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MAOA, Race, and Crime: A Simple Relationship?

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When I first got into HBD back in 2012, one of the first things I came across—along with the research on racial IQs from Rushton, Lynn, Jensen et al—was that the races differed in a gene called MAOA-L, which has a frequency in Caucasians at .1 percent (Beaver et al, 2013), 54 percent in Chinese people (Lu et al, 2013; as well as 77 percent for the 3r MAOA allele; Lea and Chambers, 2007), 56 percent in Maoris (Lea and Chambers 2007) while about 60-65 percent of Japanese people have the low-frequency version of this gene (Way and Lieberman, 2007).

So if these ethnies have a higher rate of this polymorphism and it is true that this gene causes crime, then the Chinese and Japanese should have the highest rates of crime in the world, since even apparently the effect of MAOA and violence and antisocial behavior is seen even without child abuse (Ficks and Waldman, 2014). Except East Asian countries have lower rates of crime (Rushton, 1995; Rushton and Whytney, 2002). Though, Japan’s low crime rate is relatively recent, and when compared with other countries on certain measures “Japan fares the same or worse when compared to other nations” (Barberet 2009, 198). This goes against a lot of HBD theory, and I will save that for another day. (Japan has a 99 percent prosecution rate, which could be due to low prosecutorial budgets; Ramseyer and Rasmusen, 2001. I will cover this in the future.)

The media fervor—as usual—gave the MAOA gene the nickname “the warrior gene“, which is extremely simplistic (I will have much more to say on ‘genes for’ any trait towards the end of the article). I will show how this is a very simplistic view.

The MAOA gene was first discovered in 1993 in a Dutch family who had a history of extreme violence going as far back as the 1890s. Since the discovery of this gene, it has been invoked as an ultimate cause of crime. However, as some hereditarians do note, MAOA only ’causes’ violence if one has a specific MAOA genotype and if they have been abused as a child (Caspi et al, 2002; Cohen et al, 2006; Beaver et al, 2009; Ferguson et al, 2011; Cicchetti, Rogosch, Thibodeau, 2012;). People have invoked these gene variants as ultimate causes of crime—that is, people who have the low-expressing MAOA variants are more likely to commit more crime—but the relationship is not so simple.

Maoris are more four times more likely to have the low-expressing gene variant than Europeans, the same holding for African Americans and Europeans (Lea and Chambers, 2007).

There is, however, a protective effect that protects whites (and not non-whites in certain cases) against antisocial behavior/violent attitudes if one has a certain genotype (Widom and Brzustowicz, 2006), though the authors write on page 688: “For non-whites, the effect of child abuse and neglect on the juvenile VASB was not significant (beta .08, SE .11, t 1.19, ns), whereas the effect of child maltreatment on lifetime VASB composite approached significance (beta .13, SE .12, t 1.86, p .06). For non-whites (see Figure 2), neither gene (MAOA) environment (child abuse and neglect) interaction was significant: juvenile VASB (beta .06, SE .28, t .67, ns) and lifetime VASB (beta .01, SE .29, t .14, ns).” So as you can see, there are mixed results. Whites seem to be protected against the effect of antisocial behavior and violence but only if they have a certain genotype (which implies that if they have the other genotype, then if abused they will show violent and antisocial behavior). So, we can see that the relationship between MAOA and criminal behavior is not as simple as some would make it out to be.

MAOA, like other genetic variants, of course, has been linked to numerous other traits. Steven J. Heine, author of the book DNA is Not Destiny: The Remarkable and Completely Misunderstood Relationship Between You and Your Genes:

However, any labels like “the warrior gene” are highly problematic because they suggest that the this gene is specifically associated with violence. It’s not, just as alleles from other genes do not only have one outcome. Pleiotropy is the term for how a single genetic variant can influence multiple different phenotypes. MAOA is highly pleiotropic: the traits and conditions potientially connected to the MAOA gene invlude Alzheimer’s. anoerxia, autism, body mass index, bone mineral density, chronic fatigue syndrome, depression, extraversion, hypertension, individualism, insomnia, intelligence, memory, neuroticism, obesity, openness to experience, persistence, restless leg syndrome, schizophrenia, social phobia, sudden infant death syndrome, time perception and voting behavior. (59) Perhaps it would be more fitting to call MAOA “the everything but the kitchen sink gene. (Heine, 2017: 195)

Something that I have not seen brought up when discussions of race, crime, and MAOA come up is that Japanese people have the highest chance—even higher than blacks, Maoris, and whites—to have the low repeat MAOA variant (Way and Lieberman) yet have lower rates of crime. So MAOA cannot possibly be a ‘main cause’ of crime. It is way more complex than that. “However intuitively satisfying it may be to explain cultural differences in violence in terms of genes“, Heine writes, “as of yet there is no direct evidence for this” (Heine, 2017: 196).

Numerous people have used ‘their genes’ in an attempt to get out of criminal acts that they have committed. A judge even knocked off one year off of a murder’s sentence since he found the evidence for the MAOA gene’s link to violence “particularly compelling.” I find it “particularly ridiculous” that the man got less time in jail than someone who ‘had a choice’ in his actions to murder someone. Doesn’t it seem ridiculous to you that someone gets less time in jail than someone else, all because he may have the ‘crime/warrior gene’?

Aspinwall, Brown, and Tabery (2012) showed that when evidence of a ‘biomechanic’ cause of violence/psychopathy was shown to the judges (n=191), that they reduced their sentences by almost one year if they were reading a story in which the accused was found to have the low-repeat MAOA allele (13.93 to 12.83 years). So, as you can see, this can sway judges’ perception into giving one a lighter sentence since they believe that the evidence shows that one ‘can not control themselves’, which results in the judge giving assailants lighter sentences because ‘it’s in their genes’.

Further, people would be more lenient on sentences for criminals who are found to have these ‘criminal genes’ than those who were found to not have them (Cheung and Heine, 2015). Monterosso, Royzman, and Schwartz (2010) also write: “Physiologically explained behavior was more likely to be characterized as “automatic,” and willpower and character were less likely to be cited as relevant to the behavior. Physiological explanations of undesirable behavior may mitigate blame by inviting nonteleological causal attributions.” So, clearly, most college students would give a lighter sentence if the individual in question were found to have ‘criminal genes’. But, if these genes really did ’cause’ crime, shouldn’t they be given heavier sentences to keep them on the inside more so those with the ‘non-criminal genes’ don’t have to suffer from the ‘genetically induced’ crime?

Heine (2017: 198-199) also writes:

But is someone really less any responsible for their actions if his or her genes are implicated? A problem with this argument is that we would be hard-pressed to find any actions that we engage in where our genes are not involved—our behaviors do not occur in any gene-free zones. Or, consider this: there actually is a particular genetic variant that, if you possess it, makes you about 40 times more likely to engage in same-sex homicides than those who possess a different variant. (66) It’s known as the Y chromosome—that is, people who possess it are biologically male. Given this, should we infer that Y chromosomes cause murders, and thus give a reduced sentence to anyone who is the carrier of such a chromosome because he is really not responsible for his actions? The philosopher Stephen Morse calls the tendency to excuse a crime because of a biological basis the “fundamental psycholegal error.” (67) The problem with this tendency is that it involves separating yout genes from yourself. Saying “my genes made me do it” doesn’t make sense because there is no “I” that is independent of your genetic makeup. But curiously, once genes are implicaed, people see, to feel that the accused is no longer fully in control of his or her actions.

Further, in the case of a child pornographer, one named Gary Cossey, the court said:

The court predicted that some fifty years from now Cossey’s offense conduct would likely be discovered to be caused by “a gene you were born with. And it’s not a gene you can get rid of.” The court expressed its belief that although Cossey was in therapy, it “can only lead, in my view, to a sincere effort on your part to control, but you can’t get rid of it. You are what you’re born with. And that’s the only explanation for what I see here.”

However, this judge punished Cossey more severely due to the ‘possibility’ that scientists may find ‘genes for’ child pornography use in 50 years. Cossey was then given another, unbiased judge, and was given a ‘more lenient’ sentence than the genetic determinist judge did.

Sean Last over at The Alternative Hypothesis is also a big believer in this so-called MAOA-race difference that explains racial differences in crime. However, as reviewed above (and as he writes), MAOA can be called the “everything but the kitchen sink gene” (Heine, 2017: 195), as I will touch on briefly below, to attribute ’causes’ to genes is not the right way to look at them. It’s not so easy to say that since one ‘has the warrior gene’ that they’d automatically be violent. Last cites a study saying that even those who have the MAOA allele who were not abused showed higher rates of violent behavior (Ficks and Waldman, 2014). They write (pg. 429):

The frequency of the ‘‘risk’’ allele in nonclinical samples of European ancestry ranges from 0.3 to 0.4, although the frequency of this allele in individuals of Asian and African ancestry appears to be substantially higher (*0.6 in both groups; Sabol et al. 1998).

