
Thegenetic history of the African diaspora is composed of the overall genetic history of theAfrican diaspora, within regions outside ofAfrica, such asNorth America,Central America, theCaribbean,South America,Europe,Asia, andAustralia; this includes the genetic histories ofAfrican Americans,Afro-Canadians,Afro-Caribbeans,Afro-Latinos,Afro-Europeans,Afro-Asians, andAfrican Australians.
TheSahara served as a trans-regional passageway and place of dwelling for people in Africa during varioushumid phases[1][2][3] and periods throughout thehistory of Africa.[4][5] As early as 11,000 years ago,Sub-SaharanWest Africans, bearingmacrohaplogroup L (e.g.,L1b1a11, L1b1a6a, L1b1a8, L1b1a9a1,L2a1k,L3d1b1a), may have migrated throughNorth Africa and intoEurope, mostly intosouthern Europe (e.g.,Iberia).[6]
Amid theGreen Sahara inAfrica, the mutation forsickle cell originated in theSahara[7] or in thenorthwest forest region of westernCentral 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 andBenin/Senegal haplotypes) may have first arose in the ancestors of modernWest Africans, bearing haplogroupsE1b1a1-L485 andE1b1a1-U175 or their ancestral haplogroup E1b1a1-M4732.[7] West Africans (e.g.,Yoruba andEsan of Nigeria), bearing the Benin sickle cell haplotype, may have migrated through thenortheastern region of Africa into the western region ofArabia.[7] West Africans (e.g.,Mende of Sierra Leone), bearing the Senegal sickle cell haplotype,[10][7] may have migrated intoMauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, intoNorth Africa, and from North Africa, intoSouthern Europe,Turkey, and a region near northernIraq and southern Turkey.[10] Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes intoBasra, 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%), andEgypt (80.8%).[10]
During the early period of the Holocene,Sub-Saharan African mitochondrial DNA was introduced into Europe, mostly inIberia.[11]West Africans probably migrated, acrossSahelian Africa,North Africa, and theStrait of Gibraltar, intoEurope, and introduced 63% of Sub-Saharan African mitochondrial DNA.[11] Between 15,000 BP and 7000 BP, 86% ofSub-Saharan African mitochondrial DNA was introduced into Southwest Asia byEast Africans, largely in the region ofArabia, which constitute 50% of Sub-Saharan African mitochondrial DNA in modernSouthwest Asia.[11]
In 4000 BP, there may have been a population that traversed fromAfrica (e.g.,West Africa or West-Central Africa), through theStrait of Gibraltar, into theIberian Peninsula, where admixing between Africans and Iberians (e.g., of northernPortugal, of southernSpain) occurred.[12]
AnAfrican individual, who has been dated between 1st century CE and 3rd century CE as well as carriedhaplogroup H1, may have forcibly (viaenslavement) or voluntarily migrated from the centralSahara or theNile Valley (e.g.,Sudan) toRome.[13]
During the modern period,West Africans introduced more than 75% ofSub-Saharan mitochondrial DNA into North America andSouthern Africans introduced almost 15%.[11] West Africans also introduced ~45% of Sub-Saharan African mitochondrial DNA into South America, whereas, Southern Africans, largely indigenousAngolans, 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 byWest Africans, which constitutes 50% of Sub-Saharan African mitochondrial DNA in modern Southwest Asia.[11]
Regarding theIndian Ocean slave trade, Romuald (2017) states: "From the 8th to the 19th centuries, about four million people were captured from the shores ofeastern Africa byArabMuslim andSwahili traders. It has been suggested that slaves transported before the 16th century originated from theHorn of Africa, i.e.,Nilotic orAfro-Asiatic speakers from present-dayEthiopia, whereas most Africans enslaved from the 18th century onward wereZanj, i.e.,Bantu speakers ofsoutheastern Africa."[14] Regarding theTrans-Atlantic slave trade, Fortes-Lima (2021) states:
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, fromSenegal toAngola, and even round theCape and on toMozambique. The largest number (around 95%) of slaves arrived inLatin America, with ~43% disembarked inSouth America, ~52% in theCaribbean, while the remaining 5% arrived in what has become today theUnited States. This forced and massive migration of people radically changed the genetic landscape of present-day populations inthe Americas...According to historical resources, from 1501 to 1867 enslaved Africans were embarked from eight major historical coastal regions insub-Saharan Africa: 5.7% of the captives were fromSenegambia, 3.2% fromSierra Leone, 2.7% fromWindward Coast, 9.6% fromGold Coast, 16.1% fromBight of Benin, 12.3% from theBight of Biafra, 46.3% from WestCentral Africa, and 4.1% fromSoutheast Africa. West Central Africa region (coastal region from present-dayGabon toAngola) 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]
InLisbon, Portugal, 87% ofAngolans, who were sampled in 2014, carried various haplogroups ofMacro-haplogroup L (e.g.,L0a, L0d,L1b,L1c,L2a,L2b,L2c,L3a, L3b, L3d, L3f,L4), whereas, other sampled Angolans carried different haplogroups (e.g.,H,T,R0,K,U,J,M).[16] InLisbon, Portugal, out of 80Guinea-Bissauns, who were sampled in 2017, 73 carriedMacro-haplogroup L, 5 carriedhaplogroup U, one carriedhaplogroup M, and one carriedhaplogroup V.[17] InLisbon, Portugal, 81% ofMozambicans, who were sampled in 2017, carried various haplogroups ofMacro-haplogroup L, whereas, 19% of the sampled Mozambicans carried different haplogroups (e.g.,H,U,K,J1,M4,R0,T2).[18]
