Amid the Green Sahara in Africa, the mutation for sickle cell originated in the Sahara[7] or in the northwest forest region of western Central Africa (e.g., Cameroon)[7][8] by at least 7,300 years ago,[7][8] though possibly as early as 22,000 years ago.[9][8] The ancestral sickle cell haplotype to modern haplotypes (e.g., Cameroon/Central African Republic and Benin/Senegal haplotypes) may have first arose in the ancestors of modern West Africans, bearing haplogroups E1b1a1-L485 and E1b1a1-U175 or their ancestral haplogroup E1b1a1-M4732.[7] West Africans (e.g., Yoruba and Esan of Nigeria), bearing the Benin sickle cell haplotype, may have migrated through the northeastern region of Africa into the western region of Arabia.[7] West Africans (e.g., Mende of Sierra Leone), bearing the Senegal sickle cell haplotype,[10][7] may have migrated into Mauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, into North Africa, and from North Africa, into Southern Europe, Turkey, and a region near northern Iraq and southern Turkey.[10] Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes into Basra, Iraq, where both occur equally.[10] West Africans, bearing the Benin sickle cell haplotype, may have migrated into the northern region of Iraq (69.5%), Jordan (80%), Lebanon (73%), Oman (52.1%), and Egypt (80.8%).[10]
An African individual, who has been dated between 1st century CE and 3rd century CE as well as carried haplogroup H1, may have forcibly (via enslavement) or voluntarily migrated from the central Sahara or the Nile Valley (e.g., Sudan) to Rome.[13]
During the modern period, West Africans introduced more than 75% of Sub-Saharan mitochondrial DNA into North America and Southern Africans introduced almost 15%.[11] West Africans also introduced ~45% of Sub-Saharan African mitochondrial DNA into South America, whereas, Southern Africans, largely indigenous Angolans, introduced ~55%.[11] During the modern period, West Africans introduced 75% of Sub-Saharan African mitochondrial DNA into Iberia and other parts of Europe, possibly by sea voyage.[11] During the modern period, a greater number of West Africans introduced Sub-Saharan African mitochondrial DNA than East Africans.[11] In the modern period, 68% of Sub-Saharan African mitochondrial DNA was introduced by East Africans and 22% was introduced by West Africans, which constitutes 50% of Sub-Saharan African mitochondrial DNA in modern Southwest Asia.[11]
Between the 15th and the 19th century, around twelve million Africans were forcibly displaced from their countries to be enslaved (that means around 30,000 captives a year over three and a half centuries). Enslaved Africans were taken from African slaving coasts that stretched thousands of miles, from Senegal to Angola, and even round the Cape and on to Mozambique. The largest number (around 95%) of slaves arrived in Latin America, with ~43% disembarked in South America, ~52% in the Caribbean, while the remaining 5% arrived in what has become today the United States. This forced and massive migration of people radically changed the genetic landscape of present-day populations in the Americas...According to historical resources, from 1501 to 1867 enslaved Africans were embarked from eight major historical coastal regions in sub-Saharan Africa: 5.7% of the captives were from Senegambia, 3.2% from Sierra Leone, 2.7% from Windward Coast, 9.6% from Gold Coast, 16.1% from Bight of Benin, 12.3% from the Bight of Biafra, 46.3% from West Central Africa, and 4.1% from Southeast Africa. West Central Africa region (coastal region from present-day Gabon to Angola) was always the largest regional point for captives throughout most of the TAST [Trans-Atlantic Slave Trade] period, and much of the trade there was focused in present-day Angola. As the TAST expanded after 1641, slaving regions such as Gold Coast, the Bights of Benin and Biafra, and West Central Africa became more prominent than they had been before.[15]
Out of 642 individuals from 15 populations among the African diaspora in the Americas sampled in 2016, some of which included individuals who self-identified as being of African descent, the ancestry of 328 African Americans were found to be 80% African, the ancestry of Afro-Jamaicans were found to be 89% African, and the ancestry of Puerto Ricans were found to be 27% African.[15]