So, why don’t Asians have higher rates of crime—along with blacks—if MAOA on its own causes violent and antisocial behavior? Next I know that someone would claim that “AHA! TESTOSTERONE ALSO MEDIATES THIS RELATIONSHIP!!” However, as I’ve talked about countless times (until I’m blue in the face), blacks do not have/have lower levels of testosterone than whites (Richards et al, 1992Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Though young black males have higher levels of testosterone due to the environment (honor culture) (Mazur, 2016). So that canard cannot be trotted out.

All in all, these simplistic and reductionist approaches to ‘figuring out’ the ’causes’ of crime do not make any sense. To point at one gene and say that this is ‘the cause’ of that do not make sense.

One last point on ‘genes as causes’ for behavior. This is something that deserves a piece of its own, but I will just provide a quote from Eva Jablonska and Marion Lamb’s book Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life (Jablonska and Lamb, 2014: 17; read chapter one of the book here; I have the nook version so the page number may be different):

Although many psychiatrists, biochemists, and other scientists who are not geneticists (yet express themselves with remarkable facility on genetic issues) still use the language of genes as simple causal agents, and promise their audience rapid solutions to all sorts of problems, they are no more than propagandists whose knowledge or motives must be suspect. The geneticists themselves now think and talk (most of the time) in terms of genetic networks composed of tens or hundreds of genes and gene products, which interact with each other and together affect the development of a particular trait. They recognize that whether or not a trait (a sexual preference, for example) develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule, and the environment in which an individual develops.

So to say that those who have low-functioning MAOA variants have an ‘excuse’ as to why they commit crime is incorrect. I know that most people know this, but when you read some people’s writings on things like this it’s like they think that these singular genes/polymorphisms/etc cause these things on their own. In actuality, you need to look at how the whole system interacts with these things, and not reduce whole complex physiological systems to a sum of its parts. This is why implicating singular genes/polymorphisms as explanations for racial differences in crime does not make sense (as can be seen with the Japanese example).

To reduce behaviors simply to gene X and not look at the whole system does not make any sense. There are no ‘genes for’ anything, except a few Mendelian diseases (Ropers, 2010). Stating that certain genes ’cause’ X, as I have shown does not make sense and, wrongly, in my opinion, gives criminals less of a sentencing since judges find stuff like this ‘very compelling’. If that’s the case, why implicate any murderer? ‘Their genes made them do it’, right? Though, things are not that simple to implicate one gene as a cause for crime or any other complex behavior; in this sense—like for most things to do with the human body—holism makes way more sense and not reductionism. We need to look at how these genes that are ‘implicated’ in criminal behavior interact with the whole system. Only then can we understand the causes of criminal behavior. Looking at singular genes impedes us from figuring out the true underlying reasons why people commit crime.

Remember: we can’t blame “warrior genes” for violent crime. If someone does have a ‘genetic predisposition to crime’ from the MAOA gene, then wouldn’t it make more sense to give them more time? Though, the relationship is not so simple as I have covered. So to close, there is no ‘simple relationship’ between race, crime and MAOA. Not in the way that other hereditarians would like you to believe. Because if this relationship were so simple, then East Asians (Chinese, Japanese) would have the highest rates of crime, and they do not.

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Does Testosterone Affect Human Cognition and Decision-Making?

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According to a new article published at The Guardian, testosterone does affect human cognition and decision-making. The article, titled, Now we men can blame our hormones: testosterone is trouble, by Phil Daoust, is yet more media sensationalism against testosterone. Daoust’s article is full of assumptions and conclusions that do not follow from an article he cites on testosterone and cognitive reflection and decision making.

The cited article, Single dose testosterone administration impairs cognitive reflection in menstates that endogenous testosterone (testosterone produced in the body) is correlated with physical aggression. However, I’ve shown that this is not true. They conclude overall the exogenous testosterone is related to an increase in irrational thinking and decision-making. Nothing wrong with concluding that from the data. However, Daoust’s interpretation and conclusions he draws from this study are wrong, mostly due to the same old tales and misconceptions about testosterone.

This is the largest study of the effect of exogenous testosterone and decision-making and cognition. The authors show that men administered a gel that was rubbed into the upper body that is used for TRT (testosterone replacement therapy) showed “incorrect intuitive answers were more common, and correct answers were less common in the T group, for each of the three CRT questions analyzed separately” (Nave et al, 2017: 8). However, what The Guardian article does not state is that this relationship could be mediated by more than testosterone, such as motivation and arithmetic skills.

Nevertheless, those who rubbed themselves with the testosterone gel answered 20 percent fewer questions correctly. This was attributed to the fact that they were more likely to be anxious and not think about the answer. One of the authors also states that either testosterone inhibits the action of mentally checking your work or it increases the intuitive feeling that you’re definitely right (since those who rubbed themselves with T gel gave more intuitive answers, implying that the testosterone made them go to their first thought in their head). I have no problems with the paper—other than the fact that gel has an inconsistent absorption rate and has high rates of aromatization.  The study has a good design and I hope it gets explored more. I do have a problem with Dauost’s interpretation of it, however.

A host of studies have already shown a correlation between elevated testosterone levels and aggression – and now they’re being linked to dumb overconfidence.

The ‘host of studies‘ that ‘have already shown a correlation between elevated  testosterone levels and aggression‘ don’t say what you think they do. This is another case of the testosterone sensationalism of the media—talking about a hormone they don’t really know anything about.

That won’t help with the marketing – though it may explain Donald Trump and his half-cocked willy-waggling. Perhaps it’s not the president’s brain that’s running things, but the Leydig cells in his testicles.

Nice shot. This isn’t how it works, though. You can’t generalize a study done on college-aged males to a 71-year-old man.

Women aren’t entirely off the hook – their bodies also produce testosterone, though in smaller quantities, and the Caltech study notes that “it remains to be tested whether the effect is generalisable to females” – but for now at least they now have another way to fight the scourge of mansplaining: “You’re talking out of your nuts.”

Another paragraph showing no understanding, even bringing up the term ‘mansplaining’—whatever that means. This article is, clearly, demonizing high T men, and is a great example of the media bias on testosterone studies that I have brought up in the past.

Better still, with the evils of testosterone firmly established, the world may learn to appreciate older men. Around the age of 30, no longer “young, dumb and full of cum”, we typically find our testosterone levels declining, so that with every day that passes we become less aggressive, more rational and generally nicer.

The evils of testosterone firmly established“, nice job at hiding your bias. Yes the cited article (Nave et al 2017) does bring up how testosterone is linked to aggression. But, for the millionth time, the correlation between testosterone and aggressive behavior is only .08 (Archer, Graham-Kevan, and Davies, 2005).

Even then, most of the reduction of this ‘evil hormone’ is due to lifestyle changes. It just so happens that around the ages 25-30—when most men notice a decrease in testosterone levels—that men begin to change their lifestyle habits, which involve marriage which decreases testosterone levels (Gray et al, 2002; Burnham et al, 2003; Gray, 2011; Pollet, Cobey, and van der Meij, 2013Farrelly et al, 2015;  Holmboe et al, 2017), having children (Gray et al, 2002Gray et al, 2006; Gettler et al, 2011) to obesity (Palmer et al, 2012Mazur et al, 2013; Fui, Dupuis, and Grossman, 2014; Jayaraman, Lent-Schochet, and Pike, 2014; Saxbe et al, 2017) smoking is not clearly related to testosterone (Zhao et al, 2016), and high-carb diets decrease testosterone (Silva, 2014).

So the so-called age-related decline in testosterone is not really age-related at all—it has to do with environmental and social factors which then decreases testosterone (Shi et al, 2013). Why should a man be ‘happy’ that his testosterone levels are decreasing due—largely—to his lifestyle? Low testosterone is related to cardiovascular risk (Maggio and Basaria, 2009), insulin sensitivity (Pitteloud et al, 2005Grossman et al, 2008), metabolic syndrome (Salam, Kshetrimayum, and Keisam, 2012Tsuijimora et al, 2013), heart attack (Daka et al, 2015), elevated risk of dementia in older men (Carcaillon et al, 2014), muscle loss (Yuki et al, 2013), and stroke and ischemic attack (Yeap et al, 2009).

So it seems that, contrary to Phil Daoust’s (the author of The Guardian article on testosterone) claims that low testosterone is associated with less aggressive behavior, more rationality and being nicer, in general, are wrong. Low testosterone is associated with numerous maladies, and the Daoust is trying to make low testosterone out to be ‘a good thing’, while demonizing men with higher levels of testosterone with cherry-picked studies and not large meta-analyses like I have cited that show that testosterone has an extremely low correlation with aggressive behavior.

As I have covered in the past, testosterone levels in the West are declining, along with semen count and quality. These things are due, largely in part, to social and environmental factors such as obesity, low activity, and an overall change in lifestyle. One (albeit anecdotal) reason I could conjure up has to do with dominance. Testosterone is the dominance hormone and so if testosterone levels are declining, then that means men must not be showing dominance as much. I would place part of the blame here on feminism and articles like the one reviewed here as part of the problem. So contra the author’s assertion, lower levels of testosterone into old age are not good, since that signifies a change in lifestyle—many of which are in the control of the male in question (I, of course, would not advise anyone to not have children or get married).