Out of 642 individuals from 15 populations among theAfrican diaspora in the Americas sampled in 2016, some of which included individuals who self-identified as being of African descent, the ancestry of 328African Americans were found to be 80%African, the ancestry ofAfro-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 andNative Americans,Maroonsretained and adapted theircultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such asColombia,Jamaica,French Guiana, and Suriname.[15]Alukus,Kwinti,Matawai,Ndjukas,Paramakas, andSaramakas, who areMaroons of Noir Marron, are the largest, autonomous group of Maroons in theAmericas.[15] Though Noir Marron groups and other groups among theAfrican 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 theBight of Benin; in particular, there are strong genetic connections withAfricans inBenin and a linguistic connection withGbe speakers, such as theFon people.[15]
During the Holocene, 3% ofSub-Saharan African mitochondrial DNA is indicated to have been introduced intoSouth America and 6% is indicated to have been introduced intoNorth 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% ofSub-Saharan mitochondrial DNA into North America andSouthern Africans introduced almost 15%.[11] West Africans also introduced ~45% of Sub-Saharan African mitochondrial DNA into South America, whereas, Southern Africans, largely indigenousAngolans, introduced ~55%.[11]
AtAvery's Rest inDelaware, 3 out of 11 individuals wereAfrican Americans, who were dated between 1675 CE and 1725 CE; one was ofWest African ancestry and carried haplogroupsE1b1a-CTS2447 andL3e3b, another was of westernCentral African Bantu-speaking ancestry and carriedE1b1a-Z5974 andL0a1a2, and another was ofWest African andEast African ancestry and carriedE1b1a-Z5974 andL3d2.[19]
At a burial site inDelaware,enslavedAfrican Americans, who were dated to the 17th century CE as well as hadWest African andBantu ancestry fromCentral Africa andEast Africa, carried haplogroupsL3e3,L0a1a, andL3i2.[20]
At Catoctin Furnace African American Cemetery, inCatoctin Furnace, Maryland, there were 27African Americans found who were dated between 1774 CE and 1850 CE.[21][22] One female individual, who was of 95.17%Sub-Saharan African and 1.69%European ancestry, carried haplogroupL3e1.[23] One male individual, who was of 98.14%Sub-Saharan African ancestry, carried haplogroupsE1b1a1a1a1c2c andL2a1+143+@16309.[23] One male individual, who was of 83.73%Sub-Saharan African and 7.74%European ancestry, carried haplogroupsE1b1a1a1a1c1b1 andL3e2a1b1.[23] One male individual, who was of 88.47%Sub-Saharan African and 7.92%European ancestry, carried haplogroupsR1b1a1b1a1a2c1 andL3e1.[23] One male individual, who was of 84.94%Sub-Saharan African and 9.45%European ancestry, carried haplogroupsE1b1a1a1a2a1a andL2a1+143+16189 (16192)+@16309.[23] One female individual, who was of 97.02%Sub-Saharan African and 1.06%European ancestry, carried haplogroupL3f1b1a.[23] One male individual, who was of 87.83%Sub-Saharan African and 8.23%European ancestry, carried haplogroupsE1b1a1a1a1c1a1a3a1d1 andL3d1b3.[23] One male individual, who was of 98.14%Sub-Saharan African ancestry, carried haplogroupsE1b1a1a1a1a andL3e2a1b1.[23] One male individual, who was of 53.75%Sub-Saharan African and 42.11%European ancestry, carried haplogroupsR1b1a1b1a1a2c1a1h2a~ andL3f1b3.[23] One female individual, who was of 98.12%Sub-Saharan African ancestry, carried haplogroupL2b1a3.[23] One female individual, who was of 97.94%Sub-Saharan African ancestry, carried haplogroupL3e1a1a.[23] One male individual, who was of 93.87%Sub-Saharan African and 2.58%European ancestry, carried haplogroupsE1b1a1a1 andL3e1.[23] One male individual, who was of 98.70%Sub-Saharan African ancestry, carried haplogroupsE1b1a1a1a1c1b2a andL2a1a1.[23] One male individual, who was of 97.01%Sub-Saharan African ancestry, carried haplogroupsE1b1a1a1a1c1a1 andL3e2a1b1.[23] One female individual, who was of 87.17%Sub-Saharan African and 6.93%European ancestry, carried haplogroupL2a1+143+16189 (16192)+@16309.[23] One male individual, who was of 82.31%Sub-Saharan African and 10.24%European ancestry, carried haplogroupsE1b1a1a1a1c1b andL3e2a1b1.[23] One male individual, who was of 91.82%Sub-Saharan African and 5.31%European ancestry, carried haplogroupsE1b1a1a1a1c1a1 andL3e2.[23] One female individual, who was of 75.81%Sub-Saharan African and 21.44%European ancestry, carried haplogroupL4b2b1.[23] One female individual, who was of 91.95%Sub-Saharan African and 4.47%European ancestry, carried haplogroupL3e2.[23] One male individual, who was of 87.70%Sub-Saharan African and 4.93%European ancestry, carried haplogroupsE2b andL2b1a3.[23] One female individual, who was of 97.53%Sub-Saharan African and 0.21%European ancestry, carried haplogroupL2b1a3.[23] One female individual, who was of 83.28%Sub-Saharan African and 10.72%European ancestry, carried haplogroupL3e2a1b1.[23] One male individual, who was of 41.31%Sub-Saharan African and 53.59%European ancestry, carried haplogroupsR1a1a1 andJ1b1a1a.[23] One male individual, who was of 92.70%Sub-Saharan African and 3.57%European ancestry, carried haplogroupsA1b1 andL0a1b1a.[23] One male individual, who was of 81.18%Sub-Saharan African and 14.86%European ancestry, carried haplogroupsE1b1a1~ andL2c.[23] One female individual, who was of 88.09%Sub-Saharan African and 5.44%European ancestry, carried haplogroupL2a1+143+16189 (16192)+@16309.[23] One female individual, who was of 92.32%Sub-Saharan African and 4.05%European ancestry, carried haplogroupL2b1a3.[23]
At a burial site inSchuyler Flatts,New York, 6 out of 14 individuals wereAfrican Americans, who were dated to the 18th century CE as well as ofWest African, westernCentral African, andMalagasy ancestry, carried various haplogroups; two carriedhaplogroup L2 (e.g.,L2a1,L2b1), two carriedhaplogroup L3 (e.g.,L3e2, L3e2b), one carriedhaplogroup M, and one carriedhaplogroup M7.[24]
