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Blood pressure (BP) is a physiological variable. Therefore since it is a physiological variable then it can be affected by environmental and social changes. How do racial differences come into play here, for instance? Since blacks face more (perceived) discrimination, then they should, on average, have higher BP levels than whites. This is what we find—but the effect is mostly seen in low-income blacks. How do psychosocial factors come into play here in the black-white BP gap?
BP is regulated by cardiac output, vascular resistance of blood flow, blood volume, arterial stiffness, and, of course, the individual’s emotional state which can decrease or increase BP. Neural mechanisms also exist which regulate BP (Chopra, Baby, and Jacob, 2011). Knowing how and why BP increases or decreases will have us better understand the social contexts of increased BP in low SES blacks.
BP is a complex physiological trait. It can go up and down due to what occurs in the immediate environment. Values of 120/80 mmHg are cited as ‘average’ values, but we have no idea what an ‘average’ BP is. Nevertheless—like most/all physiological variables—there is a wide range of what is considered ‘normal’. Due to the variance in human physiological systems, what is ‘normal’ for one individual is not ‘normal’ for another. Variation in BP (like, say, 120 SBP (systolic blood pressure) to 140 SBP) is ‘normal’. I believe even around 110 for SBP is within that range. For DPB (diastolic blood pressure) between 75 and 90 is within normal diurnal fluctuations due to activity/eating/etc (Taylor, Wilt, and Welch, 2011). BP, like testosterone, is one of those tricky variables to measure and so must be measured upon waking to see if there are any problems. So even for a trait like BP, there seems to be a ‘normal range’.
About 33 percent of blacks have hypertension (HTN) (Peters, Arojan, and Flack, 2006). Urban blacks are more likely to have higher BP levels than whites, but “At present, there is no complete explanation for these differences and further research is required” (Lindhorst et al, 2007). Low SES is correlated with higher levels of BP in black Americans—especially those with darker skin—but not Africans in Africa (Fuchs, 2011), suggesting that this is an American phenomenon that needs to be addressed. One good explanation, in my view, is the social environment. Physiological traits are extremely malleable due to the need to be able to ‘change gears’ in an instant, for instance to either fight or flight. Though, in our modernized world, these responses—mostly—have no need and so (due to our supposed civilized behavior), one’s BP rises due to social stress and other environmental factors and it is due to the urban environment.
What is the cause of high BP in blacks?
One explanation that has been given to explain higher rates of BP in blacks when compared to whites is discrimination. However, studies show mixed evidence on whether or not so-called discrimination raises BP (Couto, Goto, and Bastos, 2012). The same American effect (American blacks having higher BP than American whites) is seen even in the UK London area (Agyemang and Bhopal, 2003). This, yet again, is more evidence that the social environment drives these differences—again, regardless of whether or not any of the discrimination is real or imagined. Say most of it were imagined: it’d be irrelevant because the imagined discrimination leads to very real physiological outcomes in BP.
The country of birth also has an effect on BP. In one study, it was noted that Africans had significantly higher BP when compared to Asians (which is identical/lower) and native French living in France (Bahous et al, 2015). Ethnic differences in BP increase due to similar sodium intake is lower than what is usually cited (Graudal and Jurgens, 2015). However, other authors have pointed out that basing conclusions off of observational studies have problems, like the estimation of sodium intake being inaccurate since it’s a one-time measure; (Gunn et al, 2013; Cobb et al, 2014)
There is also evidence—along with pathways—that show how certain social activities work to lower stress and BP, including participation at church (Livingstone, Devine, and Moore, 1991). Black Americans can make other lifestyle changes in order to decrease BP, such as exercise and other lifestyle interventions. Redman, Baer, and Hicks state that “gene-environment interactions, job-related stress, racism, and other psychosocial factors to racial/ethnic disparities” need to be explored as causes for higher rates of HTN in blacks compared to whites. And with the knowledge of how all physiological systems work in terms of stress and other factors, should be explored as causes for this disparity.
