Home » HBD (Page 10)
Category Archives: HBD
Differing Race Concepts and the Existence of Race: Biologically Scientific Definitions of Race
2700 words
Do you need to look at genetic differences between races to see if race is real? Some may argue that you do, and when you do you’ll see that genetic variation is too small to say that race exists. However, other arguments exist that do not look at genetic differences between races, but look at geographic ancestry, reproductive isolation between races, and morphologic differences. Those three variables are enough to prove the existence of race without looking at genetic differences between races. They do correspond to genetic differences between races. The four concepts I will briefly lay out are from Michael Hardimon, professor of philosophy at University of California, San Diego. The concepts are the racialist concept of race, minimalist concept of race concept, populationist concept of race, and the socialrace concept of race. One doesn’t need to look at the racialist concept of race to prove the existence of race, which I will prove below.
Michael Hardimon published Rethinking Race: The Case for Deflationary Realism earlier this year. In the book, he makes the case that race exists if minimalist race exists (I will get into what minimalist race entails below). Nevertheless, race deniers will say that even by looking at variables such as morphology, reproductive isolation, and geographic ancestry, race as a concept is scientifically invalid. This is patently false.
Concepts of race
The racialist concept of race
Hardimon’s first race concept is the racialist concept. The racialist concept (keep in mind, this is, as Hardimon writes on page 17 of his book Rethinking Race “the specific concept I have dubbed “the racialist concept” which “is hierarchal“) as defined by Hardimon holds that “racialist race is the idea of a fundamental division between groups and individuals” (Hardimon, 2017: 17). I think that Hardimon strawmans the racialist concept as he as defined it, but that’s for another day.
He also says that the racialist concept “is closely associated with racism” while the terms racialism and racism are “sometimes used interchangeably” (Hardimon, 2017: 17).
His argument against the racialist concept of race (as he defines it) is as follows (Hardimon, 2017: 21):
A third line of argument starts from the idea that in order for racialist races to exist, certain things must be true of human genetics, namely the following:
(a) The fraction of human genetic diversity between populations must exceed the fraction of diversity between them.
(b) The fraction of human genetic diversity within populations must be small.
(c) The fraction of diversity between populations must be large.
(d) Most genes must be highly differentiated by race.
(e) The variation in genes that underlie obvious physical differences must be typical of the genome in general.
(f) There must be several important genetic differences between races apart from the genetic differences that underlie obvious physical differences.
Note: (b) says that racialist races are genetically racially homogeneous groups; (c)-(f) say that racialist races are distinguised by major biological differences.
Call (a)-(f) the racialist concept of race’s genetic profile.
Now that his argument against the racialist concept (as he defines it) is laid out, you can see why I said that I think he strawmans the racialist concept. But I’ll get into that another day.
He then cites Lewontin’s (1972) analysis of blood groups by race as evidence against the racialist concept. Lewontin found that 85.4 percent of total human variation fell within populations. He also found that populations that populations classically defined as human races (Caucasians, Africans, Mongoloids, South Asian Aborigines, American Indians, and Oceanians) accounted for 8.3 percent of total human variation. Total variation between the classically defined races accounted for 6.3 percent of the variance.
It’s worth noting that the numbers given by Lewontin are true; where he goes wrong is assuming that there is no taxonomic significance for race based on the data he got from his analysis. “Call this Lewontin’s cleaver,” writes Hardimon on page 22.
Then in 2002, 31 years after Lewontin published his analysis, A.W.F. Edwards published his paper Human Genetic Diversity: Lewontin’s Fallacy. (Edwards, 2003). In the paper, Edwards argues that Lewontin’s conclusion is incorrect. Edwards (2003: 800-801) writes in his conclusion (emphasis mine):
There is nothing wrong with Lewontin’s statistical analysis of variation, only with the belief that it is relevant to classification. It is not true that ‘‘racial classification is … of virtually no genetic or taxonomic significance’’. It is not true, as Nature claimed, that ‘‘two random individuals from any one group are almost as different as any two random individuals from the entire world’’, and it is not true, as the New Scientist claimed, that ‘‘two individuals are different because they are individuals, not because they belong to different races’’ and that ‘‘you can’t predict someone’s race by their genes’’. Such statements might only be true if all the characters studied were independent, which they are not.
Of course, Lewontin’s conclusion is fallacious because small genetic differences do not entail that racial classification that race has no taxonomic significance (Richard Dawkins accepts the taxonomic existence of race). As you can see from the quote from Edwards, he does not object to Lewontin’s analysis of the races, he objects to his conclusion—namely that races do not exist based on the within-race variation being greater than between-race variation.
On page 22-23, Hardimon writes about Edwards’ objection to Lewontin’s conclusion:
Lewontin’s locus-by-locus analysis (which does not consider the possibility of a correlation between individual loci) does not preclude the possibility that individual loci might be correlated in such a way that people could be grouped into traditional racial categories. The underlying thought is that racial classification would have “taxonomic significance” were it possible to group people into traditional racial categories by making use of correlations between individual loci. However, Lewontin’s argument that there are no racialist races because the component of within-race genetic variation is larger than the component of between-race variation is untouched by Edwards’s objection.
In 2002, Rosenberg et al, in their paper Genetic Structure of Human Populations confirmed Lewontin’s analysis. They looked at 377 autosomal loci in 1,056 individuals from 52 populations and found that within-population differences between major groups (Africa, Europe, Asia, the Middle East, Central and South Asia, East Asia, Oceania, and America) accounted for 3-5 percent of genetic variation while genetic differences between individuals accounted for 93-95 percent of genetic variation. So Rosenberg et al (2002) confirmed Lewontin’s (1972) analysis—though do recall that Lewontin’s conclusion is incorrect. According to Hardimon’s interpretation of the racialist concept of race, both Lewontin’s and Rosenberg et al’s analysis disprove the racialist concept of race, but that doesn’t mean that there is no scientific basis for the biological reality of race (Hardimon, 2012).
The minimalist concept of race
The minimalist concept of race is similar to the racialist concept, though there are some stark differences. It does not say that there are intrinsic differences between races—call them essences if you will), but it does say that you can distinguish races by patterns of different physical features such as skin color, hair type, nose shape, morphology, etc, which then correspond to differences in geographic ancestry in geographically, genetically isolated breeding populations.
The minimalist concept of race further states that (i) races are distinguised from other races by patterns of visible physical features; (ii) the members are linked by a common ancestry which is peculiar to members of the group; and (iii) this group must originate from a distinct location.
The minimalist concept of race does not require: that the fraction of human genetic diversity between minimalist races is larger than the fraction of diversity within them; it is compatible with within-race diversity being large and between-race diversity being small; it does not require most genes to be highly differentiated by race; it does not require the existence of a lot genetic differences between races that underlie more than the phenotypic differences already noticed; the concept does not imply that there can be predictions made from yet unstudied characteristics; it finally does not require any genetic differences between races other than those found in the genes that underlie differences in physical appearance between race. This is called the minimalist concept of biological race (Hardimon, 2017: 66) and it survives all objections from Lewontin’s and Rosenberg et al’s analysis of between-race genetic variation.
This is my favorite race concept, personally, because it covers any and all objections from the race-denialist crowd—people who deny any genetic differences between races—because the only genetic differences it counts on are those physical traits that are already noticed.
Hardimon (2017: 29) writes:
Such readers should feel free to regard the minimalist concept of race, that is, as a concept that, though in many respects similar to the ordinary concept, is nonetheless distinct from it. What I would insist on is that minimalist races (groups satisfying the minimalist concept of race) are *races* (that is races so properly called)—either because the minimalist concept of race just is the ordinary concept of race or because it captures enough of the ordinary concept of race for minimalist races to be counted as races. My view is that if it can be shown that minimalist races exist, races exist. And if it can be shown that *minimalist race* is real, race is real.
The populatonist concept of race
The populationist concept of race is a nonessentialist, non-hierarchical concept of race that slightly differs from the minimalist concept of race. The populationist concept of race can be said to be a scientific concept of race (as can the minimalist concept) because it characterizes races as groups belonging to different groups of biological descent, they are distinguished by patterns of phenotypic differences, and these phenotypic differences trace back to geographically separated and genetically isolated founding populations.
The populationist concept of race also holds that “A race is a subdivision of Homo sapiens—a group or population that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographical ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population” (Hardimon, 2017: 99). So with these criteria, you can see that even if you do not accept the racialist concept of race (as Hardimon defines it), you can still be a race realist. The populationist concept is likely to exist, and if the populationist concept of race exists then race is real.
Defining race as geographically and reproductively isolated breeding populations that share a common line of biological descent with similar phenotypic characters is as barebones a concept of race as you can get—and it is perfectly in line with how most people view races on the basis of phenotypic characterization. The populationist concept of race supposes that numerous concepts from the racialist concept of race are true—but do not presuppose any to-be-studied differences between those races. The strength of the populationist argument, as you can see, is very strong and it holds up to numerous lines of criticism very well. Although both the populationist and minimalist race concepts do not presupposed any to-be-studied differences between races, this still is not good enough for race deniers.
It is clear that without even looking at the brain and physiological differences between races, that race does indeed exist and it does—contrary to popular belief—have implications for people’s health of certain races.
The socialrace concept of race
Finally, the last concept of race laid out by Hardimon is the concept of socialrace. The concept of socialrace takes a race to be a racialist race, it refers to a position that is occupied by a social group that is a socialrace, and the socialrace concept refers to the system of social positions that are socialraces. This concept of race is, clearly, different from the minimalist and populationist race concepts but does indeed correlate with popular notions of race (and would correlate with the minimalist and populationist concept of race very well). The socialrace concept is, basically, what is believed to be racialist races.
The concept of socialrace is a concept of race as a social group (Hardimon, The Ontology of Race: 31)
The socialrace concept differs from the minimalist and populationist concept of race in that it looks at so-called social—not biological—correlates of race. Though, still, the socialrace concept can be said to show the reality of race since how one socially defines themselves correlates almost perfectly with geographic ancestry (which is a prerequisite for the existence of the minimalist concept of race and the populationist concept of race) (Tang et al, 2005). They showed that self-identified racial categories lined up almost perfectly with geographic ancestry (99.86 percent of the time). So, as you can see, the concept of socialrace also gives credence to the existence of the minimalist and populationist concepts of race.