At anAfrican American cemetery dated to the 18th century CE, inPortsmouth, New Hampshire,enslaved African Americans carried haplogroupsU5 andU6.[25]
At an Anson Street burial site dated to the 18th century CE, inCharleston, South Carolina, 29enslavedAfrican Americans carried the following haplogroups: one carriedhaplogroup L0 (e.g.,L0a1), six carried haplogroup L1 (e.g.,L1b,L1c), nine carriedL2 (e.g.,L2a,L2b,L2c), twelve carriedL3 (e.g.,L3e, L3b, L3d, L3f), and one carriedU6 (e.g., U6a5).[26]
At an Anson Street burial site, inCharleston, South Carolina, there were 18African Americans found who were dated to the 18th century CE.[27] Banza was of westernCentral African ancestry and carried haplogroupsE1b1a-CTS668 andL3e3b1.[27] Lima was ofWest African ancestry and carried haplogroupsE1b1a-M4671 andL3b3.[27] Kuto was of westernCentral African ancestry and carried haplogroupsE1b1a-CTS2198 andL2a1a2.[27] Anika was ofSub-Saharan African ancestry and carried haplogroupsE1b1a-CTS6126 andL2b1.[27] Nana was ofWest African ancestry and carriedhaplogroup L2b3a.[27] Zimbu was of westernCentral African ancestry and carried haplogroupsE1b1a-CTS5497 andL3e1e.[27] Wuta was ofSub-Saharan African ancestry and carried haplogroupsE1b1a-CTS7305 andL3e2b+152.[27] Daba was ofWest African ancestry and carried haplogroupsE1b1a-M4273 andL2c.[27] Fumu was ofSub-Saharan African ancestry and carried haplogroupsB2a1a-Y12201 andL3e2b+152.[27] Lisa was ofWest African ancestry and carried haplogroupsE1b1a-Z6020 andH100.[27] Ganda was ofWest African ancestry and carried haplogroupsE1b1a-CTS5612 andL1c1c.[27] Coosaw was ofWest African andNative American ancestry and carried haplogroupsE2b1a-CTS2400 andA2.[27] Kidzera was of westernCentral African ancestry and carriedhaplogroup L2a1a2c.[27] Pita was ofSub-Saharan African ancestry and carried haplogroupsE1b1a-M4287 andL3e2b.[27] Tima was of westernCentral African ancestry and carriedhaplogroup L3e1e.[27] Jode was ofSub-Saharan African ancestry and carried haplogroupsE1b1a-CTS4975 andL2a1a2c.[27] Ajana was of westernCentral African ancestry and carriedhaplogroup L2a1I.[27] Isi was of westernCentral African ancestry and carriedhaplogroup L3e2a.[27]
InMaryland, a tobacco pipe dated to the 19th century CE was determined to have been used by anenslavedAfrican American woman, who was ofMende ancestry, and carriedhaplogroup L3e.[28] She may have lived for a period of time between 1736 CE and 1864 CE.[15]
At Avondale Burial Place, inBibb County, Georgia, utilized between 1820 CE and 1950 CE, 18 out of 20 individuals were determined to beAfrican American, as they carried the following haplogroups: oneL0, two withL1, seven withL2, seven withL3, and one withU6.[29]
InPhiladelphia,Pennsylvania, an individual ofWest African ancestry, who died ofcholera during acholera pandemic in 1849 CE, carriedhaplogroup L3d1b3.[30]
60% ofAfrican Americans, who were sampled in 2007, were ofhaplogroup E1b1a, within which 22.9% were particularly ofhaplogroup E-M2; they also possessed numerousSNPs (e.g., U175, U209, U181, U290, U174, U186, and U247).[31]
An African American man, who was sampled in 2013, carriedhaplogroup A00, which likely dates back to 338,000 BP, and is a haplogroup shared with theMbo people.[32]
Torres et al. (2012) states: "One African American population, those fromSouth Carolina, cluster with the African populations. Notably, the South Carolina population falls nearest to theGrain Coast populations. Ethnohistorical records indicate a relationship between African Americans within this region of theUnited States andWest Africans fromSenegal,Gambia, andSierra 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 ofrice cultivation."[33]

Due to the X-chromosomes inAfrican Americans having high concentrations of ancestry fromAfrica, this coheres with the understanding of there being an asymmetric flow of genes from European males toAfrican females;[34][35] consequently, this can be understood as being the result ofenslavedAfrican American females beingraped by European males.[36]
African Americans, who were sampled in 2015, carried various haplogroups ofmacro-haplogroup L (e.g.,L0,L1,L1b,L1c,L2,L2a,L2b,L2c,L2e,L3,L3b, L3d, L3e, L3f, L3h, L3x,L4).[37] 10.2% of African Americans carried haplogroup L1b and 19.8% of African Americans carried haplogroup L2a.[37]
Stefflova et al. (2011) states: "Ancestry fromGuinea Bissau-Mali-Senegal-Sierra Leone predominates in otherUnited StatesAfrican American populations compared toPhiladelphia alone (43% vs. 22%). Despite the differences in coverage and sampling, this pattern may be attributed to a significant contribution of slaves fromBritish colonies in Africa to theBritish-controlled Philadelphia region compared to a more diverse contribution to other parts of the United States fromFrench,Spanish, andDutch colonies. Additional possible contributing factors include the different periods of theslave 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 theGullah/Geechee populations fromSouth 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 fromWest African populations fromSenegambia and the Rice Coast (Guinea Bissau-Mali-Senegal-Sierra Leone), followed byCentral Africans from theCongo andAngola, 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 toYoruba people thanEast 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 ofWest African and westernCentral African ancestry.[15] Approximately 7% of their ancestry derives fromWindward Coast, 13% fromSenegambia, 30% fromAngola, and nearly 50% fromBenin, westernNigeria, andTogo.[15] Additionally, 4.8% of their ancestry derives fromBantu peoples and 16% derives fromAfrican rainforest hunter-gatherers.[15]
