Why
have British women become broader-hipped over the past three thousand years?
(Wikicommons: Niek Sprakel)
British
women have become broader-hipped over the past three thousand years or so.
That's the conclusion of a recent study of alleles that influence female hip
circumference, using data from the UKBiobank. Audrey Arner and her colleagues at Penn State identified148 SNPs associated with female hip circumference and 49 SNPs associated with first child birth weight. Nine of them influence both
women's hip circumference and first child birth weight. The SNPs associated with
female hip circumference seemed to influence first child birth weight but not vice versa. There also seems to have been selection over approximately the last three thousand years for women with broader hips. The
baby's head is the biggest challenge during childbirth:
Human
birthing is difficult owing to a tradeoff between large neonatal brain size and
maternal pelvic dimensions, which are constrained by aspects of bipedal
biomechanics. The net effect is that human neonatal head size closely matches
maternal pelvic dimensions, unlike in our closest living relatives, the great
apes, whose pelvic dimensions are larger than neonatal head sizes. (Franciscus
2009)
Have
female hips become broader over the past three thousand years because the birth
canal has had to accommodate babies with larger brains? That hypothesis would
be consistent with an analysis of ancient DNA by Michael Woodley of Menie and
others, who showed that alleles for educational attainment gradually increased
in frequency between 4,560 and 1,210 years ago in Europeans and Central Asians.
That increase may have been due to gene-culture coevolution: as societies grew
larger and more complex, the average person had to perform mental tasks that
likewise became larger in number and more complex. Such an environment would
have favored the survival and reproduction of individuals with higher cognitive
ability. Mean IQ thus rose over time, as did cranial capacity.
On
the other hand, Henneberg (1988) showed that cranial capacity steadily shrank
from the Mesolithic to modern times, becoming 9.9% smaller in men and 17.4%
smaller in women. His conclusion was based on a large sample: 9,500 male skulls
and 3,300 female skulls.
So
we have a contradiction. Perhaps cranial capacity didn't really shrink from the
Mesolithic to modern times. Perhaps smaller skulls are more likely to decompose
faster. The skulls we unearth would therefore be a biased sample, and this bias
toward preservation of larger skulls would gradually increase for skulls that
have been in the ground longer.
The
problem of "preservation bias" has already been noted with respect to
female and infant remains:
There
are nearly always more males than females in skeletal collections from
archeological sites [...]. This has been explained in part by the comparatively
rapid disintegration of lightly built female skeletons.
[...]
The burial records show that most of the people buried in the Purisima cemetery
were either infants, children, or elderly adults. The skeletal remains
excavated from the cemetery, in contrast, are predominately those of young
adults. The underrepresentation of young children in the skeletal collection is
most likely a result of the comparatively rapid disintegration of their
incompletely calcified bones.
[...]
If, on the other hand, infants or elderly people are more common in a skeletal
collection from a recent cemetery than they are in an ancient one, much less
can be inferred about differences in the original age structure of the two
burial populations. Such a difference would be expected due to differential
preservation, even if the age structures of the two burial populations were
identical. (Walker et al. 1988)
The
same preservation bias might cause an overrepresentation of larger skulls among
older remains.
Franciscus,
R.G. (2009). When did the modern human pattern of childbirth arise? New
insights from an old Neandertal pelvis. Proceedings
of the National Academy of Sciences 106(23): 9125-9126. https://www.pnas.org/content/106/23/9125.short
Worldwide
frequency of the new ASPM variant (Mekel-Bobrov
et al. 2007)
Fifteen
years ago, Science published a major finding:
the human brain was still evolving well after the dawn of history. This could
be seen in the evolution of ASPM, a
gene that severely reduces brain size if it fails to function during
development.
Here,
we show that one genetic variant of ASPM
in humans arose merely about 5800 years ago and has since swept to high
frequency under strong positive selection. These findings, especially the
remarkably young age of the positively selected variant, suggest that the human
brain is still undergoing rapid adaptive evolution. (Mekel-Bobrov et al. 2007)
This
variant seems to have come from the Middle East, where it is most prevalent
today (37-52%). Its prevalence is next highest in Europe (38-50%). It is much
less common in East Asia (0-25%) and virtually absent almost everywhere else.