Grim et al (1990) state that factors that influence high BP in blacks compared to whites are inherited and that is the major source of variation between these populations. However, the other mounting social/physiological evidence deserves an explanation; that is not inherited, and what we know about how our physiology responds to stress and discrimination—whether real or imagined—are extremely important and lead to extremely real, and important, outcomes in these populations. It is also argued that since blacks en route to America during the slave trade died from salt-depletive diseases, that blacks with a higher genetic propensity to absorb salt survived and this is why blacks have a higher propensity to absorb salt and are more ‘salt-sensitive’, which also could explain higher rates of HTN in American blacks compared to their cousins in Africa (Wilson and Grim, 1991). However, Curtin (1992) disputes this because “There is no evidence that diet or the resulting patterns of disease and demography among slaves in the American South were significantly different from those of other poor southerners”.
However, in regards to the social environment, Williams (1992) drives one of the best arguments I have encountered in this literature so far, stating that while genetic factors play a small part in regards to the BP gap between blacks and whites, social factors are arguably more important than genetic ones (and with our homeodynamic physiology, this does make sense). Dressler (1990) for instance, argues that skin color is a proxy for both social class and discrimination and these factors explain a large amount of the variation. Psychosocial variables can also explain heightened BP (Marmot, 1985; Cuffee et al, 2014). Yan et al (2003) also note how “time urgency/impatience” and “hostility” “were associated with a dose-response increase in the long-term risk of hypertension.” Henry (1988) also argues that calcium, obesity and genetic factors cannot be the aetiology of HTN in blacks, while also proposing that high sodium intakes are due to psychosocial stress (Williams, 1992: 136).
Obesity also leads to hypertension (Re, 2009) while blacks are more likely to be obese than whites, however, black American men with more African ancestry are less likely to be obese (Klimentidis et al, 2016). This would imply that the greater amount of African ancestry in American blacks both protects against obesity and along with it HTN. Williams (1992) makes a convincing argument that environmental and social factors are the cause for the black-white BP gap. And while genetic factors are important, no doubt, environmental and social factors are arguably more important to this debate.
Kulkarni et al (1998) show that increased stress leads to subsequent BP elevations which, over time, will lead to HTN. In a 2009 meta-analysis, Gasparin et al show how “individuals who had stronger responses to stressor tasks were 21% more likely to develop blood pressure increase when compared to those with less strong responses.”
Further, in support for the ‘perceived stress’ hypothesis in regards to blacks ‘perceiving’ stress and discrimination, “stress denial in combination with abdominal obesity, alcohol consumption, and smoking may be proxy for a high stress level” (Suter et al, 1997). Carroll et al (2001) also show how there are is “modest support for the hypothesis that heightened blood pressure reactions to mental stress contribute to the development of high blood pressure.” Sparrenberger et al (2009) also did a systematic review of observational studies, finding that “Acute stress is probably not a risk factor for hypertension. Chronic stress and particularly the non-adaptive response to stress are more likely causes of sustained elevation of blood pressure.”
Lastly, Langford (1981) shows that when SES is controlled for, the black-white BP disparity vanishes, implying that social and environmental—not genetic—factors are the cause for elevated HTN levels in black Americans. Sweet et al (2007) showed that for lighter-skinned blacks, as SES rose BP decreased while for darker-skinned blacks BP increased as SES did while implicating factors like ‘racism’ as the ultimate causes. This is solid evidence that both skin color and SES are predictors of higher prevalence of BP in black populations, and since other studies show that this is not noticed in higher class blacks, nor is this noticed in blacks in Africa, then the main causes of this disparity are social and environmental in nature.
(Non, Gravlee, and Mulligan, 2012). Their study suggests that educating black Americans on the dangers and preventative measures of high BP will reduce BP disparities between the races. This is in-line with Williams (1992) in that the social environment is the cause for the higher rates of BP. One hypothesis explored to explain why this effect with education was greater in blacks than whites was that BP-related factors, such as stress, poverty and racial discrimination (remember, even if no racial discrimination occurs, any so-called discrimination is in the eye of the beholder so that will contribute to a rise in physiologic variables) and maybe social isolation may be causes for this phenomenon. Future studies also must show how higher education causes lower BP, or if it only serves as other markers for the social environment. Nevertheless, this is an important study in our understanding of how and why the races differ in BP and it will go far to increase our understanding of this malady. This is a very convincing argument that education and not genetic ancestry cause disparities in BP between blacks and whites.
