ArticlePDF AvailableLiterature Review

The evolution of human skin colouration and its relevance to health in the modern world

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Abstract

Functionally naked skin which comes in a range of colours is unique to the human species. This review summarises current evidence pertaining to the evolution of these attributes. The biggest changes in the integument occurred during the course of human evolution in equatorial Africa, under regimes of high daytime temperatures and high ultraviolet radiation (UVR). Loss of most functional body hair was accompanied by the evolution of an epidermis with a specialised stratum corneum and permanent, protective, eumelanin pigmentation. The main reason for the evolution of dark pigmentation was to protect against folate deficiency caused by elevated demands for folate in cell division, DNA repair, and melanogenesis stimulated by UVR. Dispersal out of tropical Africa created new challenges for human physiology especially because of lower and more seasonal levels of UVR and ultraviolet B (UVB) outside of the tropics. In these environments, the challenge of producing a vitamin D precursor in the skin from available UVB was met by natural selection acting on mutations capable of producing varying degrees of depigmentation. The range of pigmentation observed in modern humans today is, thus, the product of two opposing clines, one favoring photoprotection near the equator, the other favoring vitamin D photosynthesis nearer the poles. Recent migrations and changes in lifestyle in the last 500 years have brought many humans into UVR regimes different from those experienced by their ancestors and, accordingly, exposed them to new disease risks, including skin cancer and vitamin D deficiency.
58
education
Symposium review
The evolution of human skin colouration and
its relevance to health in the modern world
NG Jablonski
Distinguished Professor of Anthropology, The Pennsylvania State University, University Park, Pennsylvania, USA
Correspondence to NG Jablonski,
Department of Anthropology, The
Pennsylvania State University, 409
Carpenter Building, University Park,
PA 16802, USA
tel. +1 (814) 865-2509
e-mail ngj2@psu.edu
This review is based in part on Professor Jablonski’s lecture at the RCPE
Symposium on Dermatology in Edinburgh on 21 September 2011
ABSTRACT Functionally naked skin which comes in a range of colours is unique
to the human species. This review summarises current evidence pertaining to the
evolution of these attributes. The biggest changes in the integument occurred
during the course of human evolution in equatorial Africa, under regimes of high
daytime temperatures and high ultraviolet radiation (UVR). Loss of most
functional body hair was accompanied by the evolution of an epidermis with a
specialised stratum corneum and permanent, protective, eumelanin pigmentation.
The main reason for the evolution of dark pigmentation was to protect against
folate deficiency caused by elevated demands for folate in cell division, DNA
repair, and melanogenesis stimulated by UVR. Dispersal out of tropical Africa
created new challenges for human physiology especially because of lower and
more seasonal levels of UVR and ultraviolet B (UVB) outside of the tropics. In
these environments, the challenge of producing a vitamin D precursor in the skin
from available UVB was met by natural selection acting on mutations capable of
producing varying degrees of depigmentation. The range of pigmentation
observed in modern humans today is, thus, the product of two opposing clines,
one favoring photoprotection near the equator, the other favoring vitamin D
photosynthesis nearer the poles. Recent migrations and changes in lifestyle in the
last 500 years have brought many humans into UVR regimes different from those
experienced by their ancestors and, accordingly, exposed them to new disease
risks, including skin cancer and vitamin D deficiency.
KeywoRdS Melanin, natural selection, vitamin D, migration, urbanisation,
depigmentation
deClARATion of inTeReSTS No conflict of interests declared.
Human skin is functionally naked, sweaty, resistant to
abrasion, colourful, and often deliberately decorated.
This constellation of attributes makes human skin
unique1 and of great interest to comparative biologists
and anthropologists. The range of colour exhibited by
human skin is its most singular biological characteristic
and the one of greatest social import because skin
colour has been the primary trait used to classify people
into races. Skin colour has been observed and studied by
philosophers and scientists for over two millennia and
yet there is still much about it that is not known.
Research into the evolution and importance of skin
pigmentation languished during much of the twentieth
century because of legitimate concerns that study of the
causes and ramifications of skin colour variation would
be socially divisive. This situation has changed in the last
20 years partly because of the development of new
genetic tools, which have allowed for rapid and wide-
scale exploration of human variation. Study of variation in
pigmentation also gained impetus because of the recog-
nition that understanding and dispassionate discussion of
the causes of visible human variation is important to
human health and the future of societies. Here I review
recent advances in knowledge of the evolution of skin
pigmentation variation and the diverse effects that skin
pigmentation has on health and wellbeing in the
modern world.
