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I say that if you are over-weight and wish to lose weight, then you should eat less. You should keep eating less until you achieve your desired weight, and then stick to that level of calorific intake.
Why only talk about calories and assume that they do the same things once ingested into the body? See Feinman and Fine (2004) to see how and why that is fallacious. This was actually studied. Contestants on the show The Biggest Loser were followed after they lost a considerable amount of weight. They followed the same old mantra: eat less, and move more. Because if you decrease what is coming in, and expend more energy then you will lose weight. Thermodynamics, energy in and out, right? That should put one into a negative energy balance and they should lose weight if they persist with the diet. And they did. However, what is going on with the metabolism of the people who lost all of this weight, and is this effect more noticeable for people who lost more weight in comparison to others?
Fothergill et al (2016) found that persistent metabolic slowdown occurred after weight loss, the average being a 600 kcal slowdown. This is what the conventional dieting advice gets you, a slowed metabolism with you having to eat fewer kcal than one who was never obese. This is what the ‘eat less, move more’ advice, the ‘CI/CO’ advice is horribly flawed and does not work!
He seems to understand that exercise does not work to induce weight loss, but it’s this supposed combo that’s supposed to be effective, a kind of one-two punch, and you only need to eat less and move more if you want to lose weight! This is horribly flawed. He then shows a few table from a paper he authored with another researcher back in 1974 (Bhanji and Thompson, 1974).
Say you take 30 people who weigh the same, have the same amount of body fat and are the same height, they eat the same exact macronutrient composition, with the same exact foods, eating at a surplus deficit with the same caloric content, and, at the end of say, 3 months, you will get a different array of weight gained/stalled/decrease in weight. Wow. Something like this would certainly disprove the CI/CO myth. Aamodt (2016: 138-139) describes a study by Bouchard and Tremblay (1997; warning: twin study), writing:
When identical twins, men in their early 20s, were fed a thousand extra calories per day for about three months, each pair showed similar weight gains. In contrast, the gains varied across twin pairs, ranging from nine to twenty-nine pound, even though the calorie imbalance esd the same for everyone. An individual’s genes also influence weight loss. When another group of identical twins burned a thousand more calories per day through exercise while maintaining a stable food intake in an inpatient facility, their losses ranged from two to eighteen pounds and were even more similar within twin pairs than weight gain.
Take a moment to think about that. Some people’s bodies resis weight loss so well that burning an extra thousand calpires a day for three months, without eating more, leads them to lose only two pounds. The “weight loss is just math” crows we met in the last chapter needs to look at what happens when their math is applied to living people. (We know what usually happens: they accuse the poor dieter of cheating, whether or not it’s true.) If cutting 3,500 calories equals one pound of weight loss, then everyone on the twuns’ exercist protocol should have lost twenty-four pounds, but not a single participant lost that much. The average weight loss was only eleven pounds, and the individual variation was huge. Such differences can result from genetic influences on resting metabolism, which varies 10 to 15 percent between people, or from differences in the gut. Because the thousand-calorie energy imbalance was the same in both the gain and loss experiments, this twin research also illustrates that it’s easier to gain weight than to lose it.
That’s weird. If a calorie were truly a calorie, then, at least in the was CI/COers word things, everyone should have had the same or similar weight loss, not with the average weight loss less than half what should have been expected from the kcal they consumed. That is a shot against the CI/CO theory. Yet more evidence against comes from the Vermont Prison Experiment (see Salans et al, 1971). In this experiment, they were given up to 10,000 kcal per day and they, like in the other study described previously, all gained differing amounts of weight. Wow, almost as if individuals are different and the simplistic caloric math of the CI/COers doesn’t size up against real-life situations.
The First Law of Thermodynamics always holds, it’s just irrelevant to human physiology. (Watch Gary Taubes take down this mythconception too; not a typo.) Think about an individual who decreases total caloric intake from 1500 kcal per day to 1200 kcal per day over a certain period of time. The body is then forced to drop its metabolism to match the caloric intake, so the metabolic system of the human body knows when to decrease when it senses it’s getting less intake, and for this reason the First Law is not violated here, it’s irrelevant. The same thing also occurred to the Biggest Loser contestants. Because the followed the CI/CO paradigm of ‘eat less and move more’.
Processed food is not bad in itself, but it is hard to monitor what is in it, and it is probably best avoided if you wish to lose weight, that is, it should not be a large part of your habitual intake.
If you’re trying to lose weight you should most definitely avoid processed foods and carbohydrates.
In general, all foods are good for you, in moderation. There are circumstances when you may have to eat what is available, even if it is not the best basis for a permanent sustained diet.
I only contest the ‘all foods are good for you’ part. Moderation, yes. But in our hedonistic world we live in today with a constant bombardment of advertisements there is no such thing as ‘moderation’. Finally, again, willpower is irrelevant to obesity.
I’d like to know the individual weight gains in Thompson’s study. I bet it’d follow both what occurred in the study described by Aamodt and the study by Sims et al. The point is, human physiological systems are more complicated than to attempt to break down weight loss to only the number of calories you eat, when not thinking of what and how you eat it. What is lost in all of this is WHEN is a good time to eat? People continuously speak about what to eat, where to eat, how to eat, who to eat with but no one ever seriously discusses WHEN to eat. What I mean by this is that people are constantly stuffing their faces all day, constantly spiking their insulin which then causes obesity.
The fatal blow for the CI/CO theory is that people do not gain or lose weight at the same rate (I’d add matched for height, overall weight, muscle mass and body fat, too) as seen above in the papers cited. Why people still think that the human body and its physiology is so simple is beyond me.
Hedonism along with an overconsumption of calories consumed (from processed carbohydrates) is why we’re so fat right now in the third world and the only way to reverse the trend is to tell the truth about human weight loss and how and why we get fat. CI/CO clearly does not work and is based on false premises, no matter how much people attempt to save it. It’s highly flawed and assumed that the human body is so ‘simple’ as to not ‘care’ about the quality of the macro nor where it came from.
Race, aggression, and prostate cancer are all linked, with some believing that race is the cause of higher testosterone which then causes aggression and higher rates of crime along with maladies such as prostate cancer. These claims have long been put to bed, with a wide range of large analyses.
The testosterone debate regarding prostate cancer has been raging for decades and we have made good strides in understanding the etiology of prostate cancer and how it manifests. The same holds true for aggression. But does testosterone hold the key to understanding aggression, prostate cancer and does race dictate group levels of the hormone which then would explain some of the disparities between groups and individuals of certain groups?
For decades it was believed that heightened levels of testosterone caused prostate cancer. Most of the theories to this day still hold that large amounts of androgens, like testosterone and it’s metabolic byproduct dihydrotestosterone, are the two many factors that drive the proliferation of cells and therefore, if a male is exposed to higher levels of testosterone throughout their lives then they are at a high risk of prostate cancer compared to a man with low testosterone levels, so the story goes.
In 1986 Ronald Ross set out to test a hypothesis: that black males were exposed to more testosterone in the womb and this then drove their higher rates of prostate cancer later in life. He reportedly discovered that blacks, after controlling for confounds, had 15 percent higher testosterone than whites which may be the cause of differential prostate cancer mortality between the two races (Ross et al, 1986) This is told in a 1997 editorial by Hugh McIntosh. First, the fact that black males were supposedly exposed to more testosterone in the womb is brought up. I am aware of one paper discussing higher levels of testosterone in black women compared to white women (Perry et al, 1996). Though, I’ve shown that black women don’t have high levels of testosterone, not higher than white women, anyway (see Mazur, 2016 for discussion). (Yes I changed my view on black women and testosterone, stop saying that they have high levels of testosterone it’s just not true. I see people still link to that article despite the long disclaimer at the top.)
Alvarado (2013) discusses Ross et al (1986), Ellis and Nyborg (1992) (which I also discussed here along with Ross et al) and other papers discussing the supposed higher testosterone of blacks when compared to whites and attempts to use a life history framework to explain higher incidences of prostate cancer in black males. He first notes that nutritional status influences testosterone production which should be no surprise to anyone. He brings up some points I agree with and some I do not. For instance, he states that differences in nutrition could explain differences in testosterone between Western and non-Western people (I agree), but that this has no effect within Western countries (which is incorrect as I’ll get to later).
He also states that ancestry isn’t related to prostate cancer, writing “In summation, ancestry does not adequately explain variation among ethnic groups with higher or lower testosterone levels, nor does it appear to explain variation among ethnic groups with high or low prostate cancer rates. This calls into question the efficacy of a disease model that is unable to predict either deleterious or protective effects.”
He then states that SES is negatively correlated with prostate cancer rates, and that numerous papers show that people with low SES have higher rates of prostate cancer mortality which makes sense, since people in a lower economic class would have less access to and a chance to get good medical care to identify problems such as prostate cancer, including prostate biopsies and checkups to identify the condition.
He finally discusses the challenge hypothesis and prostate cancer risk. He cites studies by Mazur and Booth (who I’ve cited in the past in numerous articles) as evidence that, as most know, black-majority areas have more crime which would then cause higher levels of testosterone production. He cites Mazur’s old papers showing that low-class men, no matter if they’re white or black, had heightened levels of testosterone and that college-educated men did not, which implies that the social environment can and does elevate testosterone levels and can keep them heightened. Alvarado concludes this section writing: “Among Westernized men who have energetic resources to support the metabolic costs associated with elevated testosterone, there is evidence that being exposed to a higher frequency of aggressive challenges can result in chronically elevated testosterone levels. If living in an aggressive social environment contributes to prostate cancer disparities, this has important implications for prevention and risk stratification.” He’s not really wrong but on what he is wrong I will discuss later on this section. It’s false that testosterone causes prostate cancer so some of this thesis is incorrect.
I rebutted Ross et al (1986) December of last year. The study was hugely flawed and, yet, still gets cited to this day including by Alvarado (2013) as the main point of his thesis. However, perhaps most importantly, the assay times were done ‘when it was convenient’ for the students which were between 10 am and 3 pm. To not get any wacky readings one most assay the individuals as close to 8:30 am as possible. Furthermore, they did not control for waist circumference which is another huge confound. Lastly, the sample was extremely small (50 blacks and 50 whites) and done on a nonrepresentative sample (college students). I don’t think anyone can honestly cite this paper as any evidence for blacks having higher levels of testosterone or testosterone causing prostate cancer because it just doesn’t do that. (Read Race, Testosterone and Prostate Cancer for more information.)
