AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 139:447–450 (2009)

* News and Views
The Evolution of Light Skin Color:
Role of Vitamin D Disputed

Ashley H. Robins*
Department of Medicine,
Division of Pharmacology,
University of Cape Town Medical School,
Observatory, South Africa 7925

Vitamin D is essential for calcium and phosphorus homeostasis
and for the growth, development, and structural
integrity of the skeleton. Over 90% of the body’s
requirements for vitamin D derive from cutaneous photosynthesis,
with dietary sources accounting for the remainder.
Ultraviolet-B radiation (UVB) penetrates the
epidermis where it photolyses 7-dehydrocholesterol to
previtamin D3, which is then converted to vitamin D3.
The latter is translocated to the circulation via the dermal
vasculature; it is hydroxylated (enzymatically) in
the liver to 25-hydroxyvitamin D (25-OHD) and then in
the kidneys to 1,25-dihydroxyvitamin D (1,25-(OH)2D)
(Holick, 2007). Although the serum 25-OHD concentration
gives the best index of an individual’s vitamin D
status, 1,25-(OH)2D is the most active form biologically
in mediating the effects on intestine (calcium absorption)
and bone. The serum concentration of 1,25-(OH)2D is
tightly regulated and is not ordinarily dependent on sun
exposure or diet.


Severe vitamin D deficiency causes nutritional rickets
in children and adolescents, and osteomalacia and
osteoporosis in adults. Rickets is caused by defective
mineralization of the collagen matrix in newly formed
osteoid tissue, with resultant bone softening. It is characterized
by crippling deformities (notably bowing of
the lower limb bones and narrowing of the pelvic outlet),
muscle weakness, and, in neonates born to vitamin
D-deficient mothers, by potentially fatal hypocalcaemia
(manifesting as convulsions, heart failure) (Wharton
and Bishop, 2003; Holick, 2006b).
Rickets is a sunlight deprivation disease, which
emerged on an epidemic scale during the industrial revolution,
when cities in Europe and North America were
enveloped in a perpetual twilightlike haze of coal smoke.
By the end of the 19th century, up to 90% of children in
these centers suffered from rickets.

SKIN DEPIGMENTATION: THE VITAMIN D
HYPOTHESIS

Originated by Murray (1934), the vitamin D hypothesis
was revived and popularized by Loomis (1967),
and, more recently, refined by Jablonski and Chaplin
(2000) with the application of quantitative UVB data.
It is based on the observation that the skin color of
the world’s indigenous peoples follows a clinical distribution:
the darkest populations inhabit the equatorial
and tropical belt; the most pale-skinned the regions
above 508N; and those of intermediate pigmentation
the middle latitudes. Skin reflectances exhibit a highpositive
and high-negative correlation with latitude
and UVB measurements, respectively (Jablonski and
Chaplin, 2000; Parra, 2007), i.e., higher reflectances
(lighter skin color) are strongly associated with higher
latitudes and lower UVB. At high latitudes, UVB intensity
is reduced throughout the year but profoundly
so in the winter months. At this latitude, solar elevation
is low and UVB has to travel a more oblique and
longer course to the earth, thereby being subjected to
increased scattering and ozone absorption in the upper
atmosphere.

Anatomically modern, and presumably deeply pigmented,
humans (Homo sapiens) arose in sub-Saharan
Africa 100,000–150,000 years ago. Some of them left
the continent and advanced northward, arriving in
Europe 35,000–40,000 years ago. The hypothesis proposes
that as these northbound migrants proceeded to
higher latitudes they underwent progressive depigmentation
until they ultimately attained the light-colored
appearance typical of contemporary northern Europeans.
This pigmentary transformation was a physiological
adaptation to the less intense UVB at these
latitudes. The melanin of dark-skinned individuals
would have impeded the epidermal transmission of an
already attenuated UVB and inhibited the synthesis of
previtamin D3 and vitamin D3. (Melanin is an excellent
sunscreen.) The resultant vitamin D deficiency would
have produced rickets, which, with its deformities and
muscle weakness, would have seriously handicapped
mobility and the ability to forage for food. In the
female, a contacted pelvis would have led to obstructed
labor and death of mother and baby (in the absence of
Caesarean section); and even if the infant was successfully
delivered, there was the danger of brain damage
or life-threatening hypocalcaemia. There is little doubt
that in the hostile environment of late-Pleistocene
Europe rickets would have imperiled reproductive fitness
and survival. Natural selection would have favored
the genes for light skin color and promoted depigmentation.
Conversely, in the topics (with their intense and
perennial UVB), selection pressures would have driven
the evolution of dark pigmentation owing to the remarkable
photoprotective properties of melanin (Robins,
1991; Jablonski and Chaplin, 2000).