The evoluTion of funCTionAl nAKedneSS
And iTS RelATionShip To SKin
pigmenTATion
The evolution of skin pigmentation in humans is related
to the evolution of hairlessness and enhanced sweating
abilities.2 The common ancestor of chimpanzees and
humans lived about six million years ago in equatorial
Africa, under conditions of high daytime temperatures
and high ultraviolet radiation (UVR). This common
ancestor probably had dark hair covering pale skin on
most of its body, the condition common to catarrhine
primates. The exposed skin on the face and on the dorsal
surfaces of the hands and feet had active melanocytes
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doi:10.4997/JRCPE.2012.114
© 2012 Royal College of Physicians of Edinburgh
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capable of producing melanin in response to sun exposure,
but unexposed skin remained unpigmented.3 Loss of
functional body hair occurred early in the evolution of the
genus Homo and was associated with the evolution of an
efficient whole-body cooling system based on eccrine
sweating.3–6 Because sweating is most effective in cooling
the body when there is less hair on the surface to slow
evaporation, the evolution of increased density of
eccrine sweat glands occurred pari passu with functional
nakedness. Naked skin is more vulnerable to environ-
mental influences, and that of humans differs from that
of close but hairier primate relatives in its greater water
resistance and resistance to abrasion.1 These differences
are due in part to genes related to the epidermal
proteins that contribute to the barrier functions of the
skin, the integrity of sweat glands and the delicate and
friable nature of body hair.7,8 Naked skin is also more
vulnerable to damage from solar radiation, including
UVR,9,10 and compensation for this came from evolution
of increased thickness of the epidermis, especially the
stratum corneum1,11 and of permanent protective eumelanin
pigmentation to prevent the most energetic and damaging
wavelengths of UVR from penetrating the body.3
Melanin pigments are complex polymers that have a
great capacity to absorb visible light, UVR, and ionising
radiation, and to neutralise the reactive oxygen species
(ROS) created when these agents interact with skin
cells.12,13 Eumelanin is the dominant form of melanin
found in human skin. It is intensely dark in its concentrated
form because it absorbs broadly in the spectrum of
visible light. Eumelanin polymers are intractably stable
even when they are bombarded by high-energy radiation
or ROS.14,15 Ultraviolet radiation damages DNA and the
constituents of cell membranes, causing a toxic cascade
of events that produces ROS and disrupts normal
chemical reactions in cells.16,17 These processes are greatly
attenuated by eumelanin, especially when it is present
close to the surface of the skin.18
evoluTion of pRoTeCTive eumelAnin
pigmenTATion undeR high uvR CondiTionS
Human skin pigmentation is highly correlated with
latitude,19–21 but is even more highly correlated (r2=-0.93)
with UVR, specifically the UV minimal erythemal dose or
UVMED.3,19,22,23 Skin pigmentation as measured by skin
reflectance is more strongly correlated with UVMED than
with any other single environmental factor.22
Many hypotheses have been advanced to account for the
evolution of dark pigmentation under high UVR regimes,
and these are reviewed at length elsewhere.2 In brief,
four major hypotheses proposed have described
advantages under natural selection accruing from: 1)
lowered mortality due to protection from sunburn and
skin cancer; 2) enhancing survival through camouflage in
poorly lit forested environments; 3) the antimicrobial
properties of eumelanin in pathogen-rich environments;
and 4) protection of folate metabolism against deficiencies
caused by high UVR. Our research has focused on the last
of these hypotheses.
The mostly deleterious effects of UVR on biological
systems are well known.16,24 Darkly pigmented, eumelanin-
rich skin protects against much of the damage to DNA
caused by UVR,25 and is associated with much lower
rates of skin cancer than lightly pigmented skin.26–29
Heavily pigmented melanocytes are able to resume
proliferation after ultraviolet B (UVB) irradiation faster
than lightly pigmented ones, and DNA from lightly
pigmented melanocytes is more badly damaged after
irradiation with increasing doses of UVB than is DNA
from heavily pigmented ones.17,27 By contrast, pheomelanin
in lightly pigmented skin appears to increase the risk of
oxidation stress in melanocytes. This, combined with the
limited ability of pheomelanin to absorb UVR, leads to
elevated skin cancer risk among light-skinned
individuals.26,30,31 The damaging effects of UVR on DNA
structure are widely recognised and are associated with
the initiation of skin cancers that mostly affect people
toward the end or after their reproductive careers.3,32
Cutaneous malignant melanoma is the only type with a
high incidence rate among people of reproductive age,
and overall incidence and mortality rates for melanoma
prior to the mid-twentieth century were very low (<5
per 100,000).33 Increases in the incidence of melanoma
in the last 50 years are the result of lightly pigmented
people being exposed to more intense or longer
periods of sunlight and UVR34 and experiencing more
painful sunburns35 because of migration to sunny places
or recreational sun-tanning, the so-called ‘vacation
effect’.36–38 These conditions were not typical of our
species prior to the twentieth century, when most
people moved very little during their lifetimes because
they lacked the means of transportation to do so. It is
difficult to quantify the relative importance of sunburns
and skin cancer, specifically melanoma, as selective
factors in the evolution of skin pigmentation, but
available epidemiological evidence indicates that
mortality of individuals of young reproductive age would
have been extremely low. Thus, reduction of sunburn
and melanoma risk probably contributed only to a
minor extent in the evolution of darkly pigmented skin.
