The superposition principle, also known as superposition property, states that, for all linear systems,
the net response caused by two or more stimuli is the sum of the
responses that would have been caused by each stimulus individually. So
that if input A produces response X, and input B produces response Y, then input (A + B) produces response (X + Y).
This principle has many applications in physics and engineering because many physical systems can be modeled as linear systems. For example, a beam can be modeled as a linear system where the input stimulus is the load on the beam and the output response is the deflection
of the beam. The importance of linear systems is that they are easier
to analyze mathematically; there is a large body of mathematical
techniques, frequency-domainlinear transform methods such as Fourier and Laplace transforms, and linear operator
theory, that are applicable. Because physical systems are generally
only approximately linear, the superposition principle is only an
approximation of the true physical behavior.
The superposition principle applies to any linear system, including algebraic equations, linear differential equations, and systems of equations of those forms. The stimuli and responses could be numbers, functions, vectors, vector fields, time-varying signals, or any other object that satisfies certain axioms. Note that when vectors or vector fields are involved, a superposition is interpreted as a vector sum.
If the superposition holds, then it automatically also holds for all
linear operations applied on these functions (due to definition), such
as gradients, differentials or integrals (if they exist).
Relation to Fourier analysis and similar methods
By
writing a very general stimulus (in a linear system) as the
superposition of stimuli of a specific and simple form, often the
response becomes easier to compute.
For example, in Fourier analysis, the stimulus is written as the superposition of infinitely many sinusoids.
Due to the superposition principle, each of these sinusoids can be
analyzed separately, and its individual response can be computed. (The
response is itself a sinusoid, with the same frequency as the stimulus,
but generally a different amplitude and phase.)
According to the superposition principle, the response to the original
stimulus is the sum (or integral) of all the individual sinusoidal
responses.
Fourier analysis is particularly common for waves. For example, in electromagnetic theory, ordinary light is described as a superposition of plane waves (waves of fixed frequency, polarization, and direction). As long as the superposition principle holds (which is often but not always; see nonlinear optics), the behavior of any light wave can be understood as a superposition of the behavior of these simpler plane waves.
Waves are usually described by variations in some parameters through space and time—for example, height in a water wave, pressure in a sound wave, or the electromagnetic field in a light wave. The value of this parameter is called the amplitude of the wave and the wave itself is a function specifying the amplitude at each point.
In any system with waves, the waveform at a given time is a function of the sources (i.e., external forces, if any, that create or affect the wave) and initial conditions of the system. In many cases (for example, in the classic wave equation),
the equation describing the wave is linear. When this is true, the
superposition principle can be applied. That means that the net
amplitude caused by two or more waves traversing the same space is the
sum of the amplitudes that would have been produced by the individual
waves separately. For example, two waves traveling towards each other
will pass right through each other without any distortion on the other
side. (See image at the top.)
No-one has ever been able to define the difference between interference
and diffraction satisfactorily. It is just a question of usage, and
there is no specific, important physical difference between them. The
best we can do, roughly speaking, is to say that when there are only a
few sources, say two, interfering, then the result is usually called
interference, but if there is a large number of them, it seems that the
word diffraction is more often used.
Other authors elaborate:
The difference is one of
convenience and convention. If the waves to be superposed originate from
a few coherent sources, say, two, the effect is called interference. On
the other hand, if the waves to be superposed originate by subdividing a
wavefront into infinitesimal coherent wavelets (sources), the effect is
called diffraction. That is the difference between the two phenomena is
[a matter] of degree only, and basically, they are two limiting cases
of superposition effects.
Yet another source concurs:
In as much as the interference
fringes observed by Young were the diffraction pattern of the double
slit, this chapter [Fraunhofer diffraction] is, therefore, a
continuation of Chapter 8 [Interference]. On the other hand, few
opticians would regard the Michelson interferometer as an example of
diffraction. Some of the important categories of diffraction relate to
the interference that accompanies division of the wavefront, so
Feynman's observation to some extent reflects the difficulty that we may
have in distinguishing division of amplitude and division of wavefront.
