Death: how and why

It’s Sir Peter Medawar day. The topic is merely one of the many fascinating ideas he contributed to biology and to the world of letters in general: why we age and thereby die. It’s part two in a planned three-post series about death, which began with Death: who and when.

Let’s set this up just right. I’ve seen too many colleagues, let alone students, fall into the trap of thinking that death is a matter of wear and tear on a mechanism. OK, so it’s not “for a purpose,” they get that, but unfortunately the only one thing they can see after that is ordinary entropy. However, that does not apply at all. The question is why your tissue replacement at 60 is crap quality relative to the very same process at age 6. And why this is so time-stamped in-species, such that a virtually identical organism undergoes the very same shift in basic tissue competence in a sixth of that time.

Ooh wait. Quick vocabulary: mortality is when someone actually dies by whatever means; longevity is how long they live, or would live, until death by senescence.

Remember in the thread Adapt this how I talked about predation and selection on pepper moths? Never mind what color they are. I’m talking about how every single pepper moth gets eaten – in the real world, that’s how they die. But if you housed and nurtured and cosseted a bunch of them, they’d get old and die, sooner later. And the average age thereof would match to a bit older than the average age of getting taken down and eaten. Actually, I don’t know how thoroughly that’s known for the moths specifically, but the phenomenon has been studied pretty hard in wild populations whose logistics allow complete tracking of individual fates. Check this out, it’s a classic: Actuarial senescence and demographic heterogeneity in the Florida scrub jay. (Geez … I used to read stuff like this all the time …)

Reiteration via text to reinforce A-V learning: inherited effects (a better word than “trait” in this case) which decrease individual viability become rarer in a population and sometimes absent due to selection, if and only if they affect the organism prior to the average age of death by misadventure, in that population’s specific history. Those which – otherwise identical – affect the organism mainly after that point are not decreased in frequency by the same means, or at all. This means your genome is a walking time bomb. You personally might have a shorter or longer longevity on the average, but in your population and generation, its average value is set by that history and that variable.

Look, I’m gonna be grim – people talk about “in his sleep” or “peacefully” and so on. My father may be one of the few examples, killed by his second stroke in what seems to have been an instant. But most of the time, the words “naturally,” “of old age,” hide a multitude of sufferings.

  • Epithelia: creases, loses permeability or conversely becomes porous – and never mind your outer skin, this stuff lines your GI tract and circulatory system
  • Neural function: chemical or physical impairment, in afferent (sensing), efferent (doing), or central (processing) capacity
  • Musculoskeletal: weaker bones, poor tendon repair, patches of dead muscle
  • Endocrine: unreliable hormonal negative feedback deregulates a wide variety of metabolic and digestive actions
  • Immune: choose – your attack-dog T-cells lose their effectiveness so they can’t spot incipient cancer cells, virally-infected cells, or bacteria; or they decide your own tissues are valid targets
  • Urinary: every cell in your body floods your blood with urea (slightly less-dangerous ammonia) every minute, and your kidneys now fail to remove it
  • Circulatory: not only the epithelial problems mentioned above, but decreased removal of cholesterol blockages, and acidosis problems based on kidney and respiratory issues
  • Respiratory: lungs are inpocketings of epithelial tissues which require constant cellular turnover, so the lthings that go wrong with that are legion

Let’s think as well about one of the minor mysteries that I alluded to regarding Alex: that longevity plays hob across species relatedness. Different species have different longevities in joyous disregard of higher taxonomic grouping, i.e., phylogenetic clustering — doesn’t that strike you as odd? In terms of personal significance, longevity should be some bedrock fixed thing essential to a given creature’s “kind,” but it’s a remarkably species-specific phenomenon. There seems to be little or no developmental (a.k.a. phylogenetic) constraint involved. Medawar’s idea may be all there is.

That’s a big bird to flip at “survival of the fittest” or any mortality-centered description of selection, too. One of the finest examples of unconstrained selection available, and it’s all about dropping us dead in our tracks without any “adapting” to be found. Teachers please take note.

I better clarify my reference to Mendelian expression:

  • Progeria is reduced by selection insofar as those with the condition do not produce offspring; it’s present in the population only to the extent that an extremely diffuse and low-probability inheritance phenomenon is involved
  • Regarding a recessive deleterious effect, it’s the combination of a heretofore non-apparent allele with another one which leads to the problem, that’s what I meant by “more effective form,” not that the allele itself was different
  • Huntingdon’s results from a high-penetrance gene, specifically a dominant allele – you only need one – and such an allele is definitely susceptible to full removal from the population by selection … if it were affecting us at an earlier age

You may count me among those who do not think anyone has refuted Medawar on this topic either logically or clinically. As with so many good inductions, it is not “proven” or thoroughly investigated in deductive terms, and obviously any number of revisions and ifs-and-buts are going to show up in the actual biology when that happens. However, that investigation can’t happen until the mess of non-factual and non-necessary terms or expectations about selection gets cleaned up, and until the contradiction between the evolutionary vs. medical models for bodily function – which is primarily a professional clash – gets brought under scrutiny. Neither of these tasks has made much headway despite numerous explicit needs to do so in the past three decades, unfortunately.

If it did, I know where I’d start.

Does consistently multivariate cause-of-death lead to a squishier or more accurately wider “band” across individuals than an extremely predictable cause (e.g. predation in scrub jays)?

Is it really death due to misadventure/whatever that sets the crucial age-point, or is it more about a cost-benefit fitness curve relative to reproductive effort? This would tie well to the ongoing academic head-butts about human female menopause – if such arguments would disentangle themselves from the unhelpful “for what” language and from human exceptionalism, they’d be resolved quickly.

How evolutionarily labile is it? Selection notoriously reduces inheritable variation in a population, but this is an interesting case of retention and possibly accumulation, rather than curtailment. Therefore, is a species’ potential longevity wide-open for increased or decreased longevity based on the “crux” age-point?

So many good questions, open to investigation without shiny-special lab gear. Nary a grant to be seen.

Next: The evolution of evolution

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2 thoughts on “Death: how and why

  1. Pingback: Death: what remains | Man nor Beast

  2. Pingback: Can biology accurately describe life and death? | OUPBlog

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