Different fields of science often don't talk to each other, even when coming at the same problem from different angles. A stark example of this can be found in the literature on aging. I'm in the field of evolutionary demography, and aging is one of our central focuses. We ask why and how it happens by studying the demographic patterns of different species under different circumstances. The evolutionary demographic theory of aging is built around the idea that there are alleles that have effects at different ages and natural selection acts on these genes to sculpt the age-specific mortality at different ages. Because dying young (before you've had a chance to reproduce) is more disadvantageous than dying old (after you've already passed on some genes) natural selection acts more strongly to minimize mortality in early adulthood than later adulthood, resulting in a chance of dying that increases in age. There are decades of theory built up around this idea, and the idea is not without merit, but it does assume these age-specific gene effects, generally without bothering to say what the actual genes are or how they influence mortality.
Another field within biology that focuses heavily on understanding aging is biogerontology. Biogerontology focuses on understanding the mechanistic basis of aging at the cellular and molecular level. They describe aging as a process of narrowing of the homeodynamic space, often due to accumulation of damage. Homeodynamic space is a concept related to homeostasis (the tendency of organisms to push their physiological state back to some optimum), but with the recognition that the goal that the individual is pushing towards, and its options for pushing, change over time. For example, as the cells in an organism accumulate mutations, it becomes more dangerous to allow them to continue replicating, because this could spawn a cancer. So the cells are forced to turn down expression of genes that allow for cell replication. But if your cells are replicating less, then you should be more reluctant to allow apoptosis, programmed cell death, because cells that die can't as easily be replaced. But if you've down-regulated the genes involved in apoptosis, this means infected cells will be less likely to kill themselves, so you need to have a stronger inflammation response, so that white blood cells will be brought to areas of infection and kill the infected cells from the outside. But increased inflammation has all sorts of nasty side effects, which themselves need to be compensated for. Note that I am just making this chain up as an example. The point being that the organism, in order to deal with the accumulation of damage, has to adjust various aspects of its physiology, which can cause damage or challenges to the system, which requires further adjustments. The organism gradually loses wiggle room, paints itself into a corner as it were. When this homeodynamic space gets too small, the organism can't respond to whatever insults (internal or external) come along and gets killed.
Reading papers in biogerontology, I am struck by two things. The first is how naive and outdated their evolutionary assumptions tend to be. For example, they still will state that aging is not observed in the wild because no individual lives long enough to grow old in the wild, an opinion that evolutionary biologists began to reject in the 1960s and have now disproved with data from numerous species from plankton to humans and birds to aphids. But I am also struck by how naive they would think our assumptions about age-specific genes are. They state as one of the basic principles of biogerontology that are no genes whose roll it is to cause aging, or which act at a particular age to regulate the chance of death. You will remember I said that such age-specific gene effects, from unspecified genes, are at the center of much of the theory behind evolutionary demography. Yet biogerontologists know such genes not to exist. So our assumptions about the mechanisms are as naive and simplistic as their assumptions regarding the demography.
This lack of communication, with each field basing its thinking on ideas the other has long since rejected, is common in science. There are simply too many journals, papers, conferences, etc., too many fields that may produce important information, for anyone to keep a useful fraction of an eye on most of them. So the lack of communication between fields is to some extent inevitable, but it does have significant consequences.
This is obvious when we introduce the gerontological observation that gene expression is not highly age specific (at least not late in life) to the evolutionary literature on post-reproductive lifespan (PRLS). Much of the study of PRLS has been motivated by the idea that PRLS shouldn't exist unless post-reproductive individuals do something useful for their younger kin. This idea arises from the evolutionary demographic theory of aging I described above. If an individual has reached the age where it can no longer reproduce, the genes it is expressing at that age should be genes that selection doesn't care about at all, because whether she dies at that age has no effect on how many offspring she has. So mutations that kill post-reproductive individuals should accumulate rapidly, unopposed by natural selection. W.D. Hamilton, a preeminent evolutionary theorist of the mid-20th century, wrote in 1966 that “In the absence of complications due to parental care or other altruistic contributions due to post-reproductives, the [mortality] curve should be roughly asymptotic to the age of the ending of reproduction.” By this he means that as the individual approaches the end of her reproductive period, her chance of dying at each instant should approach 100%. This has been dubbed "Hamilton's Wall of Death." Hamilton's work is influential enough, and his basic logic sound enough, that many of my colleagues still believe we should find the Wall of Death. But in fact we can find PRLS in a huge range of organisms where there is no parental care or anything comparable, and the Wall of Death is nowhere to be found. Hamilton's prediction fails because his model is built around high age-specificity of gene expression, which we now know not to exist. Genes which are being expressed at and after the age of reproductive cessation are the same genes being expressed prior to that age, doing the same things they did prior to that age (except of course reproduction) and so they can't just suddenly cause all sorts of lethal effects. This represents a major constraint on the ways selection can shape the pattern of mortality over age, and we evolutionary demographers are just starting to come to terms with the ramifications of this. When I have time to write another longish post, I'll explain how this leads to a major question in evolutionary demography that I have been thinking about but don't yet have any plausible answer to.