The deleterious effects of UVR are not limited to DNA,
and it is probably the effects of UVR on folate
metabolism that have been of greatest importance in the
evolution of dark pigmentation in humans. The
importance of folate in human development and health
has been highlighted by studies demonstrating that
interdiction of cell proliferation because of folate
deficiency interferes with normal development, and
causes birth defects. The role of folate deficiency in
causing neural tube defects is now firmly established.39–42
Folate sufficiency is also necessary for maintenance of
The evolution of human skin colouration
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active spermatogenesis43,44 and in the formation of myelin
and the production of many neurotransmitters including
serotonin.45 Folate can only be obtained from foods such as
green leafy vegetables, citrus fruits and whole grains, or
from supplements of the synthetic form of the vitamin, folic
acid. Healthy levels of folate are difficult to maintain in the
body because natural food folates are unstable, suffer from
low bioavailability, and tend to break down when foods are
boiled or stored.46,47 Folate deficiencies can be caused by
insufficient intake of folate, improper absorption of the
vitamin from the gut, or the breakdown of folate or its main
serum form, 5-methylhydrofolate (5-MTHF) by alcohol or
UVR, in particular ultraviolet A (UVA).48–50
Ultraviolet radiation and the ROS generated by UVA
lower levels of folate 5-MTHF in the body because
competition for folate is intense when high UVR
simultaneously stimulates multiple folate-requiring
processes, including cell division, DNA repair, and
melanogenesis. Reduction of levels of folate and 5-MTHF
is particularly serious if the body’s demand for folate is
high – as in pregnancy – or if folate levels are already low
because of low intake. The essential connections between
folate metabolism and the evolution of dark skin
pigmentation are, firstly, the relationship between UVR
exposure and folate deficiency and, secondly, the
relationship between UVR-induced folate deficiency and
reduced fitness due to failures of normal embryogenesis
and spermatogenesis.3,51 High concentrations of melanin
significantly reduce folate destruction in vitro through
absorption and scattering of UVA.18 Research into the
UVR-mediated dynamics of folate metabolism is active
and continuing, especially in the laboratory of Johan
Moan of the University of Oslo.52
This evidence supports the theory that the major factor
contributing to the evolution of dark skin pigmentation
was the reduction of fitness brought about by UVR-
induced folate deficiency. Supporting evidence also
comes from epidemiological studies, which indicate
trends associating dark pigmentation with lower rates of
neural tube defects.53–55 Much research remains to be
done in this area, including further in vivo studies of folate
metabolism in humans subjected to UVR, and prospective
epidemiological studies which can further probe the
relationship that skin pigmentation and dietary intake of
folate have on rates of birth defects.
The importance of the maintenance of dark pigment-
ation under high UVR conditions has been underlined by
studies of the MC1R (melanocortin 1 receptor) locus,
one of several genes that contributes to skin, hair and
eye pigmentation. In modern Africans, this gene exhibits
no variation, but outside of Africa it is highly variable. The
absence of variation in African forms of the gene provides
evidence of strong positive selection or selective sweep
occurring around 1.2 million years ago56 and the maintenance
of a functional constraint on variation (purifying selection)
in Africa thereafter.57–59 The ancestral form of MC1R, along
with probable contributions from other pigmentation
genes (Shriver et al. 2003,60 Norton et al. 200761), makes
possible the production of large amounts of eumelanin in
the melanocytes of the skin and appears to have been so
effective in improving health and reproductive success
that people carrying it quickly outnumbered and replaced
those who did not.