WebMD states that, of course, both environmental and genetic factors are at play in regards to black’s increased propensity for acquiring HTN. Fuchs (2011) also states that “They [environmental and behavioral factors] could act directly or by triggering mechanisms of blood pressure increase that are dormant in blacks living in Africa” and explain why black Americans have higher rates of BP than Africans in Africa. Further, race and ethnicity are independent predictors of HTN (Holmes et al, 2013).
Blacks and whites do differ in BP, and its aetiology is both complex and hard to untangle Genetic factors probably don’t account for a lot of this variance since Africans in Africa have low levels of BP compared to their black American cousins. Numerous lines of evidence shows that social and environmental factors are the cause, and so to change this, all people—especially blacks—should be educated on how to change these problems in our society. Whether discrimination is real or imagined, the effects of it lead to real physiological outcomes that then lead to increased health disparities between these populations.
Research into neural plasticity has been fruitful the past few decades. However, people like Steven Pinker in his book The Blank Slate attempt to undermine the effects of neural plasticity in regards to TBI and IQ, for instance. However, the plasticity of our brains is how our brains evolved (Skoyles and Sagan, 2002). So since our brains are so plastic, then doing certain tasks may help in terms of ‘processing speed’, reaction time and overall cognitive ability, right?
Science Daily reported on a new meta-analysis that took 15 years to complete that looked at how action video games affect reaction time and cognitive performance. What they found was something that I have talked about a bit: that playing these types of games increases one’s reaction time and even their cognitive ability. Unfortunately, the paper is not on Sci-Hub yet, but when it is released on Sci-Hub I will go more in depth on it.
The authors (Benoit et al, 2017) looked at 15 years of papers on action video games and cognitive performance from the year 2000-2015. They focused on war and shooting video games to gauge whether or not there was a causal effect on action video game playing and cognitive performance. They got two meta-analyses out of all of the research they did.
They studied 8,790 people between the ages of 6-40 and gave them a battery of cognitive tests. These tests included spatial attention tasks as well as testing how well one could multi-task while changing their plans in-line with the rules of the game. “It was found that the cognition of gamers was better by one-half of a standard deviation compared to non-gamers.” Though this meta-analysis failed to answer one question: do people who play games have higher cognitive ability or do people with higher cognitive ability play more games? The classic chicken-and-the-egg problem.
They then looked at other studies of 2,883 individuals and partitioned them into 2 groups: groups of people who played action games like war and shooter games whereas the second group played games like SIMS, Tetris and Puzzle (I would loosely term these strategy games as well). They found that both groups played for 8 hours per week, netting 50 hours of gameplay over 12 weeks.
What they found was that the results were overwhelmingly in favor of war and shooting games improving cognition. The interesting thing about these analyses was that it took years to get the data and it is from all over the world, so it doesn’t only hold in America, for instance. Though, in the abstract of the paper (all I have access to at the moment) Benoit et al (2017) write:
Publication bias remains, however, a threat with average effects in the published literature estimated to be 30% larger than in the full literature. As a result, we encourage the field to conduct larger cohort studies and more intervention studies, especially those with more than 30 hours of training.
This is in-line with numerous other papers on the matter of cognitive abilities and action video games. Green and Bavelier (2007) showed that video game players “could tolerate smaller target-distractor distances” whereas “similar effects were observed in non-video-game players who were trained on an action video game; this result verifies a causative relationship between video-game play and augmented spatial resolution.” They found that action video games ‘sharpened vision’ by up to 20 percent. Green and Bavelier (2012) also show that playing action video games may enhance the ability to learn new tasks and that what is learned from playing these types of games “transfers well beyond the training task.”
Green and Bavelier (2003) show that playing action video games showed better visual attention in comparison to those who did not play games. Even those who did not game saw improvement in visual attention which, again, shows that video games have an actual causal effect on these phenomena and it’s not just ‘people with higher cognitive ability choosing to play video games’. (See also Murphy and Spencer, 2009 who show that “There were no other group differences for any task suggesting a limited role for video game playing in the modification of visual attention.“)
Dye, Green, and Bavelier (2009) show that action video games increase reaction time (RT). Variables like videogame-playing when testing cognitive abilities are a huge confound, as can be seen, since people who play action video games have a quicker reaction time than those who do not—which, as I’ve shown, has a causal relationship with game playing since even the controls who did not play action games saw an increase in their RT. Achtman, Green, and Bavelier (2008) show yet again that action video game playing enhances visual attention and overall visual processing.
