Thursday, March 28, 2024

What we know about the collapse of Baltimore's Francis Scott Key Bridge


Federal investigators unveiled new details about what occurred in the minutes before a hulking cargo ship lost power and slammed into Baltimore’s Francis Scott Key Bridge, including the pilot’s urgent call for assistance and authorities’ efforts to clear people off the bridge.

The first sign of distress came just under three minutes before the crash when the cargo ship’s pilot called over the radio requesting any tugboats in the area to respond to the vessel, National Transportation Safety Board Chair Jennifer Homendy said in a news conference Wednesday.

Within a minute, police officers on either end of the bridge were ordered to stop traffic crossing the bridge, said Marcel Muise, the NTSB investigator in charge of the collapse inquiry – an action several officials have credited with saving lives.

Investigators had their first full day at the scene Wednesday and witnessed the “utter devastation” of the mangled bridge, parts of which are still draped over the ship’s bow, Homendy said.

“When I look at something like that, I am thinking not about the container ships that are coming through, not about traffic getting back up and running on the bridge. I’m thinking about the families who’ve lost loved ones,” Homendy said.

Six construction workers who were on the bridge are now presumed dead, and two of their bodies were found trapped in a submerged truck on Wednesday, police said. Search efforts for the remaining four have been paused until salvage crews can clear heavy underwater debris that is believed to be encasing their remains.

NTSB crews used the ship’s voyage data recorder, or VDR, to piece together a rough timeline of events leading up to the collision. But it will take months for them to gather the piles of physical evidence, maintenance records, ship data and witness interviews required to deliver a full report, Homendy said.

Here’s the NTSB’s timeline in hours, minutes and seconds:

• Approximately 12:39 a.m.: The ship departed from Seagirt Marine Terminal.

• By 1:07:00 a.m.: The ship had entered the Fort McHenry Channel.

• 01:24:59 a.m.: Numerous audible alarms were recorded on the ship’s bridge audio. At about the same time, the VDR stopped recording ship system data but was able to continue recording audio using a different power source.

• 01:26:02 a.m.: The VDR resumed recording ship system data. During this time, steering commands and orders regarding the rudder were captured on audio.

• 01:26:39 a.m.: The ship’s pilot made a general very high frequency (VHF) radio call for tugboats in the vicinity to assist the vessel. Around this time, the pilot association dispatcher contacted the Maryland Transportation Authority duty officer regarding the blackout, according to transit authority data.

• Around 01:27:04 a.m.: The pilot ordered that the ship’s port anchor be dropped and issued additional steering commands.

• Around 01:27:25 a.m.: The pilot issued a radio call over the VHF radio, reporting that the vessel had lost all power and was approaching the bridge. Around this time, the transit authority duty officer radioed two of its units — one on each side of the bridge — that were already on scene and ordered them to close traffic on the bridge. All lanes were then shut down.

• Around 01:29 a.m.: The ship’s speed over ground was recorded at just under 8 miles per hour. From this moment until approximately 1:29:33, the VDR audio recorded sounds consistent with the collision with the bridge. Additionally, MDTA dash cameras show the bridge lights extinguishing.

• 01:29:39 a.m.: The pilot radioed the US Coast Guard to report the bridge was down.

There were 23 people onboard the cargo ship when it collided with one of the bridge’s columns, including 21 crew members and two pilots, who are tasked with getting the ship out of port. All crew members were safe, the Maritime and Port Authority of Singapore said previously.

There were no issues reported with the ship prior to its arrival in Baltimore, officials said Wednesday. “We were informed that they were going to conduct routine engine maintenance on it while it was in port. And that’s the only thing we were informed about the vessel in that regard,” Coast Guard Rear Admiral Shannon Gilreath said at the news conference.

As the investigation continues, NTSB and debris salvage crews face challenging and dangerous conditions, including cold and rainy weather, slick surfaces and unstable pieces of wreckage, NTSB and fire officials said.

“Naturally, we’re still very cognizant of the fact that there are hazardous materials aboard the vessel itself,” Baltimore City Fire Chief James Wallace said Wednesday.

Among the ship’s cargo, a senior NTSB hazmat investigator has identified 56 containers of hazardous material – 764 tons – mostly corrosives and flammables, as well as some lithium-ion batteries, the agency said.

Earlier, Coast Guard Vice Admiral Peter Gautier said there is no hazmat threat to the public. Of the ship’s 4,700 cargo containers, only two are missing overboard and neither contains hazardous materials, he said.

The collapse has left massive steel structures and cement debris in the Patapsco River, as well as several vehicles that may contain victim’s remains, police said. Divers stopped their search efforts Wednesday until salvage crews can remove enough of the materials for it to become safe to reenter the water, Maryland State Police’s Col. Roland L. Butler Jr. said.

Unlike most bridges built today, the Key Bridge – completed in 1977 – is “fracture critical,” Homendy explained. “What that means is if a member fails that would likely cause a portion of, or the entire bridge, to collapse. There’s no redundancy.”

The destruction of the bridge and the resulting closure of the port will have major repercussions on the city’s economy and the country’s supply chain, Transportation Secretary Pete Buttigieg said Wednesday. The Baltimore port is the largest in the US for autos and light trucks, handling a record 850,000 vehicles last year.