This concept of race—as its name implies—does not talk race is a biological manner, but a social one, as its name implies. However, due to the extremely high chance that one’s self-identified race (their socialrace) lines up with the geographic ancestry of the classical races, we can see that the socialrace concept further buttresses the argument for the existence for the reality of the minimalist concept of race and the populationist concept of race.
The socialrace concept is kind of like Templeton (2014) defines race: that human races exist in a cultural sense, but not biologic sense. I have shown, though, that races exist in a cultural, social, and biological sense with the arguments presented in this article. Socialrace, culturalrace, whatever you want to call it, it is evidence for the existence of race.
Conclusion
Race exists whether or not the racialist position of race (as Hardimon defines it) is true or not. The minimalist concept of race and populationist concept of race show that race is real while the concept of socialrace further lends credence to the biological models of the minimalist and populationist concept of race. Even still, people who deny race because the genetic distance between races is too small for their to be any meaningful differences between them do not accept that three arguments above (sans the racialist concept) for the existence of race. They’ll still talk about the genetic differences between them and, say, morphology, but the minimalist concept of race and the populationist concept of race define race in enough of a way that genetic differences do not need to be looked at—we can only look at reproductive isolation, morphology, geographic ancestry and physical differences between minimalist and populationist races such as hair, nose, and skin color along with morphological differences.
Minimalist and populationist races exist and are a biological reality. We can take those two concepts to be a scientific basis for race. While we can take the concept of socialrace not as a biological concept, but as a social concept and we can then say that socialrace is socially real while being a significant social reality. That social reality is manifested by noticing different racial phenotypes, along with differences in SES, educational attainment, etc, and placing different races in different average social positions, which would correlate with the concepts of race mentioned above. This also correlated nearly perfectly with geographic ancestry. So, I’m saying it again, the existence of race as a social reality is real; the existence of socialrace buttresses the arguments for both the existence of the minimalist concept of race and the populationist concept of race—both of which are scientific concepts of race.
Minimalist races exist, and is a superficial biological reality, populations races may exist and if they exist, they are a relatively superficial biological reality. Socialraces exist and are a social reality which also lend credence to the minimalist and populationist concepts. I personally am privy to the minimalist race concept because it is shown to be real, so race is real.
In sum, race exists whether you look at genetic differences between races or not, morphology, geographic ancestry, reproductive and genetic isolation are all you need to prove the existence of race. There is a scientific concept of race, and the minimalist and populationist race concepts provide the existence for it, while the socialrace concept does as well. It is clear that for a scientific concept of race, you only need phenotypic variation, morphologic variation between races,
(Also read the American Rennaisance review for the book, A Tactical Retreat for Race Denial. I think it is balanced and fairly written, though a bit biased and doesn’t account for Hardimon’s views well enough in my opinion.)
My Response to Jared Taylor’s Article “Breakthroughs in Intelligence”
1300 words
Here is my reply to Jared Taylor’s new article over at AmRen Breakthroughs in Intelligence:
“The human mind is not a blank slate; intelligence is biological”
The mind is not a ‘blank slate’, though there is no ‘biological’ basis for intelligence (at least in the way that hereditarians believe). They’re just correlations. (Whatever ‘intelligence’ is.)
“there is no known environmental intervention—including breast feeding”
There is a causal effect of breast feeding on IQ:
While reported associations of breastfeeding with child BP and BMI are likely to reflect residual confounding, breastfeeding may have causal effects on IQ. Comparing associations between populations with differing confounding structures can be used to improve causal inference in observational studies.
Brion, M. A., Lawlor, D. A., Matijasevich, A., Horta, B., Anselmi, L., Araújo, C. L., . . . Smith, G. D. (2011). What are the causal effects of breastfeeding on IQ, obesity and blood pressure? Evidence from comparing high-income with middle-income cohorts. International Journal of Epidemiology, 40(3), 670-680. doi:10.1093/ije/dyr020
Breastfeeding is related to improved performance in intelligence tests. A positive effect of breastfeeding on cognition was also observed in a randomised trial. This suggests that the association is causal.
Horta, B. L., Mola, C. L., & Victora, C. G. (2015). Breastfeeding and intelligence: a systematic review and meta-analysis. Acta Paediatrica, 104, 14-19. doi:10.1111/apa.13139
“before long we should be able to change genes and the brain itself in order to raise intelligence.“
Which genes? 84 percent of genes are expressed in the brain. Good luck ‘finding’ them…
These results corroborate with the results from previous studies, which have shown 84% of genes to be expressed in the adult human brain …
Negi, S. K., & Guda, C. (2017). Global gene expression profiling of healthy human brain and its application in studying neurological disorders. Scientific Reports, 7(1). doi:10.1038/s41598-017-00952-9
“Normal people can have extraordinary abilities. Prof. Haier writes about a non-savant who used memory techniques to memorize 67,890 digits of π! He also notes that chess grandmasters have an average IQ of 100; they seem to have a highly specialized ability that is different from normal intelligence. Prof. Haier asks whether we will eventually understand the brain well enough to endow anyone with special abilities of that kind.”
Evidence that intelligence is not related to expertise.
“It is only after a weight of evidence has been established that we should have any degree of confidence in a finding, and Prof. Haier issues another warning: “If the weight of evidence changes for any of the topics covered, I will change my mind, and so should you.” It is refreshing when scientists do science rather than sociology.”
Even with the “weight of evidence”, most people will not change their views on this matter.
“Once it became possible to take static and then real-time pictures of what is going on in the brain, a number of findings emerged. One is that intelligence appears to be related to both brain efficiency and structure”
Patterns of activation in response to various fluid reasoning tasks are diverse, and brain regions activated in response to ostensibly similar types of reasoning (inductive, deductive) appear to be closely associated with task content and context. The evidence is not consistent with the view that there is a unitary reasoning neural substrate. (p. 145)
Nisbett R. E., Aronson J., Blair C., Dickens W., Flynn J., Halpern D. F., Turkheimer E. Intelligence: New findings and theoretical developments. American Psychologist. 2012;67:130–159. doi: 10.1037/a0026699.
“Early findings suggested that smart people’s brains require less glucose—the main fuel for brain activity—than those of dullards.”
Cause and correlation aren’t untangled; they could be answering questions in a familiar format, for instance, and this could be why their brains show less glucose consumption.
“It now appears that grey matter is where “thinking” takes place, and white matter provides connections between different areas of grey matter. Some brains seem to be organized with shorter white-matter connections, which appear to allow more efficient communication, and there seem to be sex differences in the ways the part of the brain are connected. One of the effects of aging is deterioration of the white-matter connections, which reduces intelligence.”
Read this commentary (pg. 162): Norgate, S., & Richardson, K. (2007). On images from correlations. Behavioral and Brain Sciences, 30(02), 162. doi:10.1017/s0140525x07001379
“Brain damage never makes people smarter”
This is wrong:
You would think that cutting out one-half of people’s brains would kill them, or at least leave them vegetables needing care for the rest of their lives. But it does not. Consider this striking story. A boy starts having seizures at 10 years of age when his right cerebral hemisphere atrophies. By the time he is 12, the left side of his body is paralyzed. When he is 19, surgeons decide to operate and remove the right side of his brain, as it is causing gits in his intact left one. You might think this would lower his IQ or leave him severely retarded, but no. His IQ shoots up 14 points, to 142! The mystery is not so great when you realize that the operation has gotten rid of the source of his fits, which had previously hampered his intelligence. When doctors saw him 15 years later, they described him as “having obtained a university diploma . . . [and now holding] a responsible administrative position with a local authority.”
Skoyles, J. R., & Sagan, D. (2002). Up from dragons: the evolution of human intelligence. New York: McGraw-Hill (pg. 282)
“Prof. Haier wants a concerted effort: “What if a country ignored space exploration and announced its major scientific goal was to achieve the capability to increase every citizen’s g-factor [general intelligence] by a standard deviation?””
Don’t make me laugh. You need to prove that ‘g’ exists first. Glad to see some commentary on epigenetics that isn’t bashing it (it is a real phenomenon, though the scope of it in regards to health, disease and evolution remains to be discovered).
As most readers may know, I’m skeptical here and a huge contrarian. I do not believe that g is physiological and if it were then they better start defining it/talking about it differently because I’ve shown that if it were physiological then it would not mimick any known physiological process in the body. I eagerly await some good neuroscience studies on IQ that are robust, with large ns, their conclusions show the arrow of causality, and they’re not just making large sweeping claims that they found X “just because they want to” and are emotionally invested in their work. That’s my opinion about a lot of intelligence research; like everyone, they are invested in their own theories and will do whatever it takes to save face no matter the results. The recent Amy Cuddy fiasco is the perfect example of someone not giving up when it’s clear they’re incorrect.
I wish that Mr. Taylor would actually read some of the literature out there on TBI and IQ along with how people with chunks of their brains missing can have IQs in the normal range, showing evidence that most a lot of our brain mass is redundant. How can someone survive with a brain that weighs 1.5 pounds (680 gms) and not need care for the rest of his life? That, in my opinion, shows how incredible of an organ the human brain is and how plastic it is—especially in young age. People with IQs in the normal range need to be studied by neuroscientists because anomalies need explaining.
If large brains are needed for high IQs, then how do these people function in day-to-day life? Shouldn’t they be ‘as dumb as an erectus’, since they have erectus-sized brains living in the modern world? Well, the human body and brain are two amazing aspects of evolution, so even sudden brain damage and brain removal (up to half the brain) does not show deleterious effects in a lot of people. This is a clue, a clue that most of our brain mass after erectus is useless for our ‘intelligence’ and that our brains must have expanded for another reason—family structure, sociality, expertise, etc. I will cover this at length in the future.
Racial Differences in Physical Activity and Acquisition of Coronary Artery Calcification
1200 words
Last week a study was published stating that white men who exercised 3 times the recommendation of 1.5 hours (450 minutes, 7.5 hours) had a higher chance of getting coronary artery calcification (CAC), which is the accumulation of plaque and calcium in the arteries of the heart. You, of course see news headlines such as: “Physically active white men at high risk for plaque buildup in arteries“; “White Men Who Exercise Every Day Have 86 Per Cent Higher Risk of Heart Disease Than Black Men, Study Claims“; “Excessive Exercise May Harm The Heart, Study Suggests “; “Excessive exercise increases risk of arterial plaque buildup in white men“; (and my personal favorite headline about this study): “You can exercise yourself to death, says new study“. People just passing by and reading the title (like most do) may then conclude that “they’re saying not to exercise because of CAC.” No, this is not what they are saying at all.
