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Find the Genes: Testosterone Version

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Testosterone has a similar heritability to IQ (between .4 and .6; Harris, Vernon, and Boomsma, 1998Travison et al, 2014). To most, this would imply a significant effect of genes on the production of testosterone and therefore we should find a lot of SNPs that affect the production of testosterone. However, testosterone production is much more complicated than that. In this article, I will talk about testosterone production and discuss two studies which purport to show a few SNPs associated with testosterone. Now, this doesn’t mean that the SNPs cause high/low testosterone, just that they were associated. I will then speak briefly on the ‘IQ SNPs’ and compare it to ‘testosterone SNPs’.

Testosterone SNPs?

Complex traits are ‘controlled’ by many genes and environmental factors (Garland Jr., Zhao, and Saltzman, 2016). Testosterone is a complex trait, so along with the heritability of testosterone being .4 to .6, there must be many genes of small effect that influence testosterone, just like they supposedly do for IQ. This is obviously wrong for testosterone, which I will explain below.

Back in 2011 it was reported that genetic markers were discovered ‘for’ testosterone, estrogen, and SHGB production, while showing that genetic variants in the SHGB locus, located on the X chromosome, were associated with substantial testosterone variation and increased the risk of low testosterone (important to keep in mind) (Ohlsson et al, 2011). The study was done since low testosterone is linked to numerous maladies. 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 this is a very important study to understand the genetic determinants of low serum testosterone.

Ohlsson et al (2011) conducted a meta-analysis of GWASs, using a sample of 14,429 ‘Caucasian’ men. To be brief, they discovered two SNPs associated with testosterone by performing a GWAS of serum testosterone concentrations on 2 million SNPs on over 8,000 ‘Caucasians’. The strongest associated SNP discovered was rs12150660 was associated with low testosterone in this analysis, as well as in a study of Han Chinese, but it is rare along with rs5934505 being associated with an increased risk of low testosterone(Chen et al, 2016). Chen et al (2016) also caution that their results need replication (but I will show that it is meaningless due to how testosterone is produced in the body).

Ohlsson et al (2011) also found the same associations with the same two SNPs, along with rs6258 which affect how testosterone binds to SHGB. Ohlsson et al (2011) also validated their results: “To validate the independence of these two SNPs, conditional meta-analysis of the discovery cohorts including both rs12150660 and rs6258 in an additive genetic linear model adjusted for covariates was calculated.” Both SNPs were independently associated with low serum testosterone in men (less than 300ng/dl which is in the lower range of the new testosterone guidelines that just went into effect back in July). Men who had 3 or more of these SNPs were 6.5 times more likely to have lower testosterone.

Ohlsson et al (2011) conclude that they discovered genetic variants in the SHGB locus and X chromosome that significantly affect serum testosterone production in males (noting that it’s only on ‘Caucasians’ so this cannot be extrapolated to other races). It’s worth noting that, as can be seen, these SNPs are not really associated with variation in the normal range, but near the lower end of the normal range in which people would then need to seek medical help for a possible condition they may have.

In infant males, no SNPs were significantly associated with salivary testosterone levels, and the same was seen for infant females. Individual variation in salivary testosterone levels during mini-puberty (Kurtoglu and Bastug, 2014) were explained by environmental factors, not SNPs (Xia et al, 2014). They also replicated Carmaschi et al (2010) who also showed that environmental factors influence testosterone more than genetic factors in infancy. There is a direct correlation between salivary testosterone levels and free serum testosterone (Wang et al, 1981; Johnson, Joplin, and Burin, 1987), so free serum testosterone was indirectly tested.

This is interesting because, as I’ve noted here numerous times, testosterone is indirectly controlled by DNA, and it can be raised or lowered due to numerous environmental variables (Mazur and Booth, 1998; Mazur, 2016), such as  marriage (Gray et al, 2002Burnham et al, 2003Gray, 2011Pollet, Cobey, and van der Meij, 2013Farrelly et al, 2015;  Holmboe et al, 2017), having children (Gray et al, 2002Gray et al, 2006Gettler et al, 2011); to obesity (Palmer et al, 2012Mazur et al, 2013Fui, Dupuis, and Grossman, 2014Jayaraman, Lent-Schochet, and Pike, 2014Saxbe et al, 2017) smoking is not clearly related to testosterone (Zhao et al, 2016), and high-carb diets decrease testosterone (Silva, 2014). Though, most testosterone decline can be ameliorated with environmental interventions (Shi et al, 2013), it’s not a foregone conclusion that testosterone will sharply decrease around age 25-30.