What may explain prostate cancer rates if not for differences in testosterone like has been hypothesized for decades? Well, as I have argued, diet explains a lot of the variation between races. The etiology of prostate cancer is not known (ACA, 2016) but we know that it’s not testosterone and that diet plays a large role in its acquisition. Due to their dark skin, they need more sunlight than do whites to synthesize the same amount of vitamin D, and low levels of vitamin D in blacks are strongly related to prostate cancer (Harris, 2006). Murphy et al (2014) even showed, through biopsies, that black American men had higher rates of prostate cancer if they had lower levels of vitamin D. Lower concentrations of vitamin D in blacks compared to whites due to dark pigmentation which causes reduced vitamin D photoproduction and may also account for “much of the unexplained survival disparity after consideration of such factors as SES, state at diagnosis and treatment” (Grant and Peiris, 2012).
As mentioned above, testosterone is assumed to be higher in certain races compared to others (based on flawed studies) which then supposedly exacerbates prostate cancer. However, as can be seen above, a lot of assumptions go into the testosterone-prostate cancer hypothesis which is just false. So if the assumptions are false about testosterone, mainly regarding racial differences in the hormone and then what the hormone actually does, then most of their claims can be disregarded.
Perhaps the biggest problem is that Ross et al is a 32-year-old paper (which still gets cited favorably despite its huge flaws) while our understanding of the hormone and its physiology has made considerable progress in that time frame. So it’s in fact not so weird to see papers like this that say “Prostate cancer appears to be unrelated related to endogenous testosterone levels” (Boyle et al, 2016). Other papers also show the same thing, that testosterone is not related to prostate cancer (Stattin et al, 2004; Michaud, Billups, and Partin, 2015). This kills a lot of theories and hypotheses, especially regarding racial differences in prostate cancer acquisition and mortality. So, what this shows is that even if blacks did have 15 percent higher serum testosterone than whites as Ross et al, Rushton, Lynn, Templer, et al believed then it wouldn’t cause higher levels of prostate cancer (nor aggression, which I’ll get into later).
How high is testosterone in black males compared to white males? People may attempt to cite papers like the 32-year-old paper by Ross et al, though as I’ve discussed numerous times the paper is highly flawed and should therefore not be cited. Either way, levels are not as high as people believe and meta-analyses and actual nationally representative samples (not convenience college samples) show low to no difference, and even the low difference wouldn’t explain any health disparities.
One of the best papers on this matter of racial differences in testosterone is Richard et al (2014). They meta-analyzed 15 studies and concluded that the “racial differences [range] from 2.5 to 4.9 percent” but “this modest difference is unlikely to explain racial differences in disease risk.” This shows that testosterone isn’t as high in blacks as is popularly misconceived, and that, as I will show below, it wouldn’t even cause higher rates of aggression and therefore criminal behavior. (Rohrmann et al 2007 show no difference in testosterone between black and white males in a nationally representative sample after controlling for lifestyle and anthropometric variables. Whereas Mazur, 2009 shows that blacks have higher levels of testosterone due to low marriage rates and lower levels of adiposity, while be found a .39 ng/ml difference between blacks and whites aged 20 to 60. Is this supposed to explain crime, aggression, and prostate cancer?)
However, as I’ve noted last year (and as Alvarado, 2013 did as well), young black males with low education have higher levels of testosterone which is not noticed in black males of the same age group but with more education (Mazur, 2016). Since blacks of a similar age group have lower levels of testosterone but are more highly educated then this is a clue that education drives aggression/testosterone/violent behavior and not that testosterone drives it.
Mazur (2016) also replicated Assari, Caldwell, and Zimmerman’s (2014) finding that “Our model in the male sample suggests that males with higher levels of education has lower aggressive behaviors. Among males, testosterone was not associated with aggressive behaviors.” I know this is hard for many to swallow that testosterone doesn’t lead to aggressive behavior in men, but I’ll cover that in the last and final section.
So it’s clear that the myth that Rushton, Lynn, Templer, Kanazawa, et al pushed regarding hormonal differences between the races are false. It’s also with noting, as I did in my response to Rushton on r/K selection theory, that the r/K model is literally predicated on 1) testosterone differences between races being real and in the direction that Rushton and Lynn want because they cite the highly flawed Ross et al (1986) and 2) testosterone does not cause higher levels of aggression (which I’ll show below) which then lead to higher rates of crime along with higher rates of incarceration.
A blogger who goes by the name of ethnicmuse did an analysis of numerous testosterone papers and he found:
Which, of course, goes against a ton of HBD theory, that is, if testosterone did what HBDers believed it does (it doesn’t). This is what it comes down to: blacks don’t have higher levels of testosterone than whites and testosterone doesn’t cause aggression nor prostate cancer so even if this relationship was in the direction that Rushton et al assert then it still wouldn’t cause any of the explanatory variables they discuss.
Last year Lee Ellis published a paper outlining his ENA theory (Ellis, 2017). I responded to the paper and pointed out what he got right and wrong. He discussed strength (blacks aren’t stronger than whites due to body type and physiology, but excel in other areas); circulating testosterone, umbilical cord testosterone exposure; bone density and crime; penis size, race, and crime (Rushton’s 1997 claims on penis size don’t ‘size up’ to the literature as I’ve shown two times); prostate-specific antigens, race, and prostate cancer; CAG repeats; intelligence and education and ‘intelligence’; and prenatal androgen exposure. His theory has large holes and doesn’t line up in some places, as he himself admits in his paper. He, as expected, cites Ross et al (1986) favorably in his analysis.
Testosterone can’t explain all of these differences, no matter if it’s prenatal androgen exposure or not, and a difference of 2.5 to 4.9 percent between blacks and whites regarding testosterone (Richard et al, 2014) won’t explain differences in crime, aggression, nor prostate cancer.
Other authors have attempted to also implicate testosterone as a major player in a wide range of evolutionary theories (Lynn, 1990; Rushton, 1997; Rushton, 1999; Hart, 2007; Rushton and Templer, 2012; Ellis, 2017). However, as can be seen by digging into this literature, these claims are not true and therefore we can discard the conclusions come to by the aforementioned authors since they’re based on false premises (testosterone being a cause for aggression, crime, and prostate cancer and r/K meaning anything to human races, it doesn’t)
Finally, to conclude this section, does testosterone explain racial differences in crime? No, racial differences in testosterone, however small, cannot be responsible for the crime gap between blacks and whites.
Testosterone and aggression
Testosterone and aggression, are they linked? Can testosterone tell us anything about individual differences in aggressive behavior? Surprisingly for most, the answer seems to be a resounding no. One example is the castration of males. Does it completely take away the urge to act aggressively? No, it does not. What is shown when sex offenders are castrated is that their levels of aggression decrease, but importantly, they do not decrease to 0. Robert Sapolsky writes on page 96 of his book Behave: The Biology of Humans at Our Best and Worst (2017) (pg 96):
… the more experience a male has being aggressive prior to castration, the more aggression continues afterward. In other words, the less his being aggressive in the future requires testosterone and the more it’s a function of social learning.
He also writes (pg 96-97):
On to the next issue that lessens the primacy of testosterone: What do individual levels of testosterone have to do with aggression? If one person higher testosterone levels than another, or higher levels this week than last, are they more likely to be aggressive?
Initially the answer seemed to be yes, as studies showed correlation between individual differences in testosterone levels and levels of aggression. In a typical study, higher testosterone levels would be observed in those male prisoners with higher rates of aggression. But being aggressive stimulates testosterone secretion; no wonder more aggressive individuals had higher levels. Such studies couldn’t disentangle chickens and eggs.
Thus, a better question is whether differences in testosterone levels among individuals predict who will be aggressive. And among birds, fish, mammals, and especially other primates, the answer is generally no. This has been studied extensively in humans, examining a variety of measures of aggression. And the answer is clear. To quote British endocrinologist John Archer in a definitive 2006 review, “There is a weak and inconsistent association between testosterone levels and aggression in [human] adults, and . . . administration of testosterone to volunteers typically does not increase aggression.” The brain doesn’t pay attention to testosterone levels within the normal range.
Thus, aggression is typically more about social learning than about testosterone, differing levels of testosterone generally can’t explain why some individuals are more aggressive than others.
Sapolsky also has a 1997 book of essays on human biology titled The Trouble With Testosterone: And Other Essays On The Biology Of The Human Predicament and he has a really good essay on testosterone titled Will Boys Just Be Boys? where he writes (pg 113 to 114):
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Because of a strong bias among certain scientists, it has taken do forever to convince them of this point.
As I said, it takes a lot of work to cure people of that physics envy, and to see interindividual differences in testosterone levels don’t predict subsequent differences in aggressive behavior among individuals. Similarly, fluctuations in testosterone within one individual over time do not predict subsequent changes in the levels of aggression in the one individual—get a hiccup in testosterone secretion one afternoon and that’s not when the guy goes postal.
And on page 115 writes:
You need some testosterone around for normal levels of aggressive behavior—zero levels after castration and down it usually goes; quadruple it (the sort of range generated in weight lifters abusing anabolic steroids), and aggression typically increases. But anywhere from roughly 20 percent of normal to twice normal and it’s all the same; the brain can’t distinguish among this wide range of basically normal values.
Weird…almost as if there is a wide range of ‘normal’ that is ‘built in’ to our homeodynamic physiology…
So here’s the point: differences in testosterone between individuals tell us nothing about individual differences in aggressive behavior; castration and replacement seems to show that, however broadly, testosterone is related to aggression “But that turns out to not be true either, and the implications of this are lost on most people the first thirty times you tell them about it. Which is why you’d better tell them about it thirty-one times, because it’s the most important part of this piece” (Sapolsky, 1997: 115).
Later in the essay, Sapolsky discusses a discusses 5 monkeys that were given time to form a hierarchy of 1 through 5. Number 3 can ‘throw his weight’ around with 4 and 5 but treads carefully around 1 and 2. He then states to take the third-ranking monkey and inject him with a ton of testosterone, and that when you check the behavioral data that he’d then be participating in more aggressive actions than before which would imply that the exogenous testosterone causes participation in more aggressive behavior. But it’s way more nuanced than that.
So even though small fluctuations in the levels of the hormone don’t seem to matter much, testosterone still causes aggression. But that would be wrong. Check out number 3 more closely. Is he now raining aggression and terror on any and all in the group, frothing in an androgenic glaze of indiscriminate violence. Not at all. He’s still judiciously kowtowing to numbers 1 and 2 but has simply become a total bastard to number 4 and 5. This is critical: testosterone isn’t causing aggression, it’s exaggerating the aggression that’s already there.
The correlation between testosterone and aggression is between .08 and .14 (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan, and Davies, 2005; Book and Quinsey, 2005). Therefore, along with all of the other evidence provided in this article, it seems that testosterone and aggression have a weak positive correlation, which buttresses the point that aggression concurrent increases in testosterone.