The Coronary Artery Risk Development in Young Adults (CARDIA) study is one of the most important studies in the study of coronary heart disease that have been undertaken. It is a sample of men and women, about equal numbers of each race, from Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; and Oakland, California. The study began in 1985-86 and there were follow-up examinations at “1987-1988 (Year 2), 1990-1991 (Year 5), 1992-1993 (Year 7), 1995-1996 (Year 10), 2000-2001 (Year 15), 2005-2006 (Year 20), 2010-2011 (Year 25), and 2015-2016 (Year 30).” The CARDIA website writes:
Data have also been collected on physical measurements such as weight and body composition as well as lifestyle factors such as dietary and exercise patterns, substance use (tobacco and alcohol), behavioral and psychological variables, medical and family history, and other chemistries (e.g., insulin).
So there is a goldmine of information to be gleaned from this data. The study that is getting press in the news uses data from this cohort.
The study
The study is titled 25-Year Physical Activity Trajectories and Development of Subclinical Coronary Artery Disease as Measured by Coronary Artery Calcium by Laddu et al (2017). They studied three cohorts by the amount of time they exercised per week: below requirement, at requirements, or above requirements. It is recommended to exercise at least 150 minutes per week.
There were 3,175 men and women who participated in the CARDIA study between 1985 and 2011 who had CAC data available for 25 years. About 47.4 percent of the sample was black, with 56.6 being women. The cohort “consisted of 18.9% black men, 24.6% white men, 28.6% black women, and 28.0% white women” (Laddu et al, 2017).
Of the three activity levels they studies (below 150 minutes, 150 minutes, and over 150 minutes), they observed that white men who exercised 3 times the weekly recommendation (150 minutes(3)= 450 minutes=7.5 hours) had a higher chance of developing CAC. It’s worth noting that exercise time was self-reported (which is the only way I can see how something like this would work, are you supposed to follow people with a camera every day to see how long they engage in physical activity?).
In regards to the physical activity measurement, Laddu et al (2017) write:
At each of the 8 examinations, self-reported leisure-time PA was ascertained by the interviewer-administered CARDIA Physical Activity History Questionnaire.17 Participants were asked about the frequency of participation in 13 specific categories (8 vigorous intensity and 5 moderate intensity) of recreational sports, exercise, home maintenance, and occupational activities during the previous 12 months. Intensity for each activity was expressed as metabolic equivalents (METs), in which 1 MET is defined as the energy expended at rest, which is approximately equivalent to an oxygen consumption of 3.5 mL per 1 kg of body weight per minute.18Vigorous activities (≥6 METs) included running or jogging; racquet sports; biking; swimming; exercise or dance class; job lifting, carrying, or digging; shoveling or lifting during leisure; and strenuous sports. Moderate-intensity activities (3-5 METs) included nonstrenuous sports, walking and hiking, golfing and bowling, home exercises or calisthenics, and home maintenance or gardening.19 Each activity was scored according to whether it was performed for 1 hour or longer during any 1 month during the past year, the number of months it was performed at that level, and the number of months the activity was performed frequently. Each activity was then assigned an intensity score, ranging from 3 to 8 METs, and a duration threshold (ranging from 2-5 hours per week), above which participation was considered to be frequent.20
This is a good metric; though I would like to see a study that looks at just gym-going activity and death, time spent in the gym strength training/moderate to intense cardio. Nevertheless, white men who reported more physical activity had a higher chance of acquiring CAC. Though I can see people’s recall being hazy, people over/under reporting, etc etc.
White men who exercised 7.5 hours per week were 27 percent more likely to get CAC, whereas blacks who exercised that much were at no greater risk to acquire CAC when compared to whites (7.5 hours of exercise compared to less than 2.5 hours per week). Black women who exercised less than the recommendations had a higher chance of acquiring CAC. The researchers couldn’t ascertain why white men who exercised three times the recommendations had such a higher chance of acquiring CAC by the time they reached middle age, but Dr. Jamal Rana says “however this plaque buildup may well be of the more stable kind, and thus less likely to rupture and causes heart attack, which was not evaluated in this study.” The head author, Dr. Deepika Laddu also reiterated: “it does not suggest that anyone should stop exercising.” So people who just read these click bait headlines who say “They’re telling whites not to exercise!”, you’re wrong and you should read papers and not news articles.
This is the perfect example of people reading click baity, fear-mongering headlines and running with it. I saw some people saying “They’re telling us not to exercise!” No. If you were to read the paper and any serious news articles on the matter, you’d see that they do not recommend that people do not exercise. Now the question is, why do whites who exercise more than 7.5 hours per week have a higher chance of acquiring heart disease? I can think of a few explanations (though they are not satisfactory): 1) genes: which genes? Why? How do they interact with the body over time to lead to arterial calcification?; 2) dietary habits: I’d like to know what their diet was like and see their macro composition, carbohydrates, not saturated fat, causes heart disease (Siri-Tirino et al, 2010; de Souza et al, 2015) so that may be a huge contributing factor.
Nevertheless, this is yet another physiological race difference. Oddly enough, black men are more likely than white men to have hypertension (Hicken et al, 2013).
Even though black men, on average, have higher rates of hypertension than white men, white men who are physically active for 7.5 had a higher chance of acquiring CAC than those who exercised less than 2.5 hours per week. This effect wasn’t seen in black men who had physical activity at that level, which, of course, implies that differences in genes and SES underlie this difference. I await more papers into this matter into the mechanisms of how and why this occurs and will ruminate on this myself in the future. No, this study does not tell white men not to exercise.
Evidence for Natural Selection in Humans: East Asians Have Higher Frequency of CASC5 Brain Size Regulating Gene
1500 words
Brain size is one physical difference that the races differ on. East Asians have bigger brains than Europeans who have bigger brains than Africans (Beals et al, 1984; Rushton, 1997). What caused these average differences and the ultimate causes for them have been subject to huge debate. Is it drift? Natural/sexual selection? Mutation? Gene flow? Epigenetic? One reason why brains would need to be large in colder climates is due to heat retention, while in tropical climates heads need to be smaller to dissipate heat. One of the biggest criticisms of HBD is that there is no/little evidence of recent natural selection between human races. Well, that has changed.
CASC5 “performs two crucial functions during mitosis, being required for correct attachment of chromosome centromeres to the microtubule apparatus, and also essential for spindle-assembly checkpoint (SAC) signaling” (Shi et al, 2016). The gene has been found to be important in recent human evolution along with neurogenesis.
Shi et al (2016) genotyped 278 Han Chinese (174 females and 104 males with a mean age of 36) who were free of maladies or genetic defects. They had the coding sequences of CASC5 for humans, chimpanzees, gorillas, baboons, gibbons, orangutans, tarsiers, Denisovans, and Neanderthals. They downloaded genotypes from the Human Genome Project for their analysis.
They compared CASC5 among three human species: humans, Neanderthals, and Denisovans. Using chimpanzees as an outgroup, they discovered 45 human-specific mutations, 48 Neanderthal-specific mutations, and 41 Neanderthal-specific mutations. Further, when one exon region was aligned among modern humans, non-human primates and other mammalian species, 12 amino acid sites showed divergence between modern humans, Neanderthals, and Denisovans with 8 occurring in modern humans. Of the 8 sites in humans, 6 are preserved which implies that they were important in our evolutionary history.
Shi et al (2016) write:
At the population level, among the 8 modern human amino acid changes, two (H159R and G1086S) are fixed in current human populations, and the other six are polymorphic Fig. 1). Surprisingly, 5 of the 6 amino acid polymorphic sites showed deep between-population divergence in allele frequencies. East Asians possess much higher frequencies of the derived alleles at four sites (T43R-rs7177192, A113T-rs12911738, S486A-rs2412541 and G936R-rs8040502) as compared to either Europeans or Africans (Fig. 1), while E1285K-rs17747633 is relatively enriched in Europeans (46%), and rare in East Asians (10%) and Africans (3%). No between-population divergence was observed for T598 M-rs11858113 (Fig. 1).
So East Asians have a much higher frequency of this derived trait. This is direct evidence for natural selection in recent human evolution in regards to the physical structure of the brain.
Since most of the amino acid polymorphic sites showed between-population divergence, they decided to analyze the three classical races using 1000 genomes. The variation between the races could be due to either genetic drift or natural selection. When they analyzed certain gene regions, they observed a signal of positive selection for East Asians but not Europeans or Africans. They further tested this selection signal using “the standardized integrated haplotype score (iHS) which is used for detecting recent positive selection with incomplete sweep (i.e. the selected allele is not yet fixed)” (Shi et al, 2016). Using this method, they discovered a few SNPs with large iHS values in Europeans (7 SNPs at 4.2 percent) and none in Africans.
They also conducted a genome-wide scan of Fst, iHS, and “XPCLR (searching for highly differentiated genomimc regions as targets of selective sweeps)” (Shi et al, 2016). Several SNPs had high Fst, iHS and XPCLR scores, which indicate that these alleles have been under positive selection in East Asians. Among the fixed amino acid sites in human populations, East Asians showed 5, Europeans showed 1, and Africans showed 0 which, the authors write, “[imply] that these amino acid changes may have functional effects” (Shi et al, 2016). Furthermore, using the HDGP, they obtained the frequency of the 6 amino acid sites in 53 populations. This analysis showed that 4 of the 6 amino acid sites are “regionally enriched in East Asia .. in line with the suggested signal of population-specific selection in this area” (Shi et al, 2016).
Then, since CASC5 is a brain size regulating gene, they looked for phenotypic effects. They recruited 167 Han Chinese (89 men, 178 women) who were free of maladies. They genotyped 11 SNPs and all of the frequencies followed Harvey-Weinberg Equilibrium (which states that allele and genotype frequencies will remain constant in a population from generation to generation in the absence of evolutionary pressures; Andrews, 2010). In the female sample, 5 regions were related to gray matter volume and four were on the amino acid polymorphic sites. Interestingly, the four alleles which showed such a stark difference between East Asians and Europeans and Africans showed more significant associations in Han Chinese females than males. Those carrying the derived alleles had larger brain volumes in comparison with those who had the ancestral alleles, implying recent natural selection in East Asia for brain size.
