As promised, Coyne has published his follow-up article. Again, here’s his thesis:
In a post one week ago, “The ideological opposition to biological truth,” I argued that sexual dimorphism for body size (difference between men and women) in humans is most likely explained by sexual selection, and that it also reflects behavioral differences between males and females: males compete for females, and greater size and strength give males an advantage.
If you read part 1, you know I’ve brought forward some evidence to argue the contrary. But back then, Coyne said he hadn’t published all his evidence and would do so in his follow-up article.
So, here we are. How does Coyne’s evidence stack up?
Unfortunately, Coyne’s doing more than supporting his original thesis, he’s also defending his views against a critique by Holly Dunsworth. I don’t think he does a terribly good job: he misunderstands her assertion that he’s oversimplifying sexual selection, thinking instead that she’s denying sexual selection, and the result includes a comical section where he refutes her changes that he’s too focused on male-driven selection with a long list of how males drive sexual selection. Coyne somehow got it into his head that Dunsworth was arguing against sexual dimorphism, when her brief blog post never mentions dimorphism at all.
It’s embarrassing, sure, but it’s not why I’m writing this post. This is:
But the sexual selection theory for human sexual dimorphism is supported by a lot of evidence. It is manifestly not a mere “just-so” story. In my original piece I adduced this evidence (revised slightly):
At long last, we get to the promised evidence!
- In human societies studied by Richard Alexander, those societies that are more polygynous (in which males compete more intensively for females) show greater sexual size dimorphism than societies that are more monogamous. This was a prediction made before the data were acquired—a prediction derived from sexual selection theory. And it was fulfilled. UPDATE: I see now that Alexander’s finding wasn’t reproduced in another experiment, so consider this conclusion questionable.
- Among species of primates, there’s a good correlation between the polygyny of a species and sexual dimorphism: those species in which males have a higher variance in offspring number, and in which males thus compete more intensely for females, also show a greater ratio of male/female body size, even when corrected for phylogeny. (Too, in primate species in which males fight each other over females, the relative size of the canine teeth, used in battle, is larger than in species showing less direct male-male competition.)
… uh, Coyne? The only part of that which counts as evidence is the reference to the work of Richard Alexander, and even there you grant the findings may be “questionable.” You don’t even link to or cite Alexander’s studies, forcing anyone who wants to verify it for themselves to manually dig through the scientific literature. None of that second bullet point is cited or linked at all, it’s just naked assertion. I already dealt with both points in Part 1, anyway (short version: strong dimorphism can be plausibly linked to behavior, but humans exhibit weak dimoprhism relative to our primate peers and that doesn’t show a behavioral link).
In humans, as in many other species in which males compete for females, the sex ratio at birth favors males. They then die off at a higher rate due to higher risk-taking and exploratory behavior, and also senesce faster, which is why among older humans there are so many more females than males. (Check out any Gray Line tourbus.) This is predicted by sexual selction theory.
Whoa whoa, hold up. There are multiple claims there, none of which are cited or linked to:
- People assigned male are born at higher rates than those assigned female.
- Assigned males have higher risk-taking behavior than females, plus
- They have higher exploratory behavior, plus
- They age quicker,
- And all these reasons explain why there are more elderly women than men.
It also makes for a strange argument. Human beings exhibit body dimorphism along sexual lines; human beings exhibit behavioral dimorphism along sexual lines; ergo, body dimorphism is driving behavioral dimorphism?! Does this mean that since US science funding and suicides by hanging are correlated, science funding is driving suicide? Maybe suicide is driving science funding instead? Or maybe the two measures are correlated with something else? Or maybe the correlation is a fluke? Coyne’s argument would have him laughed out of a scientific methodology class, yet we give it a pass because it confirms our existing prejudices.
We should not let our beliefs guide our logic, though. Evidence should take that role. And what does the evidence say?