Interest
waned in the subject when several researchers found no association between the new
variant and IQ scores or brain size (Mekel-Bobrov et al. 2007; Rushton et al.
2007). At the time it was widely thought, notably by J. Philippe Rushton, that IQ
covers all aspects of mental effort. When I asked him whether the researchers
had measured mental endurance, he replied: "No, they just used the
standard IQ tests, head circumference, and (in our case) a test of altruism.
[...] Generally there isn't thought to be much left to be explained after g is taken out."
This
view has since been called into question. Some cognitive abilities correlate
poorly with IQ, like executive function (Arffa 2007). Others show no
correlation at all, like face recognition (Zhu et al. 2010). Furthermore, there
has been growing evidence that the different ASPM variants of modern humans affect only some parts of the brain,
and not the entire brain. According to a comparative study of primate species,
the evolution of ASPM does not
correlate with major changes in the whole brain or in cerebellum size:
Particularly
striking is the result that only major changes of cerebral cortex size and not
major changes in whole brain or cerebellum size are associated with positive
selection in ASPM. This is consistent
with an expression report indicating that ASPM's
expression is limited to the cerebral cortex of the brain (Bond et al. 2002).
Our findings stand in contrast to recent null findings correlating ASPM genotypes with human brain size
variation. Those studies used the relatively imprecise phenotypic trait of
whole brain instead of cerebral cortex size (Rushton, Vernon, and Bons 2006;
Woods et al. 2006; Thimpson et al. 2007). Although previous studies have shown
that parts of the brain scale strongly with one another and especially with
whole brain (e.g., Finlay and Darlington 1995), evidence here suggests that
different brain parts still have their own evolutionary and functional
differentiation with unique genetic bases. (Ali and Meier 2008)
Another
comparative study found that ASPM had
undergone accelerated change in chimpanzee, bonobo, and human lineages. Perhaps
more interestingly, the effects were confined to development of the cerebral
cortex:
Our
findings indicate that ASPM variation
is potentially associated with cerebral ventricular volume in chimpanzees, but
not with any of the other brain structure measures. Ventricles are a critical
site of neuronal proliferation in early development. Furthermore, the
cerebrospinal fluid which circulates through the ventricles throughout life
carries proteins that play important roles in central nervous system
development and maintenance, like Sonic Hedgehog protein and Insulin-like
Growth Factor 2.
Sonic
Hedgehog protein?
Thus,
variation in ventricular volume may affect the circulation of growth factors
that could potentially influence the regulation of cerebral cortical
development. Alternatively, because ASPM
has a significant effect on neural progenitor cycling along the ventricles in
fetal life, the association shown in our study may be a result of how brain
size is patterned by ASPM during
neurogenesis in early development. It has been shown that ASPM plays a role in regulating the affinity of ventricular radial
glial cells (VRGs) for the ventricular surface. (Singh et al. 2019)
While
there is also a broader role in brain development and brain size, it is usually
limited to extreme cases, like microcephaly:
The
abundance of ASPM mutations in human
patients with microcephaly suggests that the gene plays a significant role in
the regulation of brain size; however, variation in the gene has not always
shown direct impact on brain circumference, volume, and intelligence in
non-pathological populations. It is possible that ASPM interacts with other genes to affect brain volume, and thus
associations depend on genetic background. Furthermore, selective pressure on ASPM may be associated with other
aspects of neuronal function that do not lead to overt changes in brain
structure, or might have a pleiotropic effect in other areas of the body, as ASPM is also expressed outside of the
brain (Singh et al. 2019)
Possible
explanations for the new ASPM variant
Shift from tonal
to nontonal language?