Shi et al (2015) also attempted two replications on this allele writing:
We further conducted a replication analysis of the five significant CAC5 SNPs in two other independent Han Chinese samples (Li et al. 2015; Xu et al. 2015). The results showed that three SNPs (rs 7177192, rs11858113 and rs8040502) remained significant in Replication-1 for total brain volume and gray matter volume (Xu et al. 2015), but no association was detected in Replication-2 (Li et al. 2015) (Table S4).
It is very plausible that the genes that have regulated brain growth in our species further aid differences in brain morphology within and between races. This effect is seen mostly in Han Chinese girls. Shi et al (2016) write in the Discussion:
If this finding is accurate and can be further verified, it suggests that that [sic] after modern humans migrated out of Africa less than 100,000 years ago, the brain size may still be subject to selection.
I do believe it is accurate. Of course, the brain size could still be subject to selection; there is no magic field shielding the brain against selection pressure. Evolution does not stop at the neck.
So Shi et al (2016) showed that there were brain genes under recent selection in East Asians. What could the cause be? There are a few:
- Climate: In colder climates you need a smaller body size and big brain to survive the cold to better thermoregulate. A smaller body means there is less surface area to cover, while a larger head retains heat. It, obviously, would have been advantageous for these populations to have large brains and thus get selected for them—whether by natural or sexual selection. This could also have to do with the fact that one needs bigger eyes in colder environments, which would cause an increase in the size of the brain for the larger eyes, as well as being sharper visio-spatially.
- Intelligence: East Asians in this study showed that they had high levels of gray matter in the skull. Further, large brains are favored by an intermediately challenging environment (Gonzalez-Forero, Faulwasser, and Lehmann, 2017).
- Expertise: I used Skoyle’s (1999) theory on expertise and human evolution and applied it to racial differences in brain size and relating it to the number of tools they had to use which differed based on climate. Now, of course, if one group uses more tools then, by effect, they would need more expertise with which to learn how to make those tools so large brains would be selected for expertise—especially in novel areas.
- Vision: Large brains mean large eyes, and people from cold climates have large eyes and large brains (Pearce and Dunbar, 2011). Decreasing light levels select for larger eye size and visual cortex size in order to “increase sensitivity and maintain acuity“. Large eyeballs mean enlarged visual cortices. Therefore, in low light, large brains and eyes get selected for so one can see better in a low light environment.
Of course, all four of the examples below could (and probably do) work in tandem. However, before jumping to conclusions I want to see more data on this and how the whole of the system interacts with these alleles and these amino acid polymorphic sites.
In sum, there is now evidence for natural selection on East Asians (and not Africans or Europeans) that favored large brains, particularly gray matter, in East Asians with considerable sexual dimorphism favoring women. Four of the genes tested (MCPH1, ASPM, CDK5RAP2, and WDR62) are regulated by estradiol and contribute to sexual dimorphism in human and non-human primates (Shi et al, 2016). Though it still needs to be tested if this holds true for CASC5.
This is some of the first evidence that I have come across for natural selection on genes that are implicated in brain evolution/structural development between and within populations. It does show the old “Rushton’s Rule of Three“, that is, Mongoloids on top, Caucasians in the middle, and Negroids on bottom, though Caucasians were significantly closer to Africans than Mongoloids in the frequency of these derived alleles. I can see a HBDer going “They must be related to IQ”, I doubt it. They don’t ‘have’ to be related to IQ. It just infers a survival advantage in low light, cold environments and therefore it gets selected for until it reaches a high frequency in that population due to its adaptive value—whether spreading by natural or sexual selection.
MAOA, Race, and Crime: A Simple Relationship?
2400 words
When I first got into HBD back in 2012, one of the first things I came across—along with the research on racial IQs from Rushton, Lynn, Jensen et al—was that the races differed in a gene called MAOA-L, which has a frequency in Caucasians at .1 percent (Beaver et al, 2013), 54 percent in Chinese people (Lu et al, 2013; 56 percent in Maoris (Lea and Chambers 2007) while about 60-65 percent of Japanese people have the low-frequency version of this gene (Way and Lieberman, 2007).
So if these ethnies have a higher rate of this polymorphism and it is true that this gene causes crime, then the Chinese and Japanese should have the highest rates of crime in the world, since even apparently the effect of MAOA and violence and antisocial behavior is seen even without child abuse (Ficks and Waldman, 2014). Except East Asian countries have lower rates of crime (Rushton, 1995; Rushton and Whytney, 2002). Though, Japan’s low crime rate is relatively recent, and when compared with other countries on certain measures “Japan fares the same or worse when compared to other nations” (Barberet 2009, 198). This goes against a lot of HBD theory, and I will save that for another day. (Japan has a 99 percent prosecution rate, which could be due to low prosecutorial budgets; Ramseyer and Rasmusen, 2001. I will cover this in the future.)
The media fervor—as usual—gave the MAOA gene the nickname “the warrior gene“, which is extremely simplistic (I will have much more to say on ‘genes for’ any trait towards the end of the article). I will show how this is a very simplistic view.
The MAOA gene was first discovered in 1993 in a Dutch family who had a history of extreme violence going as far back as the 1890s. Since the discovery of this gene, it has been invoked as an ultimate cause of crime. However, as some hereditarians do note, MAOA only ’causes’ violence if one has a specific MAOA genotype and if they have been abused as a child (Caspi et al, 2002; Cohen et al, 2006; Beaver et al, 2009; Ferguson et al, 2011; Cicchetti, Rogosch, Thibodeau, 2012;). People have invoked these gene variants as ultimate causes of crime—that is, people who have the low-expressing MAOA variants are more likely to commit more crime—but the relationship is not so simple.
Maoris are more four times more likely to have the low-expressing gene variant than Europeans, the same holding for African Americans and Europeans (Lea and Chambers, 2007).
There is, however, a protective effect that protects whites (and not non-whites in certain cases) against antisocial behavior/violent attitudes if one has a certain genotype (Widom and Brzustowicz, 2006), though the authors write on page 688: “For non-whites, the effect of child abuse and neglect on the juvenile VASB was not significant (beta .08, SE .11, t 1.19, ns), whereas the effect of child maltreatment on lifetime VASB composite approached significance (beta .13, SE .12, t 1.86, p .06). For non-whites (see Figure 2), neither gene (MAOA) environment (child abuse and neglect) interaction was significant: juvenile VASB (beta .06, SE .28, t .67, ns) and lifetime VASB (beta .01, SE .29, t .14, ns).” So as you can see, there are mixed results. Whites seem to be protected against the effect of antisocial behavior and violence but only if they have a certain genotype (which implies that if they have the other genotype, then if abused they will show violent and antisocial behavior). So, we can see that the relationship between MAOA and criminal behavior is not as simple as some would make it out to be.
MAOA, like other genetic variants, of course, has been linked to numerous other traits. Steven J. Heine, author of the book DNA is Not Destiny: The Remarkable and Completely Misunderstood Relationship Between You and Your Genes:
However, any labels like “the warrior gene” are highly problematic because they suggest that the this gene is specifically associated with violence. It’s not, just as alleles from other genes do not only have one outcome. Pleiotropy is the term for how a single genetic variant can influence multiple different phenotypes. MAOA is highly pleiotropic: the traits and conditions potientially connected to the MAOA gene invlude Alzheimer’s. anoerxia, autism, body mass index, bone mineral density, chronic fatigue syndrome, depression, extraversion, hypertension, individualism, insomnia, intelligence, memory, neuroticism, obesity, openness to experience, persistence, restless leg syndrome, schizophrenia, social phobia, sudden infant death syndrome, time perception and voting behavior. (59) Perhaps it would be more fitting to call MAOA “the everything but the kitchen sink gene. (Heine, 2017: 195)
Something that I have not seen brought up when discussions of race, crime, and MAOA come up is that Japanese people have the highest chance—even higher than blacks, Maoris, and whites—to have the low repeat MAOA variant (Way and Lieberman) yet have lower rates of crime. So MAOA cannot possibly be a ‘main cause’ of crime. It is way more complex than that. “However intuitively satisfying it may be to explain cultural differences in violence in terms of genes“, Heine writes, “as of yet there is no direct evidence for this” (Heine, 2017: 196).
Numerous people have used ‘their genes’ in an attempt to get out of criminal acts that they have committed. A judge even knocked off one year off of a murder’s sentence since he found the evidence for the MAOA gene’s link to violence “particularly compelling.” I find it “particularly ridiculous” that the man got less time in jail than someone who ‘had a choice’ in his actions to murder someone. Doesn’t it seem ridiculous to you that someone gets less time in jail than someone else, all because he may have the ‘crime/warrior gene’?
Aspinwall, Brown, and Tabery (2012) showed that when evidence of a ‘biomechanic’ cause of violence/psychopathy was shown to the judges (n=191), that they reduced their sentences by almost one year if they were reading a story in which the accused was found to have the low-repeat MAOA allele (13.93 to 12.83 years). So, as you can see, this can sway judges’ perception into giving one a lighter sentence since they believe that the evidence shows that one ‘can not control themselves’, which results in the judge giving assailants lighter sentences because ‘it’s in their genes’.
Further, people would be more lenient on sentences for criminals who are found to have these ‘criminal genes’ than those who were found to not have them (Cheung and Heine, 2015). Monterosso, Royzman, and Schwartz (2010) also write: “Physiologically explained behavior was more likely to be characterized as “automatic,” and willpower and character were less likely to be cited as relevant to the behavior. Physiological explanations of undesirable behavior may mitigate blame by inviting nonteleological causal attributions.” So, clearly, most college students would give a lighter sentence if the individual in question were found to have ‘criminal genes’. But, if these genes really did ’cause’ crime, shouldn’t they be given heavier sentences to keep them on the inside more so those with the ‘non-criminal genes’ don’t have to suffer from the ‘genetically induced’ crime?
Heine (2017: 198-199) also writes:
But is someone really less any responsible for their actions if his or her genes are implicated? A problem with this argument is that we would be hard-pressed to find any actions that we engage in where our genes are not involved—our behaviors do not occur in any gene-free zones. Or, consider this: there actually is a particular genetic variant that, if you possess it, makes you about 40 times more likely to engage in same-sex homicides than those who possess a different variant. (66) It’s known as the Y chromosome—that is, people who possess it are biologically male. Given this, should we infer that Y chromosomes cause murders, and thus give a reduced sentence to anyone who is the carrier of such a chromosome because he is really not responsible for his actions? The philosopher Stephen Morse calls the tendency to excuse a crime because of a biological basis the “fundamental psycholegal error.” (67) The problem with this tendency is that it involves separating yout genes from yourself. Saying “my genes made me do it” doesn’t make sense because there is no “I” that is independent of your genetic makeup. But curiously, once genes are implicaed, people see, to feel that the accused is no longer fully in control of his or her actions.
