Human Evolution: some of our
traits, and what we can say about them.
Some background
A summary of the fossil data, as an evolutionary tree
A summary of genetic data and anthropological data on migration
A summary of selection pressures on
melanin production during human migration
Food-related
traits
Vitamin
requirements
Dependence on plants
Vitamins C and E are most easily obtained from
plant material, as are a great many other antioxidants that are necessary for
us. The fact that we require these
nutrients indicates that when mutations occurred eliminating our ability to
produce them, there was no penalty because fruits and leaves were a significant
part of our ancestors' diet.
Dependence on bacteria
Vitamin B12 is produced by
bacteria. We absorb some from our
intestinal bacteria, but our digestive system is too short to absorb as much as
we need. We typically obtain the rest
from animal products--milk, eggs, etc--that are produced by herbivores. Herbivores have sufficiently long
digestive systems that they can absorb plenty of B12.
Amino
acid requirements
Dependence on animal meat
Plants are a poor source of protein. Seeds are the best, but still not
great--and their distribution of the various amino acids is not uniform. Yet, we require amino acids that are
present in small quantities in some seeds. For strict herbivores, it's even worse--normal plant cells
have rather little protein overall.
We can get a clue about this problem from cows, which normally eat
grass. They swallow their food
into their rumen, the first of their stomachs, where methanogenic bacteria
break down the cellulose. Cows
regurgitate this material as "cud" and chew it further, before
swallowing it into the traditional intestinal system. Their intestinal system is very long; there is plenty of
opportunity to break down the plant material and extract every bit of nutrition
in it.
But,
whatever protein is in their food at the outset, most of it is digested and
consumed by the ruminal bacteria!
As it turns out, the lengthy intestine of a cow is a very good factory
for growing more of these bacteria--many of which die and are digested by the
cow itself. To a large extent, it
is from these digested bacteria that cows obtain most of their amino acids.
DNA
sequence data from numerous genomes indicate that animals, in general, lack the
enzymes to build the essential amino acids. Herbivores, such as cows, obtain them from their gut
bacteria--much as they obtain vitamin B12. Carnivores like wolves, and hunters like humans have too
short a digestive system to extract either vitamin B12 or amino
acids from the intestinal bacteria.
Therefore, they must eat protein, the best source of which is animal
meat.
Note
that the development of hunting parallels the shift from a wide abdomen (e.g.
in Lucy) to a narrow one (e.g the Nariokotome boy), as the herbivore's large
digestive tract diminished to an omnivore's shorter one. This was advantageous for running long
distances (something humans excel at), but had the unselected disadvantage of
making us dependent on a good source of protein in our diet, as well as unable
to absorb sufficient vitamin B12.
Fat
storage
Saving excess energy molecules for times of starvation
Hunting, particularly with stone tools, is a
rather uncertain way of life.
Sometimes, hunters come home empty-handed. During these times, alternative food sources are
necessary--hence the supplementation of hunting with the gathering of
locally-available plant material.
Sometimes, even this is uncertain.
To survive "lean times" when food is scarce, a common property
of mammals is to convert excess food into fat. When we consume more calories than we use up, we trigger
this fat-storage mechanism. This
is essential when the food supply is uncertain, but can be a liability when
supermarkets contain vast arrays of high-calorie foods at relatively low cost.
Lactose
tolerance
Mutations that result in "adult persistence
of lactase" may well have occurred several times in different human
populations. If we calculate the
probability of mutation in the region of DNA where the European persistence-of-lactase
mutation lies, we estimate that such a mutation is likely to occur somewhere in
the human population once every several years. Why, then, has the mutation not persisted in most
populations? It seems to have persisted
only in the ancestors of Europeans; similar (but not identical) mutations have
been identified in two African tribes as well. The common factor is that these populations had developed a
culture that revolved around herding cows, and using milk as a source of
protein. Being able to tolerate
lactose later in life would be advantageous if milk is available, and would be
selected for. It would be
irrelevant, and thus lost, in a culture that does not use milk as food.
Other traits
Skin
color (see also here)
The ancestral human population arose in
equatorial Africa, exposed to high-intensity ultraviolet light (UV). UV can induce mutations (which can
cause skin cancer), and can photo-inactivate a number of essential
biochemicals. Thus, too-high a UV
dose is not good. However, UV also
stimulates the production of vitamin D, and is therefore essential for calcium
absorption and depostion into bone.
To balance these competing effects of UV, it is advantageous to produce
melanin in skin cells. This
effectively shades the light-sensitive chemicals in skin cells (including DNA);
a small fraction of the UV that is not removed by shading is sufficient to
induce production of vitamin D.
Upon
migration to the north, into Europe or Asia, humans faced different
conditions. It was colder, so
clothing became necessary. Less UV
shines upon the northern latitudes.
Under these conditions, extensive melanin production is no longer an
advantage. The shading blocks the
smaller amount of UV from inducing the production of sufficient vitamin D. So, in northern latitudes, mutations
that interfere with melanin production were advantageous, and were selected.
