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It Makes Logical Sense for Santa Claus to Be a White Man
1100 words
Of course, with Christmas just around the corner, it is getting attacked like it does every year. The song ‘White Christmas‘ got attacked a few years back (a personal favorite of mine during the Holiday season). I recall the attacks on the song a few years back, I used to live in the NYC metro area and I remember very clearly that the song would get strongly attacked by ‘PoCs’ because it was ‘racist’ because it was talking about a ‘white Christmas’. Well, there has been even more crazy attacks against Christmas and this time, it’s against Santa!
This attack on ol’ Saint Nick leads to him having homosexual relations with a black man, which brings me to the point of this article: Santa is being attacked now for being white and it’s clear that people don’t know a thing about skin color and cold adaptations when it comes to skin color. Of course, people choose ideology before science. It’s ridiculous that I have to write an article like this but in #2017 I’m not too surprised.
A writer for Slate, Aisha Harris, published an article back in 2013 titled “Santa Claus Should Not Be a White Man Anymore: It’s time to give St. Nick his long overdue makeover“. In the article, Harris states that she saw two Santas while growing up: one black and the other white. Her father stated that Santa came in every color. She states that decades later America is “less and less white” and that “a melanin-deficient Santa remains the default in commercials, mall castings, and movies”. The author goes on to state that we should replace white Santa with a penguin, and call it penguin Claus. But penguins live in the South Pole, not the North Pole, so the author’s contention here, again, doesn’t make sense.
Megyn Kelly discussed this article where she brings up good points that just because white Santa makes you uncomfortable that doesn’t mean that it has to change. She’s right. Your feelings don’t really matter to a long-standing tradition; if you want to make Santa black, that’s your right to do so in your household just know that 1) it doesn’t make logical sense and 2) you can’t impose your will on what you believe Christmas should or should not be like based on your feelings. I know the world is beginning to work like that today (changes based on people’s feelings), but people need to really grow up and accept certain things, especially if these things are sound and logical.
Talking about illogical statements, Andy Ostroy in HuffPo (low-hanging fruit, I know) writes an article in response to Megyn’s small tirade and states: “Yes it does, Megyn. Just because white people have concluded that Santa is white doesn’t make it right, a fact or a status that’s immune from change. It doesn’t matter what he’s ‘always been.’ I’m sure prior to 1865 there were a lot of white folks who said about slaves, “but they’ve always been slaves!”” Here’s another guy who doesn’t logic. Sure, it ‘may not matter what he’s ‘always been”, howeber if you’re looking for logical consistency with what we know about human skin variation then you will see that, even though ‘white people have concluded that Santa is white’ literally makes logical sense due to how human skin variation has evolved. We have scientific evidence for that, as you say in your piece in regard to one of Megyn’s contributors saying that it wouldn’t work because penguins live in the South Pole.
So, sorry Andy Ostroy, but Santa Claus is white.
However, you have articles like this one from The Atlantic titled “Megyn Kelly Assures Everyone That Santa Is White Even Though Santa Does Not Exist“, well I’m here to tell you that I assure everyone that Santa is white even though he doesn’t exist because logical deductions can be made based on where he lives.
This article talks about where to find black Santas that are ‘peppered’ all over the country (do you think the author of this article realizes what he wrote there?). Even former NBA all-star Baron Davis states that “his eyes see no color”. A man was teaching that “Santa comes in all colors“. People need to be logical when talking about skin color and Santa Claus, because by making ol’ St. Nick have dark skin, they’re really showing absolutely no logical thought at all.
In my article The Evolution of Human Skin Variation, I discussed how and why those people who migrated out of Africa evolved lighter skin due to migrating into high latitudes: vitamin D production. People with lighter skin can synthesize the steroid whereas people with darker skin, for instance, get diseases like rickets from not having much vitamin D. Though, logical thought such as this escapes people when they assert that Santa should be black or a ‘PoC’, they show that they do not have any knowledge of latitude, UV rays and skin color which evolves due to the intensity of UV rays.
Santa is based on St. Nicholas, a man who lived during the third century from the village Patara, which is now modern-day Turkey. This is the basis for the Santa Claus we all know and love today, and he was a white man. Santa Claus has his origins being brought to the New World by the first European settlers. Others have claimed that Santa borrows ideas from the Germanic god Wodan and other Pagan figures. Whatever the case may be, we have a few lines of evidence that he is white: 1) the man he was based off was European; 2) he was based on European legends and gods; and perhaps most importantly, 3) he lives at the damn North Pole where it makes sense to be white and have light skin to better produce vitamin D! This attack on Santa being white literally makes no sense at all.
Santa being white is logical, if a human lives at the North Pole for an extended amount of time, he will definitely be a white man due to how skin evolves in those latitudes. If you want to create a black Santa, that’s you’re right to do so. People really should stop letting their shitty ideologies permeate into everything we as a society do in America. The people who push a black Santa should know that if this version of Santa lives at the North Pole he’d quickly die due to lack of vitamin D production. Can’t let logic get in the way of a feel-good story though! Logic and reason is a white male construct anyway!
Rebutting Ross et al (1986) on Testosterone
1300 words
Ross et al (1986) is one of the most oft-cited papers that HBDers use to attempt to show that blacks have higher levels of testosterone than whites, which then—supposedly—goes on to explain higher rates of crime, aggression, and prostate cancer. However, people 1) say this only from reading the abstract (and not reading the full paper) and 2) even if they could read the paper they would not know where the flaws were to point them out and discredit the study based on flawed methodology. I see this study getting cited every now-and-then and I’m sick of seeing it.
Ross et al (1986: 45) state that they “recently reviewed the evidence that endogenous levels of certain steroid and polypeptide hormones are causally related to a group of human cancers, including cancer of the prostate gland.” I’ve shown how even injecting a man with exogenous testosterone does not worsen his prostate cancer (Eisenberg et al, 2015; Boyle et al, 2016) and testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). So this has been falsified. Even if blacks had the testosterone levels that they claimed it still would not cause higher rates of PCa (prostate cancer) incidence.
They solicited study participants from two colleges around the Los Angeles metro area. The two universities they got their sample from were the University of Southern California and California State University of Los Angeles. They recruited individuals through postings on the school bulletin board in in the school newspaper. They got 50 blacks and 50 whites. They then write something that’s troubling to me: “A convenient time for blood collection was arranged, and students were met by a nurse epidemiologist (R. H.) at either the Student Health Center or another mutually convenient location” (Ross et al, 1986: 45). This is dumb. The students were assayed at all times between 10 am and 3 pm; testosterone levels are highest at 8 am though one study on older men shows that assaying between 8 am and 2 pm doesn’t matter (Crawford et al, 2015). However, for the purposes of discussing this paper this is irrelevant.
Table 1 from Ross et al (1986) tells us a lot about the flaws in the study—most importantly, the assay times. A majority were assayed between 10 am and 2 pm—which would depress testosterone though people assayed nearer to 10 am would have higher levels than people assayed nearer to 2 pm. Alcohol consumption only decreases testosterone while drunk, and a majority of the cohort did not consume alcohol within 12 hours of being assayed.
They come to the conclusion that the mean total testosterone level was 19 percent higher than whites whereas free testosterone was 21 percent higher. In regard to the assay collection times, Ross et al (1986: 47) write:
There was a negative correlation between time of sampling (No. of min elapsed since 0600 hr) and testosterone levels for whites (r=-O.4I) but not for blacks (r = -0.08). Adjustment for this variable caused a small reduction in geometric mean differences in levels of testosterone and free testosterone between blacks and whites. After simultaneous adjustment by analysis of covariance for time of sampling and age, weight, alcohol use, smoking, and use of prescription drugs, there
remained a 15% difference in total testosterone levels and a 13% difference in free testosterone levels between blacks and whites.
Even though they ‘adjusted for this variable’, it’s still a huge confound. Testosterone assays must be taken nearer to 8 am; the fact that people were assayed all over the place in the span of a 5 hour time period while testosterone levels decrease throughout the day is a huge red flag.
They then say that they are “uncertain why young black men have higher levels of circulating testosterone than white men“, though small sample sizes, a large range of variation in assay time, and a nonrepresentative sample is why. Other, more robust, analyses show a smaller ‘gap’, about 2.5 to 4.9 percent, favoring blacks (Richard et al, 2014). All in all, this study has huge flaws and should not be pointed to—especially today in 2017—because much larger analyses with much better methodologies have been carried out and some studies show no difference while others show a small difference favoring blacks but that still would not explain higher rates of testosterone, aggression and crime.
Ross et al (1986) is used by hereditarians such as Lynn (1990), Rushton (1997) and Hart (2007). Lynn (1990) states that these large testosterone differences discovered by Ross et al (1986) lend credence to Rushton’s r/K selection theory in which blacks have more children than whites who have more children than East Asians. Evidence for this assertion, states Lynn (1990) is the fact that blacks have higher rates of prostate cancer than whites who have higher levels of testosterone than East Asians, however this has been disproven by ethnicmuse.
Rushton (1997: 170) states that blacks had 19 percent higher levels of testosterone citing Ross et al (1986), however, Rushton didn’t cite the adjusted level which ended up being 15 percent, and, again, doesn’t mean anything to their hypothesis.