So
what made the new ASPM variant so
successful? Two British researchers, Dan Dediu and D. Robert Ladd argue that it
was a shift from tonal to non-tonal language. After showing that nontonality
correlates geographically with the new ASPM
variant (and also a new variant of the Microcephalin
gene), they note that "the fact that nontonality is associated with the
derived haplogroups suggests that tone is phylogenetically older and that the
bias favors nontonality" (Dediu Ladd 2007).
If
this is true, tonality gave way to nontonality in the Middle East when the new ASPM variant arose there some six thousand
years ago. Yet we have no evidence of such a shift. Furthermore, languages have
usually evolved from nontonality to tonality: "it seems to be the dominant
view in the literature that tones arose from a toneless state" (Abramson
2004).
Spread of
alphabetical writing?
I
have argued for another explanation: the new ASPM variant was successful because it somehow assisted a mental
task that originated in the Middle East some six thousand years ago and then
spread into Europe. The task was alphabetical writing, specifically the mental
process of transcribing speech and copying texts into alphabetical characters.
Though more easily learned than ideographs, these characters place higher
demands on the mind, especially under premodern conditions (continuous text
with little or no punctuation, real-time stenography, absence of automated
assistance for publishing or copying, etc.). This task was largely assigned to
scribes of various sorts who enjoyed privileged status and probably superior
reproductive success, thereby spreading the new ASPM variant throughout the population (Frost 2007).
Conclusion
For
a brief time, over a decade ago, it seemed we had hard evidence that the human
brain was still evolving during the time of recorded history. That evidence was
soon rejected and largely forgotten, ironically through the efforts of J.
Philippe Rushton. It didn't fit his model. As he saw it, if something fails to
correlate with IQ, specifically with the g
factor, it cannot be a cognitive ability and is unworthy of interest.
Rushton
was also held back by the idea that human evolution had largely ended with the
end of the last ice age. Though intrigued by the contrary idea of ongoing human
evolution, he never brought it into his theoretical work and generally treated
it like an unwanted strip of film on a cutting-room floor.
References
Abramson,
A.S. (2004). The plausibility of phonetic explanations of tonogenesis. In:
Fant, G., Fujisaki, H., Cao, J., Xu, Y. (Eds.), From traditional phonology to modern speech processing: Festschrift for
Professor Wu Zongji's 95th birthday. Beijing: Foreign Language Teaching and
Research Press, 17-29. http://www.haskins.yale.edu/Reprints/HL1336.pdf
Ali,
F. and R. Meier. (2008). Positive selection in ASPM is correlated with cerebral cortex evolution across primates
but not with whole brain size. Molecular
Biology and Evolution 25(11): 2247-2250. http://www.haskins.yale.edu/Reprints/HL1336.pdf
Arffa,
S. (2007). The relationship of intelligence to executive function and
non-executive function measures in a sample of average, above average, and
gifted youth. Archives of Clinical
Neuropsychology 22(8): 969-978 https://academic.oup.com/acn/article/22/8/969/3025
Dediu,
D., and R. Ladd. (2007). Linguistic tone is related to the population frequency
of the adaptive haplogroups of two brain size genes, ASPM and Microcephalin. Proceedings of the National Academy of Sciences
104(26):10944-10949 https://langev.com/pdf/dediu07linguisticTonePNAS.pdf
Rushton,
J.P., P.A. Vernon, and T.A. Bons. (2007). No evidence that polymorphisms of
brain regulator genes Microcephalin
and ASPM are associated with general
mental ability, head circumference or altruism. Biology Letters-UK 3(2):157-60. https://royalsocietypublishing.org/doi/full/10.1098/rsbl.2006.0586
A
dying man, stoned on suspicion of spreading the plague - Felix Jenewein, 1899
(Wikicommons)
SARS-CoV-2,
though novel, belongs to a long-existing group of respiratory pathogens:
coronaviruses. Until the first appearance of SARS in 2002, these pathogens did
little harm to their hosts, usually causing nothing worse than a common cold.
So they may have coevolved with us. Furthermore, this coevolution may have
taken different forms in different human populations and different cultural
environments.
Coronaviruses
infect lung tissue via a receptor, ACE2, that varies structurally not only
between Asians and other human groups but also between different Asian groups.