Recovery operations temporarily halted

Eight construction workers were believed to be mending potholes on the bridge when it fell, according to officials. Two survived but crews searched the frigid waters throughout the day Wednesday for the remaining six, who were all presumed dead.

Two of the workers, a 35-year-old and a 26-year-old, were found trapped underwater in a red truck Wednesday. They were identified by authorities as Alejandro Hernandez Fuentes, from Mexico, and Dorlian Ronial Castillo Cabrera, from Guatemala. Both lived in the Baltimore area.

Search efforts to recover the bodies of the remaining four men were paused later Wednesday until search conditions could be made safer for divers, said Butler, the state police superintendent.

Based on sonar scans, officials believe that the vehicles are “encased in the superstructure and concrete” of the bridge, Butler said.

“The sonar simply said they cannot get to that area because it was fully encased in the superstructure,” he said. “Once that salvage effort takes place and that superstructure is removed, those same divers are going to go back out there and bring those people closure,” he added.

The steel frame of the Francis Scott Key Bridge sits on top of the container ship Dali after the bridge collapsed.

Among the other victims was Miguel Luna, a father of three, and Maynor Suazo, a father and entrepreneur.

The Ministry of Foreign Affairs in Guatemala said another Guatemalan was also unaccounted for: a 35-year-old from Camotán, Chiquimula. Another of the missing is also a Mexican national, Mexican president Andrés Manuel López Obrador said.

Bridge has been struck before – and survived

Tuesday’s catastrophe was not the first time a vessel has slammed into the Key Bridge. Four decades earlier, another container ship that also lost power hit the same bridge — and it stood strong.

The dramatic difference in outcomes between the two accidents is an example of the dangers caused by the massive increase in shipping vessel size in the intervening decades.

A CNN review of public records and interviews with about a dozen bridge and shipping experts show that hundreds of bridges over US waterways were built decades ago when container ships were a fraction of the size and weight they are today. Bridges of the era when the Key Bridge was built weren’t designed to protect against collisions with ships as big as the Dali, the vessel that caused the Baltimore to topple.

The Dali has a capacity of about 10,000 twenty-foot equivalent units of cargo – compared to the approximate cap of about 2,500 twenty-foot equivalent units that could be carried by container ships in the 1970s, CNN has reported.

Some experts said that this week’s disaster should inspire engineers to reevaluate whether America’s aging infrastructure can withstand impacts from the gigantic ships that traverse our waterways today.

“It’s absolutely a wake-up call,” said Rick Geddes, a professor and director of Cornell University’s Program in Infrastructure Policy. “The people who were building the Francis Scott Key Bridge never really contemplated ships of this size. It wasn’t their fault — they just didn’t have a crystal ball.”

Ship and management company involved in previous incidents

As officials worked to investigate the collapse Tuesday, questions emerged over previous issues with the ship and its management company.

The ship was briefly held at the Port of San Antonio in Chile on June 27, 2023, when an inspector found that the pressure gauges for the vessel’s heating system were “unreadable,” a spokesperson for the Chilean Navy said.

Ships managed by the Synergy Marine Group have been involved in at least three deadly incidents since 2018 in Australia, Singapore and the Philippines, according to officials in those countries.

In 2018, a member onboard of a vessel managed by Synergy in Australia was killed in an accident involving the ship’s personnel elevator, according to a report from the Australian Transportation Safety Bureau.

In 2019, an officer on a Synergy-registered vessel in Singapore was reported missing after “likely (falling) overboard while performing inspection or cleaning jobs,” according to a report by the Transport Safety Investigation Bureau of Singapore’s Ministry of Transport.

In 2023, at least one sailor was killed when a Synergy Marine-managed tanker collided with a dredging ship in the Philippines, causing it to capsize, according to an incident report from the Philippines Coast Guard.

Synergy Marine Group is focused on the Baltimore incident, spokesperson Charlie Ridgeway told CNN in a phone call Wednesday. “It would be inappropriate to discuss any previous incidents at this time.”

CNN’s Tori B. Powell, Sarah Engel, Elise Hammond, Curt Devine, Casey Tolan, Isabelle Chapman, Daniel Medina, Sahar Akbarzai, Melissa Alonso, Hande Atay Alam and Lucas Lilieholm contributed to this report.



Bronx Homeless Shelter Petition




The 3100 Homeowners Association are committed to upholding the beauty and harmony of our community. It has come to our attention that plans for a new homeless shelter at 3240 Grace Avenue in the Bronx, NY 10469 could severely impact our neighborhood's serene atmosphere and dynamics. We acknowledge the need for such facilities but must consider the well-being and cohesiveness of our area.

We believe in taking action to address this issue and are organizing a petition to present our collective concerns. Your participation is essential, and we urge you to join us in this effort to ensure that our voices are heard.

Please make it a point to voice your opinion by signing the petition linked below. Together, we can maintain the integrity of our beloved neighborhood.