evoluTion of depigmenTATion undeR
low uvR CondiTionS
The evidence that permanent dark skin pigmentation
evolved as protection against the deleterious effects of
UVR is overwhelming, but it does not explain the clinal
distribution of increasingly lightly pigmented skin outside of
the tropics. The strength of UVR, and of UVB in particular,
declines greatly north of the Tropic of Cancer and south of
the Tropic of Capricorn.22,62–64 Low levels of UVR are not
beneficial despite the fact that most UVR radiation is
harmful. This is because UVR has one overwhelmingly
positive action, photosynthesis of vitamin D3 (cholecalciferol)
in the skin by UVB.65–67 Vitamin D3 is made in the skin when
UVR penetrates the skin and is absorbed by
7-dehydrocholesterol (7-DHC) in the epidermis and
dermis to form pre-vitamin D3. This reaction only occurs in
the presence of wavelengths of 290–315 nm in the UVB
range, with peak conversion occurring at 295–297 nm, and
is dependent upon season and latitude, time of day, and on
the amount of pigment and thickness of the skin.68,69 The
reaction becomes less efficient with advancing adult age
because of age-dependent decline in 7-DHC in the skin.70,71
Circulating levels of pre-vitamin D3 are tightly controlled
because continued sunlight exposure causes the
photoisomerisation of pre-vitamin D3 to lumisterol and
tachysterol.72 Biologically active vitamin D3 is produced by
two successive hydroxylation steps in the liver and then in
the kidney to form the active metabolite 1,25(OH)2D3
(calcitriol). This is the form that acts as a steroid hormone
through binding to its specific intranuclear receptor, the
vitamin D-receptor (VDR), and subsequently modulates
the transcription of responsive genes such as that of
calcium binding protein, which regulates mineral ion
homeostasis.68,73 Vitamin D is also available in low quantities
in some foods, but vitamin D3 is found in physiologically
significant quantities in oily fish and liver.74 Dietary sources
of vitamin D must be converted into the biologically active
form via the same hydroxylation steps undergone by
cutaneously produced vitamin D3.
The most obvious function of vitamin D in humans is in
the building and maintenance of the bony skeleton. The
essential connection between vitamin D status and bone
health was established because vitamin D in the form of
cod liver oil was found to cure nutritional rickets.75
Vitamin D exerts its effects on bone indirectly through
regulation of absorption of calcium and phosphorus from
the gut, and directly modifies the activity of osteoblasts
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NG Jablonski
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and chondrocytes, and many other non-classical target
tissues.65,73 The presence of VDRs in tissues of the brain,
heart, stomach, pancreas, skin, gonads, in the activated T
and B lymphocytes of the immune system, and many sites
elsewhere in the body has heightened awareness of the
varied and important roles vitamin D plays in the body.
Chronic deficiencies in vitamin D have been associated
recently with breast, prostate, colon, ovarian and possibly
other cancers,76,77 and research in this area is extremely
active. Low vitamin D status is also linked to impaired
immune system activity, specifically Th1-mediated
autoimmunity and infectious immunity76 and to abnormal
development and function of the brain.77,78
The theory that light skin pigmentation evolved in order
to permit cutaneous vitamin D production under
conditions of reduced sunlight at high latitudes is an old
one that has considerable new, positive support from
clinical, nutritional, epidemiological, genetic and other
observational studies.3,81,82 The extent of vitamin D’s
importance to health is evidenced by the seriousness
and diversity of problems related to hypovitamosis D83–85
afflicting people throughout the life cycle. In the
musculoskeletal system, nutritional rickets in children is
now probably overshadowed by sarcopaenia and
osteomalacia in adults, the latter being silent afflictions
that can lead to increased morbidity from accidental
falls.86 And, as mentioned earlier, vitamin D deficiency
and insufficiency, especially beginning in infancy or
childhood, are associated with increased, but still not
rigorously quantified, risk of certain cancers, autoimmune
and infectious diseases. The global disease burden linked
to the vitamin D deficiencies caused by low UVR exposure
now exceeds that connected with high UVR exposure.87
The clinical and observational evidence discussed above
provides the setting for the probable action of natural
selection. Genetic evidence now strongly supports this.