Due to their relative isolation from Europeans and Native Americans, Maroonsretained and adapted their cultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as Colombia, Jamaica, French Guiana, and Suriname.[15]Alukus,Kwinti, Matawai, Ndjukas, Paramakas, and Saramakas, who are Maroons of Noir Marron, are the largest, autonomous group of Maroons in the Americas.[15] Though Noir Marron groups and other groups among the African diaspora have been in the Americas for 400 years, the ancestry of Noir Marron individuals sampled in 2017 has shown that Maroons are 98% African, which is the highest degree of retained African ancestry among the African diaspora.[15] Noir Marron Maroons were found to be genetically linked with Africans in the region of the Bight of Benin; in particular, there are strong genetic connections with Africans in Benin and a linguistic connection with Gbe speakers, such as the Fon people.[15]
During the Holocene, 3% of Sub-Saharan African mitochondrial DNA is indicated to have been introduced into South America and 6% is indicated to have been introduced into North America.[11] However, Sá et al. (2022) provided the following rationale: “This could be explained by statistical residuals from the recent lineages, but also from a couple of lineages whose founders in Africa were likely not detected, or due to minor errors in the sequences leading to overestimates of the age estimate of specific lineages.”[11] During the modern period, West Africans introduced more than 75% of Sub-Saharan mitochondrial DNA into North America and Southern Africans introduced almost 15%.[11] West Africans also introduced ~45% of Sub-Saharan African mitochondrial DNA into South America, whereas, Southern Africans, largely indigenous Angolans, introduced ~55%.[11]
At Avondale Burial Place, in Bibb County, Georgia, utilized between 1820 CE and 1950 CE, 18 out of 20 individuals were determined to be African American, as they carried the following haplogroups: one L0, two with L1, seven with L2, seven with L3, and one with U6.[29]
60% of African Americans, who were sampled in 2007, were of haplogroup E1b1a, within which 22.9% were particularly of haplogroup E-M2; they also possessed numerous SNPs (e.g., U175, U209, U181, U290, U174, U186, and U247).[31]
An African American man, who was sampled in 2013, carried haplogroup A00, which likely dates back to 338,000 BP, and is a haplogroup shared with the Mbo people.[32]
Torres et al. (2012) states: "One African American population, those from South Carolina, cluster with the African populations. Notably, the South Carolina population falls nearest to the Grain Coast populations. Ethnohistorical records indicate a relationship between African Americans within this region of the United States and West Africans from Senegal, Gambia, and Sierra Leone. Based on such records it has been suggested that many African Americans within South Carolina originate from the Grain Coast region of West Africa. Furthermore, Africans from this region were sought-after and imported to the Americas for their knowledge of rice cultivation."[33]
X-Chromosomal DNA
Due to the X-chromosomes in African Americans having high concentrations of ancestry from Africa, this coheres with the understanding of there being an asymmetric flow of genes from European males to African females;[34][35] consequently, this can be understood as being the result of enslavedAfrican American females being raped by European males.[36]
Stefflova et al. (2011) states: "Ancestry from Guinea Bissau-Mali-Senegal-Sierra Leone predominates in other United StatesAfrican American populations compared to Philadelphia alone (43% vs. 22%). Despite the differences in coverage and sampling, this pattern may be attributed to a significant contribution of slaves from British colonies in Africa to the British-controlled Philadelphia region compared to a more diverse contribution to other parts of the United States from French, Spanish, and Dutch colonies. Additional possible contributing factors include the different periods of the slave trade influencing the Philadelphian population compared to the other parts of the United States. However, these remain tentative conclusions since we cannot rule out a contribution from sampling bias. Another example of these differences is the Gullah/Geechee populations from South Carolina/Georgia that have >78% of their source from the Guinea Bissau-Mali-Senegal-Sierra Leone region (data not shown), corresponding to the “Rice coast” around Sierra Leone that was the major source of slaves drawn by the United States in the later period of the slave trade."[38] The plurality of the African component of African Americans was found to be from West African populations from Senegambia and the Rice Coast (Guinea Bissau-Mali-Senegal-Sierra Leone), followed by Central Africans from the Congo and Angola, and lastly West-Central Africans (Nigeria-Niger-Cameroon).[38]