Please sign, share, and mail  the petition below to Hon. Carl E. Heastie or drop it off at his office 

1446 East Gun Hill Road

Bronx, NY 10469

718-654-6539

Fax: 718-654-5836

https://3100homeowners.now.site/home





Wednesday, March 27, 2024

Paranormal Encounter in Abandoned Mid-Orange Prison (PART 1) | Haunted, ...


Paranormal activity in abandoned Mid-Orange prison | Part 1

July 19, 2023 | 9:18pm

“When you are evil in life, you are evil in death,” warned Pam Crisci, of Ghost Hunts USA, outside the notorious Mid-Orange Correctional Facility in Warwick, New York. Here at this abandoned boys’ reformatory-turned-prison, paranormal investigator Colin Browen and The Post’s Danica Daniel attempt to contact the spirit of a boy named “Jimmy” in Part 1 of this terrifying tour.

Child abuse was rampant at Mid-Orange, where 500 juveniles from broken and violent homes lived over the decades. One boy, Charles, hanged himself after being abused by a staffer. In 1977, the facility was converted to a medium-security prison, where serial killer Richard Beigenwald was once held, until being shut down in 2011.

Raised on grunge rock and ghost stories, host Colin Browen has investigated hundreds of the world's most notorious locations, from Hoia Baciu Forest in Romania to the Sallie House in Kansas. As a kid, he says his family unknowingly moved into a haunted house where he learned to coexist with the spirits. By 19, he was hosting "Teen Spirit" on the Verizon GO90 Network. He went on to create the popular YouTube series "The Paranormal Files" and co-hosts a true-crime podcast, "Murder in America," with his wife, Courtney.



VIOLENT HISTORY

The former Mid-Orange Correctional Facility has an extensive, and often unsettling, history.


Its origins date back to the 1930s when it was built as a reform school for boys. The school housed about 400 teens at any given time and remained in use until 1976. It is said that at least one of the boys had prematurely ended his stay within one of the dormitories. And many others have continued to prolong their stay long after death, touching guests and closing doors on them- playing with their minds along with any possessions. But the story does not end with a few playful sprites.


In 1976, when the reformatory was closed, it was converted into a correctional facility. This was when it was at its most populated, boasting almost 1,000 inmates housed by 1989. This was its primary function until June of 2011 when it was closed alongside six other state prisons. It is from these men, some of whom had committed the vilest atrocities imaginable, that the complex gets most of its haunts. Bangs, shrieks, inaudible threats, thudding feet… apparitions. It is thanks to them that some of the floors of the schoolhouse remain inaccessible to the public. Although this is done to protect any guests from injury, locked doors mean nothing to the dead.


In 2014, the complex became the official property of the town of Warwick, and in 2019 it was finally given a new purpose with the Fuchs family, where it is currently used as a professional training facility with a focus on soccer, under its new name: The Hudson Sports Complex.


And even though it is now a place of passion and joy, the ghosts of its roots stay restless. And to this day, the complex is known far and wide as a home for the paranormal. Whether it be the ghosts of the children who never found reformation in its halls or the convicted who died within its walls, something at Hudson Sports Complex demands to be heard, and sometimes, even seen… or felt.


Prison of Horrors has found its strength in embracing the terror rather than avoiding it. And for the fourth year in a row, we seek to spread that terror to the masses. Our haunts may be an act, but the fear is real- and, for those lucky few, so are the ghosts. Come stay with us awhile, will you? But be careful when you leave us… for fear is infectious.








Saturday, March 23, 2024

Genetic history of the African diaspora

 



The genetic history of the African diaspora is composed of the overall genetic history of the African diaspora, within regions outside of Africa, such as North AmericaCentral America, the CaribbeanSouth AmericaEuropeAsia, and Australia; this includes the genetic histories of African AmericansAfro-CanadiansAfro-CaribbeansAfro-LatinosAfro-EuropeansAfro-Asians, and African Australians.

Overview

Prehistoric

The Sahara served as a trans-regional passageway and place of dwelling for people in Africa during various humid phases[1][2][3] and periods throughout the history of Africa.[4][5] As early as 11,000 years ago, Sub-Saharan West Africans, bearing macrohaplogroup L (e.g., L1b1a11, L1b1a6a, L1b1a8, L1b1a9a1, L2a1kL3d1b1a), may have migrated through North Africa and into Europe, mostly into southern Europe (e.g., Iberia).[6]

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 EuropeTurkey, 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] 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]

In 4000 BP (or even earlier during the Mesolithic), there may have been a population that traversed from Africa (e.g., West Africa or West-Central Africa), through the Strait of Gibraltar, into the Iberian peninsula, where admixing between Africans and Iberians (e.g., of northern Portugal, of southern Spain) occurred. Based on a small trace presence of sub-Saharan African components in select samples from Iberia, and the discovery of a mitogenome L2a1 found in one individual, while all others belonged to European mitochondrial haplogroups.[12]

Historic

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]

International Trade of Enslaved Africans[edit]

Regarding the Indian Ocean slave trade, Romuald (2017) states: "From the 8th to the 19th centuries, about four million people were captured from the shores of eastern Africa by Arab Muslim and Swahili traders. It has been suggested that slaves transported before the 16th century originated from the Horn of Africa, i.e., Nilotic or Afro-Asiatic speakers from present-day Ethiopia, whereas most Africans enslaved from the 18th century onward were Zanj, i.e., Bantu speakers of southeastern Africa."[14] Regarding the Trans-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, 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]