Using historical data from 1,763 birth cohorts from 1800 to 1935 in 13 developed countries, we show that what is now seen as normal—a large excess of female life expectancy in adulthood—is a demographic phenomenon that emerged among people born in the late 1800s. We show that excess adult male mortality is clearly rooted in specific age groups, 50–70, and that the sex asymmetry emerged in cohorts born after 1880 when male:female mortality ratios increased by as much as 50% from a baseline of about 1.1. Heart disease is the main condition associated with increased excess male mortality for those born after 1900. We further show that smoking-attributable deaths account for about 30% of excess male mortality at ages 50–70 for cohorts born in 1900–1935. However, after accounting for smoking, substantial excess male mortality at ages 50–70 remained, particularly from cardiovascular disease. The greater male vulnerability to cardiovascular conditions emerged with the reduction in infectious mortality and changes in health-related behaviors.
Beltrán-Sánchez, Hiram, Caleb E. Finch, and Eileen M. Crimmins. “Twentieth Century Surge of Excess Adult Male Mortality.” Proceedings of the National Academy of Sciences 112, no. 29 (July 21, 2015): 8993–98. doi:10.1073/pnas.1421942112.
Sorry, but it turns out that women outnumbering men in old age is only a few centuries old; before then, easily-preventable disease and infection tended to kill more women than men. The current age gap is mostly explained by diet, smoking, and heart disease instead of risk-taking behavior. The latter isn’t a major factor in mortality, quite frankly. Roughly 7.9% of male deaths were due to accidents, suicide, or homicide in 2012 Canada vs. 4.8% of female deaths, which sounds like a lot until you consider that 52.3% of men died from cancer or heart disease vs. 47.5% of women. Large differences in rare categories look impressive on paper, but are usually drowned out by small differences in commonplace ones.
A difference in cardiovascular or genetic disease is easy to explain without invoking natural or sexual selection. Most women have two X chromosomes. This means that if there’s a defective gene on one of them, the other might have a working backup that could take its place. Most men have only one X, however, so there’s no backup to reach for. Hence why men are much more likely to be colour-blind, as some vision genes are located on the X. Since being colour blind or dying late in life due to a heart attack has little effect on your ability to pop out babies, there’s little-to-no selective pressure to encourage the genes responsible to migrate off the X. So the real culprit is rotten luck in how our genes are laid out; had we been birds instead, females would struggle with more chromosomal-linked disease. I can find the suggestion of at least one gene on the X chromosome contributes to it.
But let’s not kid ourselves, heart disease is complex and multi-causal. Neither selective pressures nor genetics can explain it all, and the experts still don’t have a total picture. Emphasis mine:
The remarkable universality of the sex difference in CHD death rates in countries that have very different CHD mortality experiences is a case in point, particularly when deaths occurring in very elderly men and women (whose actual cause of death is often uncertain) are excluded. The now familiar Kalin and Zumoff graph shows the rather consistent male-to-female ratio of 2.5 to 4.5 for fatal CHD in countries with very different rates. Only in China are CHD death rates said not to vary by sex; this observation requires confirmation.
The virtually universal male excess of CHD implies a universal inherent female advantage that operates across populations with divergent rates of heart disease and lifestyles. The obvious explanation is that estrogen is good or that testosterone is bad. But the wide differences in CHD death rates between countries, coupled with the rather consistent sex ratios shown …, suggest that this sex effect is mediated by heart disease risk factors that exert an effect on both men and women. In fact, the differences between countries are greater than the differences between sexes, suggesting that sex is not destiny with regard to CHD.
Barrett-Connor, Elizabeth. “Sex Differences in Coronary Heart Disease.” Circulation 95, no. 1 (January 7, 1997): 252–64. doi:10.1161/01.CIR.95.1.252.
I’m not sure exactly what Coyne means by “senesce.” That isn’t a specific term in biology, and I doubt it ever will be; how do you quantify “growing old,” exactly? I’m guessing he meant to say “cellular senescence,” or the gradual shortening of the telomeres which cap the ends of the chromosomes. Once those disappear, DNA no longer copies properly and the cell containing it dies off. That can be quantified, and yes male-assigned people do tend to have shorter telomeres. But some of the genes related to telomeres are on the X chromosome, which again signals a genetic fluke rather than selective pressure.
I’ve dealt with Coyne’s argument about risk-taking before, and improving that effort isn’t worth my time. “Exploratory behavior” is almost synonymous, so I don’t think it’s worth a separate look. That leaves the sex ratio at birth. Surely he can’t be wrong on this one?