In addition to being found to have 2.6% (±2.1%) Native American and 10.6% (±2.3%) European ancestry, African-Americans who were sampled in 2008, were found to be 86.8% (±2.1%) West African.[39] In addition to being found to have 8% Asian (as a proxy for Native American ancestry) and 19.6% European ancestry, African-Americans, who were sampled in 2010, were found to be 72.5% African.[40] African Americans were found to be more closely genetically related to Yoruba people than East Africans (e.g., Luhya, Maasai).[40] Murray et al. (2010) also states: "In the analysis of AIMs [Ancestry Informative Markers], African Americans were most distant from Yorubans, followed by the Luhya, and then the Maasai and were closest to Barbadians."[40] Out of 5,244 African Americans sampled in 2017, their ancestry was found to range between 73% and 78% African; in particular, they were found to be of West African and western Central African ancestry.[15] Approximately 7% of their ancestry derives from Windward Coast, 13% from Senegambia, 30% from Angola, and nearly 50% from Benin, western Nigeria, and Togo.[15] Additionally, 4.8% of their ancestry derives from Bantu peoples and 16% derives from African rainforest hunter-gatherers.[15]
Tishkoff et al. (2009) via "Supervised STRUCTURE analysis [inferred] African American ancestry from global training populations, including both Bantu (Lemande) and non-Bantu (Mandinka) Niger-Kordofanian–speaking populations. These results were generally consistent with the unsupervised STRUCTURE analysis (table S6) and demonstrate that most African Americans have high proportions of both Bantu (~0.45 mean) and non-Bantu (~0.22 mean) Niger-Kordofanian ancestry, concordant with diasporas originating as far west as Senegambia and as far south as Angola and South Africa."[41] Moderate to modest amounts of Chadic, Fulani, Nilo-Saharan, Cushitic, and Sandawe ancestry were also inferred; this is consistent with the phylogenetic analysis of Tishkoff et al. (2009), wherein African-Americans were found to share more recent common ancestry with a clade including Hausa and Fulani from Cameroon, in addition to Chadic and Central Sudanic speakers such as the Mada, Sara, and Laka.[41]
African Americans, who have a high rate of occurrence of type 2 diabetes, have a few gene variants (e.g., several SNPs in IGF2 and HLA-B genes; the SNP, rs7903146, within the TCF7L2 gene; the intergenic SNP, rs7560163, located between the RBM43 gene and RND3 gene) that are strongly associated with type 2 diabetes.[42]
The rate of occurrence for hypertension in African Americans is 39%.[42] Several genes (e.g., EVX1-HOXA, PLEKHG1, RSPO3, SOX6, ULK4), which contributes to the signaling pathway for nitric oxide – a pathway connected with multiple functions (e.g., endothelian function, heart contraction, vasodilatation) relating to hypertension – and thus, are associated with hypertension.[42] Hypertension is also associated with the NPR3 gene.[42] These genes have all been connected with hypertension in African Americans.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
African Americans have as much as 65% of the Duffy-null genotype.[43] The cancer medicine, azathioprine, regarding its safety and when it should be discontinued, was found to be unsuitable and possibly damaging to African Americans, as the standard range was based on “normal” ranges for Europeans; the distinct genetic data from African Americans (e.g., Duffy-null phenotype) might provide a different explanation for neutropenia.[43]
A majority of Afro-Caribbean people descend from peoples in the regions of West Africa and western Central Africa.[44] In particular, their genetic ancestry, to some extent, derives from peoples in the region of Angola, but more so, from peoples in regions, such as the Bight of Benin, Bight of Biafra, Cameroon, and Ghana.[44] Additionally, between the late 19th century CE and early 20th century CE, some Haitians migrated into Cuba, thereby, resulting in the addition of ancestry from Africa.[44]
