The genetics of skin colour in people—something fishy?
by Don Batten
Biblical creationists have been at the forefront of efforts to educate the public
that the concept of separate human ‘races’ has little basis in biology.1,2
The Bible tells us that we are all descendants of Noah’s family, some 4,500
years ago. From this it can be reasonably concluded that all humans are closely
related; in other words, very similar genetically.
Only one main pigment
Indeed, the same main substance—a dark brown pigment called melanin—colours
the skin of all humans.3
Individuals that have a lot of it appear to have ‘black’ skin; people
that have little appear ‘white’. Melanin is produced by organelles called
melanosomes, contained in special cells called melanocytes. Melanocytes are located
in the bottom layer of the skin, and produce melanin with the aid of tyrosinase
and other enzymes. People with lighter-coloured skin have smaller, fewer and less
dense melanosomes than darker-skinned people.
Two varieties
‘Melanin’ actually comprises two pigments, which also influence hair
and eye colour. Eumelanin is dark brown, whereas pheomelanin is reddish in colour.
People tan when sunlight stimulates eumelanin production. Redheads, who are often
unable to develop a protective tan, have a high proportion of pheomelanin. They
have probably inherited a defective gene which makes their pigment cells ‘unable
to respond to normal signals that stimulate eumelanin production’.4 Research has implicated variants of the melanocortin-1-receptor
gene (MCR1) in this inability to tan, which also relates to the production
of freckles in childhood and photodamage to the skin that manifests in adulthood.5 When exposed to UV light,
and in the absence of sufficient eumelanin, pheomelanin produces free radicals that
may cause skin damage, including cancer.6
Skin colour, like many other human traits, varies in almost continuous fashion throughout
the spectrum from very pale to very dark.
While (eu)melanin functions in protecting the skin from the damaging effects of
exposure to the sun’s UV rays, it also apparently protects folate, an essential
vitamin particularly important for neural tube development in the unborn.7 Melanin also protects those
living in lowland equatorial regions from tropical skin ulcers through an anti-microbial
effect.8 So people with
good levels of melanin are better adapted to living in the tropics than people with
little melanin. On the other hand, melanin reduces the production of vitamin D,
a vitamin essential to normal bone development that is manufactured in the skin
on exposure to sunlight. Consequently, people with dark skin tend to suffer from
rickets at high latitudes, where the skin’s exposure to sunshine is lacking,
unless their diet is rich in vitamin D (by eating fish, for example, as the Inuit
do). In such areas people with little melanin (’whites’) are better
adapted. These factors have undoubtedly contributed to the distribution of skin
colours in different regions around the world.
Other substances, such as the coloured fibres of the protein elastin and the pigment
carotene, affect skin shading in minor ways. Humans also share these compounds in
varying degrees. Other factors may influence the shade perceived by the observer
in subtle ways, such as the thickness of the overlying (clear) skin layers and the
density and positioning of the blood capillary networks.
Skin colour, like many other human traits, varies in almost continuous fashion throughout
the spectrum from very pale to very dark. Racial discrimination on the basis of
skin colour is about as irrational as discrimination based on height, finger length,
or any other continuously varying trait—indeed, discriminating on the basis
of blood type makes more chemical sense, a reduction ad absurdum of racism.
However, little is understood about the genetics of skin colour in humans. Study
of some forms of albinism, where people with certain mutations cannot manufacture
any melanin, showed that the enzyme tyrosinase, which processes the amino acid tyrosine,
is important in the manufacture of melanin. However, mutations in the tyrosinase
gene have nothing to do with the normal variations in human skin coloration; albinism
is associated with serious eyesight problems, for example.
Recent research on origin of light skin
Images from Lamason, R.L.
Figure 1. Studies on the genetic basis of a mutant form of zebrafish
with pale stripes have led to the discovery of a gene responsible for some of the
variation in human skin colour. A) Adult wild-type. B) Golden mutant. Insets show
the lower number, size and pigment density of melanosomes in the mutant form. (Images
from Lamason et al).9
A large team of researchers centred on Penn State Cancer Institute found a gene
in zebrafish that affects the shade of the dark stripes in the fish’s coloration,
causing the golden variant. A mutation in the slc24a5 gene was
found to reduce the amount of melanin in the dark striped areas, resulting in a
paler colour (see figure 1).9
The mutants had fewer and smaller melanosomes, which also contained less pigment.
This parallels the situation in pale-skinned humans, who also have fewer and smaller
melanosomes, so the researchers wondered if the same gene could be involved.
In an elegant piece of multi-disciplinary team work, the researchers showed that
a homologue of the zebrafish gene accounts for some 25–38% (95% confidence
limits) of the variation in human skin colour between northern Europeans and Africans.
