Human Evolution: some of our traits, and what we can say about them.
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
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.
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.
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.
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 (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.
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.