Green (2008: iii-iv) in an unpublished doctoral dissertation (the first link on Google should be the dissertation) showed the video game players “acquire sensory information more rapidly than NVGPs [non-videogame players]”.
Applebaum et al (2013) showed that action game playing “may be related to enhancements in the initial sensitivity to visual stimuli, but not to a greater retention of information in iconic memory buffers.” Bejjanki et al (2014) show that action video game playing “establish[es] … the development of enhanced perceptual templates following action game play.” Cardoso-Leite and Bavelier (2014) show that video games enhance “behavior in domains as varied as perception, attention, task switching, or mental rotation.”
Boot, Blakely, and Simons (2011) show that there may be a ‘file-drawer effect’ (publication bias)in terms of action video games increasing cognition, which Benoit et al (2017) acknowledge and push for more open studies.
Unsworth et al (2015) state that “nearly all of the relations between video-game experience and cognitive abilities were near zero.” So, there are numerous studies both for and against this (most of the studies for this being done by Green and Bavelier), and so this meta-analysis done by Benoit et al (2017) may finally begin to answer the question: Does playing action video games increase cognitive ability, increase visual attention and increase reaction time? The results of this new meta-analysis suggest yes, and it may have implications for IQ testing.
Richardson and Norgate (2014) in their paper Does IQ Really Predict Job Performance? state that there are numerous other reasons why some individuals may have slower RTs, one of the variables being action video game playing, along with anxiety, motivation, and familiarity with the equipment used, meaning that if one is experienced in video game playing—action games specifically—it may cause differences between individuals that do not come down to ‘processing speed’ or native ability, as is usually claimed (and with such low correlations of .2-.3 for reaction time and IQ, other factors must mediate the relationship that are not genetic in nature).
Now, let’s say the effect is as large as Benoit et al (2017) say it is at one-third of a SD. Would this mean that one would need to attempt to control for video game playing while testing, say, IQ or RT? I believe the answer is definitely pointing in that direction because it is clear—with the mounting evidence—that action video games can reduce RT and thusly confound certain tests. Action video game playing may be a pretty large confound in terms of the outcomes of IQ tests if these new meta-analyses from Benoit et al (2017) hold up. If this does hold up and playing action video games does affect both RT and cognitive ability at one-third of an SD (about 5 points), then the case can be made that this must be controlled for due to confounding the relationship.
In sum, if these effects from this new meta-analysis hold and can be replicated by other studies, then that’s a whole other variable that needs to be accounted for when testing IQ and RT. RT is a complicated variable and, according to Khodaddi et al (2014) “The relationship between reaction time and IQ is too complicated and revealing a significant correlation depends on various variables (e.g. methodology, data analysis, instrument etc.).” This, is in my view, one reason why RT should be tossed out as a ‘predictor of g‘ (whatever that is), as it is not a reliable measure and does not ‘test’ what it is purported to test.
The New York Times published an article on December the 8th titled What Doctors Should Ignore: Science has revealed how arbitrary racial categories are. Perhaps medicine will abandon them, too. It is an interesting article and while I do not agree with all of it, I do agree with some.
It starts off by talking about sickle cell anemia (SCA) and how was once thought of as a ‘black disease’ because blacks were, it seemed, the only ones who were getting the disease. I recall back in high-school having a Sicilian friend who said he ‘was black’ because Sicilians can get SCA which is ‘a black disease’, and this indicates ‘black genes’. However, when I grew up and actually learned a bit about race I learned that it was much more nuanced than that and that whether or not a population has SCA is not based on race, but is based on the climate/environment of the area which would breed mosquitoes which carry malaria. SCA still, to this day, remains a selective factor in the evolution of humans; malaria selects for the sickle cell trait (Elguero et al, 2015).