A single nucleotide differs between Africans and Europeans in the gene, SLC24A5.
This results in one amino acid difference: residue 111 is alanine (Ala)
in Africans and threonine (Thr) in Europeans. There is a high degree of
homozygosity in Europeans for the Thr variant, the A allele,
with a frequency ranging from 98.7–100% in several European-American populations
sampled. The Ala version, the G allele, ranged from 93–100%
in various African, native American and East Asian population groups. This distribution
is quite non-random, suggesting strong selection has been applied to the alleles.
This selection could be environmental, but is more likely to be sexual, i.e. due
to marriage preferences arising from recognition of the benefits of dark skin in
tropical areas and light skin in high latitude areas.10 This would have happened after the Babel population
bottleneck, when God forced the people after the Flood to spread out and ‘fill
the earth’, as he had commanded Noah. Japheth, or his wife, might even have
carried the A allele. It would be interesting to know the frequency
of the A allele in the Caucasian people of India, whose skin colour
ranges to quite dark. Does the frequency of the A allele decline
with darker skin amongst these people?
Interestingly, East Asians and native Americans share the African G
allele, so this gene has nothing to do with the lighter skin of these people compared
to Africans; other genes must be involved here.
That most of the world’s population carries the G allele
suggests that this was the genotype of the first humans and that the European
A allele arose as a single mutation after Creation. This does not mean
that Adam and Eve were necessarily ‘black’, because other genes influence
skin colour (as in East Asians, for example).
Evidence from a study of recently admixed (African + European) populations suggests
that the European A allele is partly dominant over the G
allele. This means that the AG genotype has skin colour intensity
more like an AA than a GG.
‘Conserved’?
The paper implicitly assumes the evolutionary story that the human gene originated
in some common ancestor with zebrafish. The human and zebrafish genes are so similar
in function that the human gene (allele G) activated normal melanin
production in zebrafish that have the mutant gene (golden). So, although
the authors found about 69% homology in the amino acid sequences, it seems that
the differences do not affect function much, as least in the reverse direction.
However, it could be that the human gene is more specialized in some way, such that
the zebrafish gene would not work properly in humans. The human gene codes for 500
amino acids. All genes investigated in various taxons had about the same number
of amino acids and all apparently had eight introns in the same positions.11 The intron sequences were
not discussed. Given the supposed timescale (supposedly some 400 Ma) for such conservation,
it seems more like a just-so story—especially considering how much ‘evolution’
(the materialists’ unseen ‘creator’) has supposed to have achieved
in that time.
However, this work contains valuable data that is relevant to the phenomenon that
has been called ‘race’, showing how little genetic difference there
is between various people groups (one amino acid in this case), even differences
that superficially look significant, such as skin colour.
Further reading
Recommended Resources
References
- Bergman, J., Evolution and the origins of the biological race
theory, Journal of Creation 7(2):155–168, 1993.
Return to Text.
- Bergman, J.,
Darwinism and the Nazi race Holocaust, Journal of Creation 13(2):101–111,
1999. Return to Text.
- Batten, D., Ham, K., Sarfati, J. and Wieland, C., The
Answers Book, chapter 18, Creation Ministries International, Brisbane, Australia,
1999. Return to Text.
- Cohen, P., Redheads come out of the shade, New Scientist
147:18, 1997. Return to Text.
- Bastiaens, M., ter Huurne, J. et al., The
melanocortin-1-receptor gene is the major freckle gene, Human Molecular Genetics
10(16):1701–1708, 2001. Return to Text.
- Ranadive, N.S., Shirwadkar, et al., Effects
of melanin induced free radicals on the isolated rat peritoneal mast cells, J. Invest.
Dermatol. 86:303–307, 1986. Return to
Text.
- Jablonski, N.G. and Chaplin, G., The evolution of human skin
coloration, J. Human Evol. 39(1):57–106, 2000. Return to Text.
- Mackintosh, J.A., The antimicrobial properties of melanocytes,
melanosomes and melanin and the evolution of black skin, J. Theor. Biol.
211(2):101–113, 2001. Return to Text.
- Lamason, R.L. et al., SLC24A5, a putative
cation exchanger, affects pigmentation in zebrafish and humans, Science
310:1782–1786, 2005. Return to Text.
- Batten et al., ref. 3, pp. 216–219. Return to Text.
- Supporting online material for Lamason, R.L. et al.,
SLC24A5, a putative cation exchanger, affects pigmentation in zebrafish and humans,
Science 310:1782–1786, 2005;
www.sciencemag.org/cgi/content/full/310/5755/1782/DC1. Return
to Text.
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