"He did not like my VMAT1 gene post on Eurasians. "
Please repost.....VMAT1
there is an entire thread.
As we can see Most Europeans have some sort psychiatric dis-order(xenophobia), ie aggression and social mal-function. Africans are not immune from it either but at far less frequency. Amazingly Peruvians seems to have a big proble through genetic drift?
Btw the gene evolved AFTER divergence of humans and Neanderthals
Quote
"ESTIMATION OF HAPLOTYPE NETWORK AND
MUTATION AGE OF 136Ile IN SLC18A1
A median-joining haplotype network revealed a star-like structure, indicating that H13 (containing 136Thr) was the ancestral
haplotype (Fig. S8). 136Ile was found in H5, H12, H18, and H24, and the mutation from 136Thr to 136Ile is likely to have
occurred in H24 (Fig. S8).
This result was consistent with the observation that all the archaic hominins carried 136Thr and that
the genomic regions around this SNP did not exhibited any introgression signature from Neanderthals. We conducted coalescent
simulations using GENETREE and estimated the 136Ile mutation age as having originated 105,500 (SE: ±30,800) years ago
(Fig. S9).
VMAT1 has a higher affinity for serotonin than the other monoamines (Brunk et al. 2006). Serotonin is a phylogenetically
ancient molecule and its circuits are involved in several central brain functions,
such as mood, **social or aggressive behavior**,
sleep, and memory. In addition, dysfunctions in its transport
are major causes of a variety of PDs. Thus, its role in neurodevelopment
and the effects of genotype on the
resulting physiological or behavioral phenotype have been widely discussed; however,
few studies have addressed its importance from the perspective of human evolution. Stimpson et al. (2016) has identified an evolutionary
change in the serotonergic innervation of the amygdala between chimpanzees and bonobos, and suggested that it has
The relationship between the prevalence of the disease-risk alleles and the
Out-of-Africa event has been discussed widely, and it is generally
accepted that a significant bottleneck at that time acted to enhance the genetic drift and to increase the frequencies of
risk alleles in populations (Tishkoff and Williams 2002; Comas et al. 2013). Regarding the PDs,
it is known that the prevalence
of mental disorders in **African populations is lower** than in the other regions in the world (Gureje et al. 2006; Steel et al. 2014).
Our results, combined with those of the previous studies, suggest that the variants linked to PDs not only exist due to the historical
genetic drift but also could likely be
maintained by balancing selection
in non-African populations."
