Skin Color •Functions in many ways
–Thermoregulation
–Protection from physical and chemical injury
Human Pigmentation and Adaptation
–Protection from invasion by microorganisms
–Manufactures essential nutrient

Skin Color Measurement of Skin Color
•As one of the most conspicuous human •By the latter half of the nineteenth century, while
anthropologists still had no clear idea of the
polytypic variations, skin color has underlying causes of pigmentation, they began to
probably attracted more scholarly attention devise measurement techniques to use skin color
than any other aspect of human variability in racial classification
•Skin color has served as a primary feature •Broca established a 34 tone scale, which was
simplified by his student Topinard
in most systems of racial classification
•These techniques were used into the 20th century
until the introduction of the reflectance
spectrophotometer in the early 1950s

Reflectance Spectrophotometry
Reflectance Spectrophotometer
•A Reflectance Spectrophotometer shines a
light of a specific wave length, using a
filter, and measures the intensity of light
reflected by the skin
–The technique involves alcohol wash of the
skin on the inner upper arm
•allow time for local circulation to return to normal
•shine light and measure reflectance
Skin color is Continuous:
Mean (dot) and s.d. (bar) of skin
color, for 22 populations
Biological Determinants
of Skin Color
•The pigments Carotene, Hemoglobin and
Carotene Hemoglobin,
Melanin are involved in skin color
•Carotene, the least common skin pigment
results in a yellowing of skin
–Results primarily from the over-consumption of
carotene containing foods (like carrots)
–This pigment is significant almost exclusively
in pathological or abnormal skin coloration

Hemoglobin
Melanin
•Hemoglobin is the complex molecule
responsible for transport of oxygen throughout •The primary determinant of variability in
our bodies human skin color is the amount, density,
–It is the primary protein constituent of Red Blood and distribution of the pigment melanin
Cells •Melanin has a dark brown/purple/black
•Oxygenated hemoglobin has a reddish hue color that is intensified by denser
–Produces a pinkish tint to lightly pigmented skin
compaction of the melanin granules in the
•Deoxygenated hemoglobin has a purplish color
–Produces the bluish tint to lightly pigmented skin that is
cells of the upper layers of the skin
characteristic of oxygen deprivation and suffocation

Structure of the Epidermis
Melanocytes and Skin Color
Asian
Solomon Islanders

Native American
Australian Aborigine
African American

s
e an
ro p
Eu
Layers of the Epidermis
Layers of the Epidermis
•The stratum basale consists of columnar cells, the •The stratum granulosum consists of several
keratinocytes with about 10% of the cells layers of flattened polyhedral cells with
comprising melanocytes their long axis parallel to the skin surface
–This is the germinal level of the skin which gives rise to –Cytoplasm contains keratohylin
the outer layers of cells and the melanin granules that
pigment them –As the cells increase in size they die out
•This is also where 90% of Vitamin D synthesis takes place •The stratum corneum is composed of a
•The stratum spinosum consists of several layers varying number of layers of dead
of irregular polyhedral cells (keratinocytes) keratinized cells fused to one another except
flattened on their edges
for the outer edge where flaking takes place

Melanocytes synthesize melanin which is combined into Melanin Metabolism
granules and injected into the surrounding keratinocytes
Tyrosinase Tyrosinase
Tyrosine Dopa Dopaquinone

= contributes to
copolymerization

5,6-Dihydroxyindole- Leucodopachrome
2-carboxylic acid 5-S-Cysteinyldopa

Dopachrome
5-S-Cysteinyldopa-
quinone
5,6-Dihydroxyindole

Benzothiazine
Indole-5, Intermediaries
6-quinone

Eumelanin +protein Eumelanosome Phaeomelanosome protein+ Phaeomelanin

DOPA (path to melanin)
Tyrosinase
In dark skin, melanosomes accumulate Diet
P-hydroxyphenylpyruvic oxidase
eumelanin and remain as single particles, Phenylalanine
5%
Tyrosine
pathways
Hydroxyphenylpyruvic Acid
Thyroxine
Iodination of tyrosine is the precursor
while in lighter skins they contain increasing 95%
Diet Phenylalanine
amounts of phaeomelanin and cluster in Tyrosine
Phenylalanine hydroxylase
membrane bound organelles, lysosomes hydroxylase
DOPA
Phenylpyruvic acid (dihydroxyphenylalanine)