And Hart (2007) yet still repeats the same old stuff that “these differences in sexual behavior may be a consequence of the fact that blacks, on average, have higher levels of testosterone than whites“. These three researchers, clearly, are citing this study uncritically because it fits with their ‘racial hierarchy’. In fact, Rushton (1999) asked if testosterone was a ‘master switch’. In this paper, he cites Ellis and Nyborg (1992) who find that blacks had 3 percent higher levels of testosterone than whites. They gave the following values:
For the purposes of Rushton’s interpretation, writes Fish (2013), “These uncorrected figures are, of course, not consistent with their racial r- and K-continuum.” This, of course, is a big deal. Rushton cites this study as if it lends credence to his claims but it actually found the same result as Richard et al (2014). Thirty years after Ross et al (1986) we have numerous other studies showing a small gap between the races or no gap at all. We have numerous other studies showing that testosterone does not cause aggression, crime or violent behavior. However, people will still point to the abstract of Ross et al (1986) and think that they have proven that blacks have higher levels of testosterone than whites which proves how and why they have higher levels of testosterone, commit more crime and are all around more violent.
Though, as I have written about before, what Ross et al (1986) set out find the answer for (testosterone influencing higher levels of prostate cancer) can most definitely be explained by diet and lack of certain vitamins such as vitamin D, since low levels of this steroid hormone (it’s not a vitamin) cause prostate cancer (Schwartz and Hulka, 1990; Zhao and Feldman, 2001; Khan and Partin, 2004; Garland et al, 2006). Diet can explain a lot of the variation, as I have argued in the past.
In sum, Ross et al (1986) is the only study that I’ve found on racial testosterone differences that shows that extreme directionality favoring blacks over whites. This should set off some alarms in some people’s heads. People—psychologists included—need to learn about these hormones, how they’re produced in the body, and what they’re used for. Hormones don’t cause behavior, hormones influence behavior.
This fear of testosterone is largely overblown. We need testosterone for proper normal functioning. We need testosterone to be socially dominant; if you have lower levels you’ll be less socially dominant. This fear of testosterone—especially when it comes to race and it’s so-called causes—is largely pushed by Lynn, Rushton, Hart, and Ellis. I have spent a lot of time and thousands of words showing that they are wrong and testosterone is not a hormone to fear. It does not cause crime. It does not cause aggression. It does not cause prostate cancer. I’ve rebutted quite a few hereditarians on testosterone as well as testosterone and race, and if I come across more I will rebut them as well.
More r/K Selection Theory Rebuttals
2000 words
I was alerted to a response to my article r/K Selection Theory Rebuttals on Twitter. I enjoy when people write responses to my pieces as I can better build my arguments. It’s also fun defending what I wrote.
This Pastebin is where the response is. He states that he disagrees with AC (Anonymous Conservative) on two things: calling them liberals when he would call then progressives and his clear conservative bias.
First it refers to a criticism of Ruston’s application of r/K to humans:
https://notpoliticallycorrect.me/2017/06/24/rk-selection-theory-a-response-to rushton/
This article applies r/K selection to differences between races, I don’t see how this is relevant. AC never discusses race and I’m only interested in how r/K selection applies to individuals within a civilization too.
It is very apt when rebutting AC’s ‘theory’. Human races are not local populations therefore it doesn’t apply to human races. To then bring this wrong theory to individual differences is stupid. Hell, I agree more with Rushton’s application than AC’s application and that’s saying something. The point of bringing up Rushton’s r/K theory is that he was the one who repopularized the theory and you have to give credit where it is due (I’m certain he heard of r/K from Rushton; the fact that he doesn’t give him credit there is dishonest, but AC is a dishonest guy so this is no surprise to me).
r/K selection applies to almost all life forms, next to other selection mechanisms. So it goes much deeper than the specific situation a specific race may have lived in. Even if people in races now commonly express more r-selected or K-selected behavior, I’d expect that to change if their children grew up in a different environment.
You only say that because organisms have offspring and at different rates. I won’t even go through the different cites that show that r/K theory is bunk, but I will cite one that shows that it’s been dead for years. Reznick et al, (2002: 1518) write: “The distinguishing feature of the r- and K-selection paradigm was the focus on density-dependent selection as the important agent of selection on organisms’ life histories. This paradigm was challenged as it became clear that other factors, such as age-specific mortality, could provide a more mechanistic causative link between an environment and an optimal life history (Wilbur et al. 1974, Stearns 1976, 1977). The r- and K-selection paradigm was replaced by new paradigm that focused on age-specific mortality (Stearns 1976, Charlesworth 1980).” This is simple. Age-specific mortality replaced r/K theory. People like AC attempt to ‘show’ their ‘hypothesis’ is true. They notice something in this snapshot in time then say oh this this and that make sense therefore this! It doesn’t work like that.
On his point that ‘he’d expect that to change if their children grew up in a different environment’, to say that one race is ‘r’ or ‘K’ over another, you must study the population in question in the location where the adaptations were hypothesized to have occurred (Anderson, 1991).
RR: “It is erroneously assumed that living in colder temperatures is somehow ‘harder’ than it is in Africa”
Yes, there is much less biomass available in colder temperatures. Of course Africans would still compete with each other for resources. The idea is also that there’s more requirement to think ahead, in order to prepare for the winter. Requiring more deferral of gratification.
The idea is dumb. Africa is harsher than Eurasia (Dobzhansky, 1950: 221). Did people in Africa not have to plan ahead? This is the same old rebutted cold winter garbage in terms of ‘selection for higher IQ;.
The article generally asserts that r/K selection is a simple model:
RR: “One of the main reasons that Rushton’s r/K continuum gets pushed is because it’s a ‘simple model’ that so ‘parsimoniously’ explains racial differences … But ecological systems are never simple”:
Where was an implication that any ecological system is simple? I’d say the tropics are way more complicated than cold area’s. The relevant aspect here is that a cold area is more difficult to live in, has less resources and thus supports fewer individuals. Which is a K-selected pressure.
It is a simple model. “Simple models will be successful only if their simplifying assumptions either match reality or are unimportant” (Anderson, 1991: 57). This does neither. It is surely not easy to live in the tropics. This canard that those in Africa had an easy life in comparison to the people who migrated out of Africa doesn’t make any sense. It’s like people think that food just dropped on their laps from the trees, they didn’t have to deal with predators or heat, etc. It’s an extremely simple model which is why it doesn’t work. Africans are ‘K-selected’ if Rushton is to be believed, not r-selected (Anderson, 1991).
AC’s book is for the public, not to be the bleeding edge of science. Most people have no idea about these theories. I think it would greatly improve their understanding of reality if they knew about it, it did mine. This seems like the situation with Newton’s theory of gravity. It’s been proven wrong, but we still use it when useful.
I get that, but his premises are wrong which means his theory is false. What ‘reality’? It’s just stories, fables. Whatever sounds good to AC, whatever he thinks will buttress his theory he’ll write. Anything about the ‘rabbits’ or ‘wolves’ (so-called r- and K-selected organisms respectively). r/K has been proven wrong and it’s still not useful so we should not use it.
RR: ‘So “the actual adaptation they have” is to “wear thick clothing“? This is bullshit and you know it’
No it’s not. The clothing is far thicker and thus harder to make with a higher required investment. It requires more quality of the individuals. The writer assumes a binary difference here, where none was asserted. Of course these things are on a spectrum.
Yes it is. Sorry, you didn’t understand what I meant here. The actual adaptation is not ‘to wear thick clothing’. What is ‘more quality’, is that a scientific term? What does that even mean?
RR: “The preparation does work.” (Preparation of anti-malarial remedies as seen in Wilcox and Bodecker, 2004)
Maybe it helps, much of traditional remedy use is based in tradition and superstition. Europeans where slaughtered by all kinds of diseases. It probably depends on the situation. If you can find a cure for the disease, then maybe it is a K-selected pressure.
It’s irrelevant that ‘much of the traditional remedy use is based in tradition and superstition‘, because these remedies are proven to work (Wilcox and Bodecker, 2004). “If you can find a cure for disease, then maybe it is a K-selected pressure“, you’re clueless and don’t know what you’re talking about.
RR: “Here is what people like Samuel Skinner and AC don’t get: r/K selection theory WAS discarded; it is no longer in use. Age-specific mortality better explains these trends than r/K selection”
But age-specific mortality doesn’t apply to humans and doesn’t explain differences between individuals within a species or population.
Are you saying that we can’t apply this theory to humans at all?
Yes it does apply to humans. Why talk about something when you don’t know about it? Should I care that it doesn’t explain differences between individuals within a species or population? Not everything needs to be some grand, overarching theory to explain everything so perfectly.
RR: “We found that high K scores were related to earlier sexual debut and unrelated to either pubertal onset or number of sexual partners.”
In humans that correlation is broken because of advanced society. However, we can still find that correlation in progressive or conservative politics.
Yet Rushton et al assert that Africans are r, for instance, and have more children but as you can see from Copping, Campbell and Muncer, (2014), earlier sexual debuts were seen in the so-called K dimension, completely against Rushtonian r/K theory and against whatever theory AC cooked up in his head.
There are several links to scientific papers, several of which are no longer working, but fails to summarize how they support his position.
They don’t work because sci-hub is down. I need to fix the broken links and I did summarize how they support me which is why I did “claim then (citation)”.
RR: “Individuals WITHIN A SPECIES are not R OR K”
Since environments can change, why would species not be able to adapt to the new situation?
That’s not even what the original theory spoke about. If the liberals environment changed, would they become K (according to AC)? You’re completely missing the r/K dynamic.
A Jelly fish has several reproductive strategies available and chooses based on available resources.
Humans are much more complicated, but we could still have that ability.
This doesn’t mean that r/K selection has any utility.
RR: “Something AC doesn’t get is that using the discredited r/K continuum, conservatives would be r”
I don’t get that either.
Because the continuum comes from Pianka (1970) and Rushton adapted it to show that lower IQ peoples who had more children were r-selected. Therefore, if this did apply to individuals within the human species then conservatives would be r while liberals would be K (they have fewer children and higher IQs).