WHY THE VITAMIN D HYPOTHESIS IS FLAWED

The hypothesis was initially predicated on data from
the 1920s and 1930s, which showed that blacks in the United States had a twofold to threefold increase over
whites in the prevalence of clinical rickets (Robins, 1991).
Recent surveys also record substantially lower serum 25-
OHD levels, and a markedly higher occurrence of vitamin
D deficiency, in African Americans compared with white
Americans (Looker et al., 2002; Nesby-O’Dell et al., 2002;
Gordon et al., 2004). Exposure in vitro of isolated skin
specimens and in vivo of human volunteers to UVB
showed that hypopigmented (Caucasian) skin was five to
10 times more efficient at forming vitamin D3 than
melanized (African American) skin (Chen et al., 2007).
Moreover, the UVB doses that dramatically raised serum
vitamin D levels in whites by up to 60-fold had no significant
effect on heavily pigmented African Americans
(Clemens et al., 1982). At these doses, therefore, deep
melanin pigment reduced cutaneous synthesis of vitamin
D3 by as much as 99%, the equivalent of a sunscreen with
a sun protection factor of 15 (Holick, 2006a).

The hypothesis is weakened, however, because this epidermal
melanin barrier is not absolute; it is surmountable
provided that the UVB doses or the irradiation exposure
times are increased according to the degree of pigmentation.
For example, a sixfold increase in either of these variables
brought vitamin D production in highly melanized
skin in line with that of lightly pigmented skin (Holick
et al., 1981; Clemens et al., 1982). Furthermore, single or
repeated whole-body UVB (artificially administered)
evoked similar increases in 25-OHD concentrations in
Asian, black, and white subjects (Stamp, 1975; Lo et al.,
1986; Brazerol et al., 1988). These experiments with
simulated sunlight were confirmed in the natural setting
by Ellis et al. (1977), who noted that groups of Asian,
West Indian, and European adolescents with vitamin D
deficiency and living in England showed marked and comparable
increases respectively in serum 25-OHD concentrations
during the spring and summer months (March to
October). The conclusion from all of these studies is that
there is an intrinsic capacity for vitamin D3 synthesis
regardless of skin color, provided that UVB exposure is
adequate.

Skin pigmentation is not a primary factor in causing
rickets, as exemplified in Britain where Asian immigrants
and their families were far more susceptible to
vitamin D deficiency and rickets than the more deeply
pigmented West Indians (African Caribbeans) (Ellis
et al., 1976; Ford et al., 1976). A survey in the high-latitude
city of Glasgow, Scotland (568N), found no cases of
florid rickets in 100 African children, 100 Chinese children,
or 100 Scottish children, but there were 10 cases
in 200 Asian children (Goel et al., 1976). (The problem of
Asian rickets and osteomalacia in Britain is probably
due to multiple factors, e.g., diet, genetic predisposition,
socio-cultural attitudes to clothing, and sun exposure.)

Webb et al. (1988) demonstrated that irrespective of
skin pigmentation there was no photolysis of 7-DHC to
previtamin D3 in Boston (428N) and Edmonton (528N)
from November to February (inclusive) and from October
to March, respectively. This dormancy of vitamin D production
for up to 6 months at these latitudes is offset by
the synthesis, storage, and accrual of vitamin D3 during
sun exposure in summer. Mawer et al. (1972) established
that vitamin D and 25-OHD are stored for extended
periods in body tissues, predominantly fat. In their
vitamin D-deficient patients, a large intravenous dose of
radioactive vitamin D3 was rapidly cleared from the circulation
and, together with its 25-OHD metabolite, was
distributed to the depleted storage sites. (These findings
of Mawer et al. were misinterpreted by Jablonski and
Chaplin (2000: 78) to imply that deficient subjects had a
reduced potential for vitamin D storage.)

This cumulative storage property of vitamin D was
neatly illustrated by a study of gardeners in Dundee,
Scotland (568N), who worked outdoors throughout the
year. They not only had considerably higher serum
25-OHD levels than indoor workers, but these levels
increased from July (the month of maximum UVB exposure)
until they peaked in November and December
(when UVB was in sharp decline) (Devgun et al.,
1981). At high latitudes, therefore, where vitamin D3
photosynthesis ceases during the winter months, the
body maintains an acceptable vitamin D status on a
year-round basis by mobilizing reservoirs in fat and
other tissues that have been built up during the
summer (Webb and Holick, 1988).