In particular, the Chinese population has fewer alleles that code for weak
binding to the coronavirus S-protein (Cao et al. 2020). Different ACE2 alleles are also associated with
differences in susceptibility to diabetic retinopathy, an eye disease with a
distinct global pattern of prevalence: 22% in Italy, 23% in China, 30% in the
United Kingdom, and 40% in the United States (Adams 2020).
This
geographic pattern doesn’t exist because some populations have become more
resistant to coronaviruses. Instead, the reverse seems to have happened: some
populations have become more susceptible to coronavirus infection, perhaps as a
means to prevent more serious pulmonary infections, like tuberculosis and
pneumonic plague (Shekhar et al. 2017). Such an effect has been shown with γherpesvirus
68 and cytomegalovirus (Barton et al. 2007; Miller et al. 2019). This crude
vaccination boosts the immune response through increased production of IFN-γ
and increased activation of macrophages.
Historically,
tuberculosis was especially common in crowded environments, where people lived
in proximity not only to each other but also to domesticated animals (Comas et
al. 2013). Such environments have existed continuously for the longest time in
China, as well as in areas like the Indo-Gangetic Plain, the Fertile Crescent,
and the Mediterranean Basin. Those areas are where people should be most
susceptible to coronavirus infection.
This
may explain why COVID-19 has been more severe in southern Europe than in
northern Europe. It is surprising that infection tends to become less severe with
latitude when one would expect the opposite: respiratory viruses spread more
effectively under conditions of lower temperature, lower humidity, and lower
solar UV.
Ongoing research?
These
geographic differences have caught the interest of a molecular epidemiologist
at the University of Hawai'i, Maarit Tiirikainen:
"There
have been major differences in the rates of SARS-CoV-2 infection and the severe
disease between the different geographic regions since the beginning of the
COVID-19 pandemic, even among young individuals," Dr. Tiirikainen said.
"Epidemiological studies-so-called Genome Wide Association Studies
(GWAS)-indicate that populations carry different variants of the ACE2 gene.
This variation in the gene coding for the ACE2 receptor may have an effect on
the number of ACE2 receptors on the lung cells, as well as on how effectively
the virus binds to the receptor. There may also be genetic differences in
immune and other important genes explaining why some people get more sick than
others."
She
is collaborating with a genomics company, LifeDNA, in a study that will
initially focus on Hawai'i's multiethnic inhabitants, specifically their
diversity of ACE2 alleles in relation
to the latest coronavirus (LifeDNA 2020 – h/t to Steve Sailer).
Parting thoughts
All
humans can get infected by coronaviruses, but the infection tends to vary in
severity from one population to another. This variance may reflect differences
in genetic adaptation in different cultural environments.
Of
course, adaptation may also be cultural. Because natural selection acts on the
end result, and not on the means to that end, the means may be a purely learned
algorithm, like adding spices to food or avoiding physical contact with
strangers. One might not have understood why or how such practices worked, but
they did work and would be passed on to subsequent generations, thus becoming the
traditional way of doing things. Today, we’re likely to reject such practices as
outmoded superstitions.
Barton
E.S., White D.W., Cathelyn J.S., Brett-McClellan K.A., Engle M., Diamond M.S.,
et al. (2007). Herpesvirus latency confers symbiotic protection from bacterial
infection. Nature 447: 326-329. https://www.nature.com/articles/nature05762
Cao
Y., Li L., Feng Z., Wan S., Huang P., Sun X., et al. (2020). Comparative
genetic analysis of the novel coronavirus (2019-nCoV/SARS-CoV-2) receptor ACE2
in different populations. Cell Discovery
6(11). https://www.nature.com/articles/s41421-020-0147-1%3C/blockquote%3E
Comas
I., Coscolla M., Luo T., Borrell S., Holt K.E., Kato-Maeda M., et al. (2013).
Out-of-Africa migration and Neolithic coexpansion of Mycobacterium tuberculosis with modern humans. Nature Genetics 45(10): 1176-1182. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800747/