RR: “women who reported being religious stated that having children was more important to them”
And are in favor of investing in those children through their mother staying home to take care of them. Where progressives are more likely to be in favor of the mother working and putting the children in day-care. Progressives are also in favor of birth control and abortion. Allowing them to maintain the r-selected sexual life style, without having the burden of a child. r/K selection is about the underlying psychology, not surface level attributes like total number of children.
Liberals still have fewer children than conservatives who have more. What you’re saying is largely irrelevant. “r-selected sexual lifestyle”, this is dumb. r/K selection is predicated on number of children which conceived, supposedly, differs on the basis of differential psychology, supposedly, between two human groups. It doesn’t, it’s wrong.
“I’ve already covered that libs are more intelligent than cons (Kanazawa, 2010; Kanazawa, 2014), and that conservative countries have lower IQs”
I don’t think we should expect a correlation between IQ and r or K in modern human societies. What happens is that high IQ people raise their children in abundance, which makes them more likely to be r-selected. Availability of resources is a trigger for r-selected psychology.
Riiiiight. But you would expect a correlation between other so-called r/K measures in modern societies? You don’t even make sense.
“Conservatives are more likely to be religious”
Yes because religions like Christianity are viewed as tradition. And progressives oppose tradition where conservatives favor it.
Right, and they have more children than liberals, which is r-selected behavior (supposedly).
This guy tried, but clearly, this wasn’t good enough. r/K is dead when speaking about race and the differences between human individuals. For anyone who believes AC’s bullshit, where did liberals and conservatives evolve these different behaviors? Are they local populations? People like AC ignoring the continuum by Pianka, yet use that same hierarchy are dishonest. They’re using a discredited continuum and attempt to prove their political biases. “The other team has X, Y, and Z bad while we have A, B, and C good! The other side does X and Y while we do A and B, therefore, we are better!” AC has a huge bias; he will never admit he’s wrong because he has a book to sell that pushes this discredited garbage. (Don’t worry, I’ll review it and pick it apart soon enough.)
To conclude, people really need to stop letting their biases get in the way of rational thought. If they did, they’d be able to look at these dumb theories for what they are: pseudoscience, cherry-picking and pigeon-holing the other group, the “enemy” with all of the bad qualities while their side has all of the good ones. However, as I’ve shown countless times, real life is completely different from the fantasy world AC and his followers live in.
Sexual Selection and Intelligence
By meLo, 1340 words
Introduction
Usually within the HBD community, discussions regarding the main mechanism(s) that drove the expressions of particular phenotypes is centered around natural selection or ecological(in the strictest, most traditional sense) factors. Sexual selection is unfairly sidelined, even though sex is the base of all multicellular evolution. The point of this article is to provide a logical argument for Sexual selections tremendous involvement, and to provide examples of how these pressures have shaped neolithic and modern Homo sapiens. I excluded Australoids but for good reason. Even though the population does have sexual selected traits, like blonde and culry hair, they are an incredibly diverse group and with the amount of pocket isolation I don’t think it’s fair without breaking this group into more categories. I kept this paper short, because it’s my first one and I wanted to use this as a “prototype” for future posts. Again all criticism is more than welcome because I myself am still learning about this topic.
First, it is important to note that traits which evolved from sexual selection are not the same thing as traits that serve reproductive purposes. Reproductive organs are usually the product of sexual selection, but sexual selection does not always act upon genitalia. Sexual selection favors any trait that allows an organism to attract the opposite mate more effectively, competitively or not.
The general trend
Before I explain the respective pressures and phenotypes between subpopulations of the neolithic, it is essential to begin with a summary of the temporal trend that persisted before the aforementioned groups. This begins with a breakdown of definitions and the repair of misconceptions. Human development is extremely complicated, so this explanation will have oversimplifications for the sake of efficiency. Any questions or discussions on the matter are more than welcome. If you don’t know anything about heterochronies I suggest you read this.
Paedomorphosis=/= Neoteny. Neoteny is a heterochronic process, paedomorphism is a type of heterochrony. One of the largest or most noticeable differences between Homo sapiens and Chimpanzees is the increase in paedomorphic and peramorphic traits of the former. All heterochronic mechanisms affect the developmental outcome of homo sapiens this is mostly to do with developmental trade offs and creates a mosaic pattern of our evolution. Humans have accelerated brain growth which reaches full size before most of the other limbs and organs are finished, even though this is achieved through peramorphic heterochronies it coincides with the deceleration of the body which actually produces a more paedomorphic appearance in the population. This acceleration ends(progenesis) and is subsequently followed by a strong deceleration(neoteny) of the skulls growth (Penin, 2002). Neoteny and acceleration define growth rate, but the actual duration of the growth period is hypermorphic, meaning the duration of Human growth is delayed or extended so that our legs and brains can continue to grow. Even though the brain is not paedomorphic its still enlarged to retain its childlike plasticity.These processes underlie the “direction” of our evolution, and while a lot of important traits are a result of peramorphic processes, it would be foolish to disregard the obviously paedomorphic traits we exhibit. It doesn’t take long to see how sexual selection can favor peramorphic or paedomorphic traits. Peramorphosis tends to create exaggerated features(think Irish Elk, Peacocks or the human brain) while paedomorphosis tends to appeal to sexual selection by producing “fragile” traits associated with infants of the species, in theory members of the opposite sex should associate these traits with “cuteness” and possibly even better parental skills.
Macro races
Most don’t realize, but all races have undergone sexual selection. Each race has its own unique combination of peramorphic and paedomorphic traits as well as superficial ones that don’t relate to heterochrony. I will briefly go over each race and describe the varying degrees of pressures and the resulting phenotypes.
Caucasoids
Caucasoids have the largest concentration of hypermorphic traits. They are the tallest race, and have the most color variation, this heavily implies sexual selection is involved. While height only has a small correlation with IQ, taller specimens will generally have larger brains, because they also have larger bodies. It also been documented that taller individuals tend to be seen as more attractive. Blue eyes are disproportionately present in the scientific community and they are a recessive trait, it’s speculative but very possible that blue eyes coincides with increased intelligence. Peter frost already did most of the work for me, you can read his piece on European sexual selection here. Mate competition becomes the obvious reason for these phenotypic expressions.
Negroids
Unfortunately there isn’t much data on penis size, as a result this description will be lackluster. Which is usually the go to trait that HBDers look for when defining the sexuality of Africans. Things like Breast and buttocks size are ill defined, and studies on them are rifled with misconceptions. What we do know though, is that blacks are around the same height as Europeans but the majority of groups tend to have smaller brain sizes. It is interesting to point out that Africans display more paedomorphic facial features(except for prognathism). This makes a lot of sense, Africans are more r selected than Caucasoids, so it is expected that they display more paedomorphic traits. Because of a lack of data, I can’t make a reasonable assessment on the pressures that could of caused these expressions, however I do not think it would be far fetched to assume that it is also mate competition.
Capoids/Pygmies
Pygmies, are a result of what Shea 1984 calls “rate hypomorphosis” Essentially it is a truncation of allometric scaling. Pygmies should therefore be one of the least intelligent and most r selected races. Their body and brain size decreased from the ancestral one, and they are almost entirely paedomorphic. More than likely their body size has to do with their adaptation to fewer resources. Capoids can confuse a lot of people. At first I thought they must be intelligent because of their paedomorphosis, but their brains are only a measly 1270cc and according to the Shea and Penin studies(cited earlier) a lot of traits considered to be paedomorphic(flat nose, reduced prognathism) are actually just the result of functional innovations and are independent of developmental growth. Specimen like Homo sapien Idaltu then begin to make more sense. The pressure involved here is more than likely an increased need of childcare(or at least a decrease in aggression) but not necessarily and increased need of Intellectual faculties.
Mongoloids
Along with pygmies they are the most Paedomorphic race, and one of the most r selected. East asians have proportionally short limbs, very baby like faces, and the largest brains of any race. More than likely this is due to shape retardation following neoteny(deceleration of growth). It is necessary to define why Capoids and Mongoloids share similar facial traits yet do not share the same body proportions or absolute brain size. In this situation it is reasonable to assume that both populations had similar pressures for childcare and decreased aggression the main difference is hypothesized to lie in the varying survival pressures each group faced, I believe the ecological factors in East asia were more cognitively demanding than in Southern Africa, not in the sense that Africa is an easier place to survive but that Eurasia had a higher demand for Neuroplasticity. This is for two main reasons 1) in a novel environment there is more that you are required to learn and 2) The founder effect makes recessive genes easier to be expressed.
In Summary
Intelligence can arise from a multitude of factors and no factor is completely necessary. Caucasoids seem to have developed their intellect from mate competition and K selection. Negroids are similar but to a lesser degree. Mongoloids seem to have evolved their cranial capacity for primarily docility and cooperation. All are forms of sexual selection, just for different preferences in attraction. Europeans and Africans tend to gravitate to more masculine features while Capoids, and Mongoloids are more for feminine ones.
Musings on Testosterone and Race
1500 words
People don’t understand the relationship between testosterone, aggression, and crime. People hear the sensational media stating that testosterone causes crime, aggression, and anger. However, I have written numerous articles on this blog on the true nature of testosterone, what it’s really needed for and why we need it in high amounts. I’ve mused a lot on this hormone, which is one of my favorites to discuss due to the numerous misconceptions surrounding it.
Which way does causation run in regard to prisoners and their testosterone level?: heightened testosterone > aggression > violence or aggression > heightened testosterone > dominance > possibility (not necessarily, as I have written myself in the past) of violence.
People may use animal studies in support of their contention that testosterone causes aggressive behavior. However, for reasons I have discussed in the past, animal models only show avenues for future research and do not necessarily mean that this is the case for humans (as Mazur, 2006 point out). I don’t use animal studies. They’re good for future research, but to use them as evidence for causation in humans doesn’t make sense.