Eventually,
humans crossed the Bering sea into North America, and migrated south into
equatorial regions. Here, UV
intensity is again high, and would favor production of skin pigment. But, mutations occur at random, so
there is little likelihood that mutations would perfectly revert the
loss-of-pigmentation mutations that had previously occurred. What appears to be the case is that one
or more mutations occurred that up-regulate the tanning response, so that
modest UV exposure activates melanin production quite effectively.
Thus,
we now find that dark skin is common in equatorial parts of the world, but that
the particular characteristics of it vary. In Africa, it is common to have full-time melanin
production, as our ancestors almost certainly did. In the tropical Americas, melanin production is
UV-induced. In the north, however,
melanin production is much less pronounced; in some far-northern latitudes, it
is even common to have lost not only continuous melanin production, but the
tanning response as well.
Cystic
Fibrosis
Cystic Fibrosis (CF) is a particularly nasty
disease that, until the advent of modern medical treatments, was invariably
fatal in childhood. The disease is
characterized by excess, sticky fluid in the lungs, resulting in infection,
breathing problems, etc.
Interestingly, the prevalence of CF shows latitudinal variation the way
skin color does. What's going on?
The
gene that is responsible for CF is called CFTR.
It determines the expression of a membrane-transport regulator that is
required for the movement of salt across membranes. Different families with CF may have different mutations in
the gene. This is not because the
gene mutates more easily than any other gene, but because something seems to
select for these mutations once they occur--but in Europe, and not in
equatorial Africa.
As
with most genes, there is not complete, 100% dominance/recessiveness of
different alleles (versions of the gene).
A person who receives a good copy of the gene from one parent, and a
mutant copy of the gene from the other parent does not display the CF disease
(which requires two mutant copies), but nonetheless has some differences from
individuals who have no mutant copies of the gene. It is these differences in heterozygotes for mutant CF
alleles that determine the distribution of the CF disease.
In
hot, humid climates, it is necessary to cool our bodies by sweating. When we sweat, we lose salt. Salt is absolutely essential for the
function of neurons. Thus, too
much loss of salt can be fatal in a region that is hot and humid. As it turns out, one of the functions
of the CFTR protein is to regulate the secretion of salt in sweat glands. CF heterozygotes secrete more salt than
normal. In equatorial Africa, this
is usually fatal (or complicates recovery from other diseases). As a result, CF is relatively rare in
this part of the world.
In
Europe, however, it is not so hot that losing some extra salt through sweat is
a big problem. Thus, CF mutations
should not be selected against.
But why would they be so much more common than we would expect? Is there selection for them?
The
CFTR protein also regulates salt secretion and uptake in the large
intestine. Again, even
heterozygotes show a difference from people with two good copies of the
gene. They secrete less salt into
their intestines. An interesting
consequence of this is that they lose less salt when suffering from severe
diarrhea, a would be caused by cholera.
Therefore, they have a higher likelihood of surviving a cholera
epidemic. In historical times,
European cities were often plagued by cholera and other diseases. Any genetic trait that conferred a
higher probability of survival would be selected--including the heterozygous
condition of CF. The unfortunate
consequence is that CF heterozygotes often have CF homozygous children, who
suffer from the severe lung impairment of the disease.
Hair
Very few mammals have hair that grows to great
lengths. We do--and only on our
heads. Elsewhere on our bodies,
the growth phase of hair follicles is considerably shorter, so hair (e.g.
eyebrows and eyelashes) reach a certain length and stop. Our head hair has a growth phase
measured in years, and in some individuals, hair can reach all the way to the
ankles. This curious situation
must have an explanation.
If
we watch just a little bit of television, we are likely to see ads for
shampoo. If we listen to
conversations around us just a little bit, we are likely to hear of someone
complaining about a "bad hair day." Before we go out in the morning, we fuss with our hair. When we look at others--particularly of
the opposite sex--we pay attention to their hair. We seem to be programmed to pay inordinate attention to
hair--both our own and others.' We
certainly don't pay this much attention to, say, elbows.
There
are at least two possibilities for how this arose (and probably more). One is selection by mate choice (also
called sexual selection). If we
start using hair as a factor in choosing mates, then we simultaneously select
for an instinct to study hair, and for developmental mutations that affect hair
growth. We probably also select
for behavioral instincts to "do things" to our hair.
We
also tend to live in groups--families, tribes, nations, etc. We tend to believe that our group is
"best" and that others are somehow suspect. This, too, is a selected instinct, borne of millennia of
fighting over scarce resources.
But, how do we recognize the members of our own group?
Now,
we often use hats, colors, the insignias of our favorite teams, special dress
or rituals, by which we can tell who is who. Our ancient ancestors had fewer options, but these would
have included, body paint, tattooing, and yes, hair.
So,
hairstyles seem to be a means of recognition, and would work for group
identification as well as more personal issues such as mate choice.
There
are many, many other traits that we now have. Some of them we can look upon as being relatively recent
developments. Others are holdovers
from our even-more-ancient ancestors.
It is interesting to think about when any particular trait is likely to
have appeared, and what the environmental conditions were that enabled it to
become common.