Dopamine

• Neuromelanin reduces
Noradrenaline Adrenaline oxidative damage via the
inactivation of damaging
free radicals
• Neuromelanin also plays
Neuromelanin a role in iron chelation
Melanin Metabolism
Phenylalanine Metabolism Tyrosine
Tyrosinase
Dopa
Tyrosinase
Dopaquinone

= contributes to
• Pleiotropy: A situation whereby several seemingly unrelated copolymerization
phenotypic effects are Influenced by the action of a single gene Leucodopachrome
5,6-Dihydroxyindole-
– Phenylalanine hydroxylase insufficiency causes phyenlketonuria: PKU 5-S-Cysteinyldopa
2-carboxylic acid
• Growth retardation (small body, small head size), mental retardation (mean IQ
between 20-30), light hair and skin
– Tyrosinase deficiency causes albinism Dopachrome
• Can have reproductive implications including enhanced or reduced fertility 5-S-Cysteinyldopa-
depending on mating preferences. quinone
– P-hydroxyphenylpyruvic oxidase deficiency causes tyrosinosis 5,6-Dihydroxyindole
• Increased levels of circulating tyrosine and tyrosine metabolites
• Does not abnormally increase synthesis of melanin Benzothiazine
– Deficient enzymes in the Iodination of tyrosine on this pathway causes Indole-5, Intermediaries
hereditary cretinism 6-quinone
• Similar to iodine deficiency disease, but not treatable by diet

Eumelanin +protein Eumelanosome Phaeomelanosome protein+ Phaeomelanin

Melanin Synthesis Tyrosinase inhibition
•The metabolic pathway to melanin is extremely Dopa • Tyrosinase activity is
complicated, involving several intermediate steps inhibited by a number of
–Starts with the amino acid tyrosine oxidized by the compounds including reduced
copper-containing enzyme tyrosinase to glutathione (see G-6-P D
dihydroxyphenylalanine (dopa) and then to dopaquinone GSH notes)
•A mutation to the gene for the enzyme tyrosinase that produces a Tyrosinase Inhibit (Reduced
– In the skin, the enzyme
protein with decreased functionality will result in a reduced Glutathione)
glutathione reductase (GR) is
production of melanin
Glutathione
responsible for producing GSH

Reductase
–In the extreme, this produces a genetic form of albinism
– Africans tend to have lower
levels of GSH and GR
Tyrosine •Of the 3 GR variants, Africans
GSSG
tend to have the least efficient
(Oxidized
form
Glutathione)
– Lower GSH levels lead to
greater melanin synthesis

Melanin Synthesis, 2
–Dopaquinone undergoes a series of non-enzymatic
Genetics of Skin color
reactions and rearrangements forming the different
molecules that are co-polymerized to make up one of the •Skin color is a polygenic trait, meaning multiple
types of melanin genetic loci are involved in determining skin color
•Eumelanin is the dark brown/purple/black compound found in –Multiple genes working together produce a continuous
skin and hair
distrb
i uti
onina“ Be lSha
l pe”c urveo fdeg reeso flg
iht
•Phaeomelanin is the yellow-to-reddish-brown pigment which is to dark.
present in red hair resulting from the addition of the amino acid
cystine –Early models suggested 2 or 4 major genes
•Recent work suggests many genes working together in very
–Both forms of melanin combine with other proteins to complex, additive and non-additive combinations
form the melanosome that is distributed from the •The non-enzymatic conversion of dopaquinone into eumelanin
melanocyte to surrounding cells and phaeomelanin and their combination into melanosomes is
affected by several genetic loci
Pigmentation Genes