International Emigration of Modern Africans

Europe

In LisbonPortugal, 87% of Angolans, who were sampled in 2014, carried various haplogroups of Macro-haplogroup L (e.g., L0a, L0dL1bL1cL2aL2bL2cL3a, L3b, L3d, L3fL4), whereas, other sampled Angolans carried different haplogroups (e.g., HTR0KUJM).[16] In LisbonPortugal, out of 80 Guinea-Bissauns, who were sampled in 2017, 73 carried Macro-haplogroup L, 5 carried haplogroup U, one carried haplogroup M, and one carried haplogroup V.[17] In LisbonPortugal, 81% of Mozambicans, who were sampled in 2017, carried various haplogroups of Macro-haplogroup L, whereas, 19% of the sampled Mozambicans carried different haplogroups (e.g., HUKJ1M4R0T2).[18]

Americas[edit]

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 AmericansMaroons retained and adapted their cultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as ColombiaJamaicaFrench Guiana, and Suriname.[15] Alukus,KwintiMatawaiNdjukasParamakas, 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]

North America[edit]

United States of America[edit]

Ancient DNA[edit]

At Avery’s Rest, in ChesapeakeDelaware, 3 out of 11 individuals were African Americans, who were dated between 1675 CE and 1725 CE; one was of West African ancestry and carried haplogroups E1b1a-CTS2447 and L3e3b, another was of western Central African Bantu-speaking ancestry and carried E1b1a-Z5974 and L0a1a2, and another was of West African and East African ancestry and carried E1b1a-Z5974 and L3d2.[19]

At a burial site in ChesapeakeDelawareenslaved African Americans, who were dated to the 17th century CE as well as had West African and Bantu ancestry from Central Africa and East Africa, carried haplogroups L3e3L0a1a, and L3i2.[20]

At Catoctin Furnace African American Cemetery, in Catoctin FurnaceMaryland, there were 27 African 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 haplogroup L3e1.[23] One male individual, who was of 98.14% Sub-Saharan African ancestry, carried haplogroups E1b1a1a1a1c2c and L2a1+143+@16309.[23] One male individual, who was of 83.73% Sub-Saharan African and 7.74% European ancestry, carried haplogroups E1b1a1a1a1c1b1 and L3e2a1b1.[23] One male individual, who was of 88.47% Sub-Saharan African and 7.92% European ancestry, carried haplogroups R1b1a1b1a1a2c1 and L3e1.[23] One male individual, who was of 84.94% Sub-Saharan African and 9.45% European ancestry, carried haplogroups E1b1a1a1a2a1a and L2a1+143+16189 (16192)+@16309.[23] One female individual, who was of 97.02% Sub-Saharan African and 1.06% European ancestry, carried haplogroup L3f1b1a.[23] One male individual, who was of 87.83% Sub-Saharan African and 8.23% European ancestry, carried haplogroups E1b1a1a1a1c1a1a3a1d1 and L3d1b3.[23] One male individual, who was of 98.14% Sub-Saharan African ancestry, carried haplogroups E1b1a1a1a1a and L3e2a1b1.[23] One male individual, who was of 53.75% Sub-Saharan African and 42.11% European ancestry, carried haplogroups R1b1a1b1a1a2c1a1h2a~ and L3f1b3.[23] One female individual, who was of 98.12% Sub-Saharan African ancestry, carried haplogroup L2b1a3.[23] One female individual, who was of 97.94% Sub-Saharan African ancestry, carried haplogroup L3e1a1a.[23] One male individual, who was of 93.87% Sub-Saharan African and 2.58% European ancestry, carried haplogroups E1b1a1a1 and L3e1.[23] One male individual, who was of 98.70% Sub-Saharan African ancestry, carried haplogroups E1b1a1a1a1c1b2a and L2a1a1.[23] One male individual, who was of 97.01% Sub-Saharan African ancestry, carried haplogroups E1b1a1a1a1c1a1 and L3e2a1b1.[23] One female individual, who was of 87.17% Sub-Saharan African and 6.93% European ancestry, carried haplogroup L2a1+143+16189 (16192)+@16309.[23] One male individual, who was of 82.31% Sub-Saharan African and 10.24% European ancestry, carried haplogroups E1b1a1a1a1c1b and L3e2a1b1.[23] One male individual, who was of 91.82% Sub-Saharan African and 5.31% European ancestry, carried haplogroups E1b1a1a1a1c1a1 and L3e2.[23] One female individual, who was of 75.81% Sub-Saharan African and 21.44% European ancestry, carried haplogroup L4b2b1.[23] One female individual, who was of 91.95% Sub-Saharan African and 4.47% European ancestry, carried haplogroup L3e2.[23] One male individual, who was of 87.70% Sub-Saharan African and 4.93% European ancestry, carried haplogroups E2b and L2b1a3.[23] One female individual, who was of 97.53% Sub-Saharan African and 0.21% European ancestry, carried haplogroup L2b1a3.[23] One female individual, who was of 83.28% Sub-Saharan African and 10.72% European ancestry, carried haplogroup L3e2a1b1.[23] One male individual, who was of 41.31% Sub-Saharan African and 53.59% European ancestry, carried haplogroups R1a1a1 and J1b1a1a.[23] One male individual, who was of 92.70% Sub-Saharan African and 3.57% European ancestry, carried haplogroups A1b1 and L0a1b1a.[23] One male individual, who was of 81.18% Sub-Saharan African and 14.86% European ancestry, carried haplogroups E1b1a1~ and L2c.[23] One female individual, who was of 88.09% Sub-Saharan African and 5.44% European ancestry, carried haplogroup L2a1+143+16189 (16192)+@16309.[23] One female individual, who was of 92.32% Sub-Saharan African and 4.05% European ancestry, carried haplogroup L2b1a3.[23]