Nave et al (2017) lead the way for further research into this phenomenon. If higher doses of exogenous testosterone do indeed inhibit cognitive reflection, then, as the authors note, “The possibility that this widely prescribed treatment has unknown deleterious influences on specific aspects of decision-making should be investigated further and taken into account by users, physicians, and policy makers” (Nave et al, 2017: 11). This is perhaps one of the most important sentences in the whole article. This is about the application of testosterone-infused gel and decision-making. They’re talking about the implications of administering the gel to men and how it affects decision-making and cognitive reflection. This study is NOT generalizable for 1) endogenous testosterone and 2) non-college students. If the author understood the paper and science, he wouldn’t make those assumptions about Trump’s Leydig cells in his testicles “running the show”.

Because of the testosterone fear, good studies like Nave at al (2017) get used for an agenda by people who don’t understand the hormone. People the the Right and Left both have horrible misconceptions about the hormone, and some cannot interpret studies correctly and draw the correct conclusions from them. Testosterone—endogenous or exogenous—does not cause aggression (Batrinos, 2012). This is an established fact. The testosterone decrease between the ages of 25-30 is avoidable if you don’t change to bad habits that decrease testosterone. All in all, the testosterone scare is ridiculous. People are scared of it because they don’t understand it.

Daoust didn’t understand the article he cited and drew false conclusions from his misinterpretations. I would be interested to see how men would fare on a cognitive reflection test after, say, their favorite team scored during a game, and not after being given supraphysiological doses of testosterone gel. Drawing conclusions like Daoust did, however, is wrong and will mislead numerous more people under the guise of science.

Responses to The Alternative Hypothesis and Robert Lindsay on Testosterone

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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 Crime1) 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.

  1. No it doesn’t.
  2. Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
  3. 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)

Artificially increasing the amount of testosterone in a person’s blood has been shown to lead to increases in their level of aggression (Burnham 2007Kouri et al. 1995).

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.

Why Testosterone Does Not Cause Crime

Testosterone and Aggressive Behavior

Can racial differences in circulating testosterone explain racial differences in crime?—Race/History/Evolution Notes

Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003Lucas and Campbell, and Ellison, 2004Campbell, 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.

No they’re not.

The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.

Robert Lindsay

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, 2003Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009Kheirandish and Chinegwundoh, 2011; Williams et al, 2012Gathirua-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).

Gapstur et al (2002) help my argument, not yours.

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.

Wu et al (1995) show that Asians have the highest testosterone levels. Evidence is also mixed here as well. See above on AR sensitivity.

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.)

The Androgen Receptor and “masculinization”

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.

Conclusion

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.

Why Testosterone Does Not Cause Crime

Testosterone and Aggressive Behavior

Race, Testosterone, and Prostate Cancer

Population variation in endocrine function—Race/History/Evolution Notes


Can racial differences in circulating testosterone explain racial differences in crime?—Race/History/Evolution Notes

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.

Diet and Exercise: Don’t Do It? Part II

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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, 2008Azar, Beydoun, and Albadri, 2016Noakes and Windt, 2016Saslow 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 CravingsContrary 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)

Diet and Exercise: Don’t Do It?

1800 words

On Twitter, JayMan linked to a video about a time traveling dietician who travels back to the 70s to give nutritional advice to a couple. He kept going back on what he said, re eggs and cholesterol, Paleo diet, etc. Then at the end of the video, the ‘time traveling dietician’ says “It turns out it’s genetic. It doesn’t matter whether you exercise or what you eat.”

I then asked JayMan if he was advising people to not diet or exercise—and if he was doing so—what credentials does he have to give such advice? “Appeal to authority!” So if some random guy gave me legal advice and I asked his credentials, is that an appeal to authority? Similarly, if someone is trying to give me medical advice, is asking where he got his medical license an appeal to authority? The thing is, people have specialties for a reason. I wouldn’t take diet and exercise advice from some anon blogger with no credentials, just like I wouldn’t take legal advice from a biologist. Anyway, I’ll review some studies on exercise, dieting, and sitting in regards to all-cause mortality.

Sitting and all-cause mortality

Listening to such advice—like not dieting or exercising—will lower your quality of life and life expectancy. The longer you sit, the more likely you are to have rolled shoulders among other postural imbalances. One of the biggest reasons that sitting is related to all-cause mortality (Chau et al, 2013Biddle et al, 2016). So listening to this shitty advice to ‘not exercise’ will lead an individual to having a lower QoL and lower life expectancy.

Sitting is associated with all-cause mortality because if, say, one is sitting at a desk for 8 hours per day then goes home and sits for the rest of the day, circulation will not get not get to the lower extremities. Furthermore, even mild-to-moderate exercise attenuates the situation (Chau et al, 2013). Further, reducing sedentary behavior (and of course, watching less TV) can possibly raise life expectancy in the US (Katzmarzyk and Lee, 2012). They found that cutting daily sitting time to less than three hours can increase life expectancy by two years (and, of course, quality of life). There is a large body of research on sitting and all-cause mortality (Stamatakis et al, 2013). It’s also worth noting that too much sitting decreases life expectancy—even with exercise. So JayMan’s (unprofessional) advice will lead to someone having a shitty life quality and lower life expectancy.

Dieting, and all-cause mortality

This is a bit trickier. I know that dieting for weight loss doesn’t work (Aamodt, 2016; Fung, 2016)—that is, traditional dieting (high-carb diets). The traditional advice is to eat high-carb, low-fat and moderate protein—this is due to what occurred in the 70s—the demonization of fat and the championing of carbs. This, clearly, is wrong. This has led to the obesity epidemic and the cause is our evolutionary novel environments. The main reason is that we have constructed environments for ourselves that are novel, and thus we’ve not had enough time to adapt to what we eat/how we live our new lives in our modernized world.

Indeed, even hunter-gathers don’t have our disease rates that we have—having low to no cases of our diseases of civilization (see Taubes, 2007 for a review). Why is this? It’s because they are physically active and they do not eat the same processed carbohydrates that we in first-world societies do.

In regards to exercise and all-cause mortality, people who exercise more often have a lower chance of dying from all causes than more sedentary people (Oja et al, 2016O’Donovan et al, 2017). So it’s becoming clear that JayMan is just talking out out his ass here. I’d love to hear any MD say to a patient “Don’t diet, don’t exercise. Don’t eat well. It doesn’t work.” Because that MD will be a shill for Big Food.

Further, when I say ‘diet’, I don’t mean eating below the BMR. Your ‘diet’ is what you eat, and by changing your diet, you’re changing to healthier habits and eating higher-quality foods. People like JayMan make it seem like you should eat whatever you want and not to exercise. Following this advice, however, will lead to deleterious consequences.

It DOES matter what you put into your body; it DOES matter if you exercise or not. If you do not, you will have a lower life expectancy than who does exercise and eats well.

On a side note, I know that dieting does not work for weight loss. Traditional dieting, that is. Dr. Jason Fung, world-renowned obesity, diabetes and intermittent fasting expert, has people lose and keep their weight off. He actually understands what causes obesity—insulin. Higher insulin levels are also tied to the obesity pathway through lack of glucagon receptors (Lee et al, 2014). Why is this important? First, we have to understand what insulin does in the body. Once you understand what insulin does in the body then you will see why JayMan is wrong.

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

Does this physiologic process sound that you can ‘eat whatever you want’? Or does it tell you that you should lower your carb intake as to not induce blood glucose spikes which lead to an increase in insulin? Over time, these constant blood glucose/insulin spikes lead to insulin resistance which has the body produce more insulin due to the insulin resistance resulting in a vicious cycle.

So, it seems that in order to have a higher QoL and life expectancy, one must consume processed carbs very sparingly.

These behaviors of over consuming processed carbohydrates come down to the environments we have constructed for ourselves—obesogenic environments. An obesogenic environment “refers to an environment that helps, or contributes to,
obesity” (Powell, Spears, and Rebori, 2010).

Our current obesogenic environment also contributes to dementia and cognitive impairment. What makes environments ‘obesogenic’ “is the increased presence of food cues and the increased consumption of a diet which compromises our ability to resist those cues” (Martin and Davidson, 2015). So if our obesogenic environments change, then we should see a reduction in the number of overweight/obese people.

Diet is very important for Type II diabetics. For instance, TII diabetics can manage, and even reverse, their disease with a low-carb ketogenic diet (LCKD) lowering their hBA1c, having a better lipid profile, cardiac benefits, weight loss etc (Westman et al, 2008; Azar, Beydoun, and Albadri, 2016; Noakes and Windt, 2016; Saslow et al, 2017). I wonder if JayMan would tell TII diabetics not to diet or exercise…. That’d be a recipe for disaster. TII diabetics need to keep their insulin down and eating an LCKD will do that; taking JayMan’s ‘advice’ not to diet or exercise will quickly lead to more weight gain, an exacerbation of problems and, eventually, death due to complications from not correctly managing the disease. JayMan needs to learn the literature and understand these papers to truly understand why he is wrong.