Sapolsky then goes on to discuss the amygdala’s role in fear processing. The amygdala has its influence on aggressive behavior through the stria terminalis, which is a bunch of neuronal connections. How the amygdala influences aggression is simple: bursts of electrical excitation called action potentials go up and down the stria terminalis which changes the hypothalamus. You can then inject testosterone right into the brain and will it cause the same action potentials that surge down the stria terminalis? No, it does not turn on the pathway at all. This only occurs only if the amygdala is already sending aggression-provoking action potentials down the stria terminalis with testosterone increasing the rate of action potentials you’re shortening the rest time between them. So it doesn’t turn on this pathway, it exaggerates the preexisting pattern, which is to say, it’s exaggerating the response to environmental triggers of what caused the amygdala to get excited in the first place.
He ends this essay writing (pg 119):
Testosterone is never going to tell us much about the suburban teenager who, in his after-school chess club, has developed a particularly aggressive style with his bishops. And it certainly isn’t going to tell us much about the teenager in some inner-city hellhole who has taken to mugging people. “Testosterone equals aggression” is inadequate for those who would offer a simple solution to the violent male—just decrease levels of those pesky steroids. And “testosterone equals aggression” is certainly inadequate for those who would offer a simple excuse: Boys will be boys and certain things in nature are inevitable. Violence is more complex than a single hormone. This is endocrinology for the bleeding heart liberal—our behavioral biology is usually meaningless outside of the context of social factors and the environment in which it occurs.
Injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). This, too, is a large blow for the testosterone-induces-aggression hypothesis. Because aggressive behavior heightens testosterone, testosterone doesn’t heighten aggressive behavior. (This is the causality that has been looked for, and here it is. The causality is not in the other direction.) This tells us that we need to be put into situations for our aggression to rise and along with it, testosterone. I don’t even see how people could think that testosterone could cause aggression. It’s obvious that the environmental trigger needs to be there first in order for the body’s physiology to begin testosterone production in order to prepare for the stimulus that caused the heightened testosterone production. Once the trigger occurs, then it can and does stay heightened, especially in areas where dominance contests would be more likely to occur, which would be low-income areas (Mazur, 2006, 2016).
Lastly, one thing that gets on my nerves that people point to to attempt to show that testosterone and its derivatives cause violence, aggression etc is the myth of “roid rage” which is when an individual objects himself with testosterone, anabolic steroids or another banned substance, and then the individual becomes more aggressive as a result of more free-flowing testosterone in their bloodstream.
The problem here is that people believe what they hear on the media about steroids and testosterone, and they’re largely not true. One large analysis was done to see the effects of steroids and other illicit drug use on behavior, and what was found was that after controlling for other substance use “Our results suggest that it was not lifetime steroid use per se, but rather co-occurrring polysubstance abuse that most parsimoniously explains the relatively strong association of steroid use and interpersonal violence” (Lundholm et al, 2015). So after controlling for other drugs used, men who use steroids do not go to prison and be convicted of violence after other polysubstance use was controlled for, implying that is what’s driving interpersonal violence, not the substance abuse of steroids.
Numerous myths about testosterone have been propagated over the decades, which are still believed in the new millennium despite numerous other studies and arguments to the contrary. As can be seen, the myths that people believe about testosterone are easily debunked. Numerous papers (with better methodology than Ross et al) attest to the fact that testosterone levels aren’t as high as was believed decades ago between the races. Diet can explain a lot of the variation, especially vitamin D intake. Injecting men with supraphysiological doses of testosterone does not heighten anger nor aggression. It does not even heighten prostate cancer severity.
Racial differences in testosterone are also not as high as people would like to believe, there is even an opposite relationship with Asians having higher levels and whites having lower (which wouldn’t, on average, imply femininity) testosterone levels. So as can be seen, the attempted r/K explanations from Rushton et al don’t work out here. They’re just outright wrong on testosterone, as I’ve been arguing for a long while on this blog.
Testosterone doesn’t cause aggression, aggression causes heightened testosterone. It can be seen from studies of men who have been castrated that the more crime they committed before castration, the more crime they will commit after which implies a large effect of social learning on violent behavior. Either way, the alarmist attitudes of people regarding testosterone, as I have argued, are not needed because they’re largely myths.
Dr. James Thompson is a big proponent of ‘diet being an IQ test‘ and has written quite a few articles on this matter. Though, the one he published today is perhaps the most misinformed.
He first shortly discusses the fact that 200 kcal drinks are being marketed as ‘cures’ for type II diabetes. People ‘beat’ the disease with only 200 kcal drinks. Sure, they lost weight, lost their disease. Now what? Continue drinking the drinks or now go back to old dietary habits? Type II diabetes is a lifestyle disease, and so can be ameliorated with lifestyle interventions. Though, Big Pharma wants you to believe that you can only overcome the disease with their medicines and ‘treatments’ along with the injection of insulin from your primary care doctor. Though, this would only exacerbate the disease, not cure it. The fact of the matter is this: these ‘treatments’ only ‘cure’ the proximate causes. The ULTIMATE CAUSES are left alone and this is why people fall back into habits.
When speaking about diabetes and obesity, this is a very important distinction to make. Most doctors, when treating diabetics, only treat the proximate causes (weight, symptoms that come with weight, etc) but they never get to the root of the problem. The root of the problem is, of course, insulin. The main root is never taken care of, only the proximate causes are ‘cured’ through interventions, however, the underlying cause of diabetes, and obesity as well is not taken care of because of doctors. This, then, leads to a neverending cycle of people losing a few pounds or whatnot and then they, expectedly, gain it back and they have to re-do the regimen all over again. The patient never gets cured, Big Pharma, hospitals et al get to make money off not curing a patients illness by only treating proximate and not ultimate causes.
Dr. Thompson then talks about a drink for anorexics, called ‘Complan“, and that he and another researcher gave this drink to anorexics, giving them about 3000 kcals per day of the drink, which was full of carbs, fat and vitamins and minerals (Bhanji and Thompson, 1974).
The total daily calorific intake was 2000-3000 calories, resulting in a mean weight gain of 12.39 kilos over 53 days, a daily gain of 234 grams, or 1.64 kilos (3.6 pounds) a week. That is in fact a reasonable estimate of the weight gains made by a totally sedentary person who eats a 3000 calorie diet. For a higher amount of calories, adjust upwards. Thermodynamics.
Thermodynamics? Take the first law. The first law of thermodynamics is irrelevant to human physiology (Taubes, 2007; Taubes, 2011; Fung, 2016). (Also watch Gary Taubes explain the laws of thermodynamics.) Now take the second law of thermodynamics which “states that the total entropy can never decrease over time for an isolated system, that is, a system in which neither energy nor matter can enter nor leave.” People may say that ‘a calorie is a calorie’ therefore it doesn’t matter whether all of your calories come from, say, sugar or a balanced high fat low carb diet, all weight gain or loss will be the same. Here’s the thing about that: it is fallacious. Stating that ‘a calorie is a calorie’ violates the second law of thermodynamics (Feinman and Fine, 2004). They write:
The second law of thermodynamics says that variation of efficiency for different metabolic pathways is to be expected. Thus, ironically the dictum that a “calorie is a calorie” violates the second law of thermodynamics, as a matter of principle.
So talk of thermodynamics when talking about the human physiological system does not make sense.
He then cites a new paper from Lean et al (2017) on weight management and type II diabetes. The authors write that “Type 2 diabetes is a chronic disorder that requires lifelong treatment. We aimed to assess whether intensive weight management within routine primary care would achieve remission of type 2 diabetes.” To which Dr. Thompson asks ‘How does one catch this illness?” and ‘Is there some vaccination against this “chronic disorder”?‘ The answer to how does one ‘catch this illness’ is simple: the overconsumption of processed carbohydrates, constantly spiking insulin which leads to insulin resistance which then leads to the production of more insulin since the body is resistant which then causes a vicious cycle and eventually insulin resistance occurs along with type II diabetes.
Dr. Thompson writes:
Patients had been put on Complan, or its equivalent, to break them from the bad habits of their habitual fattening diet. This is good news, and I am in favour of it. What irritates me is the evasion contained in this story, in that it does not mention that the “illness” of type 2 diabetes is merely a consequence of eating too much and becoming fat. What should the headline have been?
Trial shows that fat people who eat less become slimmer and healthier.
I hope this wonder treatment receives lots of publicity. If you wish to avoid hurting anyone’s feelings just don’t mention fatness. In extremis, you may talk about body fat around vital organs, but keep it brief, and generally evasive.
So you ‘break bad habits’ by introducing new bad habits? It’s not sustainable to drink these low kcal drinks and expect to be healthy. I hope this ‘wonder treatment’ does not receive a lot of publicity because it’s bullshit that will just line the pockets of Big Pharma et al, while making people sicker and, the ultimate goal, having them ‘need’ Big Pharma to care for their illness—when they can just as easily care for it themselves.
‘Trial shows that fat people who eat less become slimmer and healthier’. Or how about this? Fat people that eat well and exercise, up to 35 BMI, have no higher risk of early death then someone with a normal BMI who eats well and exercises (Barry et al, 2014). Neuroscientist Dr. Sandra Aamodt also compiles a wealth of solid information on this subject in her 2016 book “Why Diets Make Us Fat: The Unintended Consequences of Our Obsession with Weight Loss“.
Dr. Thompson writes:
I see little need to update the broad conclusion: if you want to lose weight you should eat less.
This is horrible advice. Most diets fail, and they fail because the ‘cures’ (eat less, move more; Caloric Reduction as Primary: CRaP) are garbage and don’t take human physiology into account. If you want to lose weight and put your diabetes into remission, then you must eat a low-carb (low carb or ketogenic, doesn’t matter) diet (Westman et al, 2008; Azar, Beydoun, and Albadri, 2016; Noakes and Windt, 2016; Saslow et al, 2017). Combine this with an intermittent fasting plan as pushed by Dr. Jason Fung, and you have a recipe to beat diabesity (diabetes and obesity) that does not involve lining the pockets of Big Pharma, nor does it involve one sacrificing their health for ‘quick-fix’ diet plans that never work.
In sum, diets are not ‘IQ tests’. Low kcal ‘drinks’ to ‘change habits’ of type II diabetics will eventually exacerbate the problem because when the body is in extended caloric restriction, the brain panics and releases hormones to stimulate appetite while stopping hormones that cause you to be sated and stop eating. This is reality; these studies that show that eating or drinking 800 kcal per day or whatnot are based on huge flaws: the fact that this could be sustainable for a large number of the population is not true. In fact, no matter how much ‘willpower’ you have, you will eventually give in because willpower is a finite resource (Mann, 2014).