At a burial site in Schuyler FlattsNew York, 6 out of 14 individuals were African Americans, who were dated to the 18th century CE as well as of West African, western Central African, and Malagasy ancestry, carried various haplogroups; two carried haplogroup L2 (e.g., L2a1L2b1), two carried haplogroup L3 (e.g., L3e2, L3e2b), one carried haplogroup M, and one carried haplogroup M7.[24]

At an African American cemetery dated to the 18th century CE, in Portsmouth, New Hampshireenslaved African Americans carried haplogroups U5 and U6.[25]

At an Anson Street burial site dated to the 18th century CE, in Charleston, South Carolina, 29 enslaved African Americans carried the following haplogroups: one carried haplogroup L0 (e.g., L0a1), six carried haplogroup L1 (e.g., L1bL1c), nine carried L2 (e.g., L2aL2bL2c), twelve carried L3 (e.g., L3e, L3b, L3d, L3f), and one carried U6 (e.g., U6a5).[26]

At an Anson Street burial site, in CharlestonSouth Carolina, there were 18 African Americans found who were dated to the 18th century CE.[27] Banza was of western Central African ancestry and carried haplogroups E1b1a-CTS668 and L3e3b1.[27] Lima was of West African ancestry and carried haplogroups E1b1a-M4671 and L3b3.[27] Kuto was of western Central African ancestry and carried haplogroups E1b1a-CTS2198 and L2a1a2.[27] Anika was of Sub-Saharan African ancestry and carried haplogroups E1b1a-CTS6126 and L2b1.[27] Nana was of West African ancestry and carried haplogroup L2b3a.[27] Zimbu was of western Central African ancestry and carried haplogroups E1b1a-CTS5497 and L3e1e.[27] Wuta was of Sub-Saharan African ancestry and carried haplogroups E1b1a-CTS7305 and L3e2b+152.[27] Daba was of West African ancestry and carried haplogroups E1b1a-M4273 and L2c.[27] Fumu was of Sub-Saharan African ancestry and carried haplogroups B2a1a-Y12201 and L3e2b+152.[27] Lisa was of West African ancestry and carried haplogroups E1b1a-Z6020 and H100.[27] Ganda was of West African ancestry and carried haplogroups E1b1a-CTS5612 and L1c1c.[27] Coosaw was of West African and Native American ancestry and carried haplogroups E2b1a-CTS2400 and A2.[27] Kidzera was of western Central African ancestry and carried haplogroup L2a1a2c.[27] Pita was of Sub-Saharan African ancestry and carried haplogroups E1b1a-M4287 and L3e2b.[27] Tima was of western Central African ancestry and carried haplogroup L3e1e.[27] Jode was of Sub-Saharan African ancestry and carried haplogroups E1b1a-CTS4975 and L2a1a2c.[27] Ajana was of western Central African ancestry and carried haplogroup L2a1I.[27] Isi was of western Central African ancestry and carried haplogroup L3e2a.[27]

In Maryland, a tobacco pipe dated to the 19th century CE was determined to have been used by an enslaved African American woman, who was of Mende ancestry, and carried haplogroup L3e.[28] She may have lived for a period of time between 1736 CE and 1864 CE.[15]

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]

In PhiladelphiaPennsylvania, an individual of West African ancestry, who died of cholera during a cholera pandemic in 1849 CE, carried haplogroup L3d1b3.[30]

Y-Chromosomal DNA

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 SenegalGambia, 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]

African-Americans from South Carolina cluster with Senegalese Mandinka
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 enslaved African American females being raped by European males.[36]

Mitochondrial DNA

African Americans, who were sampled in 2015, carried various haplogroups of macro-haplogroup L (e.g., L0L1L1bL1cL2L2aL2bL2cL2eL3L3b, L3d, L3e, L3f, L3h, L3xL4).[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 from Guinea Bissau-Mali-Senegal-Sierra Leone predominates in other United States African 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 FrenchSpanish, 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]

Regional Ancestry of the Afro Diaspora
Autosomal DNA

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., LuhyaMaasai).[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 (MandinkaNiger-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 ChadicFulaniNilo-SaharanCushitic, 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 MadaSara, and Laka.[41]

Structured Analysis African-Americans and Caped Mixed Ancestry
African-American phylogenetic relationships
Visualization of African-American Ancestry
Medical DNA