Exercise and all-cause mortality

The relationship between vigorous exercise and all-cause mortality is well studied. Gebel et al (2015) conclude that “Independent of the total amount of physical activity, engaging in some vigorous activity was protective against all-cause mortality. This finding applied to both sexes, all age categories, people with different weight status, and people with or without cardiometabolic disease.” Reduced exercise capacity also causes higher all-cause mortality rates (McAuley et al, 2016).

Unfit thin people had two times higher mortality rate than normal weight fit people. Further, overweight and obese fit people had similar mortality rates when compared to normal weight fit people (Barry et al, 2013). Clearly, physical activity needs to be heightened if one wants to live a longer, higher quality life. This runs completely opposite of what JayMan is implying.

Exercise into old age is also related to higher cognition and lower mortality rate in when compared to individuals who do not exercise. Exercise also protects against cognitive degeneration in the elderly (Bherer, Erikson and Lie-Ambrose, 2013; Carvalho et al, 2014; Paillard, 2015). If you want to keep your cognition into old age and live longer, it seems like your best bet is to exercise at a young age in order to stave off cognitive degeneration.

Strength and mortality

Finally, one last thing I need to touch on is strength and mortality. Strength is, obviously, increased through exercise. Stronger men live longer—and are protected from more disease such as cancer—than weaker men, even when controlling for cardiorespiratory fitness and other confounds (Ruiz et al, 2008).

As I have covered in the past, differences in grip strength account for differences in mortality in men—which also has a racial component (Araujo et al, 2010; Volkalis, Halle, and Meisinger, 2015). The stronger you are, the less chance you have of acquiring cancer and other maladies. Does the advice of ‘don’t exercise’ sound good now? It doesn’t, and I don’t know why anyone would seriously imply that dieting and exercise doesn’t work.

Conclusion

Dieting (meaning eating a higher quality diet, not attempting to lose weight) and exercise do work to increase life expectancy. The advice of “don’t do anything, it’s genetic” makes no sense at all after one sees the amount of literature there is on eating mindfully and exercising. I know that exercise does not induce weight loss, but it does contribute to living longer and staving off disease.

People should stay in their lane and leave things to the professionals—the people who are actually working with individuals every day and know and understand what they are going through. The canard of ‘eat whatever, don’t exercise, it’s genetic’ is very dangerous, especially today when obesity rates are skyrocketing. JayMan needs to learn the literature and how and why exercise and eating right leads to a higher quality of life and life expectancy. Thankfully, people like JayMan who say not to diet or exercise have no pull in the real world.

Clearly, to live longer, eat right, don’t sit for too long (because even if you exercise, sitting too long will lower your life expectancy) and exercise into old age and your chance of acquiring a whole slew of deleterious diseases will be lessened.

Why Testosterone Does Not Cause Crime

1900 words

Edit: (The correlation between aggression and testosterone isn’t .14 as Book et al (2001) state; the true correlation is .08 (Archer, Graham-Kevan and Davies, 2005) So it’s even lower than I thought. This is one of the many reasons why testosterone does not cause crime. It’s just feminist bullshit and fear mongering from people who do not understand the hormone and what it does in the body. The misconceptions come from Rushton’s r/K selection bullshit which has been summarily refuted.)

Recently, I’ve written at length on racial differences in testosterone and how the correlation between testosterone and physical aggression is .14. Pitifully low to account for the cause of crime and any overall differences in racial crime (that will be touched on at length in the future). Tonight I will show, yet again, why testosterone does not cause crime by looking at what times most crimes are committed by both adults and children under the age of 18. This will definitively put the ‘testosterone causes crime’ myth to bed for good.

Before I get into the time of day that most crimes are committed, I must talk about the production of testosterone in the body. There are no ‘genes for’ testosterone (although men who had three certain alleles had a 6.5 fold higher risk of having low testosterone; Ohlsson et al, 2011, I am unaware of there being a variation by race; over 10,000 Caucasian men were studied). There is, however, an indirect control of testosterone synthesis by DNA. DNA regulates the production of testosterone by coding for enzymes that convert cholesterol to testosterone (testosterone is a cholesterol-based hormone).

There are five simple steps to the production of testosterone: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone). That’s how testosterone is produced in the body. It is indirectly controlled by DNA.

qa03401_2010

Above is a graph from the Office of Juvenile Justice and Delinquency Prevention which shows the time of day that most crimes are committed. Notice how crime goes up as the time of day goes on and since kids are at school, they’re more likely to fight. This then peaks at 3 pm when kids are getting out of school.

Now look at rates of crime for adults. At its peak of 10 pm, it’s vastly lower than that of people under the age of 18, which is important to keep in mind. You can see how at 8 am that rates of crime are low for adults and high for kids, right when they would be entering school so there would be a lot of other kids around and the chance for violence goes up. Keep the times of 8 am (kids when they enter school), 12 pm (when most kids go on lunch) and 3 pm (when most kids get out of school) along with the hours of 12 pm to 8 pm for adults (when 74 percent of crimes are committed by adults).

The OJJDP writes:

  • In general, the number of violent crimes committed by adults increases hourly from 6 a.m. through the afternoon and evening hours, peaks at 10 p.m., and then drops to a low point at 6 a.m. In contrast, violent crimes by juveniles peak in the afternoon between 3 p.m. and 4 p.m., the hour at the end of the school day.
  • Nearly one-third (29%) of all violent crime committed by juvenile offenders occurs between 3 p.m. and 7 p.m. In comparison, 26% of all violent committed by adult offenders occurs between 8 p.m. and 12 p.m.

So since testosterone varies by day and levels are highest at 8 am and lowest at 8 pm (Brambilla et al, 2009; however testing men aged 45 years of age and older is fine before 2 pm due to a blunted circadian rhythm; Long, Nguyen, and Stevermer, 2015), then how could testosterone account for why men commit most of their crimes at night and why the crime that children commit spikes when they go to school, go to lunch and get out of school? The answer is that it doesn’t because testosterone does not cause crime. What testosterone does cause, however, are feelings of confidence and dominance, which does not—surprisingly—lead to increased aggression and assault on others (Booth et al, 2006).

What testosterone does cause, however, is social dominance and success, not physical aggression and maladjustment (Shcaal et al, 1996). The effects of environment are also more notable on testosterone than are genetics at 5 months of age (Carmaschi et al, 2010). Furthermore, aggressive behavior is first noticed in infancy and reaches its peak before school age (Tremblay et al, 2004; Cote et al, 2006). Though testosterone does seem to have an effect on aggression in preschool boys, however genetic and environmental causality has not been established (Sanchez-Martin et al, 2000).

Nevertheless, the meta-analyses I cited last week show that testosterone has an extremely low correlation of .14, so other factors must be at play. However, Sanchez-Martin et al (2000:778-779) also note that “Tremblay et al (1998) suggested that associations between testosterone titer and physical aggression are likely to be observed in contexts where such attack leads to social dominance. This may be true of the preschool boys in the present study. The data generated in the present study generally support Scerbo and Kolko (1994), who studied older children (7 to 14 years of age). They found a significant relationship between testosterone levels and aggression (as assessed by clinical staff).

It’s interesting to note that in the case of Scerbo and Kolko (1994) that after controlling for age and size, testosterone correlated with aggression when rated by staff but not parents or teachers. ‘Staff’ refers to clinic staff at a facility where the children were assessed for hyperactivity disorders. Of course, the staff would rate higher levels of aggression compared to parents of teachers—people who are around the children every day—since they would want a higher chance for diagnosis for certain drugs to ‘cure’ the hyperactivity, but I digress. Testosterone does not induce aggression in children, but it does induce social dominance and confidence which does not lead to aggression (Rowe et al, 2004; Booth et al, 2006).

There was also little difference in testosterone between socially dominant prisoners and aggressive prisoners (Ehrenkraz, Bliss, and Sheard, 1974). Furthermore, the testosterone increase leading to pubertal development in boys is not associated with increased aggression (Tremblay et al, 1998; Booth et al, 2006: 171). Indeed, increased body size is a marker for physical aggression in children, and I doubt these children have high muscle mass so, I assume, they have high levels of body fat and thusly lower levels of testosterone than they would have if they were leaner. Yet another strike against the ‘testosterone causes crime/physical aggression’ hypothesis.

Indeed, this has some implications for the honor culture hypothesis of why low-income blacks have higher levels of testosterone than similarly aged blacks with some college (Mazur, 2016). The patterns for crime as shown by the OOJDP shows that crime rises as the day progresses from the morning until its peak at 3 pm for children and then sharply declines while for adults it peaks at 10 pm.