In addition to being found to have 0.2% (±2.0%) Native American and 10.2% (±2.2%) European ancestry, Afro-Barbadians, who were sampled in 2008, were found to be 89.6% (±2.0%) West African.[39] In addition to being found to have 6.7% Asian and 15.9% European ancestry, Afro-Barbadians, who were sampled in 2010, were found to be 77.4% African.[40] Afro-Barbadians were found to be more closely genetically related to Yoruba people than East Africans.[40] In addition to being found to have 6% Asian and 16% European ancestry, Afro-Barbadians, who were sampled in 2013, were found to be 77% African; most of the African ancestry of Afro-Barbadians were found to derive from the Yoruba people.[45] In addition to being found to have 0% Native American and 16% European (e.g., Northern/Western) ancestry, Afro-Barbadians, who were sampled in 2016 and self-reported their African ancestry, were found to be 84% African (e.g., Yoruba).[46][47] The ancestry of Afro-Barbadians, who were sampled in 2017, were found to be 88% African.[15]
Medical DNA
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Afro-Haitians, who were sampled in 2012, were found to have carried haplogroup E1b1a-M2 (63.4%), within which were more specific sub-haplogroups, such as haplogroups E1b1a7-M191 (26.8%) and E1b1a8-U175 (26%), and subgroups within those sub-haplogroups, such as E1b1a7a-U174 (26.8%) and E1b1a8a-P278 (13%); there were also various sub-haplogroups of haplogroup R1b (e.g., R1b1b1-M269, R1b1b1a1b2-M529, R1b1b1a1b*-S116, R-M306, R1b2*-V88) as well as haplogroup R1a-M198.[49]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Afro-Jamaicans, who were sampled in 2012, were found to have carried haplogroup E1b1a-M2 (60.4%), within which were more specific sub-haplogroups, such as E1b1a7-M191 (27.7%) and E1b1a8-U175 (23.3%), and subgroups within those sub-haplogroups, such as E1b1a7a-U174 (25.8%) and E1b1a8a-P278 (11.3%); there were also various sub-haplogroups of haplogroup R1b (e.g., R1b1b1-M269, R1b1b1a1b2-M529, R1b1b1a1b*-S116, R-M306, R1b2*-V88) as well as haplogroup R1a-M198.[49]
Afro-Jamaicans, who were sampled in 2012, were found to have mostly (97.5%) carried various forms of macro-haplogroup L as well as various other haplogroups (e.g., U6, A2, B2, D4, H, J, U2, M).[50]
In addition to being found to have 3.2% (±3.1%) Native American and 12.4% (±3.5%) European ancestry, Afro-Jamaicans, who were sampled in 2008, were found to be 84.4% (±3.1%) West African.[39] In addition to being found to have 8.3% (±13.5%) Native American and 10.3% (±8.4%) European ancestry, Afro-Jamaicans, who were sampled in 2013, were found to be 81.4% (±15.9%) West African.[48] The ancestry of Afro-Jamaicans, who were sampled in 2016, were found to be 89% African.[15] In addition to being found to have 1% Native American and 11% European (e.g., Northern/Western) ancestry, Afro-Jamaicans, who were sampled in 2016 and self-reported their African ancestry, were found to be 89% African (e.g., Yoruba).[46][47]
Medical DNA
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
At La Concepción chapel and Hospital Real de San José de los Naturales, in Mexico City, Mexico, enslavedAfricans, who carried haplogroup L, were sampled for viral genomes.[55] From among the sampled individuals, who may have died between 1472–1625 CE and 1442–1608 CE, the ancient DNA of the viruses were able to be were able to be reconstructed.[55] Due to the brutality of the Middle Passage and enslavement of the first generation of Africans, the transmission of the Hepatitis B virus and human parvovirus B19 from Africa to the Americas was facilitated by Spanish slavers and colonists; while this has not been established as causally connected, it is at least associated with the Cocoliztli epidemics.[55]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
At Pretos Novos Cemetery, in Rio de Janeiro, Brazil, 4 out 16 carried M. tuberculosis and 3 out of 16 carried haplogroups L3e2, L3d1, and L1c2; thus, indicating that the individuals, who were buried in the cemetery between the 18th century CE and the 19th century CE, were born in West Africa and/or western Central Africa, and soon died after reaching Rio de Janeiro.[56]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