The phenomenon of interference
between waves is based on this idea. When two or more waves traverse
the same space, the net amplitude at each point is the sum of the
amplitudes of the individual waves. In some cases, such as in noise-canceling headphones, the summed variation has a smaller amplitude than the component variations; this is called destructive interference. In other cases, such as in a line array, the summed variation will have a bigger amplitude than any of the components individually; this is called constructive interference.
combined waveform
wave 1
wave 2
Two waves in phase
Two waves 180° out of phase
Departures from linearity
In
most realistic physical situations, the equation governing the wave is
only approximately linear. In these situations, the superposition
principle only approximately holds. As a rule, the accuracy of the
approximation tends to improve as the amplitude of the wave gets
smaller. For examples of phenomena that arise when the superposition
principle does not exactly hold, see the articles nonlinear optics and nonlinear acoustics.
In quantum mechanics, a principal task is to compute how a certain type of wave propagates and behaves. The wave is described by a wave function, and the equation governing its behavior is called the Schrödinger equation. A primary approach to computing the behavior of a wave function is to write it as a superposition (called "quantum superposition") of (possibly infinitely many) other wave functions of a certain type—stationary states
whose behavior is particularly simple. Since the Schrödinger equation
is linear, the behavior of the original wave function can be computed
through the superposition principle this way.
The projective nature of quantum-mechanical-state space causes some confusion, because a quantum mechanical state is a ray in projective Hilbert space, not a vector.
According to Dirac: "if
the ket vector corresponding to a state is multiplied by any complex
number, not zero, the resulting ket vector will correspond to the same
state [italics in original]."
However, the sum of two rays to compose a superpositioned ray is undefined. As a result, Dirac himself
uses ket vector representations of states to decompose or split,
for example, a ket vector
into superposition of component ket vectors as:
where the .
The equivalence class of the allows a well-defined meaning to be given to the relative phases of the ., but an absolute (same amount
for all the ) phase change on the
does not affect the equivalence class of the .
Nevertheless, on the topic of quantum superposition, Kramers writes: "The principle of [quantum] superposition ... has no analogy in classical physics".
According to Dirac: "the
superposition that occurs in quantum mechanics is of an essentially
different nature from any occurring in the classical theory [italics in original]."
Though reasoning by Dirac includes atomicity of observation, which is valid, as for phase,
they actually mean phase translation symmetry derived from time translation symmetry, which is also
applicable to classical states, as shown above with classical polarization states.
A common type of boundary value problem is (to put it abstractly) finding a function y that satisfies some equation
with some boundary specification
For example, in Laplace's equation with Dirichlet boundary conditions, F would be the Laplacian operator in a region R, G would be an operator that restricts y to the boundary of R, and z would be the function that y is required to equal on the boundary of R.
In the case that F and G are both linear operators,
then the superposition principle says that a superposition of solutions
to the first equation is another solution to the first equation:
while the boundary values superpose:
Using these facts, if a list can be compiled of solutions to the first
equation, then these solutions can be carefully put into a superposition
such that it will satisfy the second equation. This is one common
method of approaching boundary-value problems.
By superposition principle, the system can be decomposed into
with
Superposition principle is only available for linear systems. However, the additive state decomposition can be applied to both linear and nonlinear systems. Next, consider a nonlinear system
where is a nonlinear function. By the additive state decomposition, the system can be additively decomposed into
with
This decomposition can help to simplify controller design.
Other example applications
In electrical engineering, in a linear circuit,
the input (an applied time-varying voltage signal) is related to the
output (a current or voltage anywhere in the circuit) by a linear
transformation. Thus, a superposition (i.e., sum) of input signals will
yield the superposition of the responses.
In physics, Maxwell's equations imply that the (possibly time-varying) distributions of charges and currents are related to the electric and magnetic fields
by a linear transformation. Thus, the superposition principle can be
used to simplify the computation of fields that arise from a given
charge and current distribution. The principle also applies to other
linear differential equations arising in physics, such as the heat equation.