The question arises as to what extent early Homo
sapiens at latitudes above 408N would have been
vulnerable to rickets. Historically, rickets is a product of
urbanization, industrialization, and civilization; it was
rampant in the smog-ridden cities of Europe and North
America during the industrial revolution but conspicuously
absent in the surrounding rural areas with their
clean air and outdoor lifestyles. Sporadic cases of rickets
were described in European skeletal material dating from
the Neolithic period until medieval times, but its prevalence
was very low; it occurred in about one percent of
skeletons from Swedish and Danish cemeteries (AD 1100–
1550), and there was no evidence of it in Anglo-Saxon
remains from East Anglia. In pre-Columbian North and
South America, it hardly existed (Wells, 1975).
Where instances of rickets occurred in preindustrial
times, these were most likely due to sunlight deprivation.
Ortner and Mays (1998) identified eight cases of
active rickets (out of a sample of 687 excavated skeletons)
from a churchyard in North Yorkshire, England,
dating to the Middle Ages.

All were infants aged from
3 to 18 months, and it was conjectured that these children
had been sickly and thus kept indoors in dark,
smoky houses. An examination of graveyard material
from medieval cities in Hungary showed an increase in
the frequency of rickets from 0.7% to 2.5% from the 10th
to the 13th centuries AD, respectively (Wells, 1975),
probably because of the proliferation of windowless
houses during that period.

The strongest case against the hypothesis is that the
smoky and rickets-producing urban environments of the
industrial revolution (and even earlier) were diametrically
opposed to the sparsely inhabited, open-air, and
unpolluted landscapes in which Upper Paleolithic Europeans
lived and roamed. These individuals would have
spent their daylight hours during late spring and
summer under open skies and, partly clad in animal
skins, they would have exposed a relatively large body
area to an intensity of UVB that was optimal for cutaneous
vitamin D3 photosynthesis. This quality and quantity
of UVB (possibly enhanced during glacial periods by
reflectivity from snow and ice), maintained daily for 4 or
5 months, would have amply fulfilled their physiological
vitamin D requirements for the rest of the year.
The decisive question though is whether early, deeply
pigmented Homo sapiens in northern Europe would have
benefited from the ambient summer UVB or whether
they would have been deprived of vitamin D by virtue of
melanin blockade. As discussed earlier, dark-skinned
persons are endowed with the same capability to
448 A.H. ROBINS

American Journal of Physical Anthropology
manufacture vitamin D3 as their lighter counterparts.
Estimates are that fair-skinned people living in North
America or Europe require only 5–10 min sun exposure
of the arms and legs between 10:00 and 15:00 three
times a week (except winter) to prevent vitamin D insufficiency
(Webb and Holick, 1988; Holick, 2006a; Holick,
2007). If we assume that very dark individuals at latitudes
above 508 need 10–20 times that duration of exposure to
override the melanin barrier, then this would equate to
about 1–3 h thrice weekly, a quota that would have been
achievable within 1 or 2 days of the hunter-gatherer life of
Upper Paleolithic Europeans. It is highly improbable that
rickets ever emerged in that setting. Thus, vitamin D status
could not have constituted the fitness differential
between lightly pigmented and darkly pigmented individuals
at high latitudes that favored the evolutionary selection
of the former. There was no risk of vitamin D toxicity
from prolonged UVB exposure, as mistakenly contemplated
by Loomis (1967), because excessive sunlight
degrades previtamin D3 and vitamin D3 into inert photoproducts
(Holick et al., 1981; Webb and Holick, 1988).
In recent times, there has been a resurgence of vitamin
D insufficiency and deficiency, not only in high-latitude
countries but in some of the sunniest regions in the
world (Holick, 2006b). The explanation is that presentday
populations receive inadequate solar insolation for
various reasons: indoor working and living conditions,
deliberate sun avoidance, and the wearing of concealing
clothing.

A survey conducted across three regions of Australia of
differing latitudes (278S, 388S, and 438S) noted the high
prevalence of vitamin D insufficiency but found, unexpectedly,
that season and latitude together accounted for less
than 20% of the variation in serum 25-OHD levels (van
der Mei et al., 2007). This indicated that interindividual
differences in sun-related behavior (duration of exposure,
amount of clothing) vastly outweighed the more obvious
seasonal and latitudinal differences in determining vitamin
D status. Similarly, the marked black–white disparity
in the United States in the occurrence of vitamin D
inadequacy is not predominantly a consequence of skin
color but rather a reflection of behavior or circumstances
that restrict sun exposure. An example is a study in Cincinnati
(398N) where black breast-fed infants had strikingly
lower 25-OHD levels compared with their white
counterparts: the former were confined indoors and had
negligible solar exposure, whereas the latter had regular
outings in the sunshine (Specker et al., 1985).

Socioeconomic circumstances largely account for the
chronic sunlight deprivation experienced by many black
babies. Compared with their white compatriots, African-
American mothers tend to be financially and educationally
disadvantaged and to live in crowded neighborhoods. Consequently,
they lack the leisure time, the amenities (ready
access to gardens and parks), and the resources (baby carriages
and cars) to take their infants on regular outdoor
excursions in spring and summer, thereby maximizing vitamin
D production. It is not surprising that, where cases of
rickets have been reported in the United States in recent
times, these have affected predominantly black children.
The above arguments do not negate the effect of melanin
pigmentation on vitamin D3 production, but they
shift its influence from a primary to a secondary role,
i.e., where UVB exposure is already marginal, a darkskin
color will accentuate the problem and contribute
significantly to vitamin D deficiency.

