The African diaspora: history, adaptation and health

Abstract

The trans-Atlantic slave trade brought millions of Africans to the New World. Advances in genomics are providing novel insights into the history and health of Africans and the diasporan populations. Recent examples reviewed here include the unraveling of substantial hunter-gatherer and 'Eurasian' admixtures across sub-Saharan Africa, expanding our understanding of ancestral African genetics; the global ubiquity of mixed ancestry; the revealing of African ancestry in Latin Americans that likely derived from the slave trade; and understanding of the ancestral backgrounds of APOL1 and LPL found to influence kidney disease and lipid levels, respectively, providing specific insights into disease etiology and health disparities.

Figure 1

Individual admixture proportions from New World samples [12]. The six samples are African Caribbean in Barbados (ACB), People with African Ancestry in Southwest USA (ASW), Puerto Ricans in Puerto Rico (PUR), Colombians in Medellín, Colombia (CLM), People with Mexican Ancestry in Los Angeles, California (MXL), and Peruvians in Lima, Peru (PEL). Conditional on eight ancestries, yellow corresponds to Western African ancestry, aquamarine corresponds to West-Central African ancestry, blue corresponds to Southern European ancestry, orange corresponds to Northern European ancestry, purple corresponds to Native American ancestry, red corresponds to South Asian ancestry, green corresponds to East Asian ancestry, and black corresponds to Southeastern Asian ancestry. Summing the Western and West-Central African ancestries, the range of individual admixture proportion across these six samples goes from 0% to 97.8%. Similarly, the range of individual admixture proportion for Native American ancestry goes from 0% to 100%.

Figure 2

Geographic distribution of Trypansoma brucei and APOL1 risk variants. (A) Cumulative incidence from 1990 to 2014 of human African trypanosomiasis due to Trypansoma brucei gambiense (gHAT) and Trypanosoma brucei rhodesiense (rHAT) [75]. Uganda is the only country reporting trypanosomiasis due to both subspecies, with a higher cumulative incidence of gHAT. (B) Global frequency distribution of the G allele of the S342G mutation [,,,,–78]. The Esan in Nigeria have the highest frequency (49.5%). (C) Global frequency distribution of the G2 deletion [12,28,32,49,77]. Bantu-speaking people in South Africa (Herero, Ovambo, Pedi, Sotho, Tswana, and Zulu) have the highest frequency (21.4%).

Figure 2

Geographic distribution of Trypansoma brucei and APOL1 risk variants. (A) Cumulative incidence from 1990 to 2014 of human African trypanosomiasis due to Trypansoma brucei gambiense (gHAT) and Trypanosoma brucei rhodesiense (rHAT) [75]. Uganda is the only country reporting trypanosomiasis due to both subspecies, with a higher cumulative incidence of gHAT. (B) Global frequency distribution of the G allele of the S342G mutation [,,,,–78]. The Esan in Nigeria have the highest frequency (49.5%). (C) Global frequency distribution of the G2 deletion [12,28,32,49,77]. Bantu-speaking people in South Africa (Herero, Ovambo, Pedi, Sotho, Tswana, and Zulu) have the highest frequency (21.4%).

Figure 2

Geographic distribution of Trypansoma brucei and APOL1 risk variants. (A) Cumulative incidence from 1990 to 2014 of human African trypanosomiasis due to Trypansoma brucei gambiense (gHAT) and Trypanosoma brucei rhodesiense (rHAT) [75]. Uganda is the only country reporting trypanosomiasis due to both subspecies, with a higher cumulative incidence of gHAT. (B) Global frequency distribution of the G allele of the S342G mutation [,,,,–78]. The Esan in Nigeria have the highest frequency (49.5%). (C) Global frequency distribution of the G2 deletion [12,28,32,49,77]. Bantu-speaking people in South Africa (Herero, Ovambo, Pedi, Sotho, Tswana, and Zulu) have the highest frequency (21.4%).