Tishkoff et al. (2009) via "Supervised STRUCTURE analysis [inferred] African American ancestry from global training populations, including bothBantu (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 asSenegambia and as far south asAngola andSouth Africa."[41] Moderate to modest amounts ofChadic,Fulani,Nilo-Saharan,Cushitic, andSandawe 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 includingHausa and Fulani fromCameroon, in addition to Chadic andCentral Sudanic speakers such as theMada,Sara, andLaka.[41]



The African ancestry inAfrican Americans have often been connected to the risk alleles and genetic components of diseases predominant among African Americans, such asblood disorders,hypertension, progressivekidney failure, andtype 2 diabetes.[42]
African Americans, who have a high rate of occurrence oftype 2 diabetes, have a few gene variants (e.g., severalSNPs inIGF2 andHLA-B genes; the SNP, rs7903146, within theTCF7L2 gene; theintergenic SNP, rs7560163, located between the RBM43 gene andRND3 gene) that are strongly associated with type 2 diabetes.[42]
The rate of occurrence forhypertension in African Americans is 39%.[42] Several genes (e.g.,EVX1-HOXA, PLEKHG1,RSPO3,SOX6, ULK4), which contributes to thesignaling pathway fornitric 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 theNPR3 gene.[42] These genes have all been connected with hypertension in African Americans.[42]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42] TheSickle Hemoglobin S trait occurs in 8% of African Americans, and, generally,sickle cell anemia occurs in 0.02% of African Americans.[42]
African Americans have as much as 65% of the Duffy-nullgenotype.[43] The cancer medicine,azathioprine, regarding its safety and when it should be discontinued, was found to be unsuitable and possibly damaging toAfrican Americans, as the standard range was based on "normal" ranges forEuropeans; the distinct genetic data from African Americans (e.g., Duffy-null phenotype) might provide a different explanation forneutropenia.[43]
A majority ofAfro-Caribbean people descend from peoples in the regions ofWest Africa and westernCentral Africa.[44] In particular, their genetic ancestry, to some extent, derives from peoples in the region ofAngola, but more so, from peoples in regions, such as theBight of Benin,Bight of Biafra,Cameroon, andGhana.[44] Additionally, between the late 19th century CE and early 20th century CE, someHaitians migrated intoCuba, thereby, resulting in the addition of ancestry fromAfrica.[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 toYoruba people thanEast 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 ofAfro-Barbadians were found to derive from theYoruba 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]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 16.2% (±10.4%)Native American and 28.1% (±12.3%)European ancestry,Afro-Dominicans, who were sampled in 2013, were found to be 55.6% (±16.1%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 9%Native American and 52%European (e.g.,Northern/Western) ancestry,Afro-Dominicans, who were sampled in 2016 and self-reported their African ancestry, were found to be 38%African (e.g.,Yoruba).[46][47]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 6.8% (±4.6%)Native American and 12.1% (±11.2%)European ancestry,Afro-Grenadians, who were sampled in 2013, were found to be 81.1% (±11.3%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Afro-Haitians, who were sampled in 2012, were found to have carried haplogroupE1b1a-M2 (63.4%), within which were more specific sub-haplogroups, such as haplogroupsE1b1a7-M191 (26.8%) andE1b1a8-U175 (26%), and subgroups within those sub-haplogroups, such as E1b1a7a-U174 (26.8%) and E1b1a8a-P278 (13%); there were also various sub-haplogroups ofhaplogroup R1b (e.g.,R1b1b1-M269, R1b1b1a1b2-M529, R1b1b1a1b*-S116, R-M306,R1b2*-V88) as well ashaplogroup R1a-M198.[49]
The ancestry ofAfro-Haitians, who were sampled in 2013, were found to be 84%African.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Afro-Jamaicans, who were sampled in 2012, were found to have carried haplogroupE1b1a-M2 (60.4%), within which were more specific sub-haplogroups, such asE1b1a7-M191 (27.7%) andE1b1a8-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 ofhaplogroup R1b (e.g.,R1b1b1-M269, R1b1b1a1b2-M529, R1b1b1a1b*-S116, R-M306,R1b2*-V88) as well ashaplogroup R1a-M198.[49]
Afro-Jamaicans, who were sampled in 2012, were found to have mostly (97.5%) carried various forms ofmacro-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 ofAfro-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]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 12%Native American and 61%European (e.g.,Northern/Western) ancestry,Afro-Puerto Ricans, who were sampled in 2016 and self-reported their African ancestry, were found to be 27%African (e.g.,Yoruba).[46][47]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 5.8% (±2.9%)Native American and 8.2% (±5.4%)European ancestry,Afro-Kittitians, who were sampled in 2013, were found to be 85.9% (±5.7%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 7.5% (±7.3%)Native American and 17.9% (±12.5%)European ancestry,Afro–Saint Lucians, who were sampled in 2013, were found to be 74.5% (±15.3%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In Zoutsteeg,Philipsburg, Saint Martin, threeenslaved Africans ofWest African (e.g.,Nigeria,Ghana) and westernCentral African (e.g.,Bantu peoples ofnorthern Cameroon) ancestry, who are estimated to date between 1660 CE and 1688 CE, were found; one carried haplogroupsR1b1c-V88 andL3b1a, another carriedhaplogroup L3d1b, and the last carriedhaplogroup L2a1f.[51] A man and woman may have been fromGhana orNigeria, and a man may have been from among theBantu peoples ofCameroon,Republic of the Congo, andDemocratic Republic of the Congo.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