Depigmentation is the result of positive selection in
humans inhabiting low UVR environments, and this has
been demonstrated in molecular genetic studies that
indicate that lightly pigmented skin phenotypes in
humans evolved multiple times and has been maintained
by purifying selection.88,89,61
Eumelanin competes with 7-DHC for UVB photons to
greatly slow production of pre-vitamin D3 to the extent
that people with lightly pigmented skin produce pre-
vitamin D3 in their skin at a rate 5–10 times faster than
those with darkly pigmented skin.3,74,90–96 This poses strict
geographic limits on the distribution of darkly pigmented
people outside of high UVB areas unless vitamin-D-rich
foods or vitamin D supplements are consumed.63 Thus,
skin pigmentation in modern humans is the result of the
action of two reciprocal clines working to promote the
UVB-induced photosynthesis of pre-vitamin D3 in the
skin on the one hand and prevent the damage caused by
UVB and UVA on the other.3,63
Members of the human lineage dispersed many times
independently into non-tropical latitudes, and evolved
depigmented phenotypes by numerous and different
genetically based means, some of which remain to be
illuminated. Habitation of middle latitudes between
approximately 23° and 46° with seasonally high loads of
UVB favored the evolution of partially depigmented
phenotypes capable of tanning.63 Among people of
European ancestry, genes related to tanning ability are
similar to those related to hair colour.97 The genetic
basis of skin pigmentation now is becoming better
understood, but considerable research remains to be
done on the relationships between skin, hair and eye
pigmentation genes,12,98 on the convergent evolution of
skin pigmentation phenotypes including those in the New
World,99 and on rates of skin pigmentation evolution.
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... Nevertheless, subpopulations of particular race groups do sometimes exhibit some genetic differences that relate to clinical outcomes (e.g., Nazha et al. 2017). One risk profile that could be argued to stereotypically face a particular race group because of a biological trait are particular kinds of skin cancer (Jablonski 2012a). It is by now mundane to point out facts such as people of paler skin are more susceptible to particular kinds of skin damage from UV rays that can affect them disproportionately in causing sunburn and thereby increasing their risk of developing certain kinds of skin cancer (Jablonski 2012a). ...
... One risk profile that could be argued to stereotypically face a particular race group because of a biological trait are particular kinds of skin cancer (Jablonski 2012a). It is by now mundane to point out facts such as people of paler skin are more susceptible to particular kinds of skin damage from UV rays that can affect them disproportionately in causing sunburn and thereby increasing their risk of developing certain kinds of skin cancer (Jablonski 2012a). Skin colour is a biological trait, and one that is interesting to biology and medicine given the differential outcomes it may have on health and reproductive success (Jablonski 2012b). ...
... It is by now mundane to point out facts such as people of paler skin are more susceptible to particular kinds of skin damage from UV rays that can affect them disproportionately in causing sunburn and thereby increasing their risk of developing certain kinds of skin cancer (Jablonski 2012a). Skin colour is a biological trait, and one that is interesting to biology and medicine given the differential outcomes it may have on health and reproductive success (Jablonski 2012b). Skin colour has been an evolutionarily significant trait as evidenced by its development through purifying selection (Jablonski 2012c). ...
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Full-text available
Lee McIntyre’s Respecting Truth chronicles contemporary challenges regarding the relationship between evidence, belief formation, and ideology. Discussion in his book focuses on the ‘politicization of knowledge’ and the purportedly growing public (and sometimes academic) tendency to choose to believe what is determined by prior ideological commitments rather than what is determined by evidence-based reasoning. In considering these issues, McIntyre posits that the claim “race is a myth” is founded on a political ideology rather than on support from scientific evidence. He contrasts this view with the argument that racially correlated biomedical outcomes for self-identified racial groups suggest that biological races are real. I explore how McIntyre’s framing of the claim “race is a myth” as fundamentally ideological results in him failing to engage with the arguments and evidence many constructionists and biological anti-realists put forward in support of their views. I also show how the biomedical evidence he thinks supports biological realism is unconvincing.
... This loss of body hair left the exposed skin vulnerable to UVR. Genomic evidence indicates that the loss of body hair in humans coincided with a gain of dark, melanin-rich skin, which is thought to be a protective, adaptive response to high UVR (Jablonski, 2012;Jablonski andChaplin, 2017, 2018;Lucock et al., 2017;Lucock et al., 2018b). ...
... This loss of body hair left the exposed skin vulnerable to UVR. Genomic evidence indicates that the loss of body hair in humans coincided with a gain of dark, melanin-rich skin, which is thought to be a protective, adaptive response to high UVR (Jablonski, 2012;Jablonski andChaplin, 2017, 2018;Lucock et al., 2017;Lucock et al., 2018b). ...