Tanning
More Tanning
•Tanning is a two-stage acclimatizational
response of the skin to increasing levels of –Delayed tanning is the durable browning
caused by repeated exposure, primarily to UV-
UV exposure B but UV-A and visible light also play a role
–Immediate tanning is the transient brownish •Gradual process of skin darkening starting 48-72
tan following exposure to UV-A and visible hours after irradiation
light –Reaches a maximum 19 days after an exposure
•Reaches a maximum within 1-2 hours after exposure –Requires 9½ months for skin to return to original melanin
content
–Fades between 3-24 hours after exposure
•Melanocytes enlarge, increase dendrite density, and
•No new melanosomes formed, so the likely
experience other internal changes
mechanism is the photo-oxidation of existing
melanin or other epidermal elements •Melanosomes increase in number and melanization

UV –Tyrosinase interaction Distribution of Skin Color
Dopa UV radiation
GSH needed to
oxidize free
•Ultraviolet radiation
radicals from
UV exposure
reduces the levels of
GSH
GSH
Tyrosinase Inhibit (Reduced –Lessens the inhibition
Glutathione) of tyrosinase activity
Glutathione

–Increases the synthesis
Reductase

Less GSH
available to
inhibit tyrosinase of melanin
Tyrosine activity –Darkens the skin in
GSSG
response to exposure
(Oxidized
Glutathione)
Distribution of Skin Color, 2
Distribution of Skin Color, 3
•The clinal nature of skin color distribution
suggests an association with environmental
factors varying with latitude
–Ultraviolet Radiation, in particular, the quantity
of UV rays striking the surface of the earth
from the sun
–Temperature

h
Noa’ ur
sc s
eo nHa ss
m’ n
o
Just-So Stories about Skin Color
Canaan
•No ah’ scurseonHa m’ ss onCa naan • An early explanation of dark skin comes from
•Response to the heat of the sun h
tebi blicalstoryo fNoa h’sc urse( Gene
s is
Chapter 9, King James Version):
•Bile theory 24. And Noah awoke from his wine, and knew what his younger
son had done unto him.
•Aerobic theory 25. And he said, Cursed be Canaan; a servant of servants shall
•Optic theory he be unto his brethren.
26. And he said, Blessed be the LORD God of Shem; and
•Pigmentation as pathology of adverse environment Canaan shall be his servant.
27. God shall enlarge Japheth, and he shall dwell in the tents of
•Result of disease Shem; and Canaan shall be his servant.
•Vitamin D, Folic Acid, Cold tolerance – Nowhere does this mention darkening of the skin,
although other sections of the bible, notably in Job
and Isaiah associate curses with darkness

A Biblical Account of Dark Skin Color Voyages of Discovery
•Lamentations chapters 4 and 5 refer to skin color •By the time the slave trade was actively
becoming dark as a result of famine operating on the West African coast in the
–Ch 4, v 8: Their visage is blacker than a coal (alternate mid to late 16th century, curiosity about the
translation: darker than blackness); they are not known
in the streets: their skin cleaveth to their bones; it is cause of dark skin color was growing
withered, it is become like a stick. •The accepted environmental explanation
–Ch 5, v 10: Our skin was black like an oven because of
the terrible famine (alternate translations: terrors or
wa stha tthea c to
i no fthes un’she atwa st he
storms) cause of the differences in the complexion
of Europeans and Africans
17th Century Developments Thomas Browne (1605 –1682)
•This English physician published his view in his
•Accumulating evidence made it clear that the 1646 Pseudodoxia epidemica:
“heto
a fthes u n”e a
xplna i
tonwa snots atisfac o
try
–“Ift hefervour of the Sun, or intemperate heat of clime
–The skin color of the aborigines of North America in did solely occasion this complexion, surely a migration
similar climates to Europeans and Africans was neither or change thereof might cause a sensible, if not a total
black nor white, but olive mutation; which notwithstanding experience will not
–Af i
r canswe ref oun dtov aryinc olorfrom“ blackt o admit. {Despite their transplantation, there remains
yellow”a ccordingt os o urcesoftheda y among their descendants} a strong shadow of their
–Africans forced into European settings were showing Originals: and if they preserve their copulations entire,
no lightening of skin and those Europeans living in they still maintain their complexion. . . .{L}ikewise,
Africa were not appreciably darkening fair or white people translated in hotter Countries
rec eiveno timpre ssionsa mo untingt ot hi scomple xo
i n”
•Thev iewe merg edt tt
ha heAf
rc
ian’
sbl
acne
k s
s
–Hea lsodi s missedt heHa m’sc u rsee xpl anai
tona sa
was innate and permanent foolish tale