In 2016, linguistic evidence (e.g., Kikongo influence and remnants from the early history of Palenque found in Palenquero), which was also compatible with a diverse origin for African Y-chromosome, supported Bakongo people being the founding population of Palenque; in 2020, the Yombe people of the Republic of the Congo were found to be genetically closest with the people of Palenque.[57]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Due to their relative isolation from Europeans and Native Americans, Maroonsretained and adapted their cultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as Colombia, Jamaica, French Guiana, and Suriname.[15]Alukus,Kwinti, Matawai, Ndjukas, Paramakas, and Saramakas, who are Maroons of Noir Marron, are the largest, autonomous group of Maroons in the Americas.[15] Though Noir Marron groups and other groups among the African diaspora have been in the Americas for 400 years, the ancestry of Noir Marron individuals sampled in 2017 has shown that Maroons are 98% African, which is the highest degree of retained African ancestry among the African diaspora.[15] Noir Marron Maroons were found to be genetically linked with Africans in the region of the Bight of Benin; in particular, there are strong genetic connections with Africans in Benin and a linguistic connection with Gbe speakers, such as the Fon people.[15]
Medical DNA
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Amid the Green Sahara in Africa, the mutation for sickle cell originated in the Sahara[7] or in the northwest forest region of western Central Africa (e.g., Cameroon)[7][8] by at least 7,300 years ago,[7][8] though possibly as early as 22,000 years ago.[9][8] The ancestral sickle cell haplotype to modern haplotypes (e.g., Cameroon/Central African Republic and Benin/Senegal haplotypes) may have first arose in the ancestors of modern West Africans, bearing haplogroups E1b1a1-L485 and E1b1a1-U175 or their ancestral haplogroup E1b1a1-M4732.[7] West Africans (e.g., Yoruba and Esan of Nigeria), bearing the Benin sickle cell haplotype, may have migrated through the northeastern region of Africa into the western region of Arabia.[7] West Africans (e.g., Mende of Sierra Leone), bearing the Senegal sickle cell haplotype,[10][7] may have migrated into Mauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, into North Africa, and from North Africa, into Southern Europe, Turkey, and a region near northern Iraq and southern Turkey.[10] Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes into Basra, Iraq, where both occur equally.[10] West Africans, bearing the Benin sickle cell haplotype, may have migrated into the northern region of Iraq (69.5%), Jordan (80%), Lebanon (73%), Oman (52.1%), and Egypt (80.8%).[10]
During the early period of the Holocene, Sub-Saharan African mitochondrial DNA was introduced into Europe, mostly in Iberia.[11]West Africans probably migrated, across Sahelian Africa, North Africa, and the Strait of Gibraltar, into Europe, and introduced 63% of Sub-Saharan African mitochondrial DNA.[11] During the modern period, West Africans introduced 75% of Sub-Saharan African mitochondrial DNA into Iberia and other parts of Europe, possibly by sea voyage.[11]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
According to some studies, Greeks share some Human Leukocyte Antigen (HLA) alleles with East Africans (e.g., Amhara, Nuba, Oromo) and West Africans (e.g., Fulani, Mossi, Rimaibe) from Burkina Faso,[70][71][72] who are viewed as having a possible earlier origin in Ethiopia.[71][73] In particular, West Africans (e.g., Fulani, Mossi, Rimaibe) and Ethiopians (e.g., Amhara, Oromo) are viewed as sharing the most HLA-DRB1 alleles with Greeks.[74][72] Greeks, West Africans, and Ethiopians are viewed as viewed as sharing chromosome 7 markers.[70] During the desertification of the Green Sahara in 5000 BCE, or during the time of ancient Egypt, admixture between Greeks and black Africans are viewed as having occurred.[70] Following the aridification of the Green Sahara, Africans are viewed as possibly having migrated from the southern region of the Sahara to the region of Athens and the islands in the Aegean.[71][73] If the migration of black Africans into Greece occurred following the drying of the Green Sahara, it is viewed that this may indicate that Pelasgians derive from black Africans.[70] More likely, if the migration of black Africans into Greece occurred during the time of ancient Egypt, then it is viewed that it may have been when black African dynasties in ancient Egypt and that those who followed them were expelled.