The ancestry of theGarifuna inSaint Vincent, who were sampled in 2013, were found to be 70%African.[15] The ancestry of theGarifuna ofSaint Vincent, who were sampled in 2019, were found to be 70%African.[15] In addition to being found to have 6.5% (±6.4%)Native American and 12.8% (±12.9%)European ancestry,Afro-Vincentians, who were sampled in 2013, were found to be 80.6% (±16.4%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 9.2% (±8.7%)Native American and 15.8% (±11.5%)European ancestry,Afro-Trinidadians, who were sampled in 2013, were found to be 75.0% (±16.6%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 2.6% (±2.1%)Native American and 10.6% (±2.3%)European ancestry,Afro–Virgin Islanders fromSaint Thomas, who were sampled in 2008, were found to be 86.8% (±2.2%)West African.[39] In addition to being found to have 5.6% (±4.9%)Native American and 16.9% (±21.1%)European ancestry,Afro–Virgin Islanders fromSaint Thomas, who were sampled in 2013, were found to be 77.4% (±21.9%)West African.[48]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 29.0%Native American and 1.0%European ancestry, someAfro-Belizeans from Livingston, who were sampled in 1981, were found to be 70.0%African.[52] In addition to being found to have 17.4%Native American and 2.7%European ancestry, someAfro-Belizeans fromStann Creek, who were sampled in 1983, were found to be 79.9%African.[52] In addition to being found to have 24.1%Native American and 4.9%European ancestry, someAfro-Belizeans fromPunta Gorda, who were sampled in 1983, were found to be 71.0%African.[52] In addition to being found to have 23.9%Native American and 0.5%European ancestry, someAfro-Belizeans fromHopkins, who were sampled in 1983, were found to be 75.6%African.[52] In addition to being found to have 7.4%Native American and 17.1%European ancestry, someAfro-Belizeans fromStann Creek, who were sampled in 1983, were found to be 75.5%African.[52] In addition to being found to have 5.2%Native American and 42.8%European ancestry, someAfro-Belizeans fromPunta Gorda, who were sampled in 1983, were found to be 52.0%African.[52] In addition to being found to have 8.6%Native American and 16.7%European ancestry, someAfro-Belizeans fromBelize City, who were sampled in 1983, were found to be 74.7%African.[52]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In addition to being found to have 17%Native American and 2%European (e.g.,Northern/Western) ancestry,Afro-Hondurans, who were sampled in 2016 and self-reported their African ancestry, were found to be 81%African (e.g.,Yoruba).[46][47]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
At a San Jose de los Naturales Royal Hospital burial site, inMexico City, Mexico, threeenslaved West Africans ofWest African andSouthern African ancestry, dated between 1453 CE and 1626 CE, 1450 CE and 1620 CE, and 1436 CE and 1472 CE, were found; one carried haplogroupsE1b1a1a1c1b/E-M263.2 andL1b2a, another carried haplogroupsE1b1a1a1d1/E-P278.1/E-M425 andL3d1a1a, and the last carried haplogroupsE1b1a1a1c1a1c/E-CTS8030 andL3e1a1a.[53]Human leukocyte antigen alleles further confirm that the individuals were ofSub-Saharan African origin.[15]
At the 11–1 burial site, inCampeche, Mexico, aWest African woman, who was in her early twenties and dated to the late 17th century CE, carriedhaplogroup L3.[54]
At La Concepción chapel and Hospital Real de San José de los Naturales, inMexico City, Mexico,enslavedAfricans, who carriedhaplogroup L, were sampled for viral genomes.[55] From among the sampled individuals, who may have died between 1472–1625 CE and 1442–1608 CE, theancient DNA of the viruses were able to be were able to be reconstructed.[55] Due to the brutality of theMiddle Passage andenslavement of the first generation of Africans, the transmission of theHepatitis B virus and humanparvovirus 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 theCocoliztli epidemics.[55]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

The ancestry ofAfro-Bolivians from theYungas Valley, who were sampled in 2016, were found to be 80%African.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
At Pretos Novos Cemetery, inRio de Janeiro, Brazil, 4 out 16 carriedM. tuberculosis and 3 out of 16 carried haplogroupsL3e2, L3d1, andL1c2; thus, indicating that the individuals, who were buried in the cemetery between the 18th century CE and the 19th century CE, were born inWest Africa and/or westernCentral Africa, and soon died after reaching Rio de Janeiro.[56]
The average ancestry ofAfro-Brazilians were found to be 70.8%African.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
AtPalenque, in addition tohaplogroup R1b being found, includinghaplogroup R1b-V88,haplogroup E1b1a-M2 was found, which includes its sub-lineages (e.g., U175, U181, U290).[57] While 37.9% was unable to be identified, the following African paternal haplogroups were able to be identified atPalenque:E1b1a-M2* (xM154, M191) (22.4% rate of occurrence) likely originates nearBight of Benin,E1b1a-M2* (xM154, M191) (12.1%) likely originates nearLoango/Angola,B2a-M150* (xM109) (5.2%) likely originates inLoango,R1b-V88 (6.9%) likely originates nearBight of Benin/Loango,E1b1b-M35* (xM78, M81, M123, V6, M293) (5.2%) likely originates nearSenegambia/Bight of Benin,Y-MRCA* (xM13,SRY10831.1) (3.4%) likely originates inUpper Guinea,E1a-M33 (1.7%) likely originates inUpper Guinea,E1a-M33 (1.7%) likely originates nearBight of Benin/Bight of Biafra,E1b1a-M191 (1.7%) likely originates nearLoango/Angola, andE1b1a-M191 (1.7%) likely originates inLoango.[58]