There are easier ways to lose weight and combat diabetes, and it doesn’t involve handing money over to Big Pharma/Big Food. You only need to intermittently fast, you’ll lose weight and your diabetes will not be a problem, you’ll be able to lose weight and will not have problems with diabetes any longer (Fung, 2016). Most of these papers coming out recently on this disease are garbage. Real interventions exist, they’re easier and you don’t need to line the pockets of corporations to ‘get cured’ (which never happens, they don’t want to cure you!)
Black-white differences in physiology can tell a lot about how the two groups have evolved over time. On traits like resting metabolic rate (RMR), basal metabolic rate (BMR), adiposity, heart rate, Vo2 max, etc. These differences in physiological variables between groups, then, explain part of the reason why there are different outcomes in terms of life quality/mortality between the two groups.
Right away, by looking at the average black and average white, you can see that there are differences in somatype. So if there are differences in somatype, then there must be differences in physiological variables, and so, this may be a part of the cause of, say, differing obesity rates between black and white women (Albu et al, 1997) and even PCOS (Wang and Alvero, 2013).
Resting metabolic rate
Resting metabolic rate is your body’s metabolism at rest, and is the largest component of the daily energy budget in modern human societies (Speakman and Selman, 2003). So if two groups, on average, differ in RMR, then one with the lower RMR may have a higher risk of obesity than the group with the higher RMR. And this is what we see.
Black women do, without a shadow of a doubt, have a lower BMR, lower PAEE (physical activity energy expenditure) and TDEE (total daily expenditure) (Gannon, DiPietro, and Poehlman, 2000). Knowing this, then it is not surprising to learn that black women are also the most obese demographic in the United States. This could partly explain why black women have such a hard time losing weight. Metabolic differences between ethnic groups in America—despite living in similar environments—show that a genetic component is responsible for this.
There are even predictors of obesity in post-menopausal black and white women (Nicklas et al, 1999). They controlled for age, body weight and body composition (variables that would influence the results—no one tell me that “They shouldn’t have controlled for those because it’s a racial confound!”) and found that despite having a similar waist-to-hip ratio (WHR) and subcutaneous fat area, black women had lower visceral fat than white women, while fasting glucose, insulin levels, and resting blood pressure did not differ between the groups. White women also had a higher Vo2 max, which remained when lean mass was controlled for. White women could also oxidize fat at a higher rate than black women (15.4 g/day, which is 17% higher than black women). When this is expressed as percent of total kcal burned in a resting state, white women burned more fat than black women (50% vs 43%). I will cover the cause for this later in the article (one physiologic variable is a large cause of these differences).
We even see this in black American men with more African ancestry—they’re less likely to be obese (Klimentidis et al 2016). This, too, goes back to metabolic rate. Black American men have lower levels of body fat than white men (Vickery et al, 1988; Wagner and Heyward, 2000). All in all, there are specific genetic variants and physiologic effects, which cause West African men to have lower central (abdominal) adiposity than European men and black women who live in the same environment as black men—implying that genetic and physiologic differences between the sexes are the cause for this disparity. Whatever the case may be, it’s interesting and more studies need to be taken out so we can see how whatever gene variants are *identified* as protecting against central adiposity work in concert with the system to produce the protective effect. Black American men have lower body fat, therefore they would have, in theory, a higher metabolic rate and be less likely to be obese—while black women have the reverse compared to white women—a lower metabolic rate.
Skeletal muscle fiber
Skeletal muscle fibers are the how and why of black domination in explosive sports. This is something I’ve covered in depth. Type II fibers contract faster than type I. This has important implications for certain diseases that black men are more susceptible to. Though the continuous contraction of the fibers during physical activity leads to a higher disease susceptibility in black men—but not white men (Tanner et al, 2001). If you’re aware of fiber type differences between the races (Ama et al, 1986; Entine, 2000; Caeser and Henry, 2015); though see Kerr (2010’s) article The Myth of Racial Superiority in Sports for another view. That will be covered here in the future.
Nevertheless, fiber typing explains racial differences in sports, with somatype being another important variable in explaining racial disparities in sports. Two main variables that work in concert are the somatype (pretty much body measurements, length) and the fiber type. This explains why blacks dominate baseball and football; this explains why ‘white men can’t jump and black men can’t swim’. Physiological variables—not only ‘motivation’ or whatever else people who deny these innate differences say—largely explain why there are huge disparities in these sports. Physiology is important to our understanding of how and why certain groups dominate certain sports.
This is further compounded by differing African ethnies excelling in different running sports depending on where their ancestors evolved. Kenyans have an abundance of type I fibers whereas West Africans have an abundance of type II fibers. (Genetically speaking, ‘Jamaicans’ don’t exist; genetic testing shows them to come from a few different West African countries.) Lower body symmetry—knees and ankles—show that they’re more symmetrical than age-matched controls (Trivers et al, 2014). This also goes to show that you can’t teach speed (Lombardo and Deander, 2014). Though, of course, training and the will to want to do your best matter as well—you just cannot excel in these competitions without first and foremost having the right physiologic and genetic make-up.
Further, although it’s only one gene variant, ACTN3 and ACE explain a substantial percentage of sprint time variance, which could be the difference between breaking a world record and making a final (Papadimitriou et al, 2016). So, clearly, certain genetic variants matter more than others—and the two best studied are ACTN3 and ACE. Some authors, though, may deny the contribution of ACTN3 to elite athletic performance—like one researcher who has written numerous papers on ACTN3, Daniel MacArthur. However, elite sprinters are more likely to carry the RR ACTN3 genotype compared to the XX ACTN3 genotype, and the RR ACTN3 genotype—when combined with type II fibers and morphology—lead to increased athletic performance (Broos et al, 2016). It’s also worth noting that 2 percent of Jamaicans carry the XX ACTN3 genotype (Scott et al, 2010), so this is another well-studied variable that lends to superior running performance in Jamaicans.
In regards to Kenyans, of course when you are talking about genetic reasons for performance, some people don’t like it. Some may say that certain countries dominate in X, and that for instance, North Africa is starting to churn out elite athletes, should we begin looking for genetic advantages that they possess (Hamilton, 2000)? Though people like Hamilton are a minority view in this field, I have read a few papers that there is no evidence that Kenyans possess a pulmonary system that infers a physiologic advantage over whites (Larsen and Sheel, 2015).
People like these three authors, however, are in the minority here and there is a robust amount of research that attests to East African running dominance being genetic/physiologic in nature—though you can’t discredit SES and other motivating variables (Tucker, Onywera, and Santos-Concejero, 2015). Of course, a complex interaction between SES, genes, and environment are the cause of the success of the Kalenjin people of Kenya, because they live and train in such high altitudes (Larsen, 2003), though the venerable Bengt Saltin states that the higher Vo2 max in Kenyan boys is due to higher physical activity during childhood (Saltin et al, 1995).
The last variable I will focus on (I will cover more in the future) is blood pressure. It’s well known that blacks have higher blood pressure than whites—with black women having a higher BP than all groups—which then leads to other health implications. Some reasons for the cause are high sodium intake in blacks (Jones and Hall, 2006); salt (Lackland, 2014; blacks had a similar sensitivity than whites, but had a higher blood pressure increase); while race and ethnicity was a single independent predictor of hypertension (Holmes et al, 2013). Put simply, when it comes to BP, ethnicity matters (Lane and Lip, 2001).
While genetic factors are important in showing how and why certain ethnies have higher BP than others, social factors are arguably more important (Williams, 1992). He cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity. SES factors, of course, lead to higher rates of obesity (Sobal and Stunkard, 1989; Franklin et al, 2015). So, of course, environmental/social factors have an effect on BP—no matter if the discrimination or whatnot is imagined by the one who is supposedly discriminated against, this still causes physiologic changes in the body which then lead to higher rates of BP in certain populations.
Poverty does affect a whole slew of variables, but what I’m worried about here is its effect on blood pressure. People who are in poverty can only afford certain foods, which would then cause certain physiologic variables to increase, exacerbating the problem (Gupta, de Wit, and McKeown, 2007). Whereas diets high in protein predicted lower BP in adults (Beundia et al, 2015). So this is good evidence that the diets of blacks in America do increase BP, since they eat high amounts of salt, low protein and high carb diets.
Still, others argue that differences in BP between blacks and whites may not be explained by ancestry, but by differences in education, rather than genetic factors (Non, Gravlee, and Mulligan, 2012). Their study suggests that educating black Americans on the dangers and preventative measures of high BP will reduce BP disparities between the races. This is in-line with Williams (1992) in that the social environment is the cause for the higher rates of BP. One hypothesis explored to explain why this effect with education was greater in blacks than whites was that BP-related factors, such as stress, poverty and racial discrimination (remember, even if no racial discrimination occurs, any so-called discrimination is in the eye of the beholder so that will contribute to a rise in physiologic variables) and maybe social isolation may be causes for this phenomenon. Future studies also must show how higher education causes lower BP, or if it only serves as other markers for the social environment. Nevertheless, this is an important study in our understanding of how and why the races differ in BP and it will go far to increase our understanding of this malady.
This is not an exhaustive list—I could continue writing about other variables—but these three are some of the most important as they are a cause for higher mortality rates in America. Understanding the hows and whys of these variables will have us better equipped to help those who suffer from diseases brought on by these differences in physiological factors.
The cause for some of these physiologic differences come down to evolution, but still others may come down to the immediate obesogenic environment (Lake and Townshend, 2006) which is compounded by lower SES. Since high carbs diets increase BP, this explains part of the reason why blacks have higher BP, along with social and genetic factors. Muscle fiber typing is set by the second trimester, and no change is seen after age 6 (Bell, 1980). Resting metabolic rate gap differences between black and white women can be closed, but not completely, if black women were to engage in exercise that use their higher amounts of type II muscle fibers (Tanner et al, 2001). This research is important to understand differences in racial mortality; because when we understand them then we can begin to theorize on how and why we see these disparities.
Physiologic differences between the races are interesting, they’re easily measurable and they explain both disparities in sports and mortality by different diseases. Once we study these variables more, we will be better able to help people with these variables—race be dammed. Race is a predictor here, only because race is correlated with other variables that lead to negative health outcomes. So once we understand how and why these differences occur, then we can help others with similar problems—no matter their race.
There are a few things I constantly see around the Internet that really irk me. One of those things is the meme that soy causes feminization in males. Some people may see a picture of a guy with soft facial features and they’ll say ‘oh that’s a soy boy.’ They do not show a good understanding of soy and its chemicals. As usual, overblown claims from people who have no specialty in what they’re talking about have an answer—just one they do not want to hear.