This is a good point brought up by the article: the assumption that SCA was a ‘black disease’ had us look over numerous non-blacks who had the sickle cell trait and could get the help they needed, when they were overlooked due to their race with the assumption that they did not have this so-called ‘black disease’. Though it is understandable why it got labeled ‘a black disease’; malaria is more prevalent near to the equator and people whose ancestors evolved there are more likely to carry the trait. In regards to SCA, it should be known that blacks are more likely to get SCA, but just because someone is black does not automatically mean that it is a foregone conclusion that one has the disease.
The article then goes on to state that the push to excise race from medicine may undermine a ‘social justice concept’: that is, the want to rid the medical establishment of so-called ‘unconscious bias’ that doctors have when dealing with minorities. Of course, I will not discount that this doesn’t have some effect—however small—on racial health disparities but I do not believe that the scope of the matter is as large as it is claimed to be. This is now causing medical professionals to integrate ‘unconscious bias training’, in the hopes of ridding doctors of bias—whether conscious or not—in the hopes to ameliorate racial health disparities. Maybe it will work, maybe it will not, but what I do know is that if you know someone’s race, you can use it as a roadmap to what diseases they may or may not have, what they may or may not be susceptible to and so on. Of course, only relying on one’s race as a single data point when you’re assessing someone’s possible health risks makes no sense at all.
The author then goes on to write that the terms ‘Negroid, Caucasoid, and Mongoloid’ were revealed as ‘arbitrary’ by modern genetic science. I wouldn’t say that; I would say, though, that modern genetic science has shown us the true extent of human variation, while also showing that humans cluster into 5 distinct geographic categories, which we can call ‘race’ (Rosenberg et al, 2002; but see Wills, 2017 for alternative view that the clusters identified by Rosenberg et al, 2002 are not races. I will cover this in the future). The author then, of course, goes on to use the continuum fallacy stating that since “there are few sharp divides where one set of traits ends and another begins“. A basic rebuttal would be, can you point out where red and orange are distinct? How about violet and blue? Blue and Cyan? Yellow and orange? When people commit the continuum fallacy then the only logical conclusion is that if races don’t exist because there are “few sharp divides where one set of traits ends and another begins“, then, logically speaking, colors don’t exist either because there are ‘few [if any] sharp divides‘ where one color ends and another begins.
The author also cites geneticist Sarah Tishkoff who states that the human species is too young to have races as we define them. This is not true, as I have covered numerous times. The author then cites this study (Ng et al, 2008) in which Craig Venter’s genome was matched with the (in)famous [I love Watson] James Watson and focused on six genes that had to do with how people respond to antipsychotics, antidepressants, and other drugs. It was discovered that Venter had two of the ‘Caucasian’ variants whereas Watson carried variants more common in East Asians. Watson would have gotten the wrong medicine based on the assumption of his race and not on the predictive power of his own personal genome.
The author then talks about kidney disease and the fact that blacks are more likely to have it (Martins, Agodoa, and Norris, 2012). It was assumed that environmental factors caused the disparity of kidney disease in blacks when compared to whites, however then the APOL1 gene variant was discovered, which is related to worse kidney outcomes and is in higher frequencies in black Americans, even in blacks with well-controlled blood pressure (BP) (Parsa et al, 2013). The author then discusses that black kidneys were seen as ‘more prone to failure’ than white kidneys, but this is, so it’s said, due to that one specific gene variant and so, race shouldn’t be looked at in regards to kidney disease but individual genetic variation.
In one aspect of the medical community can using medicine based on one’s race help: prostate cancer. Black men are more likely to be afflicted with prostate cancer in comparison to whites (Odedina et al, 2009; Bhardwaj et al, 2017) with it even being proposed that black men should get separate prostate screenings to save more lives (Shenoy et al, 2016). Then he writes that we still don’t know the genes responsible, however, I have argued in the past that diet explains a large amount—if not all of the variance. (It’s not testosterone that causes it like Ross et al, 1986 believe).
The author then discusses another medical professional who argues that racial health disparities come down to the social environment. Things like BP could—most definitely—be driven by the social environment. It is assumed that the darker one’s skin is, the higher chance they have to have high BP—though this is not the case for Africans in Africa so this is clearly an American-only problem. I could conjure up one explanation: the darker the individual, the more likely he is to believe he is being ‘pre-judged’ which then affects his state of mind and has his BP rise. I discussed this shortly in my previous article Black-White Differences in Physiology. Williams (1992) reviewed evidence that social, not genetic, factors are responsible for BP differences between blacks and whites. He reviews one study showing that BP is higher in lower SES, darker-skinned blacks in comparison to higher SES blacks whereas for blacks with higher SES no effect was noticed (Klag et al, 1991). Sweet et al (2007) showed that for lighter-skinned blacks, as SES rose BP decreased while for darker-skinned blacks BP increased as SES did while implicating factors like ‘racism’ as the ultimate causes.