While 67.1% was unable to be identified, the following African maternal haplogroups were able to be identified atPalenque:L1b1a1'4 (8.9% rate of occurrence) likely originates nearSenegambia/Upper Guinea,L1c3a1b (6.3%) likely originates nearGold Coast/Angola,L0a1a+200 (1.3%) likely originates nearUpper Guinea/Bight of Benin,L2b1a (1.3%) likely originates nearBight of Benin/Angola,L2d+16129 (1.3%) likely originates inAngola,L3e1d (12.7%) likely originates inAngola, andL3f1b+16365 (1.3%) likely originates inGold Coast.[58]
In 2016, linguistic evidence (e.g.,Kikongo influence and remnants from the early history of Palenque found inPalenquero), which was also compatible with a diverse origin for African Y-chromosome, supportedBakongo people being the founding population of Palenque; in 2020, theYombe people of theRepublic of the Congo were found to be genetically closest with the people ofPalenque.[57]
In addition to being found to have 28%Native American and 39%European (e.g.,Northern/Western) ancestry,Afro-Colombians, who were sampled in 2016 and self-reported their African ancestry, were found to be 33%African (e.g.,Yoruba).[46][47] The average ancestry ofAfro-Colombians were found to be 76.8%African.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Based on 30 genetic markers,African ancestry was shown to providestatistically significant protection against Dengue Fever in Colombians.[42]
The ancestry ofAfro-Peruvians, who were sampled in 2018, were found to be 78%African.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
InBatavia, Suriname, an enslavedWest African (e.g.,Mali) with someMiddle Eastern ancestry, who died more than a century ago, carried a strain ofM. leprae andhaplogroup L3.[59]
Due to their relative isolation from Europeans andNative Americans,Maroonsretained and adapted theircultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such asColombia,Jamaica,French Guiana, and Suriname.[15]Alukus,Kwinti,Matawai,Ndjukas,Paramakas, andSaramakas, who areMaroons of Noir Marron, are the largest, autonomous group of Maroons in theAmericas.[15] Though Noir Marron groups and other groups among theAfrican 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 theBight of Benin; in particular, there are strong genetic connections withAfricans inBenin and a linguistic connection withGbe speakers, such as theFon people.[15]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
At Finca Clavijo, inGran Canaria,Canary Islands, nine individuals, dated between 15th century CE and 17th century CE, who were ofSub-Saharan African andNorth African/Moorish origin, were enslaved and forcibly brought fromAfrica (e.g.,Morocco,Senegal River); the Sub-Saharan African individuals carried haplogroupsL1b,L1c, andL2a1, and the Moorish individuals carried haplogroupsH,HV/R,R0,I, andU6b1.[60]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
InSaint Helena, 20 freed Africans,[61][62] who were dated to the 19th century CE,[61] were also of westernCentral African[61][63][64] (e.g.,Bantu peoples ofGabon andAngola) ancestry.[61] One female individual carried haplogroupL1b1a10b.[65] One female individual carriedhaplogroup L2a1f.[65] One female individual carriedhaplogroup L2a1a3c.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1d andL1c3a.[65] One male individual carried haplogroupsE1b1a1a1a1c1a1a andL0a1b2a.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1a2a2 andL0a1e.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1 andL2a1f1.[65] One male individual carried haplogroupsE1b1a1 andL3.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1d andL3e1e.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3a1d andL3e3b2.[65] One male individual carried haplogroupsE1b1a1a1a1c1a1a3 andL3e1a3a.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1a2a2 andL2b1a.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1 andL3f1b1a.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1d1c1a andL3d3a1.[65] One male individual carried haplogroupsB2a1a1a1 andL3e2b1.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3b1d1c1a andL2a1f.[65] One male individual carried haplogroupsE1b1a1a1a1c1a1a3a1c1 andL3e1d1a.[65] One male individual carried haplogroupsE1b1a1a1a2a1a3a1d andL1b1a10.[65] One male individual carried haplogroupsE1b1a1a1a1c1a1a3a1c andL2a1f1.[65] One male individual carried haplogroupsE1b1a1a1a1c1a1 andL2b1a.[65] An enslavedAfrican American man andwoman, from the 18th century CE Anson Street burial site inCharleston, South Carolina, who carriedhaplogroup L3e1e, shared this haplogroup with freed Africans in Saint Helena.[26] Based on those who were present among enlaved Africans, the ratio of males-to-females supports the conclusion of there being a strong selection bias for males in the latter period of theTrans-Atlantic Slave Trade.[61][66][67] Consequently, due to this study on the freed Africans of Saint Helena, among other studies, greater genetic insights have been made into the Trans-Atlantic Slave Trade and its effects on thedemographics of Africa.[68]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Amid theGreen Sahara inAfrica, the mutation forsickle cell originated in theSahara[7] or in thenorthwest forest region of westernCentral 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 andBenin/Senegal haplotypes) may have first arose in the ancestors of modernWest Africans, bearing haplogroupsE1b1a1-L485 andE1b1a1-U175 or their ancestral haplogroup E1b1a1-M4732.[7] West Africans (e.g.,Yoruba andEsan of Nigeria), bearing the Benin sickle cell haplotype, may have migrated through thenortheastern region of Africa into the western region ofArabia.[7] West Africans (e.g.,Mende of Sierra Leone), bearing the Senegal sickle cell haplotype,[10][7] may have migrated intoMauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, intoNorth Africa, and from North Africa, intoSouthern Europe,Turkey, and a region near northernIraq and southern Turkey.[10] Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes intoBasra, 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%), andEgypt (80.8%).[10]