Testosterone does increase when a challenge is issued; when one man feels his reputation is threatened, the propensity for violence is increased, but this was most notably seen in Southern men (Cohen et al, 1996). So the same would be said for this ‘culture of honor’ found in low-income black neighborhoods, the so-called ‘code of the street’ as stated by Anderson (1994: 88): “Moreover, if a person is assaulted, it is important, not only in the eyes of his opponent but in the eyes of his “running buddies,” for him to avenge himself. Otherwise, he risks being “tried” (challenged) or “moved on” by any number of others. To maintain his honor, he must show he is not someone to be “messed with” or “dissed.”

This culture of honor is found all over the world, including Brazil where homicide can be explained by the need to maintain honor and can be understood by taking into account cultural factors; biological, psychological and socioeconomic factors do not explain murder in Northeast Brazil as well as honor and culture (de Souza et al, 2015). People in honor cultures also have a higher chance of self-harm (Osterman and Brown, 2011) as well as a higher chance of committing violence in school (Brown, Osterman, and Barnes, 2009).

Testosterone does not cause crime; it does not cause aggression. Increases in testosterone before, during and after events are a physiologic process to prime the body for competition. As cited above, dominant behavior does not necessarily lead to violence in most cases, which may be surprising for some. Indeed, honor and culture may explain a nice amount of the homicide and violence rate in the South. Since testosterone is highest at 8 am and lowest at 8 pm and the rates of crime committed by adults and children are vastly different than the diurnal variance in the day, then testosterone does not cause crime and its increase is not associated with crime, but social dominance and confidence which does not lead to crime.

Hopefully—if anyone still believes testosterone to be the boogeyman its made out to be—I’ve put those misconceptions to rest. Racial differences in testosterone cannot be the cause of racial differences in crime—because there is either no statistical difference in testosterone between the races or the difference is non-existent. Testosterone is clearly a beneficial hormone—as I have extensively documented. Misunderstandings of the hormone are abound—especially in the HBD sphere—only due to literally a few paragraphs in a book (Rushton, 1997) and one study that showed blacks have higher testosterone than whites which was the cause of their higher rates of prostate cancer (Ross et al, 1986). The study is hard to find so I had to buy access to it. I will cover this in the future, but I discovered that they assayed the subjects when it was convenient for them—between the hours of 10 am and 3 pm—which is unacceptable. You cannot gauge racial differences in testosterone from a small study (n=50) and a non-representative sample (college students). For these reasons, the study should be thrown in the trash—especially when formulating evolutionary hypotheses.

Testosterone is one of the most important hormones for vital functioning. By knowing how it is processed in the body and that there are no ‘genes for’ testosterone (‘low testosterone genes’ notwithstanding) along with how testosterone has a low relationship with physical aggression one should not be scared of having high levels, on the contrary, one should be scared of having low levels. I have once again proven my case that testosterone is not related to violence in showing the diurnal variation in testosterone levels in adults, as well as the time of day that crimes are committed by both adults and children. High testosterone means high confidence and high dominance—and those two traits have a lot to do with masculinity—which do not lead to violence.

I know why testosterone does not cause crime—because I have an understanding of the hormone, how its produced in the body and what its effects on the body are. The most important thing to note here, is that even if blacks had 15 percent higher testosterone than whites, it still wouldn’t explain higher rates of crime or disease such as prostate cancer. So those who try so hard to prove that blacks have higher levels of the hormone do so in vain, because even if they did it wouldn’t mean anything for any theories they may have. The myth of testosterone causing aggression and crime need to be put to bed for good.

Dinosaurs, Brains, and ‘Progressive’ Evolution: Part II

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In part I, I showed how Dale Russel’s contention that the troodon would have evolved into a bipedal ‘dinosauroid’ with human locomotion and a human-sized brain was pure fantasy. I ordered the book of his that Rushton cited in his book Race, Evolution, and Behavior and I finally received it last week. When I read the relevant parts, I yawned because it’s the same old stuff that I’ve covered here on this blog numerous times. Since literally the only relevant part in the book about the troodon is the final 7 pages, that’s what I will cover today—along with a few more lines of evidence that large brains lie outside reptilian design (Gould, 1989).

First off, all of Rushton’s contentions in the final pages of his book (Rushton, 1997) need to be rebutted. Rushton (1997: 294) writes that dinosaur brains were ‘progressing’ in size for 140 million years, but neither of Russel’s writings that I have (Russel 1983; 1989) have the statement in them.

In the book Up From Dragons: The Evolution of Human Intelligence neuroscientist, evolutionary psychologist John Skoyles and science writer Dorian Sagan—the son of Carl Sagan—speak briefly about reptilian intelligence and why they wouldn’t have reached our levels of intellect:

But cold-bloodedness is a dead-end for the great story of this book—the evolution of intelligence. Certainly reptiles could evolve huge sizes, as they did over vast sweeps of Earth as dinosaurs. But they never could have evolved our quick-witted and smart brains. Being tied to the sun restricts their behavior: Instead of being free and active, searching and understanding the world, they spend too much time avoiding getting too hot or too cold. (Skoyles and Sagan, 2002: 12)

Hopson (1977: 443) writes:

I would argue, as does Feduccia (44), that the mammalian/avian levels of activity claimed by Bakker for dinosaurs should be correlated with a great increase in motor and sensory control and this should be reflected in increased brain size. Such an increase is not indicated by most dinosaur endocasts.

Most importantly, if some dinosaurs DID have bird-sized brains, the above contention would still hold. Hopson concludes that, except for coelurosaurs “the range of behaviors that existed in dinosaurs, as inferred from trackways and skeletal morphology, may not have lain much outside the observed range in ectothermic crocodilians” (Hopson, 1977: 444).

Since the conjecture/’thought experiment’ of the troodon was rebutted last week, it’s pretty conclusive that large brains lie outside of reptilian design; they need to spend so much time avoiding getting too hot or cold—as well as hunt and eat—so exploring the world and learning was not possible for them—along with the fact that they didn’t have a primate morphology and thus didn’t have the ability to fully manipulate their environment as we do which would further select for larger brains. However, as Hopson (1977) notes, animals with higher metabolic rates had larger brains; coelurosaurs had high metabolic rates and the largest dinosaur brains (Russel, 1983; 1989)—but that doesn’t mean they would have eventually evolved human-like intelligence, bipedalism or brain size and to say otherwise is fantasy.

Furthermore, there is large variation in encephalization and encephalization is not universal in mammals (Shultz and Dunbar, 2010).

Here is the thing about brain size increases: it is a local level trend. A local level trend is a trend that occurs within one or a few related species. This is exactly what characterized brain evolution; there is large variation depending on what the environment calls for (Boddy et al, 2012; Montgomery et al, 2012; see also island gigantism; Bromham and Cardillo, 2007; Welch, 2009; and also see the deep sea rule; Mcclain, Boyer, and Rosenberg, 2006). So these local trends differ by species—even one population split by, say, 50 miles of water will speciate and become evolve a completely different phenotype due to the environment of time. That is evolution by natural selection; local change, not any inherent or intrinsic ‘progress’ (Gould, 1996).

The same local level trend occurs with parasites. Now think about parasites. The get selected for ‘complexity’ or a decrease in ‘complexity’ depending on what occurs in their host. Now, looking at it from this perspective, the body is the host’s environment while the earth is ours; so my example for an environmental change would be, as usual, the asteroid impact hitting the earth blocking out the sun and decreasing high-quality food all throughout the earth. Surely I don’t need to tell you what would occur…

Russel (1989) writes:

Examples of evolutionary changes that occured at ever-increasing speeds include the initial diversification of animals in the sea 650 and 550 million years ago, the attainment of tree stature in land plants between 410 and 360 million years ago, and the diversification of mammals between 200 million years ago and the present. Changes like this have resulted in increased organismal complexity, which, in combination with a general increase in number of species, has made the biosphere of the modern Earth so much richer than it was several hundred million years ago. It is reasonable to suppose that animals living in a complex environment might find it advantageous to possess complex nervous systems in order to have access to a greater variety of responses. Indeed, the largest proportion of brain weight in an animal has also increased at an ever-increasing rate across geological time. The brain has become evidently larger in animals as diverse as insects, mollusks, and backboned creatures. Relative brain size can be taken as an indication of biotic interactions.

He references time periods that correspond with decimations (mass extinctions). Decimations lead to diversification. Think back to the Cambrian Explosion. During the Cambrian Explosion, many more lifeforms existed than can be currently classified. Therefore, according to the decimation and diversification model, greater diversity of life existed in the past. When decimations (defined as a reduction in the anatomical forms of life from mass extinction) occur, the niches that become extinct quickly become filled.

The time periods that Russel references are when mass extinctions occurred. This is how diversification occurs. What allowed for this ‘organismal complexity’ and increase in the number of species (though body plans are limited due to the Burgess Decimation) is due to the decimations. Decimation and diversification proves that evolution is not progressive.