Article
Melanin synthesis is required for proper development and function of the visual system and for protection against ultraviolet radiation. Defects in melanin synthesis result in albinism, which is characterized by visual defects and increased skin cancer risk. Melanin is synthesized in pigment cells within specialized subcellular organelles called melanosomes. Some forms of albinism result from defects in melanosome maturation, but the underlying molecular mechanisms are incompletely understood. Melanosome maturation requires the trafficking of melanogenic cargoes to melanosome precursors and an increase in melanosome pH, thereby supporting activity of the enzyme tyrosinase to promote melanin synthesis. In this work, we investigate melanosome biogenesis and maturation in melanocytes derived from mouse models of two forms of albinism, (1) oculocutaneous albinism type 4 (OCA4) due to loss of function of SLC45A2, and (2) the Hermansky-Pudlak syndrome mouse model buff that has a missense mutation in VPS33A. (1) Here we show that SLC45A2, a putative sugar/proton symporter, localizes to melanosomes and increases organellar pH at its sites of localization. Further, we show that SLC45A2 likely functions at a later stage of melanosome maturation than the ion channel OCA2, which is also necessary to raise melanosomal pH and is defective in another subtype of OCA. Additionally, we show that a common SLC45A2-L374F variant associated with lighter pigmentation in humans is degraded more rapidly than the dark skin-associated L374 variant, indicating that decreased pigmentation reflects reduced proton export from melanosomes. (2) VPS33A, an SM protein that mediates fusion, is required in the endolysosomal and autophagosomal pathways, but whether it plays a direct role in melanosomal trafficking is unknown. Contrary to a previous report, we show that a VPS33A-D251E mutation in melan-bf cells does not prohibit pigmentation; instead, buff melanocytes cells contain enlarged, mature melanosomes despite partial mistrafficking of the mature melanosomal marker TYRP1. Replacement of wild-type VPS33A in wild-type melanocytes by VPS33A-D251E does not phenocopy buff melanocytes, suggesting that an additional mutation may be responsible for our observed buff phenotype. Our analyses of mouse albinism models have thus yielded significant insights into mechanisms of melanosome maturation.
... The teleological perspective, that it is normal for Blacks to require less vitamin D, implies that the biology of human populations living in sub-Saharan Africa somehow anticipated an eventual need to accommodate to lower 25(OH)D levels compared with Whites living in the north. But tropical environments have always provided consistent and substantial vitamin D-generating ultraviolet light, for which the skin color of Blacks is, and was appropriately suited [14,15]. Highly credible data on traditionally living Africans provide a reasonable estimate of the vitamin D nutritional status of early humans. ...
... Rickets can misshape a girl's pelvis to a fatal degree [29], and a healthy pelvis was the determining feature that drove natural selection among human populations as they migrated into temperate latitudes (Fig. 1). Without rickets to drive selection for lighter skin color, the entire human population would almost certainly have remained deeply pigmented, with type 5 or 6 skin [14]. ...
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Full-text available
The vitamin D paradox relates to the lower risk of osteoporosis in people of sub-Saharan African ancestry (Blacks) compared with people of European ancestry (Whites). The paradox implies that for bone health, Blacks require less vitamin D and calcium than Whites do. Why should populations that migrated northward out of Africa have ended up needing more vitamin D than tropical Blacks? Human skin color became lighter away from the tropics to permit greater skin penetration of the UVB light that generates vitamin D. Lack of vitamin D impairs intestinal calcium absorption and limits the amount of calcium that can deposit into the protein matrix of bone, causing rickets or osteomalacia. These can cause cephalopelvic disproportion and death in childbirth. Whiter skin was more fit for reproduction in UV-light restricted environments, but natural selection was also driven by the phenotype of bone per se. Bone formation starts with the deposition of bone-matrix proteins. Mineralization of the matrix happens more slowly, and it stiffens bone. If vitamin D and/or calcium supplies are marginal, larger bones will not be as fully mineralized as smaller bones. For the same amount of mineral, unmineralized or partially mineralized bone is more easily deformed than fully mineralized bone. The evidence leads to the hypothesis that to minimize the soft bone that causes pelvic deformation, a decrease in amount of bone, along with more rapid mineralization of osteoid improved reproductive fitness in Whites. Adaptation of bone biology for reproductive fitness in response to the environmental stress of limited availability of vitamin D and calcium came at the cost of greater risk of osteoporosis later in life.
... Ultraviolet B (UVB) radiation in the skin converts 7-dehydrocholesterol to cholecalciferol which is metabolized further to active 1α,25(OH)2D3. However, UVB radiation also degrades folic acid, which is also essential, and during evolution and adaptation a strong inverse correlation between skin pigmentation and latitude has arisen [18,19]. In more recent human history relatively rapid dispersion and lifestyle changes have resulted in many individuals living in an UVB environment which differ from those of their ancestors. ...