As early as 11,000 years ago,Sub-SaharanWest Africans, bearingmacrohaplogroup L (e.g.,L1b1a11, L1b1a6a, L1b1a8, L1b1a9a1,L2a1k,L3d1b1a), may have migrated throughNorth Africa and intoEurope, mostly intosouthern Europe (e.g.,Iberia).[6]
During the early period of the Holocene,Sub-Saharan African mitochondrial DNA was introduced into Europe, mostly inIberia.[11]West Africans probably migrated, acrossSahelian Africa,North Africa, and theStrait of Gibraltar, intoEurope, 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]
AtDalmatia, inHvar,Croatia, an adult male individual, dated between the 3rd century CE and the 5th century CE, carried haplogroupsE1b1a1a1a1c1b2a2 andHV.[69]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
AtUpdown, inKent, England,Updown Girl, who was between 11 and 13 years of age, and dated to the 7th century CE, carriedhaplogroup U5b1c2b and autosomal ancestry related toWest Africans, such asEsan,Mandenka,Mende, andYoruba.[70] She was also buried alongside a paternal grandparent, with completelySub-Saharan West African ancestry.[70] More specifically, she may descend from a southernSahelian West African who likely departed from West Africa between the mid-6th century CE and the early 7th century CE.[70]
AtWorth Matravers, inDorset, England, a male individual between 17 and 25 years of age, buried in a post-Roman gravesite in use for a span of 100 years largely between 605 CE and 650 CE, carried haplogroupsE1b1b1a1-M78 andU5b1.[71] Thegenome-wide ancestry of the individual indicates that they may descend from grandparents who were aWest African man andEuropean woman; the West African ancestor of the individual may have arrived in England via theWest African gold trade route from West Africa, throughCarthage, during theimperial Byzantine period ofNorth Africa.[71] More specifically, the individual may descend from a southernSahelian West African who likely departed from West Africa between the mid-6th century CE and the early 7th century CE.[70]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
AtPont-sur-Seine, inFrance, a male individual, dated to theMiddle Neolithic, carried haplogroupsE1b1a1a1a1c2c andU5b1-16189-@16192.[72]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
According to some studies,Greeks share someHuman Leukocyte Antigen (HLA) alleles withEast Africans (e.g., Amhara,Nuba, Oromo) and West Africans (e.g.,Fulani,Mossi,Rimaibe) fromBurkina Faso,[73][74][75] who are viewed as having a possible earlier origin inEthiopia.[74][76] In particular, West Africans (e.g., Fulani, Mossi, Rimaibe) and Ethiopians (e.g.,Amhara,Oromo) are viewed as sharing the mostHLA-DRB1 alleles with Greeks.[77][75] Greeks, West Africans, and Ethiopians are viewed as viewed as sharing chromosome 7 markers.[73] During thedesertification of theGreen Sahara in 5000 BCE, or during the time ofancient Egypt, admixture between Greeks and black Africans are viewed as having occurred.[73] Following thearidification of the Green Sahara, Africans are viewed as possibly having migrated from the southern region of the Sahara to the region ofAthens and theislands in the Aegean.[74][76] If the migration of black Africans into Greece occurred following the drying of theGreen Sahara, it is viewed that this may indicate thatPelasgians derive from black Africans.[73] More likely, if the migration ofblack 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.[73][74] 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).[77] Greeks are viewed as sharing some alleles with West Africans (e.g., Fulani, Mossi, and Rimaibe) and East Africans (e.g., Oromo, Amhara, Nubians),[78][75] the latter of which are viewed as also interrelated.[78] 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.[78] Another migration ofWest Africans may have occurred thereafter.[78] Additionally, following desertification of theGreen Sahara around 5000 BCE, it is viewed that there may have been another migration of black Africans intoGreece.[78] A shared autosomal marker, relating tocystic 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, theDanaids, who are identified as Africans, are viewed as possibly having migrated toward thenorth, intoancient Egypt, being repelled in ancient Egypt, and subsequently having migrated intoPeloponnesus.[75]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
AnAfrican individual, who has been dated between 1st century CE and 3rd century CE as well as carriedhaplogroup H1, may have forcibly (viaenslavement) or voluntarily migrated from the centralSahara or theNile Valley (e.g.,Sudan) toRome.[13]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In 4000 BP, there may have been a population that traversed fromAfrica (e.g.,West Africa or West-Central Africa), through theStrait of Gibraltar, into theIberian Peninsula, where admixing between Africans and Iberians (e.g., of northernPortugal, of southernSpain) occurred.[12]
At Valle da Gafaria, inLagos, Portugal, sevenenslaved Africans, five of which had a combination ofAfrican and European admixture, and two of which hadWest African andBantu ancestry, all of who were estimated to date between the 15th century CE and the 17th century CE; while one of their haplogroups went undetermined, it was determined that the others carried haplogroupsH2a2,L1b1,L3i1b,L3'4'6,L2b1, andL3d.[79][80]
At Cabeço da Amoreira, inPortugal, anenslavedWest African man, who may have been from theSenegambian coastal region ofGambia,Mauritania, orSenegal, and carried haplogroupsE1b1a andL3b1a, was buried amongshell middens between the 16th century CE and the 18th century CE.[81]