The African ancestry in African Americans have often been connected to the risk alleles and genetic components of diseases predominant among African Americans, such as blood disordershypertension, progressive kidney failure, and type 2 diabetes.[42]

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, RSPO3SOX6, ULK4), which contributes to the signaling pathway for nitric oxide – a pathway connected with multiple functions (e.g., endothelian function, heart contractionvasodilatation) 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42] The Sickle 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-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]

Caribbean

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 BeninBight of BiafraCameroon, 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]

Barbados

Autosomal DNA[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Dominica

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Dominican Republic

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Grenada

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Haiti

Y-Chromosomal DNA

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]

Autosomal DNA

The ancestry of Afro-Haitians, who were sampled in 2013, were found to be 84% 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Jamaica

Y-Chromosomal DNA

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]

Mitochondrial DNA

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., U6A2B2D4HJU2M).[50]

Autosomal DNA

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Puerto Rico

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Saint Kitts and Nevis

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Saint Lucia

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Saint Martin

Ancient DNA

In Zoutsteeg, Philipsburg, Saint Martin, three enslaved Africans of West African (e.g., NigeriaGhana) and western Central African (e.g., Bantu peoples of northern Cameroon) ancestry, who are estimated to date between 1660 CE and 1688 CE, were found; one carried haplogroups R1b1c-V88 and L3b1a, another carried haplogroup L3d1b, and the last carried haplogroup L2a1f.[51] A man and woman may have been from Ghana or Nigeria, and a man may have been from among the Bantu peoples of CameroonRepublic of the Congo, and Democratic Republic of the Congo.[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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Saint Vincent

Autosomal DNA

The ancestry of the Garifuna in Saint Vincent, who were sampled in 2013, were found to be 70% African.[15] The ancestry of the Garifuna of Saint 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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Trinidad and Tobago

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Virgin Islands

Saint Thomas
Autosomal DNA

In addition to being found to have 2.6% (±2.1%) Native American and 10.6% (±2.3%) European ancestry, Afro-Virgin Islanders from Saint 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 from Saint Thomas, who were sampled in 2013, were found to be 77.4% (±21.9%) West African.[48]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Central America

Belize

Autosomal DNA

In addition to being found to have 29.0% Native American and 1.0% European ancestry, some Afro-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, some Afro-Belizeans from Stann 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, some Afro-Belizeans from Punta 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, some Afro-Belizeans from Hopkins, 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, some Afro-Belizeans from Stann 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, some Afro-Belizeans from Punta 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, some Afro-Belizeans from Belize City, who were sampled in 1983, were found to be 74.7% African.[52]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Guatemala

Autosomal DNA
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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Honduras

Autosomal DNA

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]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Mexico

Ancient DNA

At a San Jose de los Naturales Royal Hospital burial site, in Mexico City, Mexico, three enslaved West Africans of West African and Southern African ancestry, dated between 1453 CE and 1626 CE, 1450 CE and 1620 CE, and 1436 CE and 1472 CE, were found; one carried haplogroups E1b1a1a1c1b/E-M263.2 and L1b2a, another carried haplogroups E1b1a1a1d1/E-P278.1/E-M425 and L3d1a1a, and the last carried haplogroups E1b1a1a1c1a1c/E-CTS8030 and L3e1a1a.[53] Human leukocyte antigen alleles further confirm that the individuals were of Sub-Saharan African origin.[15]

At the 11–1 burial site, in CampecheMexico, a West African woman, who was in her early twenties and dated to the late 17th century CE, carried haplogroup L3.[54]

Medical DNA

At La Concepción chapel and Hospital Real de San José de los Naturales, in Mexico City, Mexicoenslaved Africans, 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Nicaragua

Autosomal DNA
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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

South America

MTDNA of the Afro-Diaspora

Bolivia

Autosomal DNA

The ancestry of Afro-Bolivians from the Yungas Valley, who were sampled in 2016, were found to be 80% 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Brazil

Ancient DNA

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]

Autosomal DNA

The average ancestry of Afro-Brazilians were found to be 70.8% 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Colombia

Y-Chromosomal DNA

At Palenque, in addition to haplogroup R1b being found, including haplogroup R1b-V88haplogroup 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 at PalenqueE1b1a-M2* (xM154, M191) (22.4% rate of occurrence) likely originates near Bight of BeninE1b1a-M2* (xM154, M191) (12.1%) likely originates near Loango/AngolaB2a-M150* (xM109) (5.2%) likely originates in LoangoR1b-V88 (6.9%) likely originates near Bight of Benin/LoangoE1b1b-M35* (xM78, M81, M123, V6, M293) (5.2%) likely originates near Senegambia/Bight of BeninY-MRCA* (xM13,SRY10831.1) (3.4%) likely originates in Upper GuineaE1a-M33 (1.7%) likely originates in Upper GuineaE1a-M33 (1.7%) likely originates near Bight of Benin/Bight of BiafraE1b1a-M191 (1.7%) likely originates near Loango/Angola, and E1b1a-M191 (1.7%) likely originates in Loango.[58]