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Background African American (AA) prostate cancer (PCa) appears uniquely sensitive to 1α,25(OH) 2 D 3 signaling, compared to European American (EA) PCa, but the extent and impact of vitamin D receptor genomic functions remain poorly defined. Results A panel of EA and AA prostate epithelial cells (EA: HPr1-AR, LNCaP, AA: RC43N, RC43T, RC77N, RC77T) were analyzed with RIME to reveal the cell-specific composition of the VDR- complex. 1α,25(OH) 2 D 3 -dependent ATAC-Seq revealed the greatest impact on nucleosome positioning in RC43N and RC43T, with gain of nucleosome-free at enhancer regions. VDR ChIP-Seq identified stronger and more frequent VDR binding in RC43N and RC43T that was enriched for a larger and distinct motif repertoire, than EA cells. VDR binding significantly overlapped with core circadian rhythm transcription factors in AA cell line models. RNA-Seq also revealed significantly stronger 1α,25(OH) 2 D 3 dependent VDR transcriptional responses enriched for circadian rhythm and inflammation networks in AA cells. Whilst RC43N was most responsive, RC43T displayed distorted responses. Significantly reduced BAZ1A/SMARCA5 in AA PCa samples was identified, and restored BAZ1A expression uniquely and significantly increased 1 α ,25(OH) 2 D 3 -regulated VDR targets in AA cells. These VDR- dependent cistrome-annotated genes were also uniquely and most significantly identified in three cohorts of AA PCa patients. Conclusion These data suggest VDR transcriptional control in the prostate is more potent and dynamic in AA men, and primed to govern inflammatory and circadian pathways. Reduced BAZ1A/SMARCA5 expression and/or reduced environmentally-regulated serum vitamin D 3 levels suppress these actions. Therefore, the VDR axis lies at the cross-roads of biopsychosocial processes including stress responses, access to quality early detection and treatment, social determinants and that collectively contribute to PCa health disparities.
... UVB has important activity in human physiology [19,20]. High irradiation and time exposure of UV can conduce to cancer development as well as its prevention [21]. ...
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Ultraviolet (UV) exposure has been linked to skin damage and carcinogenesis, but recently UVB has been proposed as a therapeutic approach for cancer. Herein, we investigated the cellular and molecular effects of UVB in immortal and tumorigenic HPV positive and negative cells. Cells were irradiated with 220.5 to 1102.5 J/m2 of UVB and cell proliferation was evaluated by crystal violet, while cell cycle arrest and apoptosis analysis were performed through flow cytometry. UVB effect on cells was recorded at 661.5 J/m2 and it was exacerbated at 1102.5 J/m2. All cell lines were affected by proliferation inhibition, cell cycle ablation and apoptosis induction, with different degrees depending on tumorigenesis level or HPV type. Analysis of the well-known UV-responsive p53, E2F1 and microtubules system proteins was performed in SiHa cells in response to UVB through Western-blotting assays. E2F1 and the Microtubule-associated protein 2 (MAP2) expression decrease correlated with cellular processes alteration while p53 and Microtubule-associated Protein 1S (MAP1S) expression switch was observed since 882 J/m2, suggesting they were required under more severe cellular damage. However, expression transition of α-Tubulin3C and β-Tubulin was abruptly noticed until 1102.5 J/m2 and particularly, γ-Tubulin protein expression remained without alteration. This study provides insights into the effect of UVB in cervical cancer cell lines.
... Darker skin contains more melanin which provides greater protection against UVR and is one of the major factors determining skin pigmentation [48]. Consequently, higher levels of melanin and thus darker skin has been selected for in populations near the equator that are exposed to higher UVR [23,24]. However, modern migrations have allowed people of fairer skin to live in geographic areas with high UVR that they are not fully adapted too. ...
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Full-text available
United States will soon be a nation of color; however, much of our knowledge of normal skin disease, and treatment thereof is based on white skin. We and others have attempted to elucidate any potential differences and advantages/disadvantages in skin function that have emerged during homo sapiens evolution post major migration from Eastern Africa. We investigated differences in one stratum corneum function by examining transepidermal water loss (TEWL) measurements in skin of color compared to Caucasian skin. TEWL, a measure of insensible water loss through stratum corneum, plays a major role in human survival. A comprehensive literature search was conducted to procure relevant papers that measured baseline TEWL in skin of color and Caucasian skin. The data show wide contradiction in results for all skin of color groups and white skin and, therefore, no conclusion can be made based on this question. We suggest this variation may be due to experimental confounding variables that impact TEWL quantification, such as anatomic site and sample size subject to further analysis and focus.
... Інші ж вбачають у дефіциті вітаміну Д першопричину інсулінорезистентності і адипо-зопатіїї. Доведено, що вітамін Д може впливати на чутливість тканин до інсуліну за допомогою двох механізмів: безпосередньо стимулюючи експресію рецепторів інсуліну в клітинах та за рахунок збільшення рівня внутрішньоклітинного кальцію, який необхідний для інсулін-послідовних внутрішньоклітинних процесів в інсулінозалежних тканинах [28][29][30]. ...