I have no idea when this craze of blaming soy and other foods on ‘feminization of males’ (I have done so a few years ago, though I realize my error now), but it’s starting to get out of hand. I see this around Twitter a lot; ‘oh it’s the soy making men beta’ or ‘they know exactly what soy does to men and they still push it!’. The whole scare about soy is that soy has phytoestrogens called isoflavones, and these phytoestrogens then may mimic estrogen production in the body. (It’s worth noting that phytoestrogens do not always mimic estrogens, despite some people’s protesting to me that “It has estrogen right in the name!”.)
Many men have blamed soy and phytoestrogens/isoflavones on their growing breasts, having a flaccid penis, slow beard growth (that’d be enough motivation for me to do something about it, to be honest), loss of hair on his arms and legs, and, he says “Men aren’t supposed to have breasts … It was like my body is feminizing.” So this man went to an endocrinologist and was told that he had gynecomastia—enlarged breasts in men. He got tested for a whole slew of maladies, but they all came back negative. Then the doctor told him to be very specific with his diet. The man then said that he was lactose intolerant and that he drank soy milk instead of cow’s milk. The doctor then asked him how much soy milk he drank per day, to which the man responded 3 quarts. Was soy the cause of his gynecomastia and other negative health effects? I don’t think so.
For men and boys, soy does not seem to have an effect on estrogen and other hormone levels, nor does it seem to have an effect on development and fertility:
A handful of individuals and organizations have taken an anti-soy position and have questioned the safety of soy products. In general, this position latches to statistically insignificant findings, understates how powerfully the research refutes many of the main anti-soy points, and relies heavily on animal research studies, which are medically irrelevant to human health.
Most of those people are ‘activists’ who do not understand the intricacies of what they are talking about. In the field of nutrition, it’s dumb to take studies done on animals nd then extrapolate that data to humans. It does not make sense.
There are reasons not to eat soy that do not go along with this dumb hysteria from people who do not know what they are talking about. One reasons is that, when compared to casein protein, soy protein is inferior (Luiking et al, 2005). Further, data is “inconsistent or inadequate in supporting most of the suggested health benefits of consuming soy protein or ISF” (Xiao, 2008). People may cite studies like Lephart et al (2002) where they write in their article Neurobehavioral effects of dietary soy estrogens:
Whether these observations hold true for the human brain remains to be established and will only become apparent from long-term clinical studies. One point that needs clarification relates to the timing of brain development in the rat, which differs from that in the human. (pg. 12)
Rats and humans are different; I don’t think I need to say that. Though people who cite these studies (uncritically) as ‘evidence’ that soy lowers T, causes infertility problems, and feminization just look to grab anything that affirms their fearmongering views.
Jargin (2014) writes in his article Soy and phytoestrogens: possible side effects:
Feminizing effect of phytoestrogens and soy products may be subtle, detectable only statistically in large populations; it can be of particular importance for children and adolescents. This matter should be clarified by independent research, which can have implications for the future of soy in the agriculture.
If it’s only identifiable in statistically large populations, then it is meaningless. Though, East Asians seem to be adapted to soy and so (like all studies should note), these results should not be extrapolated to other races/ethnies (Jargin, 2014). I do agree with that assessment; I do not agree with the claim that these phytoestrogens would cause problems that would only be seen in statistically large populations.
If people want to use rat studies to show that soy supposedly raises estrogen levels, then I will use a rat study showing the opposite (Song, Hendrich, and Murphy, 1999). They showed that the effects of the isoflavones from soy were only weakly estrogenic. Further, Mitchell et al (2001) write in their article Effect of a phytoestrogen food supplement on reproductive health in normal males:
The phytoestrogen supplement increased plasma genistein and daidzein
concentrations to approx. 1 µM and 0.5 µM respectively; yet, there was no observable effect on endocrine measurements, testicular volume or semen parameters over the study period. This is the first study to examine the effects of a phytoestrogen supplement on reproductive health in males. We conclude that the phytoestrogen dose consumed had no effect on semen quality.
The men in this study took a daily isoflavone supplement containing 40 mg of isoflavone every day for two months and still did not show negative effects. Looking at rat studies and then extrapolating that to humans doesn’t make sense.
Finally, there was a large meta-analysis by Messina (2010) who writes:
The intervention data indicate that isoflavones do not exert feminizing effects on men at intake levels equal to and even considerably higher than are typical for Asian males.
And from the conclusion:
Isoflavone exposure at levels even greatly exceeding reasonable dietary intakes does not affect blood T or estrogen levels in men or sperm and semen parameters. The ED-related findings in rats can be attributed to excessive isoflavone exposure and to differences in isoflavone metabolism between rodents and humans. Thus, men can feel confident that making soy a part of their diet will not compromise their virility or reproductive health.
Now, I know that proponents of the hypothesis of soy feminizing males would say to me “Why don’t you just eat a bunch of soy and see what happens then, if it is fine for you?” Well, unlike most people, I eat a strict diet and soy is not part of it.
Soy isoflavones are currently being researched in regards to the prevention and treatment of diabetes, cardiovascular disease, cancer, osteoporosis, and neuroprotection (Kalaiselven et al, 2010), while the nutritional and health benefits of soy isoflavones are currently being studied (Friedman and Brandon, 2001; McCue and Shetty, 2004). Soy foods may also be optimal for bone health (Lanou, 2011).
In conclusion, as you can see, the claims of soy causing feminizing effects on men are largely overblown. People extrapolate data from rat studies to humans, which doesn’t make any sense. To paraphrase Dr. Jason Fung, imagine 2 lions are watching a deer eat. They see how strong and in shape the deer are eating grass. So the lions, noticing that the deer are healthy eating grass, begin to eat grass too thinking it is healthy and they die. One hundred years later, 2 deer are watching a lion eat meat and sees how strong, fast, and healthy it is. They then draw the conclusion that eating meat is healthy and will do the same for them and they eat meat and die. The point of the analogy is that just because studies on animals show X and therefore Y, that does not mean that it will hold for humans! This is something very simple for people to understand, though most do not.
Most people search for things to prove their assumptions without having an actual understanding of the biological mechanisms of what they’re talking about. People should learn some of the literature before they cite studies that supposedly back their biases, because they would then see that it is not as nuanced as they believe.
(Note: Diet changing under Doctor’s supervision only.)
I enjoy reading what other bloggers write about testosterone and its supposed link to crime, aggression, and prostate cancer; I used to believe some of the things they did, since I didn’t have a good understanding of the hormone nor its production in the body. However, once you understand how its produced in the body, then what others say about it will seem like bullshit—because it is. I’ve recently read a few articles on testosterone from the HBD-blog-o-sphere and, of course, they have a lot of misconceptions in them—some even using studies I have used myself on this blog to prove my point that testosterone does not cause crime!! Now, I know that most people don’t read studies that are linked, so they would take what it says on face value because, why not, there’s a cite so what he’s saying must be true, right? Wrong. I will begin with reviewing an article by someone at The Alternative Hypothesis and then review one article from Robert Lindsay on testosterone.
The Alternative Hypothesis
Faulk has great stuff here, but the one who wrote this article, Testosterone, Race, and Crime, 1) doesn’t know what he’s talking about and 2) clearly didn’t read the papers he cited. Read this article, you’ll see him make bold claims using studies I have used for my own arguments that testosterone doesn’t cause crime! Let’s take a look.
One factor which explains part of why Blacks have higher than average crime rates is testosterone. Testosterone is known to cause aggression, and Blacks are known to at once have more of it and, for genetic reasons, to be more sensitive to its effects.
- No it doesn’t.
- “Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
- Evidence is mixed on blacks being “… for genetic reasons … more sensitive to its effects” (Update on Androgen Receptor gene—Race/History/Evolution Notes).
Testosterone activity has been linked many times to aggression and crime. Meta-analyses show that testosterone is correlated with aggression among humans and non human animals (Book, Starzyk, and Quinsey, 2001).
Why doesn’t he say what the correlation is? It’s .14 and this study, while Archer, Graham-Kevan and Davies, (2005) reanalyzed the studies used in the previous analysis and found the correlation to be .08. This is a dishonest statement.
Women who suffer from a disease known as congenital adrenal hyperplasia are exposed to abnormally high amounts of testosterone and are abnormally aggressive.
Abnormal levels of androgens in the womb for girls with CAH are associated with aggression, while boys with and without CAH are similar in aggression/activity level (Pasterski et al, 2008), yet black women, for instance, don’t have higher levels of testosterone than white women (Mazur, 2016). CAH is just girls showing masculinized behavior; testosterone doesn’t cause the aggression (See Archer, Graham-Kevan and Davies, 2005)
Actually, no. Supraphysiological levels of testosterone administered to men (200 and 600 mg weekly) did not increase aggression or anger (Batrinos, 2012).
Finally, people in prison have higher than average rates of testosterone (Dabbs et al., 2005).
Dabbs et al don’t untangle correlation from causation. Environmental factors can explain higher testosterone levels (Mazur, 2016) in inmates, and even then, some studies show socially dominant and aggressive men have the same levels of testosterone (Ehrenkraz, Bliss, and Sheard, 1974).
Thus, testosterone seems to cause both aggression and crime.
No, it doesn’t.
Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006) so, along with the studies and articles cited on testosterone, aggression, and crime, that’s another huge blow to the testosterone/crime/aggression hypothesis.
Richard et al. (2014) meta-analyzed data from 14 separate studies and found that Blacks have higher levels of free floating testosterone in their blood than Whites do.
They showed that blacks had 2.5 to 4.9 percent higher testosterone than whites, which could not explain the higher prostate cancer incidence (which meta-analyses call in to question; Sridhar et al 2010; Zagars et al 1998). That moderate amount would not be enough to cause differences in aggression either.
Exacerbating this problem even further is the fact that Blacks are more likely than Whites to have low repeat versions of the androgen receptor gene. The androgen reception (AR) gene codes for a receptor by the same name which reacts to androgenic hormones such as testosterone. This receptor is a key part of the mechanism by which testosterone has its effects throughout the body and brain.
The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.
This one is much more basic, and tiring to rebut but I’ll do it anyway. Lindsay has a whole slew of articles on testosterone on his blog that show he doesn’t understand the hormone, but I’ll just talk about this one for now: Black Males and Testosterone: Evolution and Perspectives.
It was also confirmed by a recent British study (prostate cancer rates are somewhat lower in Black British men because a higher proportion of them have one White parent)
Jones and Chinegwundoh (2014) write: “Caution should be taken prior to the interpretation of these results due to a paucity of research in this area, limited accurate ethnicity data, and lack of age-specific standardisation for comparison. Cultural attitudes towards prostate cancer and health care in general may have a significant impact on these figures, combined with other clinico-pathological associations.”
This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Black males are exposed to higher testosterone levels from the very start.
In a study of women in early pregnancy, Ross found that testosterone levels were 50% higher in Black women than in White women (MacIntosh 1997).
