites eat less refined carbs than blacks or ‘Hispanics’, and while an anecdote, I’ve worked with hundreds of people.
Table 2 of the study shows that whites have a higher total kcal intake in comparison to blacks and ‘Hispanics’, ‘Hispanics’ have a statistically significant higher carb consumption, and blacks eat less fiber. Since whites eat more dietary fat and have a higher fiber intake, that protects them against higher rates of the *average population* that will be obese. Blacks consume less fiber. Dietary fiber actually protects against obesity, so the fact that blacks don’t eat more fiber shows that they eat more refined foods (it’s easily explainable why ‘Hispanics’ eat more fiber. They consume more beans and other fibrous, whole foods). However, since ‘Hispanics’ are more likely to be poor (correlated with low intelligence), they then cannot afford higher quality foods.
Drewnowski and Specter (2004) showed that 1) the highest rates of obesity are found in populations with the lowest incomes and education (correlated with IQ); 2) an inverse relationship between energy density and energy cost; 3) sweets and fats have higher energy density and are more palatable (food scientists work feverishly in labs to find out different combinations of foods to make them more palatable so we will eat more of them); and 4) poverty and food insecurity are associated with lower food expenditures, lower fruit and vegetable intake, and lower-quality diet. All of these data points show that those who are poor are more likely to be obese due to more energy-dense food being cheaper and fats and sugars being more palatable. it’s worth noting that dietary fat combined with carbohydrates and the subsequent insulin spike stores the dietary fat as body fat as well as the insulin telling the body to not burn fat.

I’ve written more on this here and here.

So now that I’ve established that blacks and ‘Hispanics’ consume more total carbohydrates from refined foods, now I’ll show the physiologic effects of insulin.

Insulin inhibits the breakdown of fat in the adipose tissue by inhibiting the lipase that hydrolyzes (the chemical breakdown of a compound due to a reaction with water) the fat out of the cell. Since insulin facilitates the entry of glucose into the cell, when this occurs, the glucose is synthesized into glycerol. Along with the fatty acids in the liver, they both are synthesized into triglycerides in the liver. Due to these mechanisms, insulin is directly involved with the shuttling of more fat into the adipocyte. Since insulin has this effect on fat metabolism in the body, it has a fat-sparing effect. Insulin drives most cells to prefer carbohydrates for energy. Putting it all together, insulin indirectly stimulates the accumulation of fat into the adipose tissue.

Do you see why blacks and ‘Hispanics’ are more susceptible to obesity?

Another glaring error he commits is not separating refined carb consumption with natural carb consumption. Refined carbs spike insulin much more than those foods with natural carbohydrates. East Asians do not have a “higher carbohydrate tolerance than Europeans” (2:06 in the video). This one huge error he commits completely discredits his hypothesis.

He then goes on to talk about India’s diabetes rates. But why is it increasing? Because of Western diets. It’s not about a “lower carbohydrate tolerance” as he says at 3:07, it’s about consuming more refined carbohydrates.

Then at 5:05, he says that he’s “solved Gary Taubes’s race problem in regards to diet”. He did nothing of the sort.

I, of course, have no problem with his IQ data. I have a problem with the conclusions he jumps to in regards to carbohydrates and diabetes. He clearly didn’t look at other factors that would explain why East Asians have lower rates of diabesity (which is increasing as they adopt a Western lifestyle… Weird…). The same thing explains it with the Australian Aborigines.

I have absolutely no problem with the second half of his video. My problem is the first half of it–his denigration of Taubes, non-understanding of insulin spikes in comparison to the quality of carbohydrate ingested and not controlling for refined carbs– as it’s clear he didn’t do extensive research into these populations (which Taubes and others have) to show why they don’t have higher rates of diabesity.

What he doesn’t touch on are “obesogenic environments” which is defined as “the sum of influences that the surroundings, opportunities, or conditions of life have on promoting obesity in individuals or populations”. What a huge coincidence that most of the populations he cited today with higher rates of diabesity live in first-world nations, otherwise known as obesogenic environments.

He should have spoken about the Pima Indians and their rates of diabesity. They didn’t have rates of diabesity as high 100 years ago. Why? The introduction of the obesogenic environment. Prisancho (2003) in his study on the Pima and reduced fat oxidation in first-world countries showed how the Pima preferentially burn carbs and not body fat for energy. Fat-burning would account for 9 kcal lost and CHO for 4. Since they preferentially burn carbs for energy and not fat, this shows why they have higher rates of diabesity. It’s not that it’s a genetic susceptibility to burn CHO for energy over fat (there may be a small genetic component, but it doesn’t override the effects of the actual diet). I’ve shown insulin’s role in fat storage above, do you see why the Pima have this diabesity epidemic after the introduction of refined carbohydrates and the obesogenic environment?

Added sugars and salts in foods causes us to want more of those foods. As I alluded to above, food scientists continuously work to find out which combinations of sugar, salt and fat will be more hyperpalatable to us and make us eat them more. Whites nor East Asians have a ‘higher carb tolerance’, they just eat different types of carbs (mostly unrefined, in comparison to blacks and ‘Hispanics’ anyway). If any individual were to overeat on high carb foods they would become diabetic and obese. Whites nor East Asians are exempt from that.

In sum, he didn’t look at where the carbs came from, only total carb intake. Refined carbs and unrefined carbs do different things in the body. The whiter a processed food is, the more it is refined. The more a food is processed, the more its natural nutrients such as fiber are taken out. These low-fat refined foods are one cause of obesity. However, it’s way too complicated to say that only refined carbohydrates cause diabesity.

I strongly recommend he read Taubes’s and Fung’s books. If he did, he wouldn’t have said what he said about Taubes’s theory and completely disregard the absolute total amount of carb intake and not the total amount of carbohydrates ingested.