Mitochondrial DNA

While 67.1% was unable to be identified, the following African maternal haplogroups were able to be identified at PalenqueL1b1a1’4 (8.9% rate of occurrence) likely originates near Senegambia/Upper GuineaL1c3a1b (6.3%) likely originates near Gold Coast/AngolaL0a1a+200 (1.3%) likely originates near Upper Guinea/Bight of BeninL2b1a (1.3%) likely originates near Bight of Benin/AngolaL2d+16129 (1.3%) likely originates in AngolaL3e1d (12.7%) likely originates in Angola, and L3f1b+16365 (1.3%) likely originates in Gold Coast.[58]

Autosomal DNA[edit]

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]

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 of Afro-Colombians were found to be 76.8% 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African 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 provide statistically significant protection against Dengue Fever in Colombians.[42]

Peru

Autosomal DNA

The ancestry of Afro-Peruvians, who were sampled in 2018, were found to be 78% 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Suriname

Ancient DNA

In Batavia, Suriname, an enslaved West African (e.g., Mali) with some Middle Eastern ancestry, who died more than a century ago, carried a strain of M. leprae and haplogroup L3.[59]

Autosomal DNA

Due to their relative isolation from Europeans and Native AmericansMaroons retained and adapted their cultures from Africa.[15] European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as ColombiaJamaicaFrench Guiana, and Suriname.[15] Alukus,KwintiMatawaiNdjukasParamakas, 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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Atlantic Ocean

North Atlantic Ocean

Macaronesia

Canary Islands
Ancient DNA

At Finca Clavijo, in Gran CanariaCanary Islands, nine individuals, dated between 15th century CE and 17th century CE, who were of Sub-Saharan African and North African/Moorish origin, were enslaved and forcibly brought from Africa (e.g., MoroccoSenegal River); the Sub-Saharan African individuals carried haplogroups L1bL1c, and L2a1, and the Moorish individuals carried haplogroups HHV/RR0I, and U6b1.[60]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

South Atlantic Ocean

Saint Helena, Ascension and Tristan da Cunha

Saint Helena
Ancient DNA

In Saint Helena, 20 freed Africans,[61][62] who were dated to the 19th century CE,[61] were also of western Central African[61][63][64] (e.g., Bantu peoples of Gabon and Angola) ancestry.[61] One female individual carried haplogroup L1b1a10b.[65] One female individual carried haplogroup L2a1f.[65] One female individual carried haplogroup L2a1a3c.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1d and L1c3a.[65] One male individual carried haplogroups E1b1a1a1a1c1a1a and L0a1b2a.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1a2a2 and L0a1e.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1 and L2a1f1.[65] One male individual carried haplogroups E1b1a1 and L3.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1d and L3e1e.[65] One male individual carried haplogroups E1b1a1a1a2a1a3a1d and L3e3b2.[65] One male individual carried haplogroups E1b1a1a1a1c1a1a3 and L3e1a3a.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1a2a2 and L2b1a.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1 and L3f1b1a.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1d1c1a and L3d3a1.[65] One male individual carried haplogroups B2a1a1a1 and L3e2b1.[65] One male individual carried haplogroups E1b1a1a1a2a1a3b1d1c1a and L2a1f.[65] One male individual carried haplogroups E1b1a1a1a1c1a1a3a1c1 and L3e1d1a.[65] One male individual carried haplogroups E1b1a1a1a2a1a3a1d and L1b1a10.[65] One male individual carried haplogroups E1b1a1a1a1c1a1a3a1c and L2a1f1.[65] One male individual carried haplogroups E1b1a1a1a1c1a1 and L2b1a.[65] An enslaved African American man and woman, from the 18th century CE Anson Street burial site in Charleston, South Carolina, who carried haplogroup 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 the Trans-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 the demographics of Africa.[68]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Eurasia

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 EuropeTurkey, 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]

Europe

As early as 11,000 years ago, Sub-Saharan West Africans, bearing macrohaplogroup L (e.g., L1b1a11, L1b1a6a, L1b1a8, L1b1a9a1, L2a1kL3d1b1a), may have migrated through North Africa and into Europe, mostly into southern Europe (e.g., Iberia).[6]

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]

Greece

Medical DNA

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., FulaniMossiRimaibe) from Burkina Faso,[69][70][71] who are viewed as having a possible earlier origin in Ethiopia.[70][72] In particular, West Africans (e.g., Fulani, Mossi, Rimaibe) and Ethiopians (e.g., AmharaOromo) are viewed as sharing the most HLA-DRB1 alleles with Greeks.[73][71] Greeks, West Africans, and Ethiopians are viewed as viewed as sharing chromosome 7 markers.[69] 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.[69] 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.[70][72] 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.[69] 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.[69][70] 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).[73] Greeks are viewed as sharing some alleles with West Africans (e.g., Fulani, Mossi, and Rimaibe) and East Africans (e.g., Oromo, Amhara, Nubians),[74][71] the latter of which are viewed as also interrelated.[74] 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.[74] Another migration of West Africans may have occurred thereafter.[74] 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.[74] 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.[71]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Italy[edit]

Ancient DNA[edit]

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[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Portugal[edit]

Ancient DNA[edit]