[70][71] Alternatively, during the existence of ancient Egypt, it is viewed that groups from Ethiopia may have migrated to Greece and West Africa, thereby, resulting in the possible admixture of modern Greeks and modern West African ethnic groups (e.g., Fulani, Mossi, Rimaibe).[74] Greeks are viewed as sharing some alleles with West Africans (e.g., Fulani, Mossi, and Rimaibe) and East Africans (e.g., Oromo, Amhara, Nubians),[75][72] the latter of which are viewed as also interrelated.[75] Following the expulsion of what are characterized as black African Egyptian dynasties and groups who followed the dynasties toward Greece, it is viewed that there may have been subsequent admixture between the incoming groups and Greeks.[75] Another migration of West Africans may have occurred thereafter.[75] Additionally, following desertification of the Green Sahara around 5000 BCE, it is viewed that there may have been another migration of black Africans into Greece.[75] A shared autosomal marker, relating to cystic fibrosis (3120 + 1 G), was viewed as having been found between some Africans and Greeks; as a possible historic explanation for the presence of this marker, the Danaids, who are identified as Africans, are viewed as possibly having migrated toward the north, into ancient Egypt, being repelled in ancient Egypt, and subsequently having migrated into Peloponnesus.[72]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
An African individual, who has been dated between 1st century CE and 3rd century CE as well as carried haplogroup H1, may have forcibly (via enslavement) or voluntarily migrated from the central Sahara or the Nile Valley (e.g., Sudan) to Rome.[13]
Medical DNA
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Between 15,000 BP and 7000 BP, 86% of Sub-Saharan African mitochondrial DNA was introduced into Southwest Asia by East Africans, largely in the region of Arabia, which constitute 50% of Sub-Saharan African mitochondrial DNA in modern Southwest Asia.[11] During the modern period, a greater number of West Africans introduced Sub-Saharan African mitochondrial DNA than East Africans.[11] In the modern period, 68% of Sub-Saharan African mitochondrial DNA was introduced by East Africans and 22% was introduced by West Africans, which constitutes 50% of Sub-Saharan African mitochondrial DNA in modern Southwest Asia.[11]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Local myth about Zana of Abkhazia, Georgia being an Almasty was refuted by genetic evidence from ancient DNA, which confirmed that Zana was neither closely related to chimpanzees nor closely related to archaic humans, but closely related to other modern humans.[82] Margaryan et al. (2021) speculate that Zana may have had congenital generalized hypertrichosis, which may have resulted in the development of the local myth.[82]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Out of the total amount of haplogroups carried, Siddis, who were sampled in 2011, 70% of their paternal haplogroups were found to be African; their paternal haplogroups were found to be common among Bantu-speaking peoples.[14]
In addition to being found to have 30.74% (±10.98%) South Indian and 7.05% (±10.15%) European ancestry, Siddis, who were sampled in 2011, were found to be 62.21% (±9.68%) East African.[83] Siddis, who were sampled twice in 2011, were found to be 60%-75% Sub-Saharan African.[14]
Medical DNA
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]
While the orature among Makranis narrates an origin from Abyssinia, the genetic results from 2017 show that much of the ancestry of Makranis derives from Bantu-speaking peoples (Zanj), specifically from the southeast AfricanSwahili coast.[14] In addition to being found to have 74.5% Pakistani ancestry, Makranis, who were sampled in 2017, were found to be 25.5% Sub-Saharan African.[14] Due to the African ancestry in Makranis being genetically similar to southeastern Bantu (e.g., Sotho) and eastern Bantu (e.g., Luhya) peoples, their African ancestry may derive from a source population in Mozambique.[14] Additionally, the African ancestors of the Makranis may have been enslaved by slavers from the Omani Empire during the Indian Ocean slave trade of the 18th century CE.[14]
Risk allele variants G1 and G2 are associated with chronic kidney disease, which are common among populations of Sub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of western Central African ancestry and origin.[42]