People may cite Dabbs et al showing that the more violent prisoners had higher levels of testosterone and therefore conclude that higher levels of testosterone drive the violent crime that they commit, however it is much more nuanced than that.
Does being a violent criminal raise testosterone or are violent people more likely to have high testosterone? Dabbs never untangles this; they just showed a correlation, which is small as evidenced by my other citations.
Testosterone is, as evidenced by numerous studies, related to dominance and dominance contests, however, during these dominance contests “a killing is rarely the outcome of a violent dominance contest” (Mazur, 2006: 25). Therefore, this throws a wrench in the testosterone-causes-crime hypothesis.
Some individuals may state that these dominance contests then lead to violence, however, as Mazur (2006) puts it: “Heightened testosterone is not a direct cause of male violence.”
Other animals assert dominance violently but we, necessarily, do not.
Mazur (2006) states that dominance contests rarely escalate to murder. Mazur also states that dominance contests also lead to increased T for the winners and decreased T for the losers, and these contests also don’t necessarily lead to murder/violent behavior. There is a feedback loop with high T causing behavior and behavior causing high T (Mazur, 2006) while this feedback loop may lead to “lethal effects” (Mazur and Booth, 2008).
It’s worth noting that Mazur seems to advocate for ‘testosterone-depressing drugs’. He concludes:
There are strong linkages between macro-level culture and the physiology of
individuals. We may find solutions to some of our social problems by altering these linkage.
Macro-level culture being white culture, black culture, Asian culture, etc.
The physiological differences are due to the preparation for dominance contests. So, his hypothesis goes, the culture of dominance among young black men with no education is why their T is so high. That low education was also associated with low education lends credence to the claim that this is changeable.
However, in his newer article on education, low testosterone and blacks he advocates for more sensible solutions (attempting an environmental change). I don’t know about you but I have big problems with using FDA/Big Pharma drugs to ‘reduce societal problems’, and it seems that Mazur has changed his view there. Mazur (2016) writes:
If high T does facilitate the high violence rate among young black men, there would be a troubling policy question of what, if anything, to do about it. Any notion of a medical or pharmaceutical fix, rather like prescribing Ritalin for hyperactivity, would reek of race-based chemical castration and should be regarded as outside the pale. However, social interventions might be workable and ethically acceptable.
I have railed against measures like this in the past, since proposing measures to attempt to ‘decrease crime through supposedly decreasing one of the main “causes”‘ is very Brave New World-ish, and I am highly against those measures. Social interventions are, in my view, the more sensible measures to undertake.
In regard to low education and testosterone, this same relationship was noticed by Assari, Caldwell, and Zimmerman (2014) where they note that testosterone was not associated with aggression in men, but low education was, which Mazur (2016) replicates, showing that blacks of the same age group with more education had lower levels of testosterone when compared to age-matched blacks. Mazur (2016) cites one study in support for his contention that education can decrease aggressive behavior (Carre et al, 2014)
The correlation is there, I agree. let’s take the middle value of .11 between Archer, Graham-Kevan, and Davies, 2005 at .08; and Book, Starzyk, and Quinsey, 2001 .14. So testosterone explains 3 percent of the the relationship with aggression. Not high at all.
Great evidence against the testosterone-causes-aggressive-behavior hypothesis are data on the Yanomami. About 50 percent of Yanomami men meet their deaths by other Yanomami men. So the Yanomami must have testosterone levels through the roof, right? Wrong. De Lima et al (2015) write:
We observed that Yanomamis present lower levels of testosterone (414 ng/dL) in relation to other ethnic groups (502/512 ng/dL), but still within normal limits (350-1000 ng/dL).
(Note that these values for “normal limits” changed, going into effect at the end of July.)
The Yanomami with an extremely high murder rate with nowhere near a modern society have T levels on the lower end of our range. So….. The Yanomami example is direct evidence against the assertion of testosterone directly causing crime, as some people assert (it is even evidence against an indirect cause). The evidence of the Yanomami having testosterone levels near our lower range is direct evidence against the testosterone/crime hypothesis. Clearly, other variables drive the high violence rate in this society that are not testosterone. More interestingly, these people have had little contact with Western societies, and their T levels are still low compared to ours despite constantly being vigilant for threats from other Yanomami.
Most dominance contests do not end violently in the first-world, there is numerous evidence to attest to this fact. So with the low correlation between testosterone and aggression (Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005), along with dominance contests rarely ending in murder/violent crime, then there are way more factors influencing these phenomena.
So the feedback loop goes: Testosterone rises in expectation of a challenge which then, after the dominance contest (which doesn’t always necessarily lead to violence), it affects both individuals differently depending on whether or not they won or lost that dominance contest and these values then persist over time if the dominance contests continuously end up the same.
Let’s say, for argument’s sake, that testosterone is a large cause for aggressive behavior in lower-educated blacks, what should be done about it? Mazur cites evidence that behavioral interventions seem to work to decrease violent behavior during certain circumstances (Carre et al, 2014), so that is a good way to lower violence in populations that have low education.
So heightened testosterone does lead to dominance which then facilitates a dominance contest between two individuals which does not necessarily lead to crime and aggressive, violent behavior (this outcome is rare in dominance contests among “higher primates” [Mazur’s words]) so, therefore, while testosterone does facilitate dominance contests, it rarely leads to violence in our species. Therefore, testosterone does not cause aggressive behavior and crime, but it does cause dominance which, for the most part, do not always result in violent, aggressive, murderous behavior.
I’ve shown that Mazur replicated other analyses that show that testosterone and aggressive behavior are related to lower education. Testosterone wasn’t associated with aggressive behavior in Assari, Caldwell, and Zimmerman’s (2014) study, and, as Mazur (2016) replicates, low education was. So one way to end this relationship is to educate people, as shown by Carre et al (2014), and with this education, crime will begin to fall. Heightened testosterone is not a direct cause of male violence.
(Note: I also believe that other factors such as sleep and depressed nutrition play a factor in crime, as well as racial differences in it. See Birch, 1972; Liu et al, 2003; Liu et al, 2004; Walker et al, 2007; Galler et al, 2011, 2012a, 2012b; Spratt et al, 2012; Gesch, 2013; Kuratko et al, 2013; Waber et al, 2014; Raine et al, 2015; Thompson et al, 2017 for more information, I will cover this in the future. I’m of course not daft enough to believe that no genetic differences between individuals/populations are the cause of a lot of crime between them, however, as I have laid out the case in regard to testosterone and MAOA numerous times, these two explanations for both individual differences in crime as well as racial differences in crime leave a lot to be desired. Other genetic factors, of course, influence these differences, however, I am only worried about refuting the popular notions of ‘testosterone and MAOA, the ‘warrior gene” cause crime. The relationship is a lot more nuanced as I have provided mountains of evidence for.)
Comments on Batrinos (2012)
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Batrinos (2012) is a paper titled Testosterone and Aggressive Behavior in Man. Section 2 reviews studies on prisoners. Small ns, no controls, prison isn’t a natural environment. Similar data was reported, but it has the same problems as above. Studies of sexual offenders are contradictory, with blood T not being associated, then being associated with aggression. An investigation of veterans showed T to raise aggression, again, non-representative sample (and you also have to think of PTSD and other illnesses). Then the money quote:
It is of interest, however, that supraphysiological doses of testosterone in the order of 200 mg weekly (20), or even 600 mg weekly (21), which were administered to normal men had no effect on their aggression or anger levels.
Dominance is related to testosterone increases, and dominance can lead to aggressive behavior then to violent acts, but this is not always true. Mazur and Booth’s (1997) reciprocal model shows a feedback loop on dominance and testosterone:
Ehrenkranz et al. (1974) showed that socially dominant but unaggressive prisoners had relatively high T, not significantly different from the T levels of aggressive prisoners (who may have been dominant too). Nearly all primate studies that have been interpreted as linking T to aggression (Dixson 1980) may as easily be interpreted as liking T with dominance (Mazur 1976). Recent reviewers have questioned whether, among humans, T is related to aggressiveness per se (Archer 1991; Albert et al. 1994).
Testosterone and Dominance in Men
And:
Heightened testosterone is not a direct cause of male violence.
The Role of Testosterone in Male Dominance Contests that Turn Violent
(Much more on this paper soon.)
Small studies have shown that T increases during sports (duh because it’s competition) and that watching your favorite sports team win a game increases T (has been replicated).
Batrinos then cites a study talking about circadian rhythm and testosterone/aggression here:
Interestingly enough, Brown et al (2007) lends credence to my hypothesis that I have discussed in the past. Testosterone decreases at 8pm (most crime is comitted at 10 pm for adults) with increases in testosterone at night:
It is not surprising that T levels at 2000 h and 0800 h would be important for TS-IAB relationships because the 2000 h and 0800 h values represent the evening nadir and morning zenith.
But most crime is not comitted in the morning, for both adults and children (as seen below):
Now, anyone who has read my article on why testosterone doesn’t cause crime knows where I’m going with this:
Look at the times most crimes are committed then think about when T levels are highest (8 am).
Why Testosterone Does Not Cause Crime
This does seem to show a relationship with when most crimes are comitted, a sharp decrease in crime occurs as testosterone levels hit their highest in the day, which is evidence against the testosterone-causes-crime hypothesis.
In regard to the crime chart from the OJJDP, they write:
- 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.
Using what I gave, what do you draw from the line graph? It’s clear that, since testosterone is highest in the morning aand at its lowest at 8 pm (when most violent crime is being comitted) that testosterone is not directly related to crime, since, as evidenced by Brown et al (2007), testosterone levels are lowest at 8 am with a sharp rise as the night/ morning progresses. Looking at their testosterone chart for the hours between 8 pm and 8 am, testosterone did increase at 8pm and into the night. However, as testosterone levels continued increasing into the night, crime does not linearly increase with the rise in testosterone (see fig. 3 in Brown et al, 2007).