I used to believe this, but it’s much more nuanced than that. Black women don’t have higher levels of testosterone than white women (Mazur, 2016; and even then Lindsay fails to point out that this was pregnant women).
According to Ross, his findings are “very consistent with the role of androgens in prostate carcinogenesis and in explaining the racial/ethnic variations in risk” (MacIntosh 1997).
Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue.
Testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009; Kheirandish and Chinegwundoh, 2011; Williams et al, 2012; Gathirua-Mingwai and Zhang, 2014). However in a small population-based study on blacks and whites from South Carolina, Sanderson et al (2017) “did not find marked differences in lifestyle factors associated with prostate cancer by race.”
Regular exercise, however, can decrease PCa incidence in black men (Moore et al, 2010). A lot of differences can be—albeit, not too largely— ameliorated by environmental interventions such as dieting and exercising.
Many studies have shown that young Black men have higher testosterone than young White men (Ellis & Nyborg 1992; Ross et al. 1992; Tsai et al. 2006).
Ellis and Nyborg (1992) found 3 percent difference. Ross et al (1992) have the same problem as Ross et al (1986), which used University students (~50) for their sample. They’re not representative of the population. Ross et al (1992) also write:
Samples were also collected between 1000 h and 1500 h to avoid confounding
by any diurnal variation in testosterone concentrations.
Testosterone levels should be measured near to 8 am. This has the same time variation too, so I don’t take this study seriously due to that confound. Assays were collected “between” the hours of 10 am and 3 pm, which means it was whenever convenient for the student. No controls on activities, nor attempting to assay at 8 am. People of any racial group could have gone at whatever time in that 5 hour time period and skew the results. Assaying “between” those times completely defeats the purpose of the study.
This advantage [the so-called testosterone advantage] then shrinks and eventually disappears at some point during the 30s (Gapstur et al., 2002).
This makes it very difficult if not impossible to explain differing behavioral variables, including higher rates of crime and aggression, in Black males over the age of 33 on the basis of elevated testosterone levels.
See above where I talk about crime/testosterone/aggression.
Critics say that more recent studies done since the early 2000’s have shown no differences between Black and White testosterone levels. Perhaps they are referring to recent studies that show lower testosterone levels in adult Blacks than in adult Whites. This was the conclusion of one recent study (Alvergne et al. 2009) which found lower T levels in Senegalese men than in Western men. But these Senegalese men were 38.3 years old on average.
Alvergne, Fauri, and Raymond (2009) show that the differences are due to environmental factors:
This study investigated the relationship between mens’ salivary T and the trade-off between mating and parenting efforts in a polygynous population of agriculturists from rural Senegal. The men’s reproductive trade-offs were evaluated by recording (1) their pair-bonding/fatherhood status and (2) their behavioral profile in the allocation of parental care and their marital status (i.e. monogamously married; polygynously married).
They also controlled for age, so his statement “But these Senegalese men were 38.3 years old on average” is useless.
These critics may also be referring to various studies by Sabine Rohrmann which show no significance difference in T levels between Black and White Americans. Age is poorly controlled for in her studies.
That is one study out of many that I reference. Rohrmann et al (2007) controlled for age. I like how he literally only says “age is poorly controlled for in her studies“, because she did control for age.
That study found that more than 25% of the samples for adults between 30 and 39 years were positive for HSV-2. It is likely that those positive samples had been set aside, thus depleting the serum bank of male donors who were not only more polygamous but also more likely to have high T levels. This sample bias was probably worse for African American participants than for Euro-American participants.
Why would they use diseased samples? Do you even think?
Young Black males have higher levels of active testosterone than European and Asian males. Asian levels are about the same as Whites, but a study in Japan with young Japanese men suggested that the Japanese had lower activity of 5-alpha reductase than did U.S. Whites and Blacks (Ross et al 1992). This enzyme metabolizes testosterone into dihydrotestosterone, or DHT, which is at least eight to 10 times more potent than testosterone. So effectively, Asians have the lower testosterone levels than Blacks and Whites. In addition, androgen receptor sensitivity is highest in Black men, intermediate in Whites and lowest in Asians.
Ethnicmuse also showed that, contrary to popular belief, Asians have higher levels of testosterone than Africans who have higher levels of testosterone than Caucasians in his meta-analysis. (Here is his data.)
Let us look at one study (Ross et al 1986) to see what the findings of a typical study looking for testosterone differences between races shows us. This study gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in Blacks were 19% higher than in Whites, and free testosterone levels were 21% higher. Both these differences were statistically significant.
Assay times between 10 am and 3 pm, unrepresentative sample of college men, didn’t have control for waist circumference. Horribly study.
A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk.
No, it wouldn’t (if it were true).
Higher testosterone levels are linked to violent behavior.
Causation not untangled.
Studies suggest that high testosterone lowers IQ (Ostatnikova et al 2007). Other findings suggest that increased androgen receptor sensitivity and higher sperm counts (markers for increased testosterone) are negatively correlated with intelligence when measured by speed of neuronal transmission and hence general intelligence (g) in a trade-off fashion (Manning 2007).
Who cares about correlations? Causes matter more. High testosterone doesn’t lower IQ. Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut.
Racial differences in testosterone don’t exist/are extremely small in magnitude (as I’ve covered countless times). The one article from TAH literally misrepresents studies/leaves out important figures in the testosterone differences between the two races to push a certain agenda. Though if you read the studies you see something completely different. It’s the same with Lindsay. He misunderstood a few studies to push his agenda about testosterone and crime and prostate cancer. They’re both wrong, though.
Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut. People read and write about things they don’t understand, which is the cause of these misconceptions with the hormone, as well as, of course, misinterpreting studies. Learn about the hormone and you won’t fear it. It doesn’t cause crime, prostate cancer nor aggression; these people who write these articles have one idea in their head and they just go for it. They don’t understand the intricacies of the endocrine system and how sensitive it is to environmental influence. I will cover more articles that others have written on testosterone and aggression to point out what they got wrong.
In part II, we will look at the mental gymnastics of someone who is clueless to the data and uses whatever mental gymnastics possible in order to deny the data. Well, shit doesn’t work like that, JayMan. I will review yet more studies on sitting, walking and dieting on mortality as well as behavioral therapy (BT) in regards to obesity. JayMan has removed two of my comments so I assume the discussion is over. Good thing I have a blog so I can respond here; censorship is never cool. JayMan pushes very dangerous things and they need to be nipped in the bud before someone takes this ‘advice’ who could really benefit from lifestyle alterations. Stop giving nutrition advice without credentials! It’s that simple.
JayMan published a new article on ‘The Five Laws of Behavioral Genetics‘ with this little blip:
Indeed, we see this with health and lifestyle: people who exercise more have fewer/later health problems and live longer, so naturally conventional wisdom interprets this to mean that exercise leads to health and longer life, when in reality healthy people are driven to exercise and have better health due to their genes.
So, in JayMan’s world diet and exercise have no substantial impact on health, quality of life and longevity? Too bad the data says otherwise. Take this example:
Take two twins. Lock both of them in a metabolic chamber. Monitor them over their lives and they do not leave the chamber. They are fed different diets (one has a high-carb diet full of processed foods, the other a healthy diet for whatever activity he does); one exercises vigorously/strength trains (not on the same day though!) while the other does nothing and the twin who exercises and eats well doesn’t sit as often as the twin who eats a garbage diet and doesn’t exercise. What will happen?
Jayman then shows me Bouchard et al, (1990) in which a dozen pairs of twins were overfed for three months with each set of twins showing different gains in weight despite being fed the same amount of kcal. He also links to Bouchard et al, 1996 (can’t find the paper; the link on his site is dead) which shows that the twins returned to their pre-experiment weight almost effortlessly. This, of course, I do not deny.
This actually replicates a study done on prisoners in a Vermont prison (Salans, Horton, and Sims, 1971). “The astonishing overeating paradox” is something that’s well worth a look in to. Salans et al had prisoners overeat and also limited their physical activity. They started eating 4000 kcal per day and by the end of the study they were eating about 10000 kcal per day. But something weird happened: their metabolisms revved up by 50 percent in an attempt to get rid of the excess weight. After the study, the prisoners effortlessly returned to their pre-experiment weight—just like the twins in Bouchard et al’s studies.
The finding is nothing new but it’s nice to have replication (on top of the replication that it already had), but that’s not what I was talking about. Of course, being sedentary, eating like shit and not exercising will lead to deleterious health outcomes. The fact of the matter is, the twin in my thought experiment that did not exercise, sat around all day and ate whatever would die way sooner, have a lower quality of life, and more deleterious disease due to the shitty diet while his co-twin would have less since he ate right, exercised and spent less time sitting.
JayMan says, in regards to studies that show that obese people that even do light physical activity show lower all-cause mortality, that “That’s not what large RCTs show.” I know the study that he’s speaking of—the Look AHEAD study (Action for Health and Diabetes) (The Look AHEAD Research Group, 2009). The research group studied the effects of lifestyle interventions in type II diabetics. For one of the groups they gave intensive diet and exercise information, the other they gave only the standard advice. However, the study ended early at 9.3 years because there was no difference between both groups (Pi-Sunyer, 2015). JayMan uses this study as evidence that diet and exercise have no effect on the mortality of type II diabetics; however, in actuality, the results are much more nuanced.
Annuzzi et al (2014) write in their article The results of Look AHEAD do not row against the implementation of lifestyle changes in patients with type 2 diabetes:
The intervention aimed at weight loss by reducing fat calories, and using meal replacements and, eventually, orlistat, likely underemphasizing dietary composition. There is suggestive evidence, in fact, that qualitative changes in dietary composition aiming at higher consumption of foods rich in fiber and with a high vegetable/animal fat ratio favorably influence CV risk in T2D patients.
In conclusion, the Look AHEAD showed substantial health benefits of lifestyle modifications. Prevention of CV events may need higher attention to dietary composition, contributing to stricter control of CV risk factors. As a better health-related quality of life in people with diabetes is an important driver of our clinical decisions, efforts on early implementation of behavioral changes through a multifactorial approach are strongly justified.
They reduced far calories and used meal replacements. This is the trial JayMan is hedging his assertion on. Type II diabetics need a higher fat diet and don’t need the carbs as it will spike their insulin. Eating a higher fat diet will also lower the rate of CVD as well. This trial wasn’t too vigorous in terms of macronutrient composition. This is one of many reasons why type II diabetics discard dieting and exercise just yet.
Even modest weight loss of 5 to 10 percent is associated with significant improvements in cardiovascular disease (CVD) after one year, with larger weight loss showing better improvement (Wing et al, 2011). (Also read the article The Spinning of Look AHEAD.)