In engineering, superposition is used to solve for beam and structure deflections
of combined loads when the effects are linear (i.e., each load does not
affect the results of the other loads, and the effect of each load does
not significantly alter the geometry of the structural system).
Mode superposition method uses the natural frequencies and mode shapes
to characterize the dynamic response of a linear structure.
In hydrogeology, the superposition principle is applied to the drawdown of two or more water wells pumping in an ideal aquifer. This principle is used in the analytic element method to develop analytical elements capable of being combined in a single model.
The superposition principle can be applied when small deviations from a known solution to a nonlinear system are analyzed by linearization.
History
According to Léon Brillouin, the principle of superposition was first stated by Daniel Bernoulli
in 1753: "The general motion of a vibrating system is given by a
superposition of its proper vibrations." The principle was rejected by Leonhard Euler and then by Joseph Lagrange.
Bernoulli argued that any sonorous body could vibrate in a series of
simple modes with a well-defined frequency of oscillation. As he had
earlier indicated, these modes could be superposed to produce more
complex vibrations. In his reaction to Bernoulli's memoirs, Euler
praised his colleague for having best developed the physical part of the
problem of vibrating strings, but denied the generality and superiority
of the multi-modes solution.
Later it became accepted, largely through the work of Joseph Fourier.
Amid the Green Sahara in Africa, the mutation for sickle cell originated in the Sahara or in the northwest forest region of western Central Africa (e.g., Cameroon) by at least 7,300 years ago, though possibly as early as 22,000 years ago. 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. 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. West Africans (e.g., Mende of Sierra Leone), bearing the Senegal sickle cell haplotype, may have migrated into Mauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, into North Africa, and from North Africa, into Southern Europe, Turkey, and a region near northern Iraq and southern Turkey. Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes into Basra, Iraq, where both occur equally. 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%).
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.
During the modern period, West Africans introduced more than 75% of Sub-Saharan mitochondrial DNA into North America and Southern Africans introduced almost 15%.
West Africans also introduced ~45% of Sub-Saharan African mitochondrial
DNA into South America, whereas, Southern Africans, largely indigenous Angolans, introduced ~55%.
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.
During the modern period, a greater number of West Africans introduced
Sub-Saharan African mitochondrial DNA than East Africans. 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.
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.
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.
Due to their relative isolation from Europeans and Native Americans, Maroonsretained and adapted their cultures from Africa. European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as Colombia, Jamaica, French Guiana, and Suriname. Alukus,Kwinti, Matawai, Ndjukas, Paramakas, and Saramakas, who are Maroons of Noir Marron, are the largest, autonomous group of Maroons in the Americas. 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. 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.
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.
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.” During the modern period, West Africans introduced more than 75% of Sub-Saharan mitochondrial DNA into North America and Southern Africans introduced almost 15%.
West Africans also introduced ~45% of Sub-Saharan African mitochondrial
DNA into South America, whereas, Southern Africans, largely indigenous Angolans, introduced ~55%.
In Maryland, a tobacco pipe dated to the 19th century CE was determined to have been used by an enslavedAfrican American woman, who was of Mende ancestry, and carried haplogroup L3e. She may have lived for a period of time between 1736 CE and 1864 CE.
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.
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).
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.
Torres et al. (2012) states: "One African American population, those from South Carolina, cluster with the African populations. Notably, the South Carolina population falls nearest to the Grain Coast populations. Ethnohistorical records indicate a relationship between African Americans within this region of the United States and West Africans from Senegal, Gambia, and Sierra Leone.
Based on such records it has been suggested that many African Americans
within South Carolina originate from the Grain Coast region of West
Africa. Furthermore, Africans from this region were sought-after and
imported to the Americas for their knowledge of rice cultivation."
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; consequently, this can be understood as being the result of enslavedAfrican American females being raped by European males.