Biological Differences?
•Attempts made to resolve whether differences in skin To Bile or Not To Bile
color was due to innate differences in biological structure
ortransientres ponset ot hes un’she a t •Scholars attempting to avoid the polygenistic
–Santorio Santorio (1561-1636): 1614 De statica medicina s kins
’ implications of the bile theory clung to the work
complexion was determined by the presence of black bile of the French surgeon Littré who failed to find a
•Revival of a notion from the ninth century Arabian physician black gelatinous bile in the malpighian layer of
‘Alia l
-Tabari in his medical compendium Paradise of Africans
Wisdom
–Supported by Italian anatomist Malpighi (1687) •Monogenists began advocating a more complex
•Determined that dermis and stratum corneum is colorless in view of environmental causes that harks back to
both Balcks and Whites, he agreed with Santorius that the Hippocrates’Airs, Waters, Places focusing on the
blackness of Africans must originate in the underlying differential qualities of the atmosphere
mucous and reticular body—colored by bile –Thi s“aero bic”t he
orywa sch mpi
a o nedbyDu Bos in
•Early Eighteenth century anatomists reported the presence of 1719 and picked up by others, including Blumenbach in
black bile in the Malpighian layer his Varieties of Man in 1795

Aerobic and Optic Theories A New World Perspective
•John Mitchell (1744) published the first major
•Le Cat 1765 discerned black deposits he called scientific study of skin color in the New World
“æt o
hi ps”inne rvetissueso fa ni
ma ls
–Compared skin of colonial Whites and African slaves in
–Without having any idea about the origin or role of Virginia
these æthiops he was convinced that there was a •Concluded there was no anatomical basis for the bile theory
relationship with the environment and he conjectured •Only structural difference was thicker skin among the Africans
that Negroes had more of the structures than Europeans –Applied Newtonian optics to suggest that skin color was based
did, making them the basis of the dark complexion of on thickness of the skin and its ability to transmit light
the Africans –As thickness increased, the skin appeared darker
•Af rc
ian’st hicks kinp ro hibitedt h etr ansmissi ono n
fayc
olr
o
•Patot 1733 claimed that complexion differences through them
were based on the ability of the human skin to •He also conjectured that the original skin color of man was
transmit light—the“ op tic”t heoryo k
fs inc olo r neither black nor white but something in between with
Europeans and Africans represented divergent extremes caused
by the degenerative influences of the environment
Degeneration of the Primordial Type Pigmentation as Pathology
•Buffon argued that skin color differences •Lafitau (1724) argues that dark skin color is a
congenital malformation—already present in
were reflective of the geographical African fetuses
degeneration of the primordial type •Rush (1795) claimed the skin color of the Negro
–Hes ug gestsr es
torato
ino ft he“dege nerater acs
e was derived from leprosy
tothepu ritya ndv igoro ft heo i
rgn
ia ltype ” –He argues that Africans suffer from a congenital
would require the transplantation of the these disease so mild that excess pigment was the only
symptom
people to a more temperate zone plus a change
of diet and a long span of time •Albinism and other depigmentation conditions
among Africans were seen as reversion to the
original complexion

Un
An“ ve
i s
ralFr
ec e
kl” Physiology of Pigmentation
•Samuel Stanhope Smith (1810) used the •Late in the 19th century the process of
depigmentation of Henry Moss, an African melanization in plants was discovered to be
American from Virginia to suggest that dependent on the enzyme tyrosinase
pigme nt ati
onwa sno thingmo r
et hana n“ u ni
ves
ral •German histochemist Bruno Bloch demonstrated
fre
c kle” ,occa
sione dbye nvironme ntalex pos
ureto in 1927 that this same pathway was involved in
sunlight pigmentation of human skin in vitro
•By 1950 the cells where these reactions took
•He argued that climate affected skin color place, the melanocytes, were identified and it was
–Evidence: the darkening and lightening of complexion found that these cells originate embryonically in
with the seasons the neural crest
–Colda r“
i chafesthec ountena ncea ndinc rease he
st •By 1955 the UV protective effects of melanin in
rddi
u ne sso fthecompl exion” the skin were demonstrated