In 4000 BP, there may have been a population that traversed from Africa (e.g., West Africa or West-Central Africa), through the Strait of Gibraltar, into the Iberian peninsula, where admixing between Africans and Iberians (e.g., of northern Portugal, of southern Spain) occurred.[12]

At Valle da Gafaria, in Lagos, Portugal, seven enslaved Africans, five of which had a combination of African and European admixture, and two of which had West African and Bantu 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 haplogroups H2a2L1b1L3i1bL3'4'6L2b1, and L3d.[75][76]

At Cabeço da Amoreira, in Portugal, an enslaved West African man, who may have been from the Senegambian coastal region of GambiaMauritania, or Senegal, and carried haplogroups E1b1a and L3b1a, was buried among shell middens between the 16th century CE and the 18th century CE.[77]

Mitochondrial DNA[edit]

In LisbonPortugal, 87% of Angolans, who were sampled in 2014, carried various haplogroups of Macro-haplogroup L (e.g., L0a, L0dL1bL1cL2aL2bL2cL3a, L3b, L3d, L3fL4), whereas, other sampled Angolans carried different haplogroups (e.g., HTR0KUJM).[16]

In LisbonPortugal, out of 80 Guinea-Bissauns, who were sampled in 2017, 73 carried Macro-haplogroup L, 5 carried haplogroup U, one carried haplogroup M, and one carried haplogroup V.[17]

In LisbonPortugal, 81% of Mozambicans, who were sampled in 2017, carried various haplogroups of Macro-haplogroup L, whereas, 19% of the sampled Mozambicans carried different haplogroups (e.g., HUKJ1M4R0T2).[18]

Medical DNA[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Spain[edit]

Ancient DNA[edit]

In 4000 BP, there may have been a population that traversed from Africa (e.g., West Africa or West-Central Africa), through the Strait of Gibraltar, into the Iberian peninsula, where admixing between Africans and Iberians (e.g., of northern Portugal, of southern Spain) occurred.[12]

In GranadaSpain, a Muslim (Moor) of the Cordoba Caliphate,[78] who was of haplogroups E1b1a1 and H1+16189,[79] as well as estimated to date between 900 CE and 1000 CE, and a Morisco,[78] who was of haplogroup L2e1,[79] as well as estimated to date between 1500 CE and 1600 CE, were both found to be of West African (i.e., Gambian) and Iberian descent.[78]

Medical DNA[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Asia[edit]

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]

Arabia[edit]

Mitochondrial DNA[edit]

From as early as 2500 BP, East African females migrated, as well as some who may have later been enslaved and forcibly transported, into Arabia.[80] Consequently, Arabs, who were sampled in 2003, have been shown to carry Sub-Saharan African haplogroups (e.g., L1L2L3b, L3d, L3e); specifically, 35% of Yemenese from the Hadramawt region, and between 10% and 15% among other Arabs (e.g., BedouinIraqisJordaniansPalestiniansSyrians).[80]

Medical DNA[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Georgia[edit]

Ancient DNA[edit]

In AbkhaziaGeorgia, an African woman, Zana, who carried haplogroup L2b1b, was 34% West African and 66% East African, and lived during the 19th century CE.[81] 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 of enslavement during the Ottoman Empire.[81] Khwit, who was the son of Zana and carried haplogroups R1b1a1b1 and L2b1b, was of African and European admixture.[81]

Medical DNA[edit]

Local myth about Zana of AbkhaziaGeorgia 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.[81] Margaryan et al. (2021) speculate that Zana may have had congenital generalized hypertrichosis, which may have resulted in the development of the local myth.[81]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

India[edit]

Y-Chromosomal DNA[edit]

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]

Mitochondrial DNA[edit]

Out of the total amount of haplogroups carried, Siddis, who were sampled in 2011, 24% of their maternal haplogroups were found to be African.[14]

Autosomal DNA[edit]

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.[82] Siddis, who were sampled twice in 2011, were found to be 60%-75% Sub-Saharan African.[14]

Medical DNA[edit]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Israel[edit]

Medical DNA[edit]

During the Copper Age and early Islamic era of ancient IsraelWest Africans may have migrated into ancient Israel and introduced head louse from West Africa.[83]

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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]

Pakistan[edit]

Y-Chromosomal DNA[edit]

Out of the total amount of haplogroups carried, Makranis, who were sampled in 2002 and 2004, 12% (±7%) of their paternal haplogroups were African.[14]

Mitochondrial DNA[edit]

Out of the total amount of haplogroups carried, Makranis, who were sampled in 2002 and 2004, 40% (±9%) of their maternal haplogroups were African.[14]

Autosomal DNA[edit]

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 African Swahili 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]

Medical DNA[edit]

Since enslaved Africans were brought to Pakistan, the African Duffy-null alleles in Makranis have evolved.[14] Makranis have an increased level of malarial resistance to P. vivax.[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]

Some infectious diseases are protected against due to African ancestry.[42] Hereditary blood disorders, such as sickle cell anemia and thalassemia, produce an effect on the development of hemoglobin, which, consequently, prevents the reproduction of malaria parasites within the erythrocyte.[42] Populations with West African ancestry, including among the African diaspora brought via the Trans-Atlantic slave trade, tend to have occurrences of sickle cell anemia and thalassemia.[42]