Stefflova et al. (2011) states: "Ancestry from Guinea Bissau-Mali-Senegal-Sierra Leone predominates in other United StatesAfrican American populations compared to Philadelphia
alone (43% vs. 22%). Despite the differences in coverage and sampling,
this pattern may be attributed to a significant contribution of slaves
from British colonies in Africa to the British-controlled Philadelphia region compared to a more diverse contribution to other parts of the United States from French, Spanish, and Dutch colonies. Additional possible contributing factors include the different periods of the slave trade influencing the Philadelphian
population compared to the other parts of the United States. However,
these remain tentative conclusions since we cannot rule out a
contribution from sampling bias. Another example of these differences is
the Gullah/Geechee populations from South Carolina/Georgia
that have >78% of their source from the Guinea
Bissau-Mali-Senegal-Sierra Leone region (data not shown), corresponding
to the “Rice coast” around Sierra Leone that was the major source of slaves drawn by the United States in the later period of the slave trade." 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).
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.
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. African Americans were found to be more closely genetically related to Yoruba people than East Africans (e.g., Luhya, Maasai).
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." 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. Approximately 7% of their ancestry derives from Windward Coast, 13% from Senegambia, 30% from Angola, and nearly 50% from Benin, western Nigeria, and Togo. Additionally, 4.8% of their ancestry derives from Bantu peoples and 16% derives from African rainforest hunter-gatherers.
Tishkoff et al. (2009) via "Supervised STRUCTURE analysis
[inferred] African American ancestry from global training populations,
including both Bantu (Lemande) and non-Bantu (Mandinka) Niger-Kordofanian–speaking
populations. These results were generally consistent with the
unsupervised STRUCTURE analysis (table S6) and demonstrate that most
African Americans have high proportions of both Bantu (~0.45 mean) and
non-Bantu (~0.22 mean) Niger-Kordofanian ancestry, concordant with
diasporas originating as far west as Senegambia and as far south as Angola and South Africa." Moderate to modest amounts of Chadic, Fulani, Nilo-Saharan, Cushitic, and Sandawe
ancestry were also inferred; this is consistent with the phylogenetic
analysis of Tishkoff et al. (2009), wherein African-Americans were found
to share more recent common ancestry with a clade including Hausa and Fulani from Cameroon, in addition to Chadic and Central Sudanic speakers such as the Mada, Sara, and Laka.
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.
The rate of occurrence for hypertension in African Americans is 39%. Several genes (e.g., EVX1-HOXA, PLEKHG1, RSPO3, SOX6, ULK4), which contributes to the signaling pathway for nitric oxide – a pathway connected with multiple functions (e.g., endothelian function, heart contraction, vasodilatation) relating to hypertension – and thus, are associated with hypertension. Hypertension is also associated with the NPR3 gene. These genes have all been connected with hypertension in African Americans.
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.
African Americans have as much as 65% of the Duffy-null genotype. 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.
A majority of Afro-Caribbean people descend from peoples in the regions of West Africa and western Central Africa. In particular, their genetic ancestry, to some extent, derives from peoples in the region of Angola, but more so, from peoples in regions, such as the Bight of Benin, Bight of Biafra, Cameroon, and Ghana. 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.
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. 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. Afro-Barbadians were found to be more closely genetically related to Yoruba people than East Africans. 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. 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). The ancestry of Afro-Barbadians, who were sampled in 2017, were found to be 88% African.
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.
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.
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.
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.
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.
Autosomal DNA
The ancestry of Afro-Haitians, who were sampled in 2013, were found to be 84% African.
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.
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.
Afro-Jamaicans, who were sampled in 2012, were found to have mostly (97.5%) carried various forms of macro-haplogroup L as well as various other haplogroups (e.g., U6, A2, B2, D4, H, J, U2, M).
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. 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. The ancestry of Afro-Jamaicans, who were sampled in 2016, were found to be 89% African. 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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
At the 11–1 burial site, in Campeche, Mexico, a West African woman, who was in her early twenties and dated to the late 17th century CE, carried haplogroup L3.