A ‘trend’ in biology is directional change in a group stat using the mean, median or mode. Any existence of a trend from the mean (‘progress’) tells us nothing about the underlying mechanisms behind it.

To wrap this all up, even if a trend in X were to be discovered, it still wouldn’t tell us a thing about the underlying mechanisms causing it, nor will it tell us about any increasing tendency. 

The analogy of the drunkard’s walk (Gould, 1996) is why ‘progress’ doesn’t make sense. Further, niche construction matters as well. When organisms construct their own niches, change occurs based on those niche constructions. Milk-drinking 8kya in Europe and African farmers diverting water for their crops having mosquitoes come by and gaining a resistance to malaria are two examples of niche construction (Laland et al, 2009). That’s another barrier to progress!

In sum, Dale Russel says nothing I’ve not heard before in regards to ‘progressive’ evolution. He only describes ever-increasing ‘complexity’ which is due to decimations and further diversification by organisms to fill empty niches. Any type of ‘progress’ would have been stymied by mass extinctions.

Further, the fact that species can consciously—in a way—guide their own evolution through the manipulation of the environment once again shows how evolution doesn’t mean progress—it literally only means local change and any type of local change, no matter to what type of environment, will cause concurrent increases/decreases on whichever relevant traits that will give the organism the best chance for survival in that environment.

This is why evolution is not progressive; and even if scientists were to identify one thing, still, a causal mechanism won’t be able to be inferred. Ruseel (1989) describes right and left walls of complexity—nothing more. Dinosaurs didn’t have the body plans to have our brain size, bipedalism and intelligence, nor did they have the right type of blood, nor did they have the time to search and learn about the world due to being constrained to their cold-blooded system—being a slave to the sun, always attempting to avoid overheating or getting too cold (Skoyles and Sagan, 2002). The so-called ‘dinosauroid’ is an impossibility and implies a teleological lean to evolution—as if our morphology (or something similar from an unrelated organism) will always evolve if we replay the tape of life again (Gould, 1989; 1996). This is what Russel is pretty much arguing, and he is 100 percent wrong as noted above.

References

Bromham, L., & Cardillo, M. (2007). Primates follow the ‘island rule’: implications for interpreting Homo floresiensis. Biology Letters,3(4), 398-400. doi:10.1098/rsbl.2007.0113

Boddy, A. M., Mcgowen, M. R., Sherwood, C. C., Grossman, L. I., Goodman, M., & Wildman, D. E. (2012). Comparative analysis of encephalization in mammals reveals relaxed constraints on anthropoid primate and cetacean brain scaling. Journal of Evolutionary Biology,25(5), 981-994. doi:10.1111/j.1420-9101.2012.02491.x

Gould, S. J. (1989). Wonderful life: the Burgess Shale and the nature of history. New York: Norton.

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

Hopson, J. A. (1977). Relative Brain Size and Behavior in Archosaurian Reptiles. Annual Review of Ecology and Systematics,8(1), 429-448. doi:10.1146/annurev.es.08.110177.002241

Laland, K. N., Odling-Smee, J., Feldman, M. W., & Kendal, J. (2009). Conceptual Barriers to Progress Within Evolutionary Biology. Foundations of Science, 14(3), 195–216. http://doi.org/10.1007/s10699-008-9153-8

Mcclain, C. R., Boyer, A. G., & Rosenberg, G. (2006). The island rule and the evolution of body size in the deep sea. Journal of Biogeography,33(9), 1578-1584. doi:10.1111/j.1365-2699.2006.01545.x

Montgomery, S. H., Capellini, I., Barton, R. A., & Mundy, N. I. (2010). Reconstructing the ups and downs of primate brain evolution: implications for adaptive hypotheses and Homo floresiensis. BMC Biology,8(1), 9. doi:10.1186/1741-7007-8-9

Russell, D. A. (1983). Exponential evolution: Implications for intelligent extraterrestrial life. Advances in Space Research,3(9), 95-103. doi:10.1016/0273-1177(83)90045-5

Russell, D. A. (1989). An Odyssey in Time: The Dinosaurs of North America. Minocqua, WI: Published by NorthWord Press in association with National Museum of Natural Sciences.

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

Shultz, S., & Dunbar, R. (2010). Encephalization is not a universal macroevolutionary phenomenon in mammals but is associated with sociality. Proceedings of the National Academy of Sciences,107(50), 21582-21586. doi:10.1073/pnas.1005246107

Skoyles, J. R., & Sagan, D. (2002). Up From Dragons: The Evolution of Human Intelligence. New York: McGraw-Hill.

Welch, J. J. (2009). Testing the island rule: primates as a case study. Proceedings of the Royal Society B: Biological Sciences,276(1657), 675-682. doi:10.1098/rspb.2008.1180

Between-group Differences in Obesity Rates

By Scott Jameson

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I’ve been active in the blogosphere for around 24 hours now and I’ve already gotten a negative response from someone who happens to be wrong. That’s a win in my book.
The argument we’re having is, as best I can tell, why some populations out there just don’t have obesity as an observed phenotype amongst their members. TL;DR: Pumpkin Person and Robert Lindsay believe that genetics explain why there are no obese New Guineans. But it ain’t so.

The original context is an old Pumpkin Person post. Much of what he’s saying here doesn’t seem too off-base; for example he says that behavioral genetics may explain much of the differences in BMI between individuals within the same population. True. It is possible that some people are genetically inclined to eat more or unhealthier foods, rather than simply being genetically inclined to putting on weight regardless of what they do.

As an aside, genotypes that affect how you digest things also probably explain part of the BMI gap between skinny folks and fat folks within the first world. The APOA2 gene for example has a recessive allele that is associated with higher BMI in people who eat more saturated fats. The interactions between genes and environment which determine BMI are complicated and not yet fully understood, but I’m willing to bet that being genetically worse at processing certain nutrients is a part of the problem, and that being genetically inclined to stuff your face is a part of the problem as well. PP is probably right about that issue.

Where he and Lindsay get it wrong is using examples of people from Podunk, New Guinea as evidence for obesity “being genetic” (relative term). Obesity is a gene-environment interaction such that, without certain environmental inputs, you simply won’t get the phenotype. History tells us that that input is processed carbohydrates.

There was a time when people could have used Australian Aboriginals or Inuit or Pima Indians as examples of groups of people who just don’t have obese folks amongst their numbers, just as Lindsay did with a few populations. Homo sans lardicus. Then the White Devils showed up with their refined Einkorn wheat products and their firewater and so on. Now those populations have fat people in them.

There’s an ongoing debate as to whether some populations are more resistant to the fattening effects of processed carbs or not. My guess is, the answer’s yes (and you’d look at Europeans and East Asians to see the more carb-resistant people, in theory) but that topic would merit its own post. That being said, every population in the world will almost assuredly have obese people in it after you introduce processed carbs. All of the populations that were introduced to this diet, now have fat people in them.

Heritability of BMI is high within the first world because the relevant environmental input is pretty uniform: everybody has access to potatoes, everybody has access to broccoli. As PP points out, which you’re likely to eat and how much you’re likely to eat likely depends on your genetics. As I point out, how your body processes the nutrients also has a likely genetic component. But the environmental contribution to our within-population differences in BMI is low (~20%) because we all have access to roughly the same stuff.

Rural New Guineans, lacking a bunch of processed carbs, could hardly get fat if they tried their best to. That’s a big between-population, nonheritable cause for a phenotypic difference; this means that environment probably explains most of the BMI gap between them and us. If I wanted evidence to refute Lindsay’s assertion that New Guineans are skinnier thanks to genetics, I’d find a population of urbanized New Guineans somewhere with higher average BMI. Such a group would have New Guinean genetics but a “developed” environment vaguely similar to ours; if they were fatter than their rural ken, then Lindsay’s hypothesis that New Guineans are just genetically obesity-free would be falsified.

If only such research existed!

Are There Racial Differences in Penis Size?

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Do racial differences in penis size exist? The average person may say yes, due to viewing porn and hearing ‘stories’ from their friends, ie anecdotal accounts. But is this true? JP Rushton was at the helm of this resurrected idea, stating that an inverse relationship existed between penis size and brain size. He cites a WHO study on condom size showing that African countries get the biggest condoms, yet I cannot find the paper discussing it. PP wrote an article, Non-black men are so jealous of black penis sizeciting the same study Rushton (1997) cited in his book Race, Evolution, and Behavior. I will discuss PP’s musings on racial differences in penis size.

A pet peeve of mine is that a lot of non-black men in the HBD blogosphere believe everything that professor J. Philippe Rushton said about ethnic differences in IQ and brain size, but when it comes to black men having the largest penis size, they suddenly turn into HBD deniers, ranting and raving about how the research is wrong. Well, I’m sorry but HBD is not here to serve your racist supremacy, HBD is here to celebrate ALL RACES, NOT YOURS ONLY!!!! If the data shows that black men have the largest penis size, then shut up and get over it. What kind of man gets jealous over another man’s penis size anyway? A sick, twisted, perverted sinful one. Healthy well adjusted normal guys don’t even know how large their penis is, and couldn’t care less, because they have other things going for them like a girlfriend, a career, and sports, and their mind’s not in the gutter. The only legitimate reason to care is for science, so here are the FACTS:

Exactly, the only reason to care is for science. And the science shows no differences. What data shows differences in penis size? Something you can directly access right now without relying on a secondhand source to prove your claim?

