Why have humans no evolved anymore

At the end of the Pleistocene, every continent (except Antarctica) was populated and each non-African population exhibited a subset of the common genetic variants found in Africa (Barbujani & Colonna, 2010; Campbell & Tishkoff, 2010; Henn, Cavalli-Sforza, & Feldman, 2012). See Figure 4.1. The now global human population exploded during the Holocene, almost certainly due to the transition to agriculture. This explosion generated the large number of rare variants noted earlier, most of which are of recent origin (5–10 kya) and more or less specific to the major continental populations. Thus, there has been recent genetic divergence among the continental populations, but much of this variation—perhaps 95%—is neutral or weakly deleterious (Fu et al., 2013; Fumagalli et al., 2011; Tennessen et al., 2012).

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Regarding recent cognitive evolution, Huang et al. (2013) conducted a meta analysis of 27 studies of positive selection across the human genome and found that genes that are highly expressed in the central nervous system are enriched in recent positive selection. Keeping in mind that false positives are common in studies of positive selection, possible examples of divergent positive selection on neural function include: opioid cis-regulatory alleles (Rockman et al., 2005); loci involved in the axon guidance pathway, which determines the direction the axon will grow, ultimately influencing the development of neuronal networks (Tennessen & Akey, 2011); genes in non-African populations in the neuregulin ERBB4 signaling pathway, which is involved in the development of the nervous system, heart, and other tissues (Pickrell et al., 2009); selection of downstream gene targets of FOXP2, which is implicated in language abilities, in a European sample but not an East Asian or African sample (but the selected downstream genes have multiple functions in neural and nonneural tissue) (Ayub et al., 2013); and alleles in Ashkenazi Jews that have been argued to increase intelligence in heterzygotes but cause severe disease in homozygotes (Cochran & Harpending, 2009).

Additionally, population differences in frequencies of alleles impacting neural function might be due to founder effects and drift. Such seems to be the case with the dopamine D4 alleles (Kidd, Pakstis, & Yun, 2013).12 Finally, because exposure to neurotoxins from plants, fungi, pathogens, and the environment varied across populations, some divergent neural evolution might represent protective changes in neuroreceptors and other neural functions. Nevertheless, despite the lack of compelling evidence to date, it would not be surprising if there were limited population divergence in some neural/psychological functions due to recent positive selection on cognition and behavior.
Regarding recent cognitive evolution, Huang et al. (2013) conducted a meta analysis of 27 studies of positive selection across the human genome and found that genes that are highly expressed in the central nervous system are enriched in recent positive selection. Keeping in mind that false positives are common in studies of positive selection, possible examples of divergent positive selection on neural function include: opioid cis-regulatory alleles (Rockman et al., 2005); loci involved in the axon guidance pathway, which determines the direction the axon will grow, ultimately influencing the development of neuronal networks (Tennessen & Akey, 2011); genes in non-African populations in the neuregulin ERBB4 signaling pathway, which is involved in the development of the nervous system, heart, and other tissues (Pickrell et al., 2009); selection of downstream gene targets of FOXP2, which is implicated in language abilities, in a European sample but not an East Asian or African sample (but the selected downstream genes have multiple functions in neural and nonneural tissue) (Ayub et al., 2013); and alleles in Ashkenazi Jews that have been argued to increase intelligence in heterzygotes but cause severe disease in homozygotes (Cochran & Harpending, 2009).

Additionally, population differences in frequencies of alleles impacting neural function might be due to founder effects and drift. Such seems to be the case with the dopamine D4 alleles (Kidd, Pakstis, & Yun, 2013).12 Finally, because exposure to neurotoxins from plants, fungi, pathogens, and the environment varied across populations, some divergent neural evolution might represent protective changes in neuroreceptors and other neural functions. Nevertheless, despite the lack of compelling evidence to date, it would not be surprising if there were limited population divergence in some neural/psychological functions due to recent positive selection on cognition and behavior.

Click to expand...