There is evidence for the effect of psychosocial factors and BP (Marmot, 1985). In a 2014 review of the literature, Cuffee et al (2014) identify less sleep—along with other psychosocial factors—as another cause of higher BP. It just so happens that blacks average about one hour of sleep less than whites. This could cause a lot of the variation in BP differences between the races, so clearly in the case of this variable, it is useful to know one’s race, along with their SES. Keep in mind that any actual ‘racism’ doesn’t have to occur; the person only ‘needs to perceive it’, and their blood BP will rise in response to the perceived ‘racism’ (Krieger and Sidney, 1996). Harburg et al (1978) write in regards to Detroit blacks:
For 35 blacks whose fathers were from the West Indies, pressures were higher than those with American-born fathers. These findings suggest that varied gene mixtures may be related to blood pressure levels and that skin color, an indicator of possible metabolic significance, combines with socially induced stress to induce higher blood pressures in lower class American blacks.
Langford (1981) shows that when SES differences are taken into account that the black-white BP disparity vanishes. So there seems to be good evidence for the hypothesis that psychosocial factors, sleep deprivation, diet and ‘perceived discrimination’ (whether real or imagined) can explain a lot of this gap so race and SES need to be looked at when BP is taken into account. These things are easily changeable; educate people on good diets, teach people that, in most cases, no, people are not being ‘racist’ against you. That’s really what it is. This effect holds more for darker-skinned, lower-class blacks. And while I don’t deny a small part of this could be due to genetic factors, the physiology of the heart and how BP is regulated by even perceptions is pretty powerful and could have a lot of explanatory power for numerous physiological differences between races and ethnic groups.
Krieger (1990) states that in black women—not in white women—“internalized response to unfair treatment, plus non-reporting of race and gender discrimination, may constitute risk factors for high blood pressure among black women“. This could come into play in regards to black-white female differences in BP. Thomson and Lip (2005) show that “environmental influence and psychosocial factors may play a more important role than is widely accepted” in hypertension but “There remain many uncertainties to the relative importance and contribution of environmental versus genetic influences on the development of blood pressure – there is more than likely an influence from both. However, there is now evidence to necessitate increased attention in examining the non-genetic influences on blood pressure …” With how our physiology evolved to respond to environmental stimuli and respond in real time to perceived threats, it is no wonder that these types of ‘perceived discrimination’ causes higher BP in certain groups with lower SES.
Wilson (1988) implicates salt as the reason why blacks have higher BP than whites. High salt intake could affect the body’s metabolism by causing salt retention which influences blood plasma volume, cardiac output. However, whites have a higher salt intake than blacks, but blacks still ate twice the recommended amounts from the dietary guidelines (all ethnic subgroups they analyzed from America over-consumed salt as well) (Fulgoni et al, 2014). Blacks are also more ‘salt-sensitive’ than whites (Sowers et al 1988; Schmidlin et al, 2009; Sanada, Jones, and Jose, 2014) which is also heritable in blacks (Svetke, McKeown, and Wilson, 1996). A slavery hypothesis does exist to explain higher rates of hypertension in blacks, citing salt deficiency in the parts of Africa that supplied the slaves to the Americas, to the trauma of the slave trade and slavery in America. However, historical evidence does not show this to be the case because “There is no evidence that diet or the resulting patterns of disease and demography among slaves in the American South were significantly different from those of other poor southerners” (Curtin, 1992) whereas Campese (1996) hypothesizes that blacks are more likely to get hypertension because they evolved in an area with low salt.
The NYT article concludes:
Science seeks to categorize nature, to sort it into discrete groupings to better understand it. That is one way to comprehend the race concept: as an honest scientific attempt to understand human variation. The problem is, the concept is imprecise. It has repeatedly slid toward pseudoscience and has become a major divider of humanity. Now, at a time when we desperately need ways to come together, there are scientists — intellectual descendants of the very people who helped give us the race concept — who want to retire it.