Now, finally, in regards to the claim about “locally produced testosterone”, it is true that the brain can produce testosterone de novo from cholesterol; but wait! Luteinizing hormone signaling in the neurons promotes the secretion and production of steroids (Liu et al, 2007), along with the de novo production of testosterone through cholesterol (literally the only way testosterone can be produced).
Good paper, shaky claims (the prisoner claims suck, circadian rhythm claims suck). The only novel thing in this paper is saying how the brain can produce testosterone de novo from cholesterol (though luteinizing hormones are still involved, see above cite). Injecting a man with supraphysiologic doses of testosterone does not increase aggression nor anger levels. It’s definitive that testosterone does not directly cause crime, as evidenced by the low correlation between testosterone and aggression. Numerous other studies (which I have reviewed in the past), however, show that aggression precedes the testosterone increase which is only seen in certain social situations. These specific situations, by themselves, drive the production of the hormone.
Race and Nutrition
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What we eat is important. What we eat can increase or decrease our lifespan. But do different races digest and metabolize different macro and micronutrients differently? On a racial level in terms of individual diet, would one individual benefit from adopting the diet of their ancestors over another diet? Many claims have been made like this in the past few years, such as Europeans evolving to eat plants and grains. This, some people would presume, implies that if you have a certain ancestry then you must eat a certain diet or take different steps in regard to nutrition. I will show this is wrong and that, at least in regard to health and nutrition, individual variation matters more than racial variation (don’t call Lewontin’s fallacy on me. This is not a fallacy).
Different genetically isolated breeding populations evolved eating different diets based on what they had in their environment. Over time, humans eventually developed agriculture and then changed the course of human evolution forever (Cochran and Harpending, 2009). This then leads to large changes in how our genes are expressed and how our microbiome metabolizes nutrients and food we ingest. The advent of farming was, obviously, pivotal to human evolution (Cochran and Harpending, 2009). This then lead to heritable changes in the genome brought on by new foods the farmers ate. This also started the environmental mismatches we now have in our modern world, which is the cause for rising obesity rates and a large part of the cause of so-called diseases of civilization (for a discussion of these matters, see Taubes, 2008, chapter 5; see also page 8 in this summary of his book on diseases of civilization and also see Burkitt, 1973; Cordain, Eades, and Eades, 2003; Sharma and Majumdar, 2009; Sikter, Rihmer, and Guevara, 2017. For an outstanding review on the subject, read Daniel Lieberman’s 2013 book The Story of the Human Body: Evolution, Health, and Disease for in-depth discussions on this point and more in regard to nutrition and our evolutionary history).
Studies come out all the time saying that X population evolved eating Y food therefore Z. Then, people not privy to nutrition science, jump to large sweeping conclusions (mostly laymen and journalists, who are also laymen). These assumptions imply that people’s metabolic systems aren’t, first and foremost, based on an individual level with individual variation in physiologic and metabolic traits. This, I will show, is the reason why these studies don’t mean you should change your diet to what your ancestors supposedly ate based on these studies (though as I have argued in the past, high consumption of processed foods lead to obesity, insulin resistance, diabetes etc which is the cause of a lot of the modern-day maladies currently present in our population today). This assumption is wrong on numerous levels.
Buckley et al (2017), using data from the 1000 Genomes Project (see also Via, Gignoux, and Burchard, 2010), identified novel potential selections in the FADs region. The 1000 Genomes Project tested the genomes of 101 Bronze Age Europeans. They show that SNPs which are associated with arachidonic acid and eicosapentaenoic acid has been favored in Europeans since the Bronze Age (the selection for arachidonic acid being due to milk consumption which is a form of niche construction; see Laland, Odling-Smee, and Feldman, 1999; Laland, Odling-Smee, and Feldman, 2001; Laland and Brown, 2006; Rendell, Fogarty, and Laland, 2011; Laland, et al, 2016; but see Gupta et al, 2017 for a different view which will be covered in the future). They also hypothesize that differences in the selection of these regions is different in different population, implying different epigenetic changes brought on by diet (more on this later).
The FADS1 gene codes for an enzyme called fatty acid desaturase 1 which desaturates n3 and n6 which then catalyzes eicosapentaenoic and Arachidonic acid (Park et al, 2009). These genes code for enzymes that then aid in the breakdown of fatty acids. So, by testing Bronze Age Europeans and comparing their genomes with modern-day Europeans, researchers can see how the expression of genes changed and then work backward and hypothesize how and why the differing gene expression occurred.
The regions selected for are involved in processing n3 and n6 fatty acids. We need a certain ratio of them, and if either is thrown out of whack then deleterious effects occur. This, of course, can be seen by comparing our ratio of n3 to n6 fatty acid consumption with our ancestors’, who ate a 1:1 ratio of n3 to n6 (Kris-Etherson et al, 2000) which you can then compare to our n3 to n6 ratio, which is 14 to 25 times higher than it should be. The authors state that n6 is important, but it’s only important to have the correct ratio, having too much n6 is not a good thing (as I have covered here).
Twenty percent of the dry weight of the brain is made up of long-chain polyunsaturated fatty acids (Lassek and Gaulin, 2009). Therefore it is pivotal we get the correct amount of n3 fatty acids for brain development both in vitro and during infancy, the best bet being to breastfeed the babe as the mother packs on fat during pregnancy so the babe can have PUfAs during its time on the womb as well as during infancy through breastfeeding.
About 85kya selective sweeping occurred in Africa on the FADs genes. Buckley et al (2017) write: “Humans migrating out of Africa putatively carried mostly the ancestral haplotype, which remained in high frequency in non-African populations, while the derived haplotype came close to fixation in Africa. It is unclear why positive selection for the derived haplotype appears to be restricted to Africa. Mathias et al. (2012) suggested that the emergence of regular hunting of large animals, dated to ∼50 kya, might have diminished the pressure for humans to endogenously synthesize LC-PUFAs.” This is true. There is a wealth of important fatty acids in the fatty and muscle tissue of animals, which we need for proper brain functioning and development.
They also write about a study on the Inuit that proves that certain alleles have been selected for that have to do with fatty acid metabolism, which I have also covered in the past in a response to Steve Sailer. Nevertheless, on a population level, this is worth it, but individual variation in metabolism matters more than population. In the article, Sailer implied—with a quote from New York Times science editor Carl Zimmer—that the Inuit have certain gene variants that influence fatty acid metabolism in that population. Sailer goes on to write “So maybe you should try different diets and see if one works better for you.” Of course, you should. However individual variation is more important than racial variation. (It’s also interesting to note that these genes that are expressed on the Inuit are also related to height.)
Nevertheless, it is true that selection occurred on these parts of the genome in these populations studied by Buckley et al (2017), but to claim that all populations wouldn’t benefit from a low carb, high fat diet is not true. I do agree with Sailer on, in the future, the scanning of individual genomes to see which diet would have a better effect. Though I would insist that most, if not all, humans should eat a higher fat lower carb diet.
Buckley et al (2017) cite a study (Mathieson et al, 2015) which “provides strong evidence of selection in the FADSregion in Europe over the past 4,000 years, in addition to the patterns of selection already reported in Africans, South Asians, and the Inuit.” Buckley et al (2017) also cite a study (Pan et al, 2017) which shows an SNP, rs174557, regulates FADS1.
In their analysis, they showed that “this variation is largely attributable to high differentiation between two haplotype clusters: a cluster widespread in Africa, largely containing derived alleles and possibly subject to a selective sweep (Mathias et al. 2011,, 2012), and an ancestral cluster, which is present across Eurasia.” They also showed that Neanderthal genomes cluster with the derived cluster, which is present in Africans, while Denisovans cluster with the ancestral cluster, which Eurasians also have.
Buckley et al (2017) write: “Thus the derived alleles appear to promote expression of FADS1 while simultaneously abating the expression of FADS2.” This is important to keep in mind for the end of this article when I talk about nutrition and how it affects the epigenome which can then become heritable in a certain population.
Buckley et al (2017) also confirm the results of the European sample using the Nurses Health Study and the Health Professionals follow-up study GWASs: “These results reinforce the associations with cholesterol from the GLGC GWAS. This confirms the hypothesized phenotypic effect of the selected variants in terms of increased EPA and ARA levels of the putatively positively selected variants in the European population.”
Selective (dietary) pressures on the three populations tested (Africans, Europeans and South Asians) have “have driven allele frequency changes in different FADS SNPs that are only in weak LD with each other [LD is linkage disequilibrium which is the nonrandom associations of alleles at different loci in a given population]” (Buckley et al, 2017). Further, the alleles (FADS1 and FADS2) that were under selection in Europeans were strongly associated with lipid metabolism, specifically reduced linoleic acid levels. An opposite pattern was noticed in the Inuit, where selection acted to “decrease conversion of SC-PUFAs to LC-PUFAs to compensate for the relative high dietary intake of LC-PUFAs.” The allele under selection was associated with a decrease in linoleic acid levels and an increase in eicosapentaenoic acid, which may possibly be due to improved metabolism in converting LC-PUFAs from SC-PUFAs.
Buckley et al (2017) hypothesize that the cause is eating a more plant-based diet which is rich in fatty acids (n6 and n3) while a subsequent decrease in fatty animal meats occurred. Of course, relative to hunter-gatherer populations, the increased plant consumption brought on by agriculture caused different methylation on the genome which then eventually became part of the heritable variation. So, of course, farmers would have eaten more plants and the like, which one then select for the production of SC-PUFAs to LC-PUFAs. This of course began at the dawn of agriculture (Cochran and Harpending, 2009).