Medical DNA
At La Concepción chapel and Hospital Real de San José de los Naturales, in Mexico City, Mexico, enslavedAfricans, who carried haplogroup L, were sampled for viral genomes. 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. 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.
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.
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.
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.
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.
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.
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.
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.
The ancestry of Afro-Peruvians, who were sampled in 2018, were found to be 78% African.
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.
Due to their relative isolation from Europeans and Native Americans, Maroonsretained and adapted their cultures from Africa. European colonial forces relinquished and recognized the territorial sovereignty of areas occupied by Maroons, such as Colombia, Jamaica, French Guiana, and Suriname. Alukus,Kwinti, Matawai, Ndjukas, Paramakas, and Saramakas, who are Maroons of Noir Marron, are the largest, autonomous group of Maroons in the Americas. 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. 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.
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.
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.
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.
Amid the Green Sahara in Africa, the mutation for sickle cell originated in the Sahara or in the northwest forest region of western Central Africa (e.g., Cameroon) by at least 7,300 years ago, though possibly as early as 22,000 years ago. 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. 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. West Africans (e.g., Mende of Sierra Leone), bearing the Senegal sickle cell haplotype, may have migrated into Mauritania (77% modern rate of occurrence) and Senegal (100%); they may also have migrated across the Sahara, into North Africa, and from North Africa, into Southern Europe, Turkey, and a region near northern Iraq and southern Turkey. Some may have migrated and introduced the Senegal and Benin sickle cell haplotypes into Basra, Iraq, where both occur equally. 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%).
During the early period of the Holocene, Sub-Saharan African mitochondrial DNA was introduced into Europe, mostly in Iberia. 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.
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.
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.
According to some studies, Greeks share some Human Leukocyte Antigen (HLA) alleles with East Africans (e.g., Amhara, Nuba, Oromo) and West Africans (e.g., Fulani, Mossi, Rimaibe) from Burkina Faso, who are viewed as having a possible earlier origin in Ethiopia. In particular, West Africans (e.g., Fulani, Mossi, Rimaibe) and Ethiopians (e.g., Amhara, Oromo) are viewed as sharing the most HLA-DRB1 alleles with Greeks. Greeks, West Africans, and Ethiopians are viewed as viewed as sharing chromosome 7 markers. 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. 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. 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. 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.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).
Greeks are viewed as sharing some alleles with West Africans (e.g.,
Fulani, Mossi, and Rimaibe) and East Africans (e.g., Oromo, Amhara,
Nubians), the latter of which are viewed as also interrelated.
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. Another migration of West Africans may have occurred thereafter. 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. 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.
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.
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.
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.
In Lisbon, Portugal, 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., H, U, K, J1, M4, R0, T2).
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.
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.
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.
During the modern period, a greater number of West Africans introduced
Sub-Saharan African mitochondrial DNA than East Africans. 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.
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.
In Abkhazia, Georgia, an African woman, Zana, who carried haplogroup L2b1b, was 34% West African and 66% East African, and lived during the 19th century CE.
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 enslavementduring the Ottoman Empire. Khwit, who was the son of Zana and carried haplogroups R1b1a1b1 and L2b1b, was of African and European admixture.
Medical DNA
Local myth about Zana of Abkhazia, Georgia being an Almasty was refuted by genetic evidence from ancient DNA,
which confirmed that Zana was neither closely related to chimpanzees
nor closely related to archaic humans, but closely related to other modern humans. Margaryan et al. (2021) speculate that Zana may have had congenital generalized hypertrichosis, which may have resulted in the development of the local myth.
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.
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.
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. Siddis, who were sampled twice in 2011, were found to be 60%-75% Sub-Saharan African.
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.
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.
While the orature among Makranis narrates an origin from Abyssinia, the genetic results from 2017 show that much of the ancestry of Makranis derives from Bantu-speaking peoples (Zanj), specifically from the southeast AfricanSwahili coast. 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. 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. 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.
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.