20th Century Just-So Stories Selection Favoring Dark Skin
•The discovery of the interaction between melanin •Selection favoring high levels of melanin
and UV led to a number of explanations of skin
color
pigmentation in areas of high Ultraviolet
•The association between vitamin D synthesis, UV
(UV) radiation may involve several
radiation, and skin pigmentation was suggested in selective agents
the 1930s but it was largely ignored until revived –Sunburn can cause skin lesions and infections,
by Loomis in 1967 preventing some degree of heat loss
–Loomis proposed that the rate of vitamin D synthesis is
governed by pigmentation and keratinization which –Also predisposes to skin cancer
affect the amount of UV penetrating to the stratum •Highly pigmented skin provides partial protection so
granulosum, making skin color responsive to UV levels selection would favor dark skins in high UV areas
Skin Cancer
Folic Acid Deficiency
–Skin cancer is found to be prevalent among
light skinned individuals in tropical latitudes
–UV light causes denaturization (a chemical
–In Nigeria and Tanzania no albino over the age breakdown) of Folic Acid circulating in the
of 20 years was found to be free of malignant
blood
or pre-malignant skin lesions
•This can induce a deficiency even if the diet
–In Tanzania chronic skin damage was found in supplies adequate folic acid
every albino infant by the end of the first year –Deficiency symptoms include anemia, infertility, and birth
of life defects, especially neural tube defects
•This high rate and early evidence of skin damage •High melanin content in the epidermis can protect
suggests that cancer may have been a strong circulating Folic Acid, thereby selecting for dark
selective pressure in tropical areas skin in low latitude areas

Immune Suppression Selection for Depigmentation
–Ultraviolet light is known to suppress immune •Selection favoring low levels of melanin
function pigmentation in ecosystems where there are
•It has been hypothesized that increased melanization low levels of UV radiation (primarily in the
could protect the immune system by shielding the
blood borne components of the system from UV high latitudes) may also involve different
•A recent study demonstrated that differences in skin factors:
color were not associated with differences in UV- –The regulation of Vitamin D synthesis
induced immune deficits
–Frost bite sensitivity and cold tolerance

Regulation of Vitamin D Regulation of Vitamin D, 2
–Regulation of Vitamin D synthesis
–Previtamin D is transformed into vitamin D by a
•Vitamin D in the body is derived primarily from the temperature dependent process over 2-3 days
skin and secondarily from the diet –Vitamin D then diffuses into the blood vessels of the
•Vitamin D is synthesized in skin by the action of dermis
UV-B –The liver and kidney further transform the Vitamin D into
1,25-dihydroxyvitamin D which is the most active form of
–Precursor molecule is 7-DHC or 7-dehydrocholesterol,
the vitamin
which occurs in the strata granulosum and basale of the
epidermis •The function of Vitamin D is to actively cause
–UV-B exposure causes a photochemical (non-enzymatic) calcium absorption across the wall of the small
conversion of 7-DHC into previtamin D intestine into the blood stream
•High melanin content in skin reduces UV-B exposure
and cuts photochemical conversion
Regulation of Vitamin D, 4
Regulation of Vitamin D, 3 •A deficiency of Vitamin D in infants and children causes
Rickets, in adults a deficiency causes osteomalacia
•Calcium is used for bone and tooth development as –Rickets refers to a defect in the calcification of growing bone
well as for nervous and muscle action so that the bones are structurally weak and unable to withstand
mechanical pressure
–The skeleton serves as a calcium reservoir
•Symptoms include muscle weakness, deformity of the long bones
–If calcium levels in intracellular fluid drops, hormones are including bowed legs, knuckle-like projections along the rib cage
released to cause resorption of bone, placing calcium into (rachitic rosary), deformities of the pelvis that are often permanent
circulation –Long bone deformity impairs locomotion
–Pelvic distortion can make childbearing dangerous–potentially killing
mother and baby
•Prior to widespread Vitamin D supplementation in the 1930s, Black
women in the U.S. showed nearly 8 times greater pelvic deformity than
White women