Race is a useful concept. Whether in medicine, population genetics, psychology, evolution, physiology, etc it can elucidate a lot of causes for differences between races and ethnic groups—whether or not they are genetic or psychosocial in nature. That just attests to both the power of suggestion along with psychosocial factors in regards to racial differences in physiological factors.
Finally let’s see what the literature says about race in medicine. Bonham et al (2009) showed that both black and white doctors concluded that race is medically relevant but couldn’t decide why however they did state that genetics did not explain most of the disparity in relation to race and disease aside from the obvious disorders like Tay Sachs and sickle cell anemia. Philosophers accept the usefulness of race in the biomedical sciences (Andreason, 2009; Efstathiou, 2012; Hardimon, 2013; Winther, Millstein, and Nielsen, 2015; Hardimon, 2017) whereas Risch et al (2002) and Tang et al (2002) concur that race is useful in the biomedical sciences. (See also Dorothy Roberts’ Ted Talk The problem with race-based medicine which I will cover in the future). Richard Lewontin, naturally, has hang-ups here but his contentions are taken care of above. Even if race were a ‘social construct‘, as Lewontin says, it would still be useful in a biomedical sense; but since there are differences between races/ethnic groups then they most definitely are useful in a biomedical sense, even if at the end of the day individual variation matters more than racial variation. Just knowing someone’s race and SES, for instance, can tell you a lot about possible maladies they may have, even if, utltimately, individual differences in physiology and anatomy matter more in regards to the biomedical context.
In conclusion, race is most definitely a useful concept in medicine, whether race is a ‘social construct’ or not. Just using Michael Hardimon’s race concepts, for instance, shows that race is extremely useful in the biomedical context, despite what naysayers may say. Yes, individual differences in anatomy and physiology trump racial differences, but just knowing a few things like race and SES can tell a lot about a particular person, for instance with blood pressure, resting metabolic rate, and so on. Denying that race is a useful concept in the biomedical sciences will lead to more—not less—racial health disparities, which is ironic because that’s exactly what race-deniers do not want. They will have to accept a race concept, and they would accept Hardimon’s socialrace concept because that still allows it to be a ‘social construct’ while acknowledging that race and psychosocial factors interact to cause higher physiological variables. Race is a useful concept in medicine, and if the medical establishment wants to save more lives and actually end the racial disparities in health then they should acknowledge the reality of race.
If you look at the winners of the Mr. Olympia contest over the past ten years you will see a trend. Although there were only three winners in this time period, 2 were black while one was white. Dexter Jackson, a black man, won in 2008, with the apt nickname “The Blade” due to his body type and how sliced and diced he is. Jay Cutler then won in 2009 and 2010, with previous wins in 2006 and 2007. Then Phil Heath came along and has dominated for the past 7 years while it looks like no one will dethrone him for a while (I personally think that Shaun Rhoden has a chance). So why do blacks dominate this sport?
A few things come into play here: somatype, fat-free body mass, grit, determination, and of course mass amounts of steroids. However, everyone uses steroids when it comes to these elite competitions so that’s a non-factor. What comes into play is how bad you want it, along with, of course, outstanding genetics.
When talking about bodybuilding, discussions on fat-free mass almost always pop up. Blacks have lower fat-free mass than whites, with thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). So taking an elite white and black bodybuilder at similar body fat levels, the black bodybuilder will show more cuts and thusly, in theory, place better than the white bodybuilder, all things being equal.
The reigning Mr. Olympia (seven years in a row) states that “I definitely had the genetics on my side – no question about it – because without that, you’re only gonna go so far in bodybuilding.” And he is right. He has some crazy genetics, especially to get and maintain that level of leanness he does. Of course, his training regimen comes into play here. He, for instance, trains at latitude since he lives in Denver, Colorado which is called altitude training where he gets certain physiological advantages compared to those who do not train at altitude.