Of course, this can help guide individual diets as we better map the human genome. These studies, for instance, can be used as guides for individual diets based on ancestral evolution. More studies, of course, are needed.
Also, in an email with correspondence with Arstechnica, one of the authors, Nelson Rasmussen, stated: “Of course, within the last century there have been drastic changes in the diets in many areas of Europe. Diets have typically become more caloric with a higher intake of simple sugars, and perhaps also more rich in proteins and fat from animals. So selection is unlikely to be working in exactly the same way now.”
Though the strong claim from Arstechnica that “This is another nail in the coffin for the scientific validity of paleo diets” is a strong claim which needs much more evidence because low carb high-fat diets are mostly best for people since their insulin levels aren’t spiked too much which then leads to obesity, diabetes and along with it hyperinsulinemia.
Now I need to talk about how epigenetics is involved here. Nutrition can alter the genome and epigenome (Niculescu and Lupu, 2011; Niculescu, 2012; Anderson, Sant, and Dolinoy, 2012) and cause permanent heritable variation in a population if a certain allele reaches fixation, since there is evidence that maternal and paternal dietary changes possibly affecting multiple generations (Rosenfeld, 2017; though see Burggren, 2016 for the view that there is no evidence for heritable epigenetic phenotype in the genome. I will return to this in the future; see also the Dutch Famine Study showing heritable epigenetic change from famine; Lumey et al, 1993; Heijmans, 2008; Stein et al, 2009; Tobi et al, 2009; Schulz, 2010; Lumey, Stein, and Susser, 2011; Hajj et al, 2014; Jang and Serra, 2014; Tobi et al, 2014). Of course, based on what a population eats (or does not eat), epigenetic changes can and will occur. This not only affects the expression of genes in the body, but also the trillions of gut microbiota in our microbiome that partly drive our metabolic functions. Diet can change the composition of the microbiome, diet can change the epigenome and gene expression, and the microbiome can also up- and down-regulate genes (Hullar and Fu, 2014) Lipid metabolism is also related to developmental epigenetic programming (Marchlewicz et al, 2016). They showed that circulating fatty lipids in the mother during pregnancy are associated with DNA methylation in the genomes of the child. This can also, of course, contribute to health and disease risk in the future for the affected infant. FADS1 is also involved here.
Nutritional factors also come into play in regards to epigenetic inheritance (Alam et al, 2015). The n3 PUFAs also affect gene expression and DNA methylation (Hussey, Lindley, and Mastana, 2017). Further, DNA methylation is also associated with FADS1 and, to a lesser extent, FADS2 (Howard et al, 2014). This is strong evidence that, of course, that what was reviewed above in regards to selection for certain alleles for fatty acid metabolism in certain populations was strongly driven by the consumption of certain foods. Epigenetic changes that occur both in the womb and previous generations like the grandparents’, for instance, also have an effect in regard to which genes are expressed in the baby in vitro as well as consequences for future generations. The study of epigenetics, along with transgenerational epigenetic inheritance, of course, will be very important for our future understanding of both the evolution of humans and the evolution of the human diet.
Finally, I need to touch on why this doesn’t really matter in terms of individual diet choice. The fact of the matter is, anatomic, physiologic, and metabolic variation within race trumps variation between it. Two different randomly selected individuals will have different anatomy, along with different organs missing (Saladin, 2010). This implies that the individual differences in these traits trump whatever racial selection occurred since the dawn of agriculture 10kya. This is why, in my opinion, one should not look to just their ancestry when choosing a diet and should always choose a diet based that’s good for them, individually. Now, I’m not saying that this research is useless in regards to healthy diets, however, increased consumption of processed foods is the cause of obesity since processed foods (high in carbs) spike insulin which lead to obesity and diabetes (insulin causes weight gain). So, obviously, full-on plant-based diets will lead to these maladies. Contrary to the Alternative Hypothesis’ thesis on race and nutrition, this doesn’t really matter, not at the individual level, anyway. This could have small implications in regard to the population as a whole, but as an effect on the diet of individuals? No. Individual variation in traits matters much more than racial variation here (again, don’t call Lewontin’s fallacy because I’ve explained my reasoning which is logically sound).
In sum, the SNPs associated with the increased expression of FADs1 and increased the production of eicosapentaenoic and Arachidonic acid in Europeans occurred around 5kya. These studies are interesting to see how diet and how we construct our niches leads to changes in the genome based on those changes that we enact ourselves. However, laypersons who read these popular science articles on the evolution of diet in human populations will then assume that since they have X ancestry then they must eat how their immediate ancestors ate. The Arstechnica article makes some strong claims that Buckley et al (2017) prove that the paleo diet is not a viable solution for diseases of civilization. Do not make sweeping claims about eating X and Y because your ancestors evolved in Z environment, because individual variation in metabolic and physiologic functioning is greater and matters way more than racial variation
[Note: Diet changes under Doctor’s supervision only.]
Sex Differences in Aggressive Behavior and Testosterone
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Many long-time readers may know of the numerous tirades of been on in regards to the “testosterone causes crime and aggression” myth. It’s a fun subject to talk about because the intelligent human physiological system is an amazing system. However, people who are not privy to the literature on testosterone in regards to race, aggression, crime, sex differences etc are only aware of whatever they read in pop science articles. So since they never read the actual papers themselves, they get a clouded view of a subject.
In my last article, I wrote about how there are no “testosterone genes”. In previous articles on the hormone, I have proven that there is no causal link between testosterone and aggression. But when comparing the sexes, how do the results look? Do they look the same with men being more violent while women—who have substantially less testosterone than men—do not have any higher levels of aggression or crime? The most recent study I’m aware of is by Assari, Caldwell, and Zimmerman (2014) titled: Sex Differences in the Association Between Testosterone and Violent Behaviors.
To make a long story short, there was no relationship between testosterone and aggression in men, but a significant relationship between testosterone and aggression in women. This data comes from the Flint Adolescent Study, a longitudinal study conducted between the years of 1994 to 2012. In regards to testosterone collection, saliva was used which has a perfect correlation with circulating testosterone. The eligibility to be included in the testosterone assay was “provided consent for the procedure, not being pregnant, not having anything to eat, drinking nothing except water, and not using tobacco, 1 hour prior to collection” (Assari, Caldwell, and Zimmerman, 2014).
The adolescent who contributed saliva gave a whole slew of demographic factors including SES, demographics, psychological factors, family relations, religion, social relations, behavior, and health. They were aged 14 to 17 years of age. They collected data during face-to-face interviews,
Age and SES were used as control variables in their multivariate analysis. For violent behaviors, the authors write:
Youths were asked how often they had engaged in the following behaviors; ‘had a fight in school’, ‘taken part in a rumble where a group of your friends were against another group’, injured someone badly enough to need bandages or a doctor’, ‘hit a teacher or supervisor at work (work supervisor)’, used a knife or gun or other object (like a club) to get something romantic a person’, ‘carried a knife or razor’, or ‘carried a gun’. All items used a Likert response, ranging from 1 (0 times) to 5 (4 or more times). Responses to each item were averages to calculate the behavior during the last year. Total score was calculated as the average of all items. Higher scores indicated more violent behaviors (a = 0.79). This measure has shown high reliability and validity and it has been used previously in several published reports.
This is a great questionnaire. The only thing I can think of that’s missing is fighting/arguing with parents.
In regards to testosterone assaying, they were assayed after 11 am to “control for changes due to diurnal rhythm” (Assari, Caldwell, and Zimmerman, 2014). I’m iffy on that since testosterone levels are highest at 8 am but whatever. This analysis is robust. Saliva was not taken if the subject had smoked or ingested something other than water or if a subject was pregnant. Assays should be taken as close to 8 am, as that’s when levels are highest. However one study does argue to extend the range to 8 am to 2 pm (Crawford et al, 2015) while other studies show that this only should be the case for older males (Long, Nguyen, and Stevermer, 2015). Even then assays were done at the higher end of the range as stated by Crawford et al (2015), so differences shouldn’t be too much.
86.4 percent of the sample was black whereas 13.4 percent were white. 41.2 percent of the subjects had some college education whereas 58.2 percent of the subjects lived with a partner or relative. 21.4 percent of the subjects were unemployed.
The mean age was 20.5 for both men and women, however, which will be a surprise to some, testosterone did not predict aggressive behavior in men but did in women. Testosterone and aggressive behavior were positively correlated, whereas there was a negative correlation between education and testosterone and aggressive behavior. Though education was associated with aggressive behavior in men but not women. So sex and education was associated with aggressive behavior (the sex link being women more privy to aggressive behavior while men are more privy to aggressive behavior due to lack of education). Females who had high levels of education had lower levels of aggressive behavior. Again: testosterone wasn’t associated with violent behavior in men, but it was in women. This is a very important point to note.
This was a community sample, so, of course, there were different results when compared to a laboratory setting, which is not surprising. Laboratory settings are obviously unnatural settings whereas the environment you live in every day obviously is more realistic.
This study does contradict others, in that it shows that there is no association between testosterone and aggression in men. However, still other research shows that testosterone is not linked to aggression or impulsivity, but to sensation-seeking, sexual experience or sociality (Daitzman and Zuckerman, 1980; Zuckerman, 1984). Clearly, testosterone is a beneficial hormone and due to the low correlation of testosterone with aggression (between .08 and .14; Book, Starzyk, and Quinsey, 2001; Archer, Graham-Kevan and Davies, 2005; Book and Quinsey, 2005). This paper, yet again, buttresses my arguments in regards to testosterone and aggressive behavior.