Further, in the case of a child pornographer, one named Gary Cossey, the court said:
The court predicted that some fifty years from now Cossey’s offense conduct would likely be discovered to be caused by “a gene you were born with. And it’s not a gene you can get rid of.” The court expressed its belief that although Cossey was in therapy, it “can only lead, in my view, to a sincere effort on your part to control, but you can’t get rid of it. You are what you’re born with. And that’s the only explanation for what I see here.”
However, this judge punished Cossey more severely due to the ‘possibility’ that scientists may find ‘genes for’ child pornography use in 50 years. Cossey was then given another, unbiased judge, and was given a ‘more lenient’ sentence than the genetic determinist judge did.
Sean Last over at The Alternative Hypothesis is also a big believer in this so-called MAOA-race difference that explains racial differences in crime. However, as reviewed above (and as he writes), MAOA can be called the “everything but the kitchen sink gene” (Heine, 2017: 195), as I will touch on briefly below, to attribute ’causes’ to genes is not the right way to look at them. It’s not so easy to say that since one ‘has the warrior gene’ that they’d automatically be violent. Last cites a study saying that even those who have the MAOA allele who were not abused showed higher rates of violent behavior (Ficks and Waldman, 2014). They write (pg. 429):
The frequency of the ‘‘risk’’ allele in nonclinical samples of European ancestry ranges from 0.3 to 0.4, although the frequency of this allele in individuals of Asian and African ancestry appears to be substantially higher (*0.6 in both groups; Sabol et al. 1998).
So, why don’t Asians have higher rates of crime—along with blacks—if MAOA on its own causes violent and antisocial behavior? Next I know that someone would claim that “AHA! TESTOSTERONE ALSO MEDIATES THIS RELATIONSHIP!!” However, as I’ve talked about countless times (until I’m blue in the face), blacks do not have/have lower levels of testosterone than whites (Richards et al, 1992; Gapstur et al, 2002; Rohrmann et al, 2007; Mazur, 2009; Lopez et al, 2013; Hu et al, 2014; Richard et al, 2014). Though young black males have higher levels of testosterone due to the environment (honor culture) (Mazur, 2016). So that canard cannot be trotted out.
All in all, these simplistic and reductionist approaches to ‘figuring out’ the ’causes’ of crime do not make any sense. To point at one gene and say that this is ‘the cause’ of that do not make sense.
One last point on ‘genes as causes’ for behavior. This is something that deserves a piece of its own, but I will just provide a quote from Eva Jablonska and Marion Lamb’s book Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life (Jablonska and Lamb, 2014: 17; read chapter one of the book here; I have the nook version so the page number may be different):
Although many psychiatrists, biochemists, and other scientists who are not geneticists (yet express themselves with remarkable facility on genetic issues) still use the language of genes as simple causal agents, and promise their audience rapid solutions to all sorts of problems, they are no more than propagandists whose knowledge or motives must be suspect. The geneticists themselves now think and talk (most of the time) in terms of genetic networks composed of tens or hundreds of genes and gene products, which interact with each other and together affect the development of a particular trait. They recognize that whether or not a trait (a sexual preference, for example) develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule, and the environment in which an individual develops.
So to say that those who have low-functioning MAOA variants have an ‘excuse’ as to why they commit crime is incorrect. I know that most people know this, but when you read some people’s writings on things like this it’s like they think that these singular genes/polymorphisms/etc cause these things on their own. In actuality, you need to look at how the whole system interacts with these things, and not reduce whole complex physiological systems to a sum of its parts. This is why implicating singular genes/polymorphisms as explanations for racial differences in crime does not make sense (as can be seen with the Japanese example).
To reduce behaviors simply to gene X and not look at the whole system does not make any sense. There are no ‘genes for’ anything, except a few Mendelian diseases (Ropers, 2010). Stating that certain genes ’cause’ X, as I have shown does not make sense and, wrongly, in my opinion, gives criminals less of a sentencing since judges find stuff like this ‘very compelling’. If that’s the case, why implicate any murderer? ‘Their genes made them do it’, right? Though, things are not that simple to implicate one gene as a cause for crime or any other complex behavior; in this sense—like for most things to do with the human body—holism makes way more sense and not reductionism. We need to look at how these genes that are ‘implicated’ in criminal behavior interact with the whole system. Only then can we understand the causes of criminal behavior. Looking at singular genes impedes us from figuring out the true underlying reasons why people commit crime.
Remember: we can’t blame “warrior genes” for violent crime. If someone does have a ‘genetic predisposition to crime’ from the MAOA gene, then wouldn’t it make more sense to give them more time? Though, the relationship is not so simple as I have covered. So to close, there is no ‘simple relationship’ between race, crime and MAOA. Not in the way that other hereditarians would like you to believe. Because if this relationship were so simple, then East Asians (Chinese, Japanese) would have the highest rates of crime, and they do not.
Testosterone: “The Crime Gene?”
1150 words
I came across this video on YouTube last night by a geneticist/science writer Steve Jones. He is also the Emeritus Professor of genetics at University College London. This makes what he says in the video I will speak about below very troubling—especially to a man of his caliber with the knowledge he has—views he has on the hormone.
In the very beginning of the video titled Testosterone and Crime: What Can Genes Tell Us About Behavior?, Jones says “But in fact, there are genes—there is a gene—for crime, which causes nearly all the crime, and is widely used and we understand a great deal about it. It’s a chemical gene it produces a particular chemical, which we understand in detail is the chemical testosterone. Testosterone—we all have it but some of us have rather more than others—testosterone is of course a gene that is made—switched on by the Y chromosome and makes males male. Women have a small amount but only a small amount and as they get older … Now testosterone is a dangerous, dangerous thing to have. I don’t recommend it, those of you who have it, don’t get it. And if you’ve got some, don’t get any more.” What bullshit! This guy is a literal genetics Ph.D. saying this; this is proof that knowledge/educational attainment does not stop you from saying dumb, untrue things.
“I don’t know that this character does it, but certainly plenty of bodybuilders inject steroids—testosterone—into themselves. They damage themselves severely. Their life expectancy goes down strikingly. They die for all those male reasons. They die from violence, they die from suicide, they die from car accidents, they die from heart disease, all those things are true of males. … But even if you look at males and females in general, there is kind of a depressing picture for half of the room, I’m not sure which half.” Jones then talks about how men die at a much higher rate than women for a slew of reasons. This is his logic: Men have higher testosterone than women. Testosterone is shown to cause violence, aggression, heart disease, risk-taking, etc. Men have way more testosterone than women. Therefore testosterone is the reason why men die more than women and commit more violence than women. This is horrible logic—coming from a geneticist no less!
“Men actually—less expectedly perhaps—are much less good at dealing with parasites and infectious disease than women are. And that’s because testosterone—the male hormone—suppresses the immune system. Now the immune system fights off the parasites and we don’t do nearly as well.” There is actually some empirical data for his argument here. Back in 2013, it was shown that testosterone, gene expression, and the immune system were linked. They discovered that higher levels of testosterone prevented Module 52 genes from turning on. So higher levels of testosterone result in more Module 52 expression. Testosterone also does exert immune-suppressing effects, “increasing the severity of malaria, leishmaniasis, amebiasis, and tuberculosis, while at the same time supporting the clearance of toxoplasmosis (Bernin & Lotter, 2014; Nhamoyebonde & Leslie, 2014)” (Giefing-Kroll et al, 2015). The suppressive effects of testosterone on the immune system and how down-regulates “the systemic immune response by cell type specific effects in the context of immunological disorders.” (Trigunaite, Dimo, and Jorgensen, 2015).
The effects of testosterone replacement therapy (TRT) on the immune system have not been looked into, but it has a positive effect on elderly men (Osterberg, Bernie, and Ramasamy, 2014). However, Braude, Tang-Martinez, and Taylor (1999) challenge the wisdom that testosterone is an immuno-depressor. This is Jones’ only claim that is not outright wrong; there is data out there for both positions (of course I think that Braude, Tang-Martinez and Taylor, 1999 drive a solid argument against the testosterone-causes-immuno-suppression hypothesis).
The Jones says one of the dumbest things I’ve ever heard “And men, of course, are murdered much more than women. And who murders them—of course—other men. … Men murder at a much higher rate than women. … And that effect is striking—that effect is true worldwide—all over the world men, testosterone, murder at 10 times the rate of women. … So it’s a universal, it’s a biological universal, it’s clearly due to testosterone. There’s no question. The evidence is absolutely clear. So it’s a genetic phenomenon, it’s a gene for crime.” Should I be nice here and assume that whatever ‘gene’ he’s proposing that ’causes’ testosterone production actually causes the crime? Or should I take what he said at face value—that testosterone is a literal gene that causes crime? I think I’ll go with the second one.
“It’s certainly genetic, it’s also environmental. And you can’t disentangle it. You can change part of it—the environment—you can’t change the other part—the genes. And I always find it kind of odd that the public is so interested in the bit you can’t change—the genes—and is so uninterested in the bit you can—the environment.” This is wrong. Not all of it, but most of it. I don’t think that people are more interested in genes and toss aside environment—especially for testosterone. Because, as I documented yesterday, hereditarians assume that since testosterone has a heritability of around .6 then it must be mostly genetic in nature. This is wrong. As Jones said, the environment effects testosterone production too (though he didn’t go into the mechanisms).
The Left goes to the environment side—change the environment, change hormone production (this is true)—whereas the Right goes to the genes side—can’t change genes and environment is a product of genes so nothing can be done. (Oversimplified, don’t crucify me.) Both are wrong. Strong genetic determinism (gene G almost always leads to the development of trait T. (G increases the probability of T and the probability of T, given G, is 95% or greater) doesn’t make sense because a large majority of traits are moderately or weakly determined by genetics (Resnick and Vorhaus, 2006).