... However, other studies have shown the contrary, with levels higher in northern than in southern Europe [45,62]. This may partly be explained by skin pigmentation [29,30,54,55]. People in warmer climates tend to have darker skin pigmen tation, which may affect their capacity to synthesise vitamin D. White women in South England had median 25(OH)D levels of 62.5 nmol/l in summer and 39.9 nmol/l in winter, while in Asian women living in the same geographical region the median levels were considerably lower at 24.9 nmol/l and 16.9 nmol/l respectively [38]. ...
Article
Full-text available
In this study, we investigated the remains of an individual that were recovered during cleansing work of the Church of St Hripsime. Macroscopic and X-Ray inspections yielded pathological criteria which indicated osteomalacic origin. The findings of the study suggest that the individual who lived in the Late Medieval period may have gone through multiple episodes of vitamin D deficiency. Vitamin D deficiency as an effect of deficient exposure to sunlight (in particular, in rural individuals who lived in underground houses) and nourishment deficiency could be described as the main causes leading to osteomalacia in Armenia.
Chapter
Solar radiation comprises a continuum of wavelengths including ultraviolet radiation (UVR; 280–400 nm), visible light (VL; 400–760 nm), and infrared radiation (IR; 760 nm – 1 mm) (Sklar et al. Photochem Photobiol Sci 12(1):54–64, 2013). This chapter describes the molecular and clinical consequences of exposure to UVR and VL across different skin types. It also provides a review of the more common idiopathic photodermatoses, photosensitivity reactions to systemic medications and dermatoses, which are aggravated by sunlight.
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Full-text available
Lee McIntyre’s Respecting Truth chronicles the contemporary challenges regarding the relationship amongst evidence, belief formation and ideology. The discussion in his book focusses on the ‘politicisation of knowledge’ and the purportedly growing public (and sometimes academic) tendency to choose to believe what is determined by prior ideological commitments rather than what is determined by evidence-based reasoning. In considering these issues, McIntyre posits that the claim “race is a myth” is founded on a political ideology rather than on support from scientific evidence. He contrasts this view with the argument that racially correlated biomedical outcomes for self-identified racial groups suggest that biological races are real. I explore how McIntyre’s framing of the claim “race is a myth” as fundamentally ideological results in him failing to engage with the arguments and evidence many constructionists and biological anti-realists put forward in support of their views. I also show how the biomedical evidence he thinks supports biological realism is unconvincing.
Chapter
Models of atmospheric transmission allow the estimation of spectral and biologically-weighted ultraviolet (UV) radiation reaching the Earth’s surface. The theory of radiative transfer is well established, but information about the atmosphere (e.g., ozone profiles, cloud morphology), which is required as input to the models, is often incomplete. Still, model sensitivity studies provide many useful insights that, when combined with measurements, give us a more complete understanding of the complex UV environment.
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A total of 1633 cases of neural tube defects were analysed, registered between 1980 and 1983 in liveborn and stillborn babies and in fetuses aborted as a result of prenatal diagnosis of malformation in 16 EUROCAT Registries (total births =766 603). A clear geographical pattern was observed. The highest neural tube defect (NTD) rates were seen in Dublin (Ireland), Belfast (UK) and Glasgow (UK) with 40 cases per 10 000 births and in these centres there was a significant decrease in prevalence over the years. In Galway (Ireland) and Liverpool (UK), the rates were approximately 20 cases per 10 000 births, the rate decreasing over years in Liverpool. In the registries situated in continental Europe, the prevalence varied between 6 and 13 cases per 10 000 births and there was no apparent change in the prevalence with time. The spina bifida/anencephaly ratio and the male proportion among the NTD cases were both lower in the British Istes than in continental Europe. Cases of prenatal diagnosis of NTD resulting in termination of pregnancy formed 19% of the total NTD cases, this proportion increasing over years. A large variation between centres was seen in the effectiveness of prenatal screening for NTD.
Article
Until the 1990s, the criterion for appropriate vitamin D nutrition was simply the absence of overt rickets or osteomalacia (Blumberg et al., 1963). Now, circulating 25-hydroxyvitamin D [25(OH)D] concentrations are the appropriate measure of vitamin D nutritional status (Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, 1997). It is now possible to make more quantitative comparisons of vitamin D nutrition through primate and human evolution, and to draw inferences about how differences in vitamin D nutrition may have affected susceptibility to disease.