In regards to the contrast in the literature the authors describe, they write:
One of the many factors that may explain the inconsistency in these findings is the community versus clinical setting, which has been shown to be a determinant of these associations. Literature has previously shown that many of the findings that can be found in clinical samples may not be easily replicated in a community setting (36).
This is like the (in)famous, unreplicable stereotype threat (see Stroessner and Good). It can only be replicated in a lab, not in an actual educational setting. And it also seems that this is the case for testosterone and aggressive behavior.
Just because women have lower testosterone and are less likely to engage in aggressive behavior, that doesn’t mean that a relationship does not exist between females. “It is also plausible to attribute sex differences in the above studies to differential variations in the amount of testosterone among men and women” (Assari, Caldwell, and Zimmerman, 2014). This view supports the case that testosterone is linked to aggression in females, even though their range of testosterone is significantly lower than men’s, while it may also be easier to assay women for testosterone due to less diurnal variation in comparison to men (Book, Starzyk, and Quinsey, 2001).
Assari, Caldwell, and Zimmerman, (2014) also write (which, again, buttresses my arguments):
Age may explain some of the conflicting results across the studies. A meta-analysis of community and selected samples suggested that there might be only low to modest association between testosterone and aggression, with mean weighted correlations ranging from 0.08 to 0.14, in males. Overall, these meta-analyses suggest that the testosterone-aggression association is equally strong in 12 to 21-year-olds, as it is in 22 to 35-year-olds, but that it may be less strong in age groups younger than 12, than in those who are older.
So, testosterone may be associated with aggressive behavior and violence in women but not in men. In men, the significant moderator was education. It’s interesting to note that Mazur (2016) noted that young black males with little education had higher levels of testosterone than age-matched samples of other blacks. This, along with the evidence provided here, may be a clue that if the social environment changes, then so will higher levels of testosterone (as I have argued here).
They, perhaps taking too large of a leap here, argue that “aggressive behaviors may be more social and less biologically based among men” (Assari, Caldwell, and Zimmerman, 2014). Obviously social factors are easier to change than biological ones (in theory), so, they argue, preventative measures may be easier for men than women. More studies need to be done on the complex interactions between sex, testosterone, aggression, biology and the social environment which then shapes the aggressive behaviors of those who live there.
Testosterone and aggression studies are interesting. However, you must know a good amount of the literature to be able to ascertain good studies from the bad, what researchers should and should not have controlled for, time of assay, etc because these variables (some not in the author’s hands, however) can and do lead to false readings if certain variables are not controlled for. All in all, the literature is clearly points to, though other studies contest this at times, the fact that testosterone does not cause aggressive behavior in men. The myth needs to die; the data is piling up for this point of view and those who believe that testosterone causes aggressive behavior and crime (which I have shown it does not, at least for men) will soon be left in the dust as we get a better understanding of this pivotal hormone.
(In case anyone was going to use this as evidence that black women have higher levels of testosterone than white women, don’t do it because it’s not true. You’ll only embarrass yourself like this guy did. Read the comments and see him say that you don’t need scientific measurements, you only need to ‘observe it’ and through ‘observation’ we can deduce that black women have higher levels of testosterone than white women. This is not true. Quoting Mazur, 2016:
The pattern [high testosterone] is not seen among teenage boys or among females.
…
There is no indication of inordinately high T among young black women with low education.
Whoever still pushes that myth is an idealogue; I have retracted my article ‘Black Women and Testosterone‘, but idealogues just gloss over it and read what they think will bolster their views when I have provided the evidence to the contrary. It pisses me off that people selectively read things then cite my article because they think it will confirm their pre-conceived notions. Well too bad, things don’t work like that.)
My Response to (Ir)RationalWiki
1100 words
I was alerted to an article on the website (Ir)”RationalWiki” which in their own words “critique[s] and challenge[s] pseudoscience and the anti-science movement, explore[s] authoritarianism and fundamentalism, and analyze[s] how these subjects are handled in the media.” Unfortunately, it seems like the one who wrote this article (and is still adding to it) just selectively read certain articles and quote mined them.
The article on this website about me is an unfair mischaracterization of my views. Quotes will follow from the article with my comments.
In the opening paragraph they write:
NotPoliticallyCorrect is an Alt-right blog that promotes racialist pseudoscience and white nationalism; the owner posts as RaceRealist using the euphemism “racial realist” coined by the white supremacist J. P. Rushton who is extensively quoted on the blog.
- I’m not alt-right nor am I a white nationalist.
- I don’t promote ‘racialist pseudoscience’ nor do I promote ‘white nationalism’.
- Correct, Rushton did coin the term ‘race realist’, but he was not a ‘white supremacist’.
They continue, quoting an article of mine that I wrote almost two years ago titled Non-Western People are Abnormal to Our Society. I still stand by everything that I wrote in that article.
They continue:
A racist crank obsessed with controversial topics such as race and IQ and eugenics, RaceRealist argues in a 2016 blog essay “Non-Western People are Abnormal to Our [Western] Societies”[1] and its comments[2] that “MENA” and “SSA’s” (i.e. people from the Middle-East, North Africa and Sub-Saharan Africa) as well as other non-Westerners are somehow abnormal to the US and Europe:
They then quote me:
MENA and SSA people are abnormal to Western societies. It’s clear that, on average, full-on acclimation is not possible.
One only needs to look at what is occurring in Western European countries to see that, on average, this is true.
They continue:
In the same essay, RaceRealist goes on to post crude racism, such as “Negros” are biologically inferior:
Quoting me writing:
The same can be said for Negros[sic] in America as well. They are deviant, dysfunctional, they cause distress in our country and finally, they pose a danger to us, our families and societies as a whole. Just like those immigrants we have come into our countries who cannot assimilate because it’s not in their biology.
Except everything I wrote here was logically sound (last sentence notwithstanding). Look at the 4 d’s of abnormal psychology (which is the next quote they provide):
The “4 d’s of abnormality” and how they relate to our culture and the current culture/biology of those non-Western immigrants coming into our country is extremely telling. It’s clear that those people cannot assimilate into our societies because of differing biology and differing locations in which they evolved in. We chose our environments based on our biology. Environment increasingly depends on their genes, rather than being the cause of their exogenous behavior.
The 4 d’s of abnormality are deviance, dysfunction, distress and danger. Everything I wrote and then provided examples for in regards to the 4 d’s of abnormality are sound.
You can read my article Diversity in the Social Context for more evidence for this argument.
They then quote my article The Evolution of Jewish Nepotism writing:
RaceRealist is an anti-Semite who dislikes Ashkenazi Jews, accusing them of “derogating other ethnicities”; when discussing Ashkenazi Jews, he bizarrely maintains their higher average IQ is partly a product of “breeding with beautiful Roman women a few thousand years ago”,[3] for which there exists no evidence.
I admit it is conjecture. Evidence exists for Jewish men migrating to Rome to mate with Roman women (Atzmon et al, 2010). I never stated that I ‘dislike Ashkenazi Jews’. In regards to the derogation, it’s true. Close-knit ethnic groups derogate the out-group (Sampasivam et al, 2016). Further, oxytocin promotes human ethnocentrism, which caused in-group favoritism and out-group derogation (Drew et al, 2010). In-groups derogate out-groups. Read the literature.
And the final thing the page shows is my tweet saying that “I finally made it on (Ir)”RationalWiki””:
to which they wrote:
Twitter contributor Race Realist Eighty frickin’ Eight wishes to make it absolutely clear to everyone that he does not in fact consider himself “altright” and certainly not a “white nationalist”.[4]
Just because I have the numbers “88” in my handle doesn’t make me “alt-right” nor does it make me a “white nationalist.” I thought about changing it, then I realized that it’s good to weed out the people who aren’t serious about discussion and just look for things to discredit people that are meaningless to the conversation at hand. It tells you a lot about someone when they bring up irrelevant things. I’m not a white nationalist, nor am I an alt-righter. Just because I write about politics rarely and use them as an example (like in my article The Rise of Ethnocentrism and the Alt-Right: The Rebirth of Selfish Genes which I also disavow now that I realize that ‘selfish genes’ are a metaphor; Noble, 2011; Noble, 2013; Noble et al, 2014).
Take a look at the tags it tagged the article with: “Alt-righters, Pseudoscience, Racists, Internet kooks, Psuedoscience promoters, Alt-right, Internet Hate Sites.” Not an alrighter, I don’t push psuedoscience, I’m not a ‘racist’ (whatever that means). If you don’t like what I write, respond to any article you disagree with and explain why with logical, rational arguments. This piece is garbage and mischaracterizes my views using selective quotations (which, even then, failed to prove their point. No, numbers after a username are not evidence).
All in all, this article is garbage. It says that Rushton is ‘extensively quoted’, which is true for what I wrote in the beginning of this blog’s history, but not so for the past, say, 18 months. Rushton has been the target of my attacks on penis size, testosterone, and my personal favorite, r/K selection theory. But sure, go and dig in the archives for old articles to quote mine. This article written about me is dumb, doesn’t characterize my views correctly (calls me a ‘white nationalist’ and ‘alt-righter’). Selectively quote certain articles, assert that Rushton is ‘extensively quoted’ when I hardly discuss him anymore and when I do it’s about testosterone/to rebut him. (Ir)RationalWiki should think about reading a bit of my blog before characterizing me as something I’m not.
For the record, I don’t care about politics. I am not alt-right. I am not a white nationalist. I’m not an anti-semite. This will be updated to cover whatever else they decide to write about me. Hopefully it’s at least a bit closer to reality next time, because this article sucks.
Black-White Differences in Physiology
2050 words
Black-white differences in physiology can tell a lot about how the two groups have evolved over time. On traits like resting metabolic rate (RMR), basal metabolic rate (BMR), adiposity, heart rate, Vo2 max, etc. These differences in physiological variables between groups, then, explain part of the reason why there are different outcomes in terms of life quality/mortality between the two groups.