Telling diabetics not to eat right and exercise is, clearly, a recipe for disaster. This canard that dieting/exercise doesn’t work to decrease all-cause mortality—especially for diabetics and others who need the lifestyle interventions—is dangerous and a recipe for disaster.
Intentional weight loss needs to be separated from intentional weight loss as to better study the effects of both variables. Kritchevsky et al (2015) meta-analyzed 15 RCTs that “reported mortality data either as an endpoint or as an adverse event, including study designs where participants were randomized to weight loss or non-weight loss, or weight loss plus a co-intervention (e.g. weight loss plus exercise) or the weight stable co-intervention (i.e. exercise alone).” They conclude that the risk for all-cause mortality in obese people who intentionally lose weight is 15 percent lower than people not assigned to lose weight.
This study replicates a meta-analysis by Harrington, Gibson, and Cottrell (2009) on the benefits of weight loss and all-cause mortality. They noted that in unhealthy adults, weight loss accounted for a 13 percent decrease in all-cause mortality increase while in the obese this accounted for a 16 percent decrease. Of course, since the weights were self-reported and there are problems with self-reports of weight (Mann et al, 2007), then that is something that a skeptic can rightfully bring up. However, it would not be a problem since this would imply that they weighed the same/gained more weight yet had a decrease in all-cause mortality.
Even light physical activity is associated with a decrease in all-cause mortality. People who go from light activity, 2.5 hours a week of moderate physical intensity compared to no activity, show a 19 percent decrease in all-cause mortality while people who did 7 hours a week of moderate activity showed a 24 percent decrease in all-cause mortality (Woodcock et al, 2011). Even something as simple as walking is associated with lower incidence of all-cause mortality, with the largest effect being seen in individuals who went from no activity to light walking. Walking is inversely associated with disease incidence (Harner and Chida, 2008) but their analysis indicated publication bias so further study is needed. Nevertheless, the results line up with what is already known—that low-to-moderate exercise is associated with lower all-cause mortality (as seen in Woodcock et al, 2011).
What is needed to change habits/behavior is behavioral therapy (BT) (Jacob and Isaac, 2012; Buttren, Webb, and Waddren, 2012; Wilfley, Kolko, and Kaas, 2012; ). BT can also be used to increase adherence to exercise (Grave et al, 2011). BT has been shown to have great outcomes in the behaviors of obese people, and even if no weight loss/5-10 percent weight loss is seen (from Wing and Hill, 2001), better habits can be developed, and along with ‘training’ hunger hormones with lifestyle changes such as fasting, people can achieve better health and longevity—despite what naysayers may say. Though I am aware that outside of clinics/facilities, BT does not have a good track record (Foster, Makris, and Bailer, 2005). However, BT is the most studied and effective intervention in managing obesity at present (Levy et al, 2007). This is why people need to join gyms and exercise around people—they will get encouragement and can talk to others about their difficulties. Though, people like JayMan who have no personal experience doing this would not understand this.
In regards to dieting, the effect of macronutrient composition on blood markers is well known. Type II diabetics need to eat a certain diet to manage their insulin/blood sugar, and doing the opposite of those recommendations will lead to disaster.
Low-carb ketogenic diets are best for type II diabetics. There are benefits to having ketones circulating in the blood, which include (but are not limited to): weight loss, improved HbA1c levels, reduced rate of kidney disease/damage, cardiac benefits, reversing non-alcoholic fatty liver, elevated insulin, and abnormal levels of cholesterol in the blood (Westman et al, 2008; Azar, Beydoun, and Albadri, 2016; Noakes and Windt, 2016; Saslow et al, 2017). These benefits, of course, carry over to the general non-diabetic population as well.
Of course, JayMan has reservations about these studies wanting to see follow-ups—but the fact of the matter is this: dieting and eating right is associated with good blood markers, exactly what type II diabetics want. In regards to food cravings, read this relevant article by Dr. Jason Fung: Food Cravings. Contrary to JayMan’s beliefs, it’s 100 percent possible to manage food cravings and hunger. The hormone ghrelin mediates hunger. There are variations in ghrelin every day (Natalucci et al, 2005) and so if you’re feeling hungry if you wait a bit it will pass. This study lines up with most people’s personal experience in regards to hunger. One would have to have an understanding of how the brain regulates appetite to know this, though.
JayMan also cannot answer simple yes or no questions such as: Are you saying that people should not watch what they eat and should not make an effort to eat higher-quality foods? I don’t know why he is so anti-physical activity. As if it’s so bad to get up, stop sitting so much and do some exercise! People with more muscle mass and higher strength levels live longer (Ruiz et al, 2008). This anti-physical activity crusade makes absolutely no sense at all given the data. If I were to stop eating well and strength training, along with becoming a couch potato, would my chance of dying early from a slew of maladies decrease? Anyone who uses basic logic would be able to infer that the answer is yes.
I also need to address JayMan’s last comment to me which he censored:
No intervention shows that lifestyle changes extend life – or even improve health. Even if they did, their generalizability would depend on their actual prescription. In any case, the point is moot, since they don’t even show such improvements in the first place.
You’re only saying that because you’re literally hand waving away data. It’s clear that going from no exercise to some exercise will decrease all-cause mortality. I’m sorry that you have a problem reading and understanding things that you don’t agree with, but this is reality. You don’t get to construct your own reality using cherry-picked studies that don’t mean what you think they mean (like Look AHEAD; Dr. Sharma states that we may never know if weight reduction can save lives in type II diabetics, however the three studies on low-carb diets cited above lend credence to the idea that we can).
Please see my previously linked Obesity Facts page for more. Once you’ve read that, get back to me. Until then, I’m putting the brakes on this discussion.
Of course, you’re putting the brakes on this discussion, you have substantial replies other than your one-liners. You need to censor people when you have no substantial response, that’s not intellectually honest.
All in all, JayMan is giving very dangerous ‘advice’, when the literature says otherwise in regards to lifestyle interventions and all-cause mortality. You can talk about genes for this or that all you want; you’re just appealing to genes. Light physical exercise shows that mortality risk can be decreased; that’s not too hard for most people.
I know JayMan talks about genes for this and that, yet he does not understand that obesogenic environments drive this epidemic (Lake and Townshend, 2006; Powell, Spears, and Rebori, 2011; Fisberg et al, 2016). He doesn’t seem to know about the food reward hypothesis of obesity either. Think about obesogenic environments and food reward and how our brains change when we eat sugar and then things will begin to become clearer.
JayMan is giving out deadly ‘advice’, again, without the correct credentials. Clearly, as seen in both of my responses to him, taking that ‘advice’ will lead to lower quality of life and lower life expectancy. But I’m sure my readers are smart enough to not listen to such ‘advice’.
(Note: Diet and exercise under Doctor’s supervision only)
by Scott Jameson
An earlier post established that Omega 3 fatty acids are an important nutrient of which hardly anybody is getting enough, and that this deficiency is making us Westerners a bit dumber and a bit crazier on the whole. Description sometimes obligates prescription, so this post is where I spitball about possible solutions, and welcome you to join me in the comments.
I’m reminded of the gubbermint mandating the lacing of our salt with sorely needed iodine, or the enrichment of white flour with nutrients lost in the removal of the bran and germ as well as the bleaching of the endosperm.
For yourself and your family, fish oil pills are fine- kelp oil if you’re one of those people. But we need solutions that work for nearly everybody, and the brilliance of the examples I listed above is that everybody eats that stuff (bread and salt) and now it’s laced with nutrients they’ve been needing. So we could produce N3s at low cost and legally mandate that certain foods contain them. Chia is a promising source: it’s cheap, it’s loaded with N3s, and it doesn’t taste fishy. Flax also works, but it’s loaded with phytoestrogens. Tons of seeds have those, I think Chia as well, but I’ve been told (incorrectly?) that flax is a particularly bad offender. Anyway, how do we load Chia or a similar seed into people’s diets?
Omega 3 eggs are one way to go. Chickens metabolize plant ALA (such as from chia or flax) into DHA and store both in their eggs. Just as we made use of the auroch and tarpan’s efforts to have a brain, we can hijack the chicken’s futile attempts to provide brain-material for her nonexistent offspring, using her eggs as a vehicle to get N3s into ourselves. It’s as simple as a mandate that a certain percentage of all chicken feed must be N3 rich seeds and/or insects.
Another obvious place to look is the plant oils that go into our food. Check out the table on the Wikipedia page for ALA: soybean and rapeseed oils have a pathetic showing for ALA content, and they’re put in absolutely everything. The State mandates that all gas will be a bit ethanol: why not all soybean and canola be 10, 20% Chia or some comparably high ALA crop?
It’s worth pointing out that you can genetically modify ALA rich vegetable oil to be on a quality closer to par with fish oil, having some of the ALA converted into the more useful EPA. Forget any concerns about GMOs you may have because the oils I’m talking about lacing with GMOs are already themselves GMOs.
We also must mandate that all infant formula be laced with N3s: EPA and DHA in particular, and tested for stuff like mercury if it comes from fish. You probably know at least one person who is autistic because they were bottlefed.
Comment your potential solutions below. I want to hear them. Double points for anyone playing the game on hard mode: free market solutions (libertarians) or animal-free solutions (vegans). If you try both, you’re a masochist and you need help.
Homo Neanderthalis vs. Homo Sapiens Sapiens: Who is Stronger? Implications for Racial Strength Differences
Unfortunately, soft tissue does not fossilize (which is a problem for facial reconstructions of hominins; Stephan and Henneberg, 2001; I will cover the recent ‘reconstructions’ of Neanderthals and Nariokotome boy soon). So saying that Neanderthals had X percent of Y fiber type is only conjecture. However, to make inferences on who was stronger, I do not need such data. I only need to look at the morphology of the Neanderthals and Homo sapiens, and from there, inferences can be made as to who was stronger. I will argue that Neanderthals were stronger which is, of course, backed by solid data.
Neanderthals had wider pelves than Homo sapiens. Wider pelves in colder climes are due to adaptations. Although Neanderthals had wider pelves than ours, they had infants around the same size as Homo sapiens, which implies that Neanderthals had the same obstetric difficulties that we do. Neanderthals also had a pelvis that was similar to Heidelbergensis, however, most of the pelvic differences Neanderthals had that were thought to be derived traits are, in fact, ancestral traits—except for the cross-sectional shape of the pubic ramus (Gruss and Schmidt, 2015). Since Neanderthals had wider pelves and most of their pelvis were ancestral traits, then wide pelves may have been a trait of ancestral Homo (Trinkaus, Holliday, and Aurbach, 2014).