It is crucial to recognize that the overwhelming majority
of people worldwide with vitamin D insufficiency and deficiency
have the subclinical form; they are apparently
healthy and free of skeletal deformities (Gordon et al.,
2004; Rockell et al., 2005; Holick, 2006b). A survey of 232
black (East African) immigrant children living in Melbourne,
Australia (378S), found that although vitamin D
insufficiency and the more severe vitamin D deficiency
occurred in 81% and 44%, respectively, none showed clinical
signs of rickets (McGillivray et al., 2007). In the event that
early, dark-skinned humans at high latitudes did develop
vitamin D deficiency, it is highly probable that they would
have remained asymptomatic. In an evolutionary context,
vitamin D deficit per se would not have exerted a negative
selective action against dark pigmentation unless it translated
into florid rickets, with the attendant deformities and
disabilities that curtailed reproductive fitness and survival.
There is another perspective that undermines the hypothesis.
Matsuoka et al. (1991) demonstrated that after
single-dose, whole-body UVB exposure black subjects
had distinctly lower serum vitamin D3 levels than
whites; but differences between the two groups narrowed
after liver hydroxylation to 25-OHD and disappeared after
kidney hydroxylation to 1,25-(OH)2D. These findings
suggest that there is a compensatory mechanism
whereby, in the presence of vitamin D3 suppression by
melanin, the liver and kidney hydroxylating enzymes
are activated in tandem to ensure that the concentration
of the biologically active 1,25-(OH)2D metabolite is normalized
and kept constant regardless of ethnic pigmentation
(Matsuoka et al., 1991, 1995).

Homeostatic control of bone metabolism and function is
mediated by a complex series of feedback interactions
between vitamin D, calcium, phosphorus, and parathyroid
hormone (one action of which is to enhance the enzymatic
conversion of 25-OHD to 1,25-(OH)2D) (Holick, 2007).
Blacks have optimally modulated this vitamin D endocrine
system to protect the skeleton from the adverse consequences
of reduced vitamin D3 synthesis (Looker et al.,
2002; Harris, 2006). These adaptive processes fail in
extreme vitamin D deficiency (and possibly also in the elderly),
but they are decidedly effective in the moderate
vitamin D deficit state that affects nearly half of African
Americans. The latter, for example, have a lower prevalence
of osteoporosis, a lower incidence of fractures and a
higher bone mineral density than white Americans, who
generally exhibit a much more favorable vitamin D status
(Henry and Eastell, 2000; Hannan et al., 2008).

In the past decade, there has been an increasing focus
on the nonskeletal functions of vitamin D. The biologically
active metabolite 1,25-(OH)2D is produced locally in
organs such as breast, colon, and prostate, where it is
believed to regulate cellular growth and potentially to inhibit
cancer development and progression. It is active in
the immune system (macrocytes and lymphocytes) and it
may promote immunity against infectious diseases such
as tuberculosis. It is also claimed to prevent conditions
such as cardiovascular disease, hypertension, diabetes,
and rheumatoid arthritis (Holick 2006a, 2007). Much of
this work is still speculative and experimental, and the
evidence linking vitamin D to the various disease states
is inconsistent and dogged by confounding variables
(Wolpowitz and Gilchrest, 2006).

Proponents of the vitamin
D hypothesis have not yet been able to structure
these ideas into a specific evolutionary formulation;
indeed many of the diseases mentioned above manifest
LIGHT SKIN COLOR AND VITAMIN D 449
American Journal of Physical Anthropology
later in life (after the reproductive period) and so have
negligible fitness consequences. Infectious diseases tend
to occur within high-density populations and not within
small and scattered nomadic groups such as those that
characterized Upper Paleolithic humans. But, since the
thrust of this work has been to exclude vitamin D deficiency
in these early Europeans, neither the skeletal nor
the nonskeletal effects of such deficiency would pertain
to the skin color debate.

CONCLUSION

The vitamin D hypothesis has gained widespread acceptance
as the standard explanation for light skin color
in northern Europe. It has received strong endorsement
in two recent and reputable review publications
(Jablonski, 2004; Parra, 2007), and it threatens to become
enshrined in evolutionary lore. Although I have previously
advanced detailed counter-arguments (Robins,
1991), in this work I have reformulated and updated the
opposing position in the hope that it will evoke discussion
and reassessment. I believe that this hypothesis, which
superficially appears elegant and convincing, is invalidated
by current research. Alternative hypotheses deserve
to be revisited but, more important, new ideas need to be
sought to unravel the enigma of human depigmentation.

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