According to the CIA World Factbook, 59 countries out of 228 have a sex ratio less than 104:100 males to females. Here’s 14 of them:
|Saint Kitts and Nevis||1.02|
What could be going on here? My first guess is poverty; both South Africa and Haiti are known for high poverty levels, for instance, and Nauru is a wee island that’s heavily dependent on foreign aid. So let’s link this dataset to a measure of poverty, specifically the percentage of a country’s population that lives on less than $3.10 a day, in PPP-adjusted 2011 USD.
While there’s a fair bit of noise, it’s clear there’s some correlation between living standards and sex ratio at birth. This is backed up by more rigorous science, too. While the USA is quite close to the 1.05 mark, subtle changes in the rate track with gross economic trends. Comparing birth rates in East and West Germany, researchers found that the East had a lower sex ratio precisely when the economy collapsed.
Why does all this matter? Well, if the sex ratio at birth is effected by living standards, with lower standards triggering a ratio closer to parity, and the living standards of our ancestors were worse than those “enjoyed” by anyone today, isn’t it reasonable to suspect the sex ratio was lower in the past? This challenges the sex ratio as a universal trait, something that hasn’t fluctuated, and gives us reason to doubt Coyne’s claim that the male:female ratio is and always was greater than 1.
So, of Coyne’s five main assertions in that third bullet point, we find all of them are either unsupported or contradicted by the evidence. Maybe his fourth bullet point will offer something new.
- In line with the above, in humans and other primates, males show from the outset great exploratory and risk-taking behaviors, and as adults show many other behaviors that differ from those of females, such as greater dispersal. Is this due to the Primate Patriarchy? Probably not, given that these differences in behavior are shown in many species besides ours and make evolutionary sense.
Not really, he’s just recycled two assertions from the prior one, made some vague handwaving towards “many other behaviors,” and added “men are more likely to disperse than women.” Of three relevant studies I’ve tracked down on that last point, all three claim women tend to disperse more than men.
For a biology teacher who claims to value evidence, this is an embarrassing show. As charged, Coyne has spinning stories instead of grounding his work in evidence. Maybe the rest of his post will be better?
Please let it be better, I’m getting sick of writing “maybes…”
 Statistics Canada. Table 102-0561 – Leading causes of death, total population, by age group and sex, Canada, annual, CANSIM (database).
 Kaur, Navjot, and Kawalpreet Singh. “Comparative Review of Color Blindness in Different Ethnic Populations.” Journal of Evolution of Medical and Dental Sciences 1, no. 2 (2013): 6977–6981.
 Stevens, L. “Sex Chromosomes and Sex Determining Mechanisms in Birds.” Science Progress 80 ( Pt 3) (1997): 197–216.
 Pajukanta, Päivi, Michele Cargill, Laura Viitanen, Ilpo Nuotio, Anu Kareinen, Markus Perola, Joseph D. Terwilliger, et al. “Two Loci on Chromosomes 2 and X for Premature Coronary Heart Disease Identified in Early- and Late-Settlement Populations of Finland.” The American Journal of Human Genetics 67, no. 6 (December 2000): 1481–93. doi:10.1086/316902.
 Mayer, S., S. Brüderlein, S. Perner, I. Waibel, A. Holdenried, N. Ciloglu, C. Hasel, T. Mattfeldt, K. V. Nielsen, and P. Möller. “Sex-Specific Telomere Length Profiles and Age-Dependent Erosion Dynamics of Individual Chromosome Arms in Humans.” Cytogenetic and Genome Research 112, no. 3–4 (February 10, 2006): 194–201. doi:10.1159/000089870.
 Nawrot, Tim S., Jan A. Staessen, Jeffrey P. Gardner, and Abraham Aviv. “Telomere Length and Possible Link to X Chromosome.” The Lancet 363, no. 9408 (2004): 507–510.
 Leung, Justin Wai-Chung, Gargi Ghosal, Wenqi Wang, Xi Shen, Jiadong Wang, Lei Li, and Junjie Chen. “Alpha Thalassemia/Mental Retardation Syndrome X-Linked Gene Product ATRX Is Required for Proper Replication Restart and Cellular Resistance to Replication Stress.” Journal of Biological Chemistry 288, no. 9 (March 1, 2013): 6342–50. doi:10.1074/jbc.M112.411603.