In sum, Jones is clueless about testosterone. He only really said one thing that is not outright wrong (but it is questionable). It doesn’t cause crime, it doesn’t cause men to murder more. The press has gotten all of these views into people’s heads because they want to demonize men—and the hormone that is largely responsible for male-ness. It’s incredible that this guy is both a geneticist, science writer and professor of genetics and still calls testosterone a ‘gene’ saying that it is responsible for ‘most of the crime’ committed. Anyone who has been reading this blog for the past year or so since I have began revising many of my main views knows how wrong this is. People really need to get a clue on testosterone and stop spreading bullshit. I know that I’ll have to keep correcting misconceptions on testosterone for a good long time (like with r/K theory) but I enjoy writing about both things so it’s not too big a deal. I just wish people would actually educated themselves on basic physiology so that the trainwreck of a video that Jones made does not get made.
Responses to The Alternative Hypothesis and Robert Lindsay on Testosterone
2300 words
I enjoy reading what other bloggers write about testosterone and its supposed link to crime, aggression, and prostate cancer; I used to believe some of the things they did, since I didn’t have a good understanding of the hormone nor its production in the body. However, once you understand how its produced in the body, then what others say about it will seem like bullshit—because it is. I’ve recently read a few articles on testosterone from the HBD-blog-o-sphere and, of course, they have a lot of misconceptions in them—some even using studies I have used myself on this blog to prove my point that testosterone does not cause crime!! Now, I know that most people don’t read studies that are linked, so they would take what it says on face value because, why not, there’s a cite so what he’s saying must be true, right? Wrong. I will begin with reviewing an article by someone at The Alternative Hypothesis and then review one article from Robert Lindsay on testosterone.
The Alternative Hypothesis
Faulk has great stuff here, but the one who wrote this article, Testosterone, Race, and Crime, 1) doesn’t know what he’s talking about and 2) clearly didn’t read the papers he cited. Read this article, you’ll see him make bold claims using studies I have used for my own arguments that testosterone doesn’t cause crime! Let’s take a look.
One factor which explains part of why Blacks have higher than average crime rates is testosterone. Testosterone is known to cause aggression, and Blacks are known to at once have more of it and, for genetic reasons, to be more sensitive to its effects.
- No it doesn’t.
- “Testosterone is known to cause aggression“, but that’s the thing: it’s only known that it ’causes’ aggression, it really doesn’t.
- Evidence is mixed on blacks being “… for genetic reasons … more sensitive to its effects” (Update on Androgen Receptor gene—Race/History/Evolution Notes).
Testosterone activity has been linked many times to aggression and crime. Meta-analyses show that testosterone is correlated with aggression among humans and non human animals (Book, Starzyk, and Quinsey, 2001).
Why doesn’t he say what the correlation is? It’s .14 and this study, while Archer, Graham-Kevan and Davies, (2005) reanalyzed the studies used in the previous analysis and found the correlation to be .08. This is a dishonest statement.
Women who suffer from a disease known as congenital adrenal hyperplasia are exposed to abnormally high amounts of testosterone and are abnormally aggressive.
Abnormal levels of androgens in the womb for girls with CAH are associated with aggression, while boys with and without CAH are similar in aggression/activity level (Pasterski et al, 2008), yet black women, for instance, don’t have higher levels of testosterone than white women (Mazur, 2016). CAH is just girls showing masculinized behavior; testosterone doesn’t cause the aggression (See Archer, Graham-Kevan and Davies, 2005)
Artificially increasing the amount of testosterone in a person’s blood has been shown to lead to increases in their level of aggression (Burnham 2007; Kouri et al. 1995).
Actually, no. Supraphysiological levels of testosterone administered to men (200 and 600 mg weekly) did not increase aggression or anger (Batrinos, 2012).
Finally, people in prison have higher than average rates of testosterone (Dabbs et al., 2005).
Dabbs et al don’t untangle correlation from causation. Environmental factors can explain higher testosterone levels (Mazur, 2016) in inmates, and even then, some studies show socially dominant and aggressive men have the same levels of testosterone (Ehrenkraz, Bliss, and Sheard, 1974).
Thus, testosterone seems to cause both aggression and crime.
No, it doesn’t.
Why Testosterone Does Not Cause Crime
Testosterone and Aggressive Behavior
Furthermore, of the studies I could find on testosterone in Africans, they have lower levels than Western men (Campbell, O’Rourke, and Lipson, 2003; Lucas and Campbell, and Ellison, 2004; Campbell, Gray, and Ellison, 2006) so, along with the studies and articles cited on testosterone, aggression, and crime, that’s another huge blow to the testosterone/crime/aggression hypothesis.
Richard et al. (2014) meta-analyzed data from 14 separate studies and found that Blacks have higher levels of free floating testosterone in their blood than Whites do.
They showed that blacks had 2.5 to 4.9 percent higher testosterone than whites, which could not explain the higher prostate cancer incidence (which meta-analyses call in to question; Sridhar et al 2010; Zagars et al 1998). That moderate amount would not be enough to cause differences in aggression either.
Exacerbating this problem even further is the fact that Blacks are more likely than Whites to have low repeat versions of the androgen receptor gene. The androgen reception (AR) gene codes for a receptor by the same name which reacts to androgenic hormones such as testosterone. This receptor is a key part of the mechanism by which testosterone has its effects throughout the body and brain.
The rest of the article talks about CAG repeats and aggressive/criminal behavior, but it seems that whites have fewer CAG repeats than blacks.
Robert Lindsay
This one is much more basic, and tiring to rebut but I’ll do it anyway. Lindsay has a whole slew of articles on testosterone on his blog that show he doesn’t understand the hormone, but I’ll just talk about this one for now: Black Males and Testosterone: Evolution and Perspectives.
It was also confirmed by a recent British study (prostate cancer rates are somewhat lower in Black British men because a higher proportion of them have one White parent)
Jones and Chinegwundoh (2014) write: “Caution should be taken prior to the interpretation of these results due to a paucity of research in this area, limited accurate ethnicity data, and lack of age-specific standardisation for comparison. Cultural attitudes towards prostate cancer and health care in general may have a significant impact on these figures, combined with other clinico-pathological associations.”
This finding suggests that the factor(s) responsible for the difference in rates occurs, or first occurs, early in life. Black males are exposed to higher testosterone levels from the very start.
In a study of women in early pregnancy, Ross found that testosterone levels were 50% higher in Black women than in White women (MacIntosh 1997).
I used to believe this, but it’s much more nuanced than that. Black women don’t have higher levels of testosterone than white women (Mazur, 2016; and even then Lindsay fails to point out that this was pregnant women).
According to Ross, his findings are “very consistent with the role of androgens in prostate carcinogenesis and in explaining the racial/ethnic variations in risk” (MacIntosh 1997).
Testosterone has been hypothesized to play a role in the etiology of prostate cancer, because testosterone and its metabolite, dihydrotestosterone, are the principal trophic hormones that regulate growth and function of epithelial prostate tissue.
Testosterone doesn’t cause prostate cancer (Stattin et al, 2003; Michaud, Billups, and Partin, 2015). Diet explains any risk that may be there (Hayes et al, 1999; Gupta et al, 2009; Kheirandish and Chinegwundoh, 2011; Williams et al, 2012; Gathirua-Mingwai and Zhang, 2014). However in a small population-based study on blacks and whites from South Carolina, Sanderson et al (2017) “did not find marked differences in lifestyle factors associated with prostate cancer by race.”
Regular exercise, however, can decrease PCa incidence in black men (Moore et al, 2010). A lot of differences can be—albeit, not too largely— ameliorated by environmental interventions such as dieting and exercising.
Many studies have shown that young Black men have higher testosterone than young White men (Ellis & Nyborg 1992; Ross et al. 1992; Tsai et al. 2006).
Ellis and Nyborg (1992) found 3 percent difference. Ross et al (1992) have the same problem as Ross et al (1986), which used University students (~50) for their sample. They’re not representative of the population. Ross et al (1992) also write:
Samples were also collected between 1000 h and 1500 h to avoid confounding
by any diurnal variation in testosterone concentrations.
Testosterone levels should be measured near to 8 am. This has the same time variation too, so I don’t take this study seriously due to that confound. Assays were collected “between” the hours of 10 am and 3 pm, which means it was whenever convenient for the student. No controls on activities, nor attempting to assay at 8 am. People of any racial group could have gone at whatever time in that 5 hour time period and skew the results. Assaying “between” those times completely defeats the purpose of the study.
This advantage [the so-called testosterone advantage] then shrinks and eventually disappears at some point during the 30s (Gapstur et al., 2002).
Gapstur et al (2002) help my argument, not yours.
This makes it very difficult if not impossible to explain differing behavioral variables, including higher rates of crime and aggression, in Black males over the age of 33 on the basis of elevated testosterone levels.
See above where I talk about crime/testosterone/aggression.
Critics say that more recent studies done since the early 2000’s have shown no differences between Black and White testosterone levels. Perhaps they are referring to recent studies that show lower testosterone levels in adult Blacks than in adult Whites. This was the conclusion of one recent study (Alvergne et al. 2009) which found lower T levels in Senegalese men than in Western men. But these Senegalese men were 38.3 years old on average.
Alvergne, Fauri, and Raymond (2009) show that the differences are due to environmental factors:
This study investigated the relationship between mens’ salivary T and the trade-off between mating and parenting efforts in a polygynous population of agriculturists from rural Senegal. The men’s reproductive trade-offs were evaluated by recording (1) their pair-bonding/fatherhood status and (2) their behavioral profile in the allocation of parental care and their marital status (i.e. monogamously married; polygynously married).
They also controlled for age, so his statement “But these Senegalese men were 38.3 years old on average” is useless.
These critics may also be referring to various studies by Sabine Rohrmann which show no significance difference in T levels between Black and White Americans. Age is poorly controlled for in her studies.
That is one study out of many that I reference. Rohrmann et al (2007) controlled for age. I like how he literally only says “age is poorly controlled for in her studies“, because she did control for age.
That study found that more than 25% of the samples for adults between 30 and 39 years were positive for HSV-2. It is likely that those positive samples had been set aside, thus depleting the serum bank of male donors who were not only more polygamous but also more likely to have high T levels. This sample bias was probably worse for African American participants than for Euro-American participants.
Why would they use diseased samples? Do you even think?