According to data from the World Health Organization Global Programme on AIDS Specification and Guidelines for Condom Procurement (1991, p 33, Table 5), assuming a normal distribution, I estimate the average white American man has a penis length of 162 mm (SD = 19) , and the average African American man has a penis length of 170 mm (SD = 19). (since 5% of black men are longer that 200 mm, and 2% of white men are, while 27% of white men have penises shorter than 151 mm, while 15% of black men do).

No hyperlink to the study? Why do you rely on a secondhand account? Why didn’t you show the table?

Just found some information on the WHO study he cited. The information from which the WHO data is derived is derived from American blacks and Caucasians, not any subjects from Europe or Africa. He also asked 150 people on a Toronto shopping mall what their penis size was (back to garbage self-reports), and finally, who is this French army surgeon he brings up? So many questions. 

Also, PP, asking the questions and questioning his data and what he wrote isn’t “disagreeing on him on this and agreeing with him on everything else”, as you of all people know how critical o am of Lyn  and Rushton. Yet you seem to eat up everything they write, thinking they can never be wrong. Why is that? 

Rushton (1997) writes on pg 169 of Race, Evolution, and Behavior:

Data provided by the Kinsey Institute have confirmed the black-white difference in penis size (Table 8.2, and items 70-72 of Table 8.4). Alfred Kinsey and his colleagues instructed their respondents on how to measure their penis along the top surface, from belly to tip. The respondents were given cards to fill out and return in preaddressed stamped envelopes. Nobile (1982) published the first averages of these data finding the length and circumferences of the penis for the white samples was smaller than for the black sample. (Flaccid length = 3.86 inches [9.80 cm] vs. 4.34 inches [11.02 cm]; erect length = 6.15 inches [15.62 cm] vs. 6.44 inches [16.36 cm]; erect circumference = 4.83 inches [12.27 cm] vs. 4.96 inches [12.60 cm] respectively.)

Self-reports? Please. Self-reports are notoriously embellished. Moreover, the amount of black Americans in the Kinsey study was in double digits.

I can never find certain papers online, so that really hinders any further discussion on this.

If anyone can find any of these papers, leave a comment.

Harvey, P. H., & May, R. M. (1989). Out for the sperm count. Nature, 337, 508-9.

Short, R. V. (1979). Sexual selection and its component parts, somatic and genital selection, as illustrated by man and the great apes. In J. S. Rosenblatt, R. A. Hinde, C. Beer, & M-C Busnel (Eds.), Advances in the Study of Behavior, Vol. 9. New York: Academic

When it comes to scrotal circumference, I don’t have exact figures, but Rushton cites scholars showing that Africans exceed Europeans: Short, 1979; Ajmani, Jain & Saxena, 1985.

I found Ajmani et al (1985), they state that in 320 healthy Nigerians, average penile length was 3.21 inches, while scrotal circumference was 8.37 inches. PP says he didn’t have exact figures, but they were in Rushton’s references (which I see he didn’t check). Rushton doesn’t cite data on European scrotal circumference so how is that saying that ‘Africans exceed Europeans’ when only Nigerians were examined? Remember: studies are only applicable to the demographic tested. Extrapolating that data on to the whole of Africa makes no sense. Moreover, any data on Europeans is only for that specific ethny tested. Unless the whole of the European continent is averaged out, you cannot say that these differences exist.

This doesn’t even touch on Lynn’s “data” on penis size:

  Lynn attempts to justify his belief that there are differences between races in penis length on the basis that European and Asian males have lower levels of testosterone than Africans and that the “reduction of  testosterone had the effect of reducing penis length, for which evidence is given by Widodsky and Greene (1940).” Widodsky and Greene (1940) is actually a study of the effects of sex hormones on the penises of rats. This is hardly convincing evidence that there are racial differences in testosterone levels or that a reduction in penis length ever occurred in human history.

Lynn’s claims about differences in penis length between races build on earlier claims by Rushton and Bogaert (1987). The Rushton and Boagert paper is striking for its use of non-scholarly sources (Weizmann, Wiener, Wiesenthal, & Ziegler, 1991). These include a book of semi-pornographic “tall tales” by an anonymous nineteenth century French surgeon that makes wildly inconsistent claims about genital sizes in people of different races. Lynn also refers to this book without mentioning any problems with this as a source of information. Another odd data source cited by Rushton and Bogaert is an article authored by a certain “P. Nobile” published in Forum: International Journal of Human Relations. This publication is better known to the public as “The Penthouse Forum”, a popular men’s magazine. [This is pretty well known and embarrassing that Rushton did that.]

The data sources that Lynn uses in his recent paper are hardly much better. One of them is a book by Donald Templer (another self-professed race realist[1]) called Is Size Important? Templer is not a urologist but a psychologist so why he would claim to be an authority on this subject is unclear.[2] Lynn’s other source is the world penis size website. These are both self-published sources that have not been independently verified. A blogger named Ethnic Muse has carefully examined this site’s references and found that a number of articles listed on the site either do not exist under the name given or do not discuss penis size at all. There are also numerous discrepancies between the values provided by the website and the actual values given by the references.[3] Therefore, the information on this website cannot be trusted and no conclusions should be drawn from it.

Pretty embarrassing for race-realism, to be honest. Looks like the data from “P. Nobile” is from a Penthouse webforum that he ‘published’ his ‘results’ in, instead of a scholarly journal. Rushton did state ‘forum’ (not stating it was the ‘Penthouse forum’, though), but why should we take this as proof of anything?

The sadder one is multiple ‘references’ of Lynn’s that either don’t exist or don’t discuss penis size. Why trust these ‘sources’, when they aren’t controlled scientific studies?

Veale et al (2014) write:

It is not possible from the present meta-analysis to draw any conclusions about any differences in penile size across  different races. Lynn [31] suggest that penis length and girth are greatest in Negroids (sub-Saharan Africans), intermediate in Caucasoids (Europeans, South Asians and North African), and smallest in Mongoloids (East Asians), but this is baseupon studies that did not meet our present inclusion and

The greatest proportion of the participants in the present meta-analysis were Caucasoids. There was only one study of 320 men in Negroids and two studies of 445 men in Mongoloids. There are no indications of differences in

racial variability in our present study, e.g. the study from Nigeria was not a positive outlier. The question of racial variability can only be resolved by the measurements with large enough population being made by practitioners following the same method with other variables that mainfluence penis size (such as height) being kept constant. Future studies should also ensure they accurately report the race of their participants and conduct inter-rater reliability.

This meta-analysis was only done on Caucasians, but from the previous study on 320 Nigerians cited from Rushton (Ajmani et al, 1985) and 445 Mongoloids, no racial differences were found. When an actual study gets carried out on this, I doubt that there would be any differences between races.

Orakwe and Ebuh (2007) again test Nigerians (5.2 inches), then compare them with Italians (4.92 inches), Greeks (4.79 inches), Koreans (3.78), British (5.11 inches), and American Caucasians (4.9 inches). The only statistical difference was between Nigerians and Koreans. They conclude:

There is the possibility of racial differences in penile sizes, but there is no convincing scientific background to support the ascription of bigger penile dimensions to people of the Black race.

I wouldn’t say there is a ‘possibility’ that it’s true, based on a population of Nigerians. We can say that ethnic differences may exist between Koreans and Nigerians, but to extrapolate that to all five races and say that racial differences exist and that it fits neatly into Rushton’s outdated 3-way racial model is incorrect. It wasn’t a  representative sample of Nigerians (and I obviously don’t have access to the methods of the other papers, I will update this in the future when I find more data), and the bigger sample of the two samples that I cited showed a smaller size.

 

Do racial differences in penis size exist? We can’t really come to a conclusion based on the data we currently have. Using “””data””” from the Penthouse webforum and a self-reported survey online is embarrassing and the data shouldn’t be used in the discussion of whether these differences exist. The only reliable data on Africans, as far as I know, is on Nigerians; the study with the higher n showed a smaller length. The data so far, shows that no difference exist exists (Veale et al, 2014: 983).