Studies on ‘testosterone genes’ only show associations, not causes, genes don’t directly cause testosterone production, it is indirectly controlled by DNA, as I will explain below. These studies on the numerous environmental variables that decrease testosterone is proof enough of the huge effects of environment on testosterone production and synthesis.

How testosterone is produced in the body

There are five simple steps to testosterone production: 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) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.

Cells in the testes enzymatically convert cholesterol into the steroid hormone testosterone. Quoting Saladin (2010: 137):

But to make it [testosterone], a cell of the testis takes in cholesterol and enzymatically converts it to testosterone. This can occur only if the genes for the enzymes are active. Yet a further implication of this is that genes may greatly affect such complex outcomes as behavior, since testosterone strongly influences such behaviors as aggression and sex drive. [RR: Most may know that I strongly disagree with the fact that testosterone *causes* aggression, see Archer, Graham-Kevan and Davies, 2005.] In short, DNA codes only for RNA and protein synthesis, yet it indirectly controls the synthesis of a much wider range of substances concerned with all aspects of anatomy, physiology, and behavior.

testosterone production

 

(Figure from Saladin (2010: 137; Anatomy and Physiology: The Unity of Form and Function)

Genes only code for RNA and protein synthesis, and thusly, genes do not *cause* testosterone production. This is a misconception most people have; if it’s a human trait, then it must be controlled by genes, ultimately, not proximately as can be seen, and is already known in biology. Genes, on their own, are not causes but passive templates (Noble, 2008; Noble, 2011Krimsky, 2013; Noble, 2013; Also read Exploring Genetic Causation in Biology). This is something that people need to understand; genes on their own do nothing until they are activated by the system. 

What does this have to do with ‘IQ genes’?

My logic here is very simple: 1) Testosterone has the same heritability range as IQ. 2) One would assume—like is done with IQ—that since testosterone is a complex trait that it must be controlled by ‘many genes of small effect’. 3) Therefore, since I showed that there are no ‘genes for’ testosterone and only ‘associations’ (which could most probably be mediated by environmental interventions) with low testosterone, may the same hold true for ‘IQ genes/SNPS’? These testosterone SNPs I talked about from Ohlsson et al (2011) were associated with low testosterone. These ‘IQ SNP’ studies (Davies et al, 2017; Hill et al, 2017; Savage et al, 2017) are the same—except we have an actual idea of how testosterone is produced in the body, we know that DNA is indirectly controlling its production, and, most importantly, there is/are no ‘gene[s] for’ testosterone.

Conclusion

Testosterone has the same heritability range as IQ, is a complex trait like IQ, but, unlike how IQ is purported to be, it [testosterone] is not controlled by genes; only indirectly. My reasoning for using this example is simple: something has a moderate to high heritability, and so most would assume that ‘numerous genes of small effect’ would have an influence on testosterone production. This, as I have shown, is false. It’s also important to note that Ohlsson et al (2011) showed associated SNPs in regards to low testosterone—not testosterone levels in the normal range. Of course, only when physiological values are outside of the normal  range will we notice any difference between men, and only then will we find—however small—genetic differences between men with normal and low levels of testosterone (I wouldn’t be surprised if lifestyle factors explained the lower testosterone, but we’ll never know that in regards to this study).

Testosterone production is a real, measurable physiologic process, as is the hormone itself; which is not unlike the so-called physiologic process that ‘g’ is supposed to be, which does not mimic any known physiologic process in the body, which is covered with unscientific metaphors like ‘power’ and ‘energy’ and so on. This example, in my opinion, is important for this debate. Sure, Ohlsson et al (2011) found a few SNPs associated with low testosterone. That’s besides the point. They are only associated with low testosterone; they do not cause low testosterone. So, I assert, these so-called associated SNPs do not cause differences in IQ test scores; just because they’re ‘associated’ doesn’t mean they ’cause’ the differences in the trait in question. (See Noble, 2008; Noble, 2011Krimsky, 2013; Noble, 2013.) The testosterone analogy that I made here buttresses my point due to the similarities (it is a complex trait with high heritability) with IQ.

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

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

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

Some interesting articles to read:

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

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

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

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

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

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

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

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

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

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

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

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

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

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