Young Black males have higher levels of active testosterone than European and Asian males. Asian levels are about the same as Whites, but a study in Japan with young Japanese men suggested that the Japanese had lower activity of 5-alpha reductase than did U.S. Whites and Blacks (Ross et al 1992). This enzyme metabolizes testosterone into dihydrotestosterone, or DHT, which is at least eight to 10 times more potent than testosterone. So effectively, Asians have the lower testosterone levels than Blacks and Whites. In addition, androgen receptor sensitivity is highest in Black men, intermediate in Whites and lowest in Asians.
Wu et al (1995) show that Asians have the highest testosterone levels. Evidence is also mixed here as well. See above on AR sensitivity.
Ethnicmuse also showed that, contrary to popular belief, Asians have higher levels of testosterone than Africans who have higher levels of testosterone than Caucasians in his meta-analysis. (Here is his data.)
The Androgen Receptor and “masculinization”
Let us look at one study (Ross et al 1986) to see what the findings of a typical study looking for testosterone differences between races shows us. This study gives the results of assays of circulating steroid hormone levels in white and black college students in Los Angeles, CA. Mean testosterone levels in Blacks were 19% higher than in Whites, and free testosterone levels were 21% higher. Both these differences were statistically significant.
Assay times between 10 am and 3 pm, unrepresentative sample of college men, didn’t have control for waist circumference. Horribly study.
A 15% difference in circulating testosterone levels could readily explain a twofold difference in prostate cancer risk.
No, it wouldn’t (if it were true).
Higher testosterone levels are linked to violent behavior.
Causation not untangled.
Studies suggest that high testosterone lowers IQ (Ostatnikova et al 2007). Other findings suggest that increased androgen receptor sensitivity and higher sperm counts (markers for increased testosterone) are negatively correlated with intelligence when measured by speed of neuronal transmission and hence general intelligence (g) in a trade-off fashion (Manning 2007).
Who cares about correlations? Causes matter more. High testosterone doesn’t lower IQ. Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut.
Conclusion
Racial differences in testosterone don’t exist/are extremely small in magnitude (as I’ve covered countless times). The one article from TAH literally misrepresents studies/leaves out important figures in the testosterone differences between the two races to push a certain agenda. Though if you read the studies you see something completely different. It’s the same with Lindsay. He misunderstood a few studies to push his agenda about testosterone and crime and prostate cancer. They’re both wrong, though.
Why Testosterone Does Not Cause Crime
Testosterone and Aggressive Behavior
Race, Testosterone, and Prostate Cancer
Population variation in endocrine function—Race/History/Evolution Notes
Racial differences in testosterone are tiring to talk about now, but there are still a few more articles I need to rebut. People read and write about things they don’t understand, which is the cause of these misconceptions with the hormone, as well as, of course, misinterpreting studies. Learn about the hormone and you won’t fear it. It doesn’t cause crime, prostate cancer nor aggression; these people who write these articles have one idea in their head and they just go for it. They don’t understand the intricacies of the endocrine system and how sensitive it is to environmental influence. I will cover more articles that others have written on testosterone and aggression to point out what they got wrong.
Racial Differences in Jock Behavior: Implications for STI Prevalence and Deviance
1350 words
The Merriam-Webster dictionary defines jock as “a school or college athlete” and “a person devoted to a single pursuit or interest“. This term, as I previously wrote about, holds a lot of predictive power in terms of life success. What kind of racial differences can be found here? Like with a lot of life outcomes/predictors, there are racial differences and they are robust.
Male jocks get more sex, after controlling for age, race, SES and family cohesion. Being involved in sports is known to decrease sexual promiscuity, however, this effect did not hold for black American jocks, with the jock label being associated with higher levels of sexual promiscuity (Miller et al, 2005). Black American jocks reported significantly higher levels of sexual activity than non-black jocks, but they did not find that white jocks too fewer risks than their non-jock counterparts.
Black Americans do have a higher rate of STDs compathe average population (Laumann et al, 1999; Cavanaugh et al, 2010; CDC, 2015). Black females who are enrolled in, or have graduated from college had a higher STI (sexually transmitted infection) rate (12.4 percent self-reported; 13.4 percent assayed) than white women with less than a high school diploma (6.4 percent self-reported; 2.3 percent assayed) (Annang et al, 2010). I would assume that these black women would be more attracted to black male jocks and thusly would be more likely to acquire STIs since black males who self-identify as jocks are more sexually promiscuous. It seems that since black male jocks—both in high school and college—are more likely to be sexually promiscuous, this then has an effect on even the college-educated black females, since higher educational status has one less likely to acquire STIs.
Whites use the ‘jock identity’ in a sports context whereas blacks use the identity in terms of the body. Black jocks are more promiscuous and have more sex than white jocks, and I’d bet that black jocks have more STDs than white jocks since they are more likely to have sex than white jocks. Jock identity—but not athletic activity and school athlete status—was a better predictor of juvenile delinquency in a sample of 600 Western New York students, which was robust across gender and race (Miller et al, 2007a). Though, surprisingly, the ‘jock effect’ on crime was not as you would expect it: “The hypothesis that effects would be stronger for black adolescents than for their white counterparts, derived from the work of Stark et al. 1987 and Hughes and Coakley (1991), was not supported. In fact, the only clear race difference that did emerge showed a stronger effect of jock identity on major deviance for whites than for blacks” (Miller et al, 2007a).
Miller et al (2007b) found that the term jock means something different to black and white athletes. For whites, the term was associated with athletic ability and competition, whereas for blacks the term was associated with physical qualities. Whites, though, were more likely to self-identify with the label of jock than blacks (37 percent and 22 percent respectively). They also found that binge drinking predicted violence amongst family members, but in non-jocks only. The jock identity, for whites and not blacks, was also associated with more non-family violence while whites were more likely to use the aggression from sports in a non-sport context in comparison to blacks.
For black American boys, the jock label was a predictor of promiscuity but not for dating. For white American jocks, dating meant more than the jock label. Miller et al (2005) write:
We suggest that White male jocks may be more likely to be involved in a range of extracurricular status-building activities that translate into greater popularity overall, as indicated by more frequent dating; whereas African American male jocks may be “jocks” in a more narrow sense that does not translate as directly into overall dating popularity. Furthermore, it may be that White teens interpret being a “jock” in a sport context, whereas African American teens see it more in terms of relation to body (being strong, fit, or able to handle oneself physically). If so, then for Whites, being a jock would involve a degree of commitment to the “jock” risk-taking ethos, but also a degree of commitment to the conventionally approved norms with sanctioned sports involvement; whereas for African Americans, the latter commitment need not be adjunct to a jock identity.
It’s interesting to speculate on why whites would be more prone to risk-taking behavior than blacks. I would guess that it has something to do with their perception of themselves as athletes, leading to more aggressive behavior. Though certain personalities would be more likely to be athletic and thusly refer to themselves as a jock. The same would hold true for somatype as well.
So the term jock seems to mean different things for whites and blacks, and for whites, leads to more aggressive behavior in a non-sport context.
Black and females who self-identified as jocks reported lower grades whereas white females who self-identified as jocks reported higher grades than white females who did not self-report as jocks (Miller et al, 2006). Jocks also reported more misconduct such as skipping school, cutting class, being sent to the principals office, and parents having to go to the school for a disciplinary manner compared to non-jocks. Boys were more likely to engage in actions that required disciplinary intervention in comparison to girls, while boys were also more likely to skip school, have someone called from home and be sent to the principal’s office. Blacks, of course, reported lower grades than whites but there was no significant difference in misconduct by race. However, blacks reported fewer absences but more disciplinary action than whites, while blacks were less likely to cut class, but more likely to have someone called from home and slightly more likely to be sent to the principal’s office (Miller et al, 2006).
This study shows that the relationship between athletic ability and good outcomes is not as robust as believed. Athletes and jocks are also different; athletes are held in high regard in the eyes of the general public while jocks are seen as dumb and slow while also only being good at a particular sport and nothing else. Miller et al (2006) also state that this so-called ‘toxic jock effect‘ (Miller, 2009; Miller, 2011) is strongest for white boys. Some of these ‘effects’ are binge drinking and heavy drinking, bullying and violence, and sexual risk-taking. Though Miller et al (2006) say that, for this sample at least, “It may be that where academic performance is concerned, the jock label constitutes less of a departure from the norm for white boys than it does for female or black adolescents, thus weakening its negative impact on their educational outcomes.”
The correlation between athletic ability and jock identity was only .31, but significant for whites and not blacks (Miller et al, 2007b). They also found, contrary to other studies, that involvement in athletic programs did not deter minor and major adolescent crime. They also falsified the hypothesis that the ‘toxic jock effect’ (Miller, 2009; Miller, 2011) would be stronger for blacks than whites, since whites who self-identified as jocks were more likely to engage in delinquent behavior.
In sum, there are racial differences in ‘jock’ behavior, with blacks being more likely to be promiscuous while whites are more likely to engage in deviant behavior. Black women are more likely to have higher rates of STIs, and part of the reason is sexual activity with black males who self-identify as jocks, as they are more promiscuous than non-jocks. This could explain part of the difference in STI acquisition between blacks and whites. Miller et al argue to discontinue the use of the term ‘jock’ and they believe that if this occurs, deviant behavior will be curbed in white male populations that refer to themselves as ‘jocks’. I don’t know if that will be the case, but I don’t think there should be ‘word policing’, since people will end up using the term more anyway. Nevertheless, there are differences between race in terms of those that self-identify as jocks which will be explored more in the future.
The West’s Sperm Decline: Is It True?
2200 words
Another day, another slew of articles full of fear mongering. This one is on sperm decline in the West. Is it true? I have recently covered on this blog that as of July 17th, 2017, the testosterone range for men decreased (more on that when I get access to the paper). I have also covered the obesity epidemic a bit, and that also factors in to lowered testosterone and, of course, low spermatoza count. Due to these environmental factors, we can logically deduce that sperm counts have fallen as well. However, as I will cover, it may not be so cut and dry due to analyzing numerous studies with different counting methodologies among numerous other confounds that will be addressed below. First I will cover the physiology of sperm production and what may cause decreases in production. Next, I will cover the new study that is being passed around. Finally, I will talk about why you should worry about this.