You can even see this in tribes like the Kalenjin, the subgroup in Kenya that pumps out the most long-distance runners. The highest point in Kenya is 5,197 meters. You’d need certain physiological advantages to be able to live and work at that high of an altitude. These trends are noticed in America too, even. For instance, Colorado is one of the leanest states whereas near the Gulf of Mexico—basically at sea level—obesity rates are higher. Now I’m aware that correlation doesn’t equal causation, however, people that live in Colorado are more likely to be active and partake in activities such as hiking, whereas there are large amounts of physical inactivity near the Gulf.
Living and training at altitude may cause other pertinent changes in the body and how it uses energy. For instance, fatty acid oxidation may be higher while there is evidence that appetite is suppressed at altitude. In Denver, there are physiological changes that lead to fat loss:
Denver has seasonal variations that range from tolerably cold but freezing lows for five months of the year, to pleasantly warm highs in the mid-60s to upper 80s the remainder of the year. Temperatures thst for not impede outdoor activities but rouse the body to react to thermal change. The thermoneutral temperature for humans is about 82 degrees Fahrenheit, so Denver residents are forced to maintain body temperature through activity, brown fat activation (which burns fat for heat instead of energy) or wearing more insulated clothing.
This is something I touched on in my article Human Physiological Adaptations to Climate. Our physiology is homeodynamic, not homeostatic as is commonly stated (Lloyd, 2001). Due to this, our physiology can change to match the environment, and thus is due to our intelligent physiological systems which is driven by intelligent cells.
Nevertheless, altitude training is at least part of the reason why Phil Heath is the best of the best in bodybuilding. Though, what other advantages do blacks have other than thinner skin folds which gives them a more ‘3d’ look, on average?
Training is why bodybuilders look different from powerlifters. It has also been reported that bodybuilders have “unusually high values of type IIx fibers” while other studies show no difference while there may be a difference between type IIa and type IIx fibers between strength and power athletes. Nevertheless, there are somatypic differences between bodybuilders and weightlifters (I’ll provide the cite here later, I’m typing this on my phone; for the time being, the paper is titled A Comparative Study of Body Builders and Weight Lifters on Somatotypes):
The result of the study showed that there was a significant difference between body builders and weight lifters of their endomorph. Weightlifters are tend to have more fat percentage as compared to bodybuilders. There was not much difference found in the mesomorphy status of the bodybuilders and weightlifters but the bodybuilders showed slightly more musculature than the weightlifters and in the ectomorphy status bodybuilders tend to be more ectomorph than weightlifters.
On the basis of obtained results it is concluded that there was a statistical significant difference between body builders and weight lifters in their Endomorph and Ectomorph. Insignificant difference found in Ectomorph of Body Builders and Weight Lifters.
This makes sense. In the study, bodybuilders skewed more meso whereas weightlifters skewed more endo, with bodybuilders skewing more ecto than weightlifters. (For an overview of somatypes read my article Racial Differences in Somatype.) Champion bodybuilders skew extremely meso with little skew in endomorphy. Again, knowing about the average proportions of a somatype will tell you a lot about someone and which things, on average, they will excel at due to levers, bone density, body proportions etc. The same proportions are seen in Brazilian bodybuilders (Silva et al, 2003).
In conclusion, why do blacks dominate bodybuilding? Well, it may possibly be due to fiber type distribution, but that is contested by other studies. Their main advantage seems to be—and that is why they dominate other sports as well—their somatype. Another reason is thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000) gives a more ‘3D look’. Look at champion bodybuilders and their levers and overall body frame. They differ widely from weightlifters and powerlifters. Some—or most—of the difference in look between bodybuilders and weightlifters is due to differences in training.
In regards to the current best in the world with seven straight wins at the Olympia, Phil Heath, he does a special type of training, but he also has ridiculous genetics. Now, I’m not saying that genetics is the be-all-end-all here because training and intensity set the men apart from the boys. But, as is the case in a lot of areas in life, if you don’t have the right genetics you won’t excel in certain areas. Phil Heath’s nickname is “The Gift”, and it’s a very apt one at that.
I will cover why whites dominate powerlifting and strength competitions later, and the same holds there: somatype (along with muscle fiber differences) is one of the main predictive variables that cause differences in these sports.
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!
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.
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:
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.
By meLo, 1340 words
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.
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 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.
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.
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.
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.
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.
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.)
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).
Heightened testosterone is not a direct cause of male violence.
(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).
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.