Hominins do need wider pelves in colder climates, as it is good for heat retention, however (see East Asians and Northern Europeans). Also, keep in mind that Neanderthals were shorter than us—with the men averaging around 5 feet five inches, and the women averaging about 5 feet, about 5.1 inches shorter than post-WW II Europeans (Helmuth, 1998).
So what does a wider pelvis mean? Since the Neanderthals were shorter than us and also had a wider pelvis, they had a lower center of gravity in comparison to us. Homo sapiens who came Out of Africa, had a narrower pelvis since narrow pelves are better to dissipate heat (Gruss and Schmidt, 2015). Homo sapiens would have been better adapted to endurance running and athleticism, in comparison to the wide-pelved Neanderthals.
People from tropical climates have longer limbs, and are tall and narrow (which is also good for endurance running/sprinting) while people from colder climates are shorter and more ‘compact’ (Lieberman, 2015: 113-114) with a wide pelvis for heat retention (Gruss and Schmidt, 2015). So, clearly, due to the differences in pelvic anatomy between Homo sapiens and Neanderthals,
Furthermore, due to the length of Neanderthal clavicles, it was thought that they had long clavicles which would have impeded strength. However, when the clavicles were reanalyzed it was discovered that when the clavicles were adjusted with the body size of Neanderthals—and not compared with the humeral lengths—Neanderthals had a similar clavicular length, which implies a similar shoulder breadth as well, to Homo sapiens (Trinkaus, Holliday, and Aurbach, 2014). This is another clue that Neanderthals were stronger.
Yet more evidence comes from comparing the bone density of Neanderthal bones to that of Homo sapiens. Denser bones would imply that the body would be able to handle a heavier load, and thusly generate more power. In adolescent humans, muscle power predicts bone strength (Janz et al, 2016). So if the same holds true for Neanderthals—and I don’t see why not—then Neanderthals would have higher muscle power since it predicts bone strength.
Given the “heavy musculature” of Neanderthals, along with high bone robusticity, then they must have had denser bones than Homo sapiens (Friedlander and Jordan, 1994). So since Neanderthals had denser bones, then they had higher muscle power; they had a lower center of gravity due to having a wider pelvis and being shorter than Homo sapiens whose body was heat-adapted. Putting this all together, the picture is now becoming clearer that Neanderthals were, in fact, way stronger than Homo sapiens.
Another cause for these anatomical differences between Neanderthals and Homo sapiens is completely independent of cold weather. Neanderthals had an enlarged thorax (rib cage), which evolved to hold an enlarged liver, which is responsible for metabolizing large amounts of protein. Since protein has the highest thermic effect of food (TEF), then they would have had a higher metabolism due to a higher protein diet which would also have resulted in an enlarged bladder and kidneys which are necessary to remove urea, which possibly would have also contributed to a wider pelvis for Neanderthals (Ben-Dor, Gopher, and Barkai, 2016).
During glacial winters, Neanderthals would have consumed 74-85 percent of their calories from fat, with the rest coming from protein (Ben-Dor, Gopher, and Barkai, 2016). Neanderthals also consumed around 3,360-4,480 kcal per day (Steegman, Cerny, and Holliday, 2002). Let’s assume that Neanderthals averaged 3800 kcal per day. Since the upper limit of protein intake is 3.9 g/bw/day (erectus) and 4.0 g/bw/day for Homo sapiens (Ben-Dor et al, 2011), then Neanderthals would have had a theoretical higher upper limit due to having larger organs, which are useful in processing large amounts of protein. The protein intake for a Neanderthal male was between estimated to be between 985 kcal (low end) to 1170 kcal (high end). It was estimated that Neanderthal males had a protein intake of about 292 grams per day, or 1,170 kcal (Ben-Dor, Gopher, and Holliday, 2016: 370).
Assuming that Neanderthals did not eat carbohydrates during glacial winters (and even if a small amount were eaten, the model would not be affected) and an upper limit of protein intake of 300 grams per day for Neanderthal males, this implies that 74-85 percent of their diet came from animal fat—the rest being protein. Protein is the most thermogenic macro (Corvelli et al, 1997; Eisenstein et al, 2002; Buchholz and Schoeller, 2004; Halton and Hu, 2004; Gillingham et al, 2007; Binns, Grey, and Di Brezzo, 2014). So since Neanderthals ate a large amount of protein, along with their daily activities, they had to have had a high metabolic rate.
To put into perspective how much protein Neanderthals ate, the average American man eats about 100 grams of protein per day. In an analysis of the protein intake of Americans from 2003-2004, it was found that young children ate about 56 grams of protein per day, adults aged 19-30 ate about 91 grams of protein per day, and the elderly ate about 56 grams of protein per day (Fulgoni, 2008). Neanderthals ate about 3 times the amount of protein than we do, which would lead to organ enlargement since larger organs are needed to metabolize said protein as well. Another factor in the increase of metabolism for Neanderthals was the fact that it was, largely, extremely cold. Shivering increases metabolism (Tikuisis, Bell, and Jacobs, 1985; van Ooijen et al, 2005). So the Neanderthal metabolism would have been revved up close to a theoretical maximum capacity.
The high protein intake of Neanderthals is important because high amounts of protein are needed to build muscle. Neanderthals consumed a sufficient amount of kcal, along with 300 grams of protein per day on average for a Neanderthal male, which would have given Neanderthals yet another strength advantage.
I am also assuming that Neanderthals had slow twitch muscle fibers since they have wider pelves, along with evolving in higher latitudes (see Kenyans, East Asians, European muscle fiber distribution), they would have an abundance of type slow twitch muscle fibers, in comparison to fast twitch muscle fibers, however, they also have more slow twitch fibers which Europeans have, while African-Americans (West-African descendants) have a higher amount of fast twitch fibers. (Caesar and Henry, 2015). So now, thinking of everything I explained above and replacing Neanderthals with Europeans and Homo sapiens with Africans, who do you think would be stronger? Clearly, Europeans, which is what I have argued for extensively. African morphology (tall, lanky, high limb ratio) is not conducive to strength; whereas European morphology (wide pelvis, low limb ratio, an abundance of slow twitch fibers) is.
The implications for these anatomic differences between Neanderthals and Homo sapiens and how it translates into racial differences will be explored more in the future. This was just to lay the anatomic and morphologic groundwork in regards to strength and cold weather adaptations. Nevertheless, the evidence that Neanderthals were stronger/more powerful than Europeans stands on solid ground, and the same does hold for the differences in strength between Africans and Europeans. The evolution of racial pelvic variation is extremely important to understand if you want to understand racial differences in sports.
by Scott Jameson
I’ve been thinking about Omega 3 fatty acids (N3s) recently. We’re clearly adapted to getting more of them than we’re actually getting.
Children whose mothers took fish oil (chock full of N3s EPA and DHA) during pregnancy have higher coordination, and they are smarter, although that difference may not persist later in development. RaceRealist has written about N3s and PISA math scores before.
Here’s a paper summarizing many of the known benefits of fish oil supplementation. Goes over some of the aforementioned results regarding kids, and also shows random improvements such as helping people with Alzheimer’s maintain weight.
A lack of N3s is associated with depression, coronary artery disease, maybe even autism. N3s are known to lessen autism symptoms. This is probably an immune thing. Sulforaphane, an anti-inflammatory agent, is known to reduce autism symptoms, and other research has elucidated the relationship between N3s and the immune system.
This is delicious fodder for a post of its own. There’s a mass of papers about the relationship between autism and the immune system; N3s being neuroprotective and correlating negatively with likelihood of autism/severity of autism symptoms vindicates the idea that autism happens when your immune system cooks your brain (neuroinflammation). You would expect males to be whacked harder by this because they’re not good at producing the important N3 docosahexaenoic acid (DHA). Thus, males ought to have higher autism rates- and they do.
Anyway, here’s what I’m getting at. Either N3s are a counter-intuitive miracle drug, or they’re just an important nutrient of which many of us do not get enough. The latter, I should think! The lemonade that can and will be made from these lemons is that widespread N3 deficiency gives us an opportunity to understand one of the ways that a human brain can get messed up. But we still want to fix the problem- more on that in my next post.
Our ancestors probably got more N3s than we do. They’ve been estimated to, anyway. (Second study mentioning our ancestors’ higher N3 intake.) If they didn’t, they might’ve been selected for better processing of alpha linoleic acid into eicosapentaenoic acid and subsequently docosahexaenoic acid, which real-life humans aren’t great at. As it stands, humans need either a whole bunch of excess ALA to convert to EPA and DHA, or we could have EPA and DHA straight. The excess ALA idea probably isn’t something you can rely on for your N3 needs, but certainly ALAs are better than nothing.
Seeds would’ve been a part of the diet back in the Paleolithic. Flax, an example of a seed rich in ALA, was known to humans quite a darned while ago, so seeds might have been a source of these critical nutrients. It’s worth noting that the first paleolithic diet estimation study linked in the previous paragraph pegs hunter gatherers as getting way more ALA than modern folks do.
Of course, many populations would’ve lived near oceans or at least rivers and lakes, where they could’ve gotten N3s from fish and seafood.
Some of it must have come from insects, themselves actually having a decent amount of N3s.
I’ve got an even weirder guess, though: bioaccumulation in land animal tissue. This possibility must have been important for peoples like the Botai culture with extremely narrow (Tarpan-based) diets, which likely didn’t include enough seeds, insects, and/or seafood. Animals can’t produce N3s of their own, but they eat ALA, convert it into EPA and DHA, and send a lot of it up to the brain, where it’s needed, with the result being that the brain has a lot more and higher quality N3s than any of the plants from which the N3s were derived.
Grog the caveman could’ve gotten a bunch of N3s from his favorite treat: scrambled auroch brains. Many of his progeny carry the practice into the present day, to the disgust of other living humans. Being that humans and our relatives are disgusting in general, Neanderthals occasionally even ate each other’s brains, and according to CNN, they’re still at it!
Nonhuman brains had to be the more popular option, then as now; mentioning the whole cannibalism thing is a bit of a non sequitur I shoved in for sheer entertainment value. But I suspect that there are several reasons we Westerners don’t get enough N3s: we don’t eat brains anymore, we don’t eat bugs anymore, and we don’t get as many ALA-rich plant oils as we used to. Perhaps we’re not getting enough fish, or perhaps the fish we’re getting are less likely to be fatty (e.g. salmonids, tuna, schooling fish) and more likely to be lean (cod, pollock).
Somehow or other we ought to get N3s back in our diet. Could save some kids from autism or, failing that, improve their prognosis. Again, it could increase our math scores, too, particularly in women. Closing part of the gap with other nations and between our sexes- two birds with one stone for our educators- and a boon for our engineering departments as well. Which is a boon for everyone.
The stakes are high. Who can save us from our collective state of starved brains? I’ll post my ideas soon.