Physiology of sperm production
The accumulation of testosterone by ABP leads to the onset and rising rate of sperm production. So if testosterone production ceases or decreases, then subsequent decreases in sperm count and spermatogenesis should follow. If this change is drastic, infertility will soon follow. The process of sperm production is called spermatogenesis. It occurs in the seminiforous tubules and involves three main events: 1) remodeling relatively large germ cells into smaller mobile cells with flagella, 2) reducing the chromosome number by half, and 3) shuffling the genes so that each chromosome in the sperm carries novel gene combinations that differ from the parents. This is what ensures that a child will differ from their parents but still, at the same time, will be similar to them. The process by which this occurs is called meiosis, in which four daughter cells split which subsequently differentiate sperm (Saladin, 2010: 1063).
After the conclusion of meiosis I, each chromosome is still double stranded, except each daughter cell only has 23 chromosomes becoming a haploid while at the end of meiosis II, there are four haploid cells with 23 single-stranded chromosomes. Fertilization then combined the 23 chromosomes from the father and mother, which “reestablishes the diploid number of 46 chromosomes in the zygote“(Saladin, 2010: 1063-1064).
Spermatogonia divide by mitosis and then enlarge to become primary spermatocyte. The cell is then protected from the immune system since it is going to become genetically different from the rest of the cells in the body. Since the cells are guarded from the body’s immune system, the main spermatocyte undergoes meiosis I, giving rise to equal size haploid and genetically unique secondary spermatocytes. Then, each secondary spermatocyte undergoes meiosis II dividing into two spermatids with a total of four spermatogoniom. Lastly, the spermatozoa undergo no further division but undergoes spermiogenesis in which it differentiates into a single spermatozoon (Saladin, 2010: 1065-1066). Young men produce about 300,000 sperm per minute, about 400 million per day.
Sperm decrease?
The new study was published on July 25, 2017, in the journal Human Reproduction Update titled Temporal trends in sperm count: a systematic review and meta-regression analysis. Levine et al (2017) used 185 studies (n=42,935) and showed a sperm count (SC) decline of .75 percent per year, coming out to a 28.5 percent decrease between 1975 and 2011. Similar declines were seen in total sperm count (TSC) while 156 estimates of serum volume showed little change.
Figure 2a shows the mean sperm concentration between the years 1973 and 2011. Figure 2b shows the mean total sperm count between those same years.
Figure 3a shows sperm concentration for the West (North America, Australia, Europe and New Zealand) vs Other (South America, Asia, and Africa), adjusted for potential confounders such as BMI, smoking etc. Figure 3b shows total sperm count by fertility and the West and Other. You can see that Fertile Other had a sharp increase, but the increase may be due to limited statistical power and a lack of studies of unselected men from those countries before 1985. There is a sharp increase for Other, however and so the data does not support as sharp of a decline as observed in Western countries.
If this is true, why is this happening? Factors that decrease spermatogenesis include (but are not limited to): obesity, smoking, exposure to traffic exhaust fumes, and combustion products. Though there is no data (except animal models) that lend credence to the idea that pesticides, food additives, etc decrease spermatogenesis (Sharpe, 2010). Other factors are known to cause lower SC which includes maternal smoking, alcohol, stress, endocrine disruptors, persistent and nonpersistent chemicals, and, perhaps most importantly today, the use of mobile phones and the wireless Internet (Virtanen, Jorgansen, and Toparri, 2017). Radiation exposure due to constant mobile phone use may cause DNA fragmentation and decreased sperm mobility (Gorpinchenko et al, 2014). Clearly, most of this decrease can largely be ameliorated. Exercise, eating right, and not smoking seem to be the most immediate changes that can and will contribute to an increase in SC in Western men. This will also increase testosterone levels. The cause is largely immobility due to the comfortable lifestyles that we in the West have. So by becoming more active and putting down smartphones, we can then begin to reverse this downward trend.
Saladin (2010: 1067) also states that pollution has deleterious effects on reproduction—and by proxy, sperm production. He states that the evidence is mounting that we are showing declining fertility due to “anatomical abnormalities” in water, meat, vegetables, breast milk and the uterus. He brings up that sperm production decreased in 15,000 men in 1990, decreasing from 113 million/ml in 1940 to 66 million/ml in 1990. Sperm production decreased more, he says, since “the average volume of semen per ejaculate has dropped 19% over this period” (Saladin, 2010: 1067).
Saladin (2010: 1067) further writes:
The pollutants implicated in this trend include a wide array of common herbicides, inseciticides, industrial chemicals, and breakdown products of materials ranging from plastics to dishwashing detergents. Some authorities think these chemicals act by mimicking estrogens by blocking the action of testosterone by binding to its receptors. Other scientists, however, question the data and feel the issue may be overstated. While the debate continues, the U.S. Environmental Protection Agency is screening thousands of industrial chemicals for endocrine effects.
Is it really true?
As seen above, the EPA is investigating whether thousands of industrial chemicals of effects on our endocrine system. If this is true, it occurs due to the binding of these chemicals to androgen receptors, blocking the production of testosterone and thusly sperm production. However, some commentators have contested the results of studies that purport to show a decrease in SC in men over the decades.
Sherins and Delbes are critical of such studies. They rightly state that most of these studies have numerous confounds such as:
1) lack of standardized counting measures, 2) bias introduced by using different counting methodologies, 3) inadequate within-individual semen sampling in the analysis, 4) failure to account for variable abstinence intervals and ejaculatory frequency, 5) failure to assess total sperm output rather than concentration, 6) failure to assess semen parameteres other than the number of sperm, 7) failure to account for age of subject, 8) subject selection bias among comparitive studies, 9) inappropriate statistical analysis, 10) ignoring major geographic differences in sperm counts, and 11) the causal equating of male ferility with sperm count per se.
Levine et al (2017) write:
We controlled for a pre-determined set of potential confounders: fertility group, geographic group, age, abstinence time, whether semen collection and counting methods were reported, number of samples per man and indicators for exclusion criteria (Supplementary Table S1).
So they covered points 1, 2, 4, 5, 6, 7, 8, 9, and 10. This study is very robust. Levine et al (2017) replicate numerous other studies showing that sperm count has decreased in Western men (Centola et al, 2015; Senputa et al, 2017; Virtanen, Jorgensen, and Toparri, 2017). Men Southern Spain show normal levels (Fernandez et al, 2010), while Southern Spanish University students showed a decrease (Mendiola et al, 2013). The same SC decrease has been noted in Brazil in the last ten years (Borges Jr. et al, 2015).
However, te Velde and Bonde (2013) in their paper Misconceptions about falling sperm counts and fertility in Europe contest the results of studies that argue that SC has decreased within the last 50 years stating that, for instance in Denmark, the median values remained between 40-45 million sperm per ml in the 15 years analyzed. They also state that declining birth rates can be explained by cultural and social factors, such as contraception, the female emancipation, and the second demographic transition. Clearly, ferility rates are correlated with the human development index (HDI) meaning that more developed countries have a lower birth rate in comparison to less developed countries. I believe that part of the reason why we in the West have lower birth rates is because there are too many things to for us to do to occupy our time, time that could be used to have children, like going to school to pursue Masters degrees and PhDs, to just wanting more ‘me time’.
Te Velde and Bonde (2013) conclude:
‘Whether the sperm concentration and human fecundity have declined during the past 50 years is a question we will probably never be able to answer’. This statement by Olsen and Rachootin in 200348 still holds for sperm concentration despite the report in 1992. In the meantime, we know that the results of oft-repeated studies from Copenhagen and Malmö do not indicate any notable change in sperm count during the last 10–15 years. Moreover, none of the available evidence points to a decline in couple fecundity during the last 30–40 years, including Denmark.28 Moreover, birth rates and TFRs instead of declining are on the increase in many EU countries, including the spectacular rise in Denmark.34
Echoing the same sentiments, Cocuzza and Esteves (2014) conclude “that there is no enough evidence to confirm a worldwide decline in sperm counts or other semen parameters. Also, there is no scientific truth of a causative role for endocrine disruptors in the temporal decline of sperm production as observed in some studies. We conjecture that a definite conclusion would only be achieved if good quality collaborative long-term research was carried out, including aspects such as semen quality, reproductive hormones, and xenobiotics, as well as a strict definition of fecundity.” Merzenich, Zeeb, and Blettner (2010) also caution that “The observed time trend in semen quality might be an artefact, since the methodological differences between studies might be time dependent as well. Intensive research will be necessary in both clinical and epidemiological domains. More studies are needed with strict methodological standards that investigate semen quality obtained from large samples of healthy men representative for the normal male population.”
Clearly, this debate is long and ongoing, and I doubt that even Levine et al (2017) will be good enough for some researchers.
Conclusion
There are various papers for and against a decrease in sperm production in the West, just like with testosterone. However, there are ways we can deduce that SC has fallen in the West, since we have definitive data that testosterone levels have decreased. This, then, would lead to a decrease in sperm production and then fecundity and number of children conceived by couples. Of course, sociocultural factors are involved, as well as immediate environmental ones that are immediately changeable. Even if there is no scientific consensus on industrial chemicals and effects on the endocrine system, you should stay away from those too. One major reason for the decrease in sperm production—if the decrease is true—is increased mobile phone usage. Mobile phone usage has increased and so this would lower SC over time.
Whether or not the decrease in SC is true or not, every man should take steps to lead a healthier lifestyle without their cell phone. Because if this decrease is true (and Other doesn’t show a decrease as well) then it would be due to the effects of our First World societies, which would mean that we need to change how we live our lives to get back on the right track. Clearly, we must change our diets and our lifestyles. I’ve written numerous articles about how testosterone is strongly mediated by the environment, and that testosterone production in men has decreased since Western men have been, in a way, feminized and not been as dominant. This can and does decrease testosterone production which would, in turn, decrease sperm production and decrease fertility rates.
Nevertheless, taking steps to leading a healthier lifestyle will ameliorate a ton of the problems that we have in the West, which are mainly due to low birth rates, and by ameliorating these problems, the quality of life will the increase in the West. I am skeptical of the decrease due to what was brought up above, but nevertheless I assume that it is true and I hope my readers do too—if only to get some fire under you to lead a healthier lifestyle if you do not do so already as to prevent these problems before they occur and lead to serious deleterious health consequences.
(I am undecided leaning towards yes. There are too many behaviors linked to lower SC which Western men partake in. There are numerous confounds which may have not been controlled for, however knowing the main reasons why men have lower sperm count and the increased prevalence in these behaviors, we can logically deduce that sperm count has fallen too. Look to the testosterone decrease, that causes both low sperm count and lower fertility.)
NotPoliticallyCorrect 