Right away, by looking at the average black and average white, you can see that there are differences in somatype. So if there are differences in somatype, then there must be differences in physiological variables, and so, this may be a part of the cause of, say, differing obesity rates between black and white women (Albu et al, 1997) and even PCOS (Wang and Alvero, 2013).
Resting metabolic rate
Resting metabolic rate is your body’s metabolism at rest, and is the largest component of the daily energy budget in modern human societies (Speakman and Selman, 2003). So if two groups, on average, differ in RMR, then one with the lower RMR may have a higher risk of obesity than the group with the higher RMR. And this is what we see.
Black women do, without a shadow of a doubt, have a lower BMR, lower PAEE (physical activity energy expenditure) and TDEE (total daily expenditure) (Gannon, DiPietro, and Poehlman, 2000). Knowing this, then it is not surprising to learn that black women are also the most obese demographic in the United States. This could partly explain why black women have such a hard time losing weight. Metabolic differences between ethnic groups in America—despite living in similar environments—show that a genetic component is responsible for this.
There are even predictors of obesity in post-menopausal black and white women (Nicklas et al, 1999). They controlled for age, body weight and body composition (variables that would influence the results—no one tell me that “They shouldn’t have controlled for those because it’s a racial confound!”) and found that despite having a similar waist-to-hip ratio (WHR) and subcutaneous fat area, black women had lower visceral fat than white women, while fasting glucose, insulin levels, and resting blood pressure did not differ between the groups. White women also had a higher Vo2 max, which remained when lean mass was controlled for. White women could also oxidize fat at a higher rate than black women (15.4 g/day, which is 17% higher than black women). When this is expressed as percent of total kcal burned in a resting state, white women burned more fat than black women (50% vs 43%). I will cover the cause for this later in the article (one physiologic variable is a large cause of these differences).
We even see this in black American men with more African ancestry—they’re less likely to be obese (Klimentidis et al 2016). This, too, goes back to metabolic rate. Black American men have lower levels of body fat than white men (Vickery et al, 1988; Wagner and Heyward, 2000). All in all, there are specific genetic variants and physiologic effects, which cause West African men to have lower central (abdominal) adiposity than European men and black women who live in the same environment as black men—implying that genetic and physiologic differences between the sexes are the cause for this disparity. Whatever the case may be, it’s interesting and more studies need to be taken out so we can see how whatever gene variants are *identified* as protecting against central adiposity work in concert with the system to produce the protective effect. Black American men have lower body fat, therefore they would have, in theory, a higher metabolic rate and be less likely to be obese—while black women have the reverse compared to white women—a lower metabolic rate.
Skeletal muscle fiber
Skeletal muscle fibers are the how and why of black domination in explosive sports. This is something I’ve covered in depth. Type II fibers contract faster than type I. This has important implications for certain diseases that black men are more susceptible to. Though the continuous contraction of the fibers during physical activity leads to a higher disease susceptibility in black men—but not white men (Tanner et al, 2001). If you’re aware of fiber type differences between the races (Ama et al, 1986; Entine, 2000; Caeser and Henry, 2015); though see Kerr (2010’s) article The Myth of Racial Superiority in Sports for another view. That will be covered here in the future.
Nevertheless, fiber typing explains racial differences in sports, with somatype being another important variable in explaining racial disparities in sports. Two main variables that work in concert are the somatype (pretty much body measurements, length) and the fiber type. This explains why blacks dominate baseball and football; this explains why ‘white men can’t jump and black men can’t swim’. Physiological variables—not only ‘motivation’ or whatever else people who deny these innate differences say—largely explain why there are huge disparities in these sports. Physiology is important to our understanding of how and why certain groups dominate certain sports.
This is further compounded by differing African ethnies excelling in different running sports depending on where their ancestors evolved. Kenyans have an abundance of type I fibers whereas West Africans have an abundance of type II fibers. (Genetically speaking, ‘Jamaicans’ don’t exist; genetic testing shows them to come from a few different West African countries.) Lower body symmetry—knees and ankles—show that they’re more symmetrical than age-matched controls (Trivers et al, 2014). This also goes to show that you can’t teach speed (Lombardo and Deander, 2014). Though, of course, training and the will to want to do your best matter as well—you just cannot excel in these competitions without first and foremost having the right physiologic and genetic make-up.
Further, although it’s only one gene variant, ACTN3 and ACE explain a substantial percentage of sprint time variance, which could be the difference between breaking a world record and making a final (Papadimitriou et al, 2016). So, clearly, certain genetic variants matter more than others—and the two best studied are ACTN3 and ACE. Some authors, though, may deny the contribution of ACTN3 to elite athletic performance—like one researcher who has written numerous papers on ACTN3, Daniel MacArthur. However, elite sprinters are more likely to carry the RR ACTN3 genotype compared to the XX ACTN3 genotype, and the RR ACTN3 genotype—when combined with type II fibers and morphology—lead to increased athletic performance (Broos et al, 2016). It’s also worth noting that 2 percent of Jamaicans carry the XX ACTN3 genotype (Scott et al, 2010), so this is another well-studied variable that lends to superior running performance in Jamaicans.
In regards to Kenyans, of course when you are talking about genetic reasons for performance, some people don’t like it. Some may say that certain countries dominate in X, and that for instance, North Africa is starting to churn out elite athletes, should we begin looking for genetic advantages that they possess (Hamilton, 2000)? Though people like Hamilton are a minority view in this field, I have read a few papers that there is no evidence that Kenyans possess a pulmonary system that infers a physiologic advantage over whites (Larsen and Sheel, 2015).
People like these three authors, however, are in the minority here and there is a robust amount of research that attests to East African running dominance being genetic/physiologic in nature—though you can’t discredit SES and other motivating variables (Tucker, Onywera, and Santos-Concejero, 2015). Of course, a complex interaction between SES, genes, and environment are the cause of the success of the Kalenjin people of Kenya, because they live and train in such high altitudes (Larsen, 2003), though the venerable Bengt Saltin states that the higher Vo2 max in Kenyan boys is due to higher physical activity during childhood (Saltin et al, 1995).
Blood pressure
The last variable I will focus on (I will cover more in the future) is blood pressure. It’s well known that blacks have higher blood pressure than whites—with black women having a higher BP than all groups—which then leads to other health implications. Some reasons for the cause are high sodium intake in blacks (Jones and Hall, 2006); salt (Lackland, 2014; blacks had a similar sensitivity than whites, but had a higher blood pressure increase); while race and ethnicity was a single independent predictor of hypertension (Holmes et al, 2013). Put simply, when it comes to BP, ethnicity matters (Lane and Lip, 2001).
While genetic factors are important in showing how and why certain ethnies have higher BP than others, social factors are arguably more important (Williams, 1992). He cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity. SES factors, of course, lead to higher rates of obesity (Sobal and Stunkard, 1989; Franklin et al, 2015). So, of course, environmental/social factors have an effect on BP—no matter if the discrimination or whatnot is imagined by the one who is supposedly discriminated against, this still causes physiologic changes in the body which then lead to higher rates of BP in certain populations.
Poverty does affect a whole slew of variables, but what I’m worried about here is its effect on blood pressure. People who are in poverty can only afford certain foods, which would then cause certain physiologic variables to increase, exacerbating the problem (Gupta, de Wit, and McKeown, 2007). Whereas diets high in protein predicted lower BP in adults (Beundia et al, 2015). So this is good evidence that the diets of blacks in America do increase BP, since they eat high amounts of salt, low protein and high carb diets.
Still, others argue that differences in BP between blacks and whites may not be explained by ancestry, but by differences in education, rather than genetic factors (Non, Gravlee, and Mulligan, 2012). Their study suggests that educating black Americans on the dangers and preventative measures of high BP will reduce BP disparities between the races. This is in-line with Williams (1992) in that the social environment is the cause for the higher rates of BP. One hypothesis explored to explain why this effect with education was greater in blacks than whites was that BP-related factors, such as stress, poverty and racial discrimination (remember, even if no racial discrimination occurs, any so-called discrimination is in the eye of the beholder so that will contribute to a rise in physiologic variables) and maybe social isolation may be causes for this phenomenon. Future studies also must show how higher education causes lower BP, or if it only serves as other markers for the social environment. Nevertheless, this is an important study in our understanding of how and why the races differ in BP and it will go far to increase our understanding of this malady.
Conclusion
This is not an exhaustive list—I could continue writing about other variables—but these three are some of the most important as they are a cause for higher mortality rates in America. Understanding the hows and whys of these variables will have us better equipped to help those who suffer from diseases brought on by these differences in physiological factors.
The cause for some of these physiologic differences come down to evolution, but still others may come down to the immediate obesogenic environment (Lake and Townshend, 2006) which is compounded by lower SES. Since high carbs diets increase BP, this explains part of the reason why blacks have higher BP, along with social and genetic factors. Muscle fiber typing is set by the second trimester, and no change is seen after age 6 (Bell, 1980). Resting metabolic rate gap differences between black and white women can be closed, but not completely, if black women were to engage in exercise that use their higher amounts of type II muscle fibers (Tanner et al, 2001). This research is important to understand differences in racial mortality; because when we understand them then we can begin to theorize on how and why we see these disparities.
Physiologic differences between the races are interesting, they’re easily measurable and they explain both disparities in sports and mortality by different diseases. Once we study these variables more, we will be better able to help people with these variables—race be dammed. Race is a predictor here, only because race is correlated with other variables that lead to negative health outcomes. So once we understand how and why these differences occur, then we can help others with similar problems—no matter their race.
NotPoliticallyCorrect 