InLisbon, Portugal, 87% ofAngolans, who were sampled in 2014, carried various haplogroups ofMacro-haplogroup L (e.g.,L0a, L0d,L1b,L1c,L2a,L2b,L2c,L3a, L3b, L3d, L3f,L4), whereas, other sampled Angolans carried different haplogroups (e.g.,H,T,R0,K,U,J,M).[16]
InLisbon, Portugal, out of 80Guinea-Bissauns, who were sampled in 2017, 73 carriedMacro-haplogroup L, 5 carriedhaplogroup U, one carriedhaplogroup M, and one carriedhaplogroup V.[17]
InLisbon, Portugal, 81% ofMozambicans, who were sampled in 2017, carried various haplogroups ofMacro-haplogroup L, whereas, 19% of the sampled Mozambicans carried different haplogroups (e.g.,H,U,K,J1,M4,R0,T2).[18]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
In 4000 BP, there may have been a population that traversed fromAfrica (e.g.,West Africa or West-Central Africa), through theStrait of Gibraltar, into theIberian Peninsula, where admixing between Africans and Iberians (e.g., of northernPortugal, of southernSpain) occurred.[12]
InGranada, Spain, a Muslim (Moor) of theCordoba Caliphate,[82] who was of haplogroupsE1b1a1 andH1+16189,[83] as well as estimated to date between 900 CE and 1000 CE, and aMorisco,[82] who was ofhaplogroup L2e1,[83] as well as estimated to date between 1500 CE and 1600 CE, were both found to be ofWest African (i.e.,Gambian) andIberian descent.[82]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Between 15,000 BP and 7000 BP, 86% ofSub-Saharan African mitochondrial DNA was introduced into Southwest Asia byEast Africans, largely in the region ofArabia, which constitute 50% of Sub-Saharan African mitochondrial DNA in modernSouthwest 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 byWest Africans, which constitutes 50% of Sub-Saharan African mitochondrial DNA in modern Southwest Asia.[11]
From as early as 2500 BP,East African females migrated, as well as some who may have later beenenslaved and forcibly transported, intoArabia.[84] Consequently,Arabs, who were sampled in 2003, have been shown to carrySub-Saharan African haplogroups (e.g.,L1,L2,L3b, L3d, L3e); specifically, 35% ofYemenese from theHadramawt region, and between 10% and 15% among other Arabs (e.g.,Bedouin,Iraqis,Jordanians,Palestinians,Syrians).[84]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
InAbkhazia, Georgia, anAfrican woman, Zana, who carriedhaplogroup L2b1b, was 34%West African and 66%East African, and lived during the 19th century CE.[85] Between the 16th century CE and the 19th century CE, the ancestors of Zana, who were of West African and East African ancestry, may have arrived in Abkhazia, Georgia as a result ofenslavementduring theOttoman Empire.[85] Khwit, who was the son of Zana and carried haplogroupsR1b1a1b1 andL2b1b, was ofAfrican andEuropean admixture.[85]
Local myth about Zana ofAbkhazia, Georgia being anAlmasty was refuted by genetic evidence fromancient DNA, which confirmed that Zana was neither closely related to chimpanzees nor closely related to archaic humans, but closely related to othermodern humans.[85] Margaryan et al. (2021) speculate that Zana may have hadcongenital generalized hypertrichosis, which may have resulted in the development of the local myth.[85]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Out of the total amount of haplogroups carried,Siddis, who were sampled in 2011, 70% of their paternal haplogroups were found to beAfrican; their paternal haplogroups were found to be common amongBantu-speaking peoples.[14]
Out of the total amount of haplogroups carried,Siddis, who were sampled in 2011, 24% of their maternal haplogroups were found to beAfrican.[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.[86] Siddis, who were sampled twice in 2011, were found to be 60%-75%Sub-Saharan African.[14]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
During theCopper Age andearly Islamic era ofancient Israel,West Africans may have migrated into ancient Israel and introducedhead louse fromWest Africa.[87]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
Out of the total amount of haplogroups carried,Makranis, who were sampled in 2002 and 2004, 12% (±7%) of their paternal haplogroups wereAfrican.[14]
Out of the total amount of haplogroups carried,Makranis, who were sampled in 2002 and 2004, 40% (±9%) of their maternal haplogroups wereAfrican.[14]
While theorature among Makranis narrates an origin fromAbyssinia, the genetic results from 2017 show that much of the ancestry ofMakranis derives fromBantu-speaking peoples (Zanj), specifically from thesoutheast 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 inMozambique.[14] Additionally, the African ancestors of the Makranis may have been enslaved by slavers from theOmani Empire during theIndian Ocean slave trade of the 18th century CE.[14]
Sinceenslaved Africans were brought toPakistan, the AfricanDuffy-null alleles in Makranis have evolved.[14]Makranis have an increased level ofmalarial resistance toP. vivax.[14]
Risk allele variants G1 and G2 are associated withchronic kidney disease, which are common among populations ofSub-Saharan African ancestry; the G2 variant occurs at a 3%-8% rate among populations of westernCentral African ancestry and origin.[42]
Someinfectious diseases are protected against due toAfrican ancestry.[42] Hereditaryblood disorders, such assickle cell anemia andthalassemia, produce an effect on the development ofhemoglobin, which, consequently, prevents the reproduction ofmalaria parasites within theerythrocyte.[42] Populations withWest African ancestry, including among theAfrican diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]
{{cite journal}}:Cite journal requires|journal= (help)