There is a constant tension in any animal science between the impact of nature and the impact of nurture. How much of who we are and what we do is the result of our genetic predispositions, and how much because of our environment?
This tension is made a little more complicated by the fact that the dichotomy doesn't really exist. Rather, our genetic predispositions are a form of nurture.
1. Genetic evolution is the product of the environment, and it's fast
Our genetic code is the product our environmental past. This much information is available to any fourth grade student. What might surprise you is the timeframe at which genetic evolution can occur. Not millions of years, certainly thousands of years, and maybe even faster still.
Genetic adaptations to our efficiency at breathing can happen even faster—within thousands, if not hundreds of years. The most common example of this are populations that live at high altitudes, like those in Tibet, the Andes, and Ethiopia. The Tibetan population in particular appears to have genetically diverged within the last 3,000 years. But the more recent discovery of the genetic divergence of the sea-dwelling Bajou peoples reduces that timeframe to within about 1,000 years.
Various other studies also indicate that the genetic makeup of populations may well change in mere centuries, rather than thousands of years. Like this one on the increasing prevelence of an artery in the human forearm, or this one which suggests western populations are developing lower blood pressure and cholesterol levels. Or most jarringly, this one, which suggests that having more or less resources available in a community group can create natural selection pressures that work over the course of as little as two generations.
These particular evolutions are the result of classic natural selection–those who are better adapted out-survive and out-reproduce their peers. But modern health innovation means that natural selection no longer takes precedence.
The theory of neutral evolution or 'genetic drift' suggests that most genetic developments are not significant enough to be weeded out by natural selection—stochastic mutations that aren't particularly helpful or harmful. As we get better at keeping ourselves alive, more mutations fall into this category of neutrality—harms that may develop aren't so harmful anymore. But this effect is biased in an interesting way.
Typically, any mutation that causes a big change—helpful or harmful—will need to contend with the environment. When the cost of a mutation outweighs it's benefits, it will likely (literally) die out. Too much change towards a benefit might incur too many costs from a less mutable environment.
But health innovation is targeted at mitigating these costs. We care much more about keeping people from getting sick than we do keeping them from flourishing, for obvious reasons. When the costs are made less costly, we may well see beneficial mutations proliferate at a more rapid rate than the natural world would have allowed without our intervention.
In short, genetic evolution is far faster and possibly happening far more often than most people recognise.
2. Our genes change within our lifetime, and we pass these changes on
The most alarming example of how mutable our genes are come in the form of so-called 'jumping genes'. These are DNA sequences that can move their position, changing the form and function of other genes. The role of these genes are fairly mysterious still, but are abundant enough. One jumping sequence, ALU, is though to make up between 1/6 to 1/5 of the entire human genome. These genes likely serve innumerable roles in the regulation of gene expression for adaptive purposes. We know, for example, that bacteria use them to develop antibiotic resistence. They can be so useful, in fact, that another series of jumping genes took a mere 50-100 years to spread through the entire fruit fly population (although admittedly, that is a couple hundred generations of fly-lifespan).
A less enigmatic form of gene transformation, and probably not unrelated to our jumping genes, comes from epigenetic research. At the risk of oversimplification, epigenetics is the study of changes in genetic expression. Of interest to us is one aspect in particular.
We have many more genes than we use in our DNA. Some of these genes are so-called 'junk'. But many of these genes are simply 'turned off'. For example, we all have the code for a tail, but reports indicate that only a busload of people have had that genetic pattern 'turned on'.
Some genes are far easier to 'turn on' than our tail code, however. This is perhaps best illustrated by the epigenetics of anxiety-related disorders. A fairly substantial amount of research into animal models suggests that stress modifies which genes are expressed, and how, with emphasis on DNA methylation—a regulator of gene expression.
An example of this might be the effects of social rejection and isolation. Within an hour of a rejection event, genes involved in virus resistence stop being expressed and genes involved in the inflammatory response start being expressed in new cells. Essentially, cell by cell, you become more prone to the effects of illness. The cumulatative effect of social isolation, then, appears grim (and it is).
Another example might be the variation between so-called 'identical twins'. Typically, when monozygotic twins differ, we suspect that different environmental impacts are the cause. But in fact, a non-trivial number of changes in the genetic code of these twins occur throughout development. These changes may be due to the environment, or they may not. For example, stochastic gene jumping might simply explain the differences. The result however, is that despite starting out identically, these twins certainly don't end up identically and changes in their genes tell part of that story.
These changes can not only come within our lifetime, but change what genes are 'turned on' in our children too. Trauma, stress, and exercise all seem to have an impact not only on your own gene expression, but the gene expression of your offspring. Entire generations of a population can incur genetic evolution in a single step, should the stressor be widespread enough.
Inherited genetic inclinations don't stop at the abstract. Mice can inherit their parents fear of a specific odour. Birds can inherit the mating behaviour or song patterns of their parents as an innate, instinctual behaviour. Honeybees can develop aggression towards another race of honeybees. These examples demonstrate that other animals develop a genetic predisposition for behaviour in a single step, based on the environment. This is a far cry from even the shortest timeframe proposed by natural selection.
All such changes are sensible mechanisms. Before our capacity to share ideas amongst one another, our adaptability came solely from our genetic code and our ability to learn from our immediate environment. To wait for even the shortest period of selection by the attrition of the unfit would leave us vulnerable to the speedier environmental impacts. The ability to transmit information intergenerationally these ways means far faster, and more localised development of the behavioural repertoire.
Genetics is nurture
We must, of course, be sympathetic to biological accounts of mind and behaviour. We're constrained necessarily by our somatic architecture and so it's no use ignoring biological facts simply because they're inconvenient.
But our enthusiasm to explain our capacities as nature or nurture isn't sensible either. Instead, we can see that nature is influenced at many timepoints by nurture. The immediate genetic changes from gene jumps or changes in genetic expression. The inheritance of those changes. Evolution at a hundred years. Evolution at a thousand. And more distant evolution still.
Living organisms are, at their core, robust to the effects of nature. To do that, they must be able to bend to face the changing fortunes of time. Perhaps time, then, is a better instrument to examine ourselves against.