Stephen Jay Gould and Anti-Hereditarianism

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Stephen Jay Gould was one of the biggest opponents of hereditarianism, one of Rushton and Jensens’s biggest opponents. He is the author of The Mismeasure of Man, which is still given to college students to read as a “definitive refutation of The Bell Curve” and an all out attack on factor analysis, IQ testing and the whole hereditarian position at large. A passage from the very end of his book Full House perfectly explains his thought process on this matter:

“The most impressive contrast between natural evolution and cultural evolution lies embedded in the major fact of our history. We have no evidence that the modal form of human bodies or brains has changed at all in the past 100,000 years—a standard phenomenon of stasis for successful and widespread species, and not (as popularly misconceived) an odd exception to an expectation of continuous and progressive change. The Cro-Magnon people who painted the caves of the Lascaux and Altamira some fifteen thousand years ago are us—and one look at the incredible richness and beauty of this work convinces us, in the most immediate and visceral way, that Picasso held no edge in mental sophistication over these ancestors with identical brains. And yet, fifteen thousand years ago no human social grouping had produced anything that would conform with our standard definition of civilization. No society had yet invented agriculture; none had built permanent cities. Everything that we have accomplished in the unmeasurable geological moment of the last ten thousand years—from the origin of agriculture to the Sears building in Chicago, the entire panoply of human civilization for better or for worse—has been built upon the capacities of an unaltered brain. Clearly, cultural change can vastly outstrip the maximal rate of natural Darwinian evolution.” (Gould, 1996: 220)

He wrote Full House as a sequel of sorts to his book Wonderful Life: The Burgess Shale and the Nature of History (currently on the way to my home which I will read in a few days of getting it), where he argues that progress is not the driver to evolution and that complexity does not rule as bacteria rule the planet. He argues that we are not in the “Age of Mammals”, but the “Age of Bacteria”. But how could you argue that there was no change in humanity from our most recent ancestors to today?

Eldredge and Gould pioneered the theory of punctuated equilibria in 1972. The theory states that species lie in a state of stasis (that is, a period of inactivity or equilibrium) and there is little morphological change before there is a rapid burst of change, which perfectly explains why there are few transitional fossils to be found. Punctuated equilibria is the missing piece to Darwin’s theory of evolution. But what does it have to do wth the evolution of Man?

As you can see, Eldredge and Gould’s theory states that all species spend an extremely long time in stasis, and for any phenotypic change to be noticed in the fossil record, the rapid burst in change had to occur.

Quoting Gould on culture and evolution (1996, page 219-20):

But human cultural change is an entirely distinct process operating under radically different principals that do allow for the strong possibility of a driven trend for what we may legitamately call “progress” (at least in a technological sense, whether or not the changes ultimately do us any good in a practical or moral way). In this sense, I deeply regret that common usage refers to the history of our artifacts and social orginizations as “cultural evolution.” Using the same term—evolution—for both natural and cultural history obfuscates far more than it enlightens. Of course, some aspects of the two phenomena must be similar, for all processes of genealogicallt constrained historical change must share some features in common. But the differences far outweigh the similarities in this case. Unfortunately, when we speak of “cultural evolution,” we unwittingly imply that this process shares essential similarity with the phenomenon most widely described by the same name—natural, or Darwinian, change. The common designation of “evolution” then leads to one of the most frequent and portentious errors in our analysis of human life and history—the overly reductionist assumption that the Darwinian natural paradigm will fully encompass our social and technological history as well. I do wish that the term “cultural evolution” would drop from use. Why not speak of something more neutral and descriptive—“cultural change,” for example?

From the two passages I cited above, to his work on punctuated equilibria, I can definitely see how and why he would believe that there has been no relevant human evolution in the past 50,000 years. These two quotes, one from Stephen Jay Gould and the other from evolutionist Ernst Mayr show the “conventional wisdom” about human evolution:

There’a been no biological changes in humans in 40,000 or 50,000 years. Everything we call culture we’ve built with the same body and brain

—Stephen Jay Gould

Something must have happened to weaken the selective pressure drastically. We cannot escape the conclusion that man’s evolution towards manness suddenly came to a halt.

—Ernst Mayr

These quotes are from page 1 of The Ten Thousand Year explosion. Many great thinkers have suggested that human evolution has halted ever since the emergence of behavioral modernity, however, this couldn’t be further from the truth. I fully understand why such great evolutionists like Gould and Mayr believe that human evolution has halted and their arguments make complete sense based on the data (punctuated equilibria for one). But to any knowledgeable race-realist, they know that these claims are bunk and that human evolution has most definitely accelerated within the last 10,000 years (due to agriculture, the advent of farming) that made it possible for a bigger population and, along with it, a higher chance for high IQ alleles and other positive traits to spread throughout the population as it increased fitness in the environment.

HOWEVER, agriculture was good and bad for us. The good increased our population size that made it possible for high IQ alleles to spread throughout the population. The bad was along with an increase in population size, living in one spot with large groups of people upped the chances for disease acquisition, that of which are not found in hunter-gatherer populations (because they’re constantly moving, not staying in one place). According to John Hawks, our brain size has decreased, going from 1500 cc on average to 1350 cc on average, and the cause is, and this is hard to believe with the advent of agriculture (and thus, supposedly better nutrition) worse nutrition due to the advent of agriculture. Another reason I can posit is that due to more group behavior and social cohesion, we could work together with others and that, over time, would shrink our brains since we wouldn’t have to “do all the thinking”, a type of “self-domestication”, if you will.

The denial of any human change over the past 50,000 years is clearly ridiculous, however it is grounded in solid science. But with the advent of The Ten Thousand Year Explosion by Cochran and Harpending, they blasted all of the misconceptions away about no genetic change in humanity over the past 50,000 years. But, to the dismay of those who believe in “progressive evolution”, the same agriculture that was responsible for this boom—this explosion—over the past ten thousand years is also the cause of our decreasing brain size and stature. I’ve documented the change of erectus or habilis into floresiensis, this is proof enough that evolution can “work backward” (whatever that means) and have an organism become “less complex” (going back to left and right walls of complexity, which I just wrote on last night). Floresiensis is the perfect example that an organism can become less complex than a predecessor and the cause, in this context, is due to less energy on the island which led to a decrease in caloric consumption and along with it a decrease in brain size since that was what was best for that environment (due to less caloric energy being available).

While Gould makes a compelling argument in arguing against the explosion of Man in the past 50,000 years, modern data tells us otherwise. This explosion was due, in part, to agriculture which led to more social cohesion (both of those variables are also leading to a decrease in brain size). With the understanding of Eldredge and Gould’s punctuated equilibria theory, you can then see how and why Gould denied the genetic change in anatomically modern humans over the last 50,000 years. He, however, is wrong here.

I fully agree with Gould that cultural change can outstrip Darwinian evolution—he is right there. But, to make the leap and then say that there is no basis for genetic change in AMH (anatomically modern humans) is clearly wrong. I know that Gould was driven by his politics, partly, to deny any change in human nature and genetics in the past 50,000 years. Though, I don’t care about that. I care about looking at one’s perspective through a scientific lens. While Gould is wrong on his views of hereditarianism, he is 100 percent correct on “progressive” evolution and that there is no so-called “drive to complexity”. It’s his views on human evolution as a whole that are wrong. We know that faster evolution gives rise to more racial differences, and, obviously, more “differences” can either be “good” or “bad” depending on the environmental context. In my tirades over the past 6 weeks on the non-progressiveness and non-linearity of evolution, I’ve shown that these differences can either go to the “left wall” or “right wall” of complexity.

To deny the speed of evolution ever since modern behavior, and even the agricultural revolution is wrong. Too much evidence has piled up for that position. I do, after reading a lot of Gould’s work recently, understand how and where he came from with that argument, all though he was clearly wrong. Culture is learned—not biologically inherited. The cultural norms we know well are learned behaviors.

Finally, and what it seems Gould didn’t realize, is that there is gene-culture coevolution. Learned social information is central to our adaptations as humans. New cultural tendencies may force a novel and new evolutionary selection pressure that may incur new phenotypic changes. In this sense, genes and culture simultaneously evolve side-by-side with each other. Again, stressing that there is no “unilateral direction” in which these changes go, they just occur based on new environmental pressures. Thusly, to say that there is any “progress” or any inherent “drive” in evolution makes no sense. Due to which cultures we “inherit” that will drive which changes occur in that population but not another, they’d be different (as we know all genetically isolated humans are), but none would be “better” than another since they have incurred new traits to better survive in that environment; each different culture will further gain a different phenotype due to the differing culture which puts a differing selective pressure on that population.

The notion of no change in humans over the last 50,000 years is wrong. It has been driven by the rise in agriculture (giving us both positive and negative traits) along with each culture that each population adopted due to the differing selection pressures and environments over the course of their evolution genetically isolated from every other human culture. These differing cultural tendencies also gave rise to slightly faster evolution and different and novel environments in comparison to other populations. With these variables working in harmony with each other, these then accelerated human evolution (for better or worse). That same advent of behavioral modernity 50,000 years ago gave rise to the Out of Africa event. Humans then spread across the planet. In time, after being differing “founding populations” for the current races/ethnies today, differing cultures were adopted due to the differing evolutionary pressures. This is the main reason why genetically isolated human populations show such stark differences between them: Because evolution has sped up since the advent of behavioral modernity, agriculture and the adoption of culture by humans that have all contributed to making Man so different compared to the rest of the Animal Kingdom.