Rickets
Regulation of Vitamin D, 5
•Assuming that our ancestors had dark skin in the
tropics, as hominids moved into higher latitudes
there would have been substantial selection favoring
lower melanin content in the skin to improve
Vitamin D synthesis

Potential for synthesis of previtamin D3 in lightly Areas in which UV is not sufficient over the year
pigmented human skin based on annual average UV for lightly, moderately, and highly melanized skin

Not sufficient UV radiation,
averaged over the entire year, to
Zone 1: adequate UV Zone3: not2:sufficient UV UV
radiation throughout
Zone not sufficient form previtamin
Not sufficient UV in lightlyaveraged over the
D3radiation,
radiation on average
radiation during atforleast
the year the whole year
one month
pigmented
entire year,human skin
for moderately pigmented human skin

Not sufficient UV radiation for
highly pigmented human skin
Gradation of skin colors for known
Predicted shading of skin colors for indigenous humans
indigenous human populations

African
pastoralists
Alternatives to skin production of with high
reliance on
Vitamin D for Calcium Absorption fresh milk

•Lactose appears to promote the absorption of
calcium
–Hu ma nmi ki
l s50% hi gherinlactos ethanc o w’smi k,
l ne
Li
infants show better calcium absorption when nursing d
en
–Milk drinking increases calcium and lactose intake, Tr Lapps and
Inuit with
may lessen selection on UV-Vitamin D substantial
•Fish consumption increases intake of vitamin D reliance on
fish
–Fish eating would decrease selection for light skin color resources

and biosynthesis of Vitamin D

Frost Bite and Cold Tolerance Frost Bite and Cold Tolerance, 2
–Frost bite sensitivity and cold tolerance •Experiments with guinea pigs, cooling both dark and
•As our ancestors moved into higher latitudes they light skinned areas on the same animal, showed dark
also would have been subject to colder temperatures skin more susceptible to frost bite
•There is a great deal of anecdotal evidence and some •Frost bite cripples hands and feet causing survival
medical record evidence (most from the Korean problems, and secondary infections including
War) suggesting that individuals with heavily gangrene may be fatal
pigmented skin are more susceptible to frostbite
•Animal studies demonstrate that melanocytes are
more easily destroyed by freezing than the rest of
the skin cells
Sexual Selection Sexual selection and skin color
•Mating preference for skin color was • Aoki argues that selection is unidirectional favoring dark
skin to prevent sun burn, skin cancer, folate denaturation,
promoted by Darwin as being one of the etc.
primary reasons for differences in skin color – This selection would be relaxed at higher latitudes with lower UV
stress
between the races of man • He suggests that there is a near universal preference for
light skin in human mate selection
•Recently Aoki (2002) has argued that this is – As selection lessened at higher latitudes, this intersexual selection
the primary reason for the distribution of for lighter skin color would become a stronger force driving skin
color genes in the direction of less pigmentation
aboriginal skin color • The clinal distribution of skin color results from the
balance between natural and sexual selection

References
Aoki K. 2002. Sexual selection as a cause of human skin colour v ara
iti
on: Darwin’s
hypothesis revisited. Ann. Hum. Biol., 29:589-608.
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O’ Rour keD( eds .
)Huma nBi olog y:AnEv oluto
i naya
r ndBi oc t
ulurlPerspective.
a
New York: Wiley-Liss. Pp. 163-224.
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Jablonsky NG, and G Chaplin (2000) Evolution of human skin color. Journal of Human
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Montellano, BR Ortiz (1993) Melanin, Afrocentricity, and pseudoscience. Yearbook of
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Robins AH (1991) Biological perspectives on human pigmentation. Cambridge:
Cambridge University Press.
Sturm, RA (1998) Human pigmentation genes and their response to solar UV radiation.
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