notes-science-bio-bioMisc

human outliers:

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" Angela A Stanton PhD? • 2 years ago

I think that a very important element was left out of this extremely elegant and well-written article. Thank you; I truly enjoyed reading it. I am a scientist and constantly bump into damage caused (to protein, to mitochondrial DNA, and similar others) by modern medicine! Some medicines deliberately modify the shape of proteins. For example, SSRIs use an "inhibitor" to plug up a neurotransmitter sensor similar to how a cork plugs up a bottle of wine. Unfortunately the cork is not the shape and polarity as what the protein expects and it damages it in the process.

The same with medicines that are ligands (such as Ambien)--they mimic the properties of a real neurotransmitter but they are not and modify the shape of the receptor to behave like they were that neurotransmitter, damaging the proteins. We also have an antibiotics class (quinolones, such as Cipro, a very common medicine many of us have taken) that damages bacterial DNA, which is great...it kills bacteria except our mitochondria is bacteria as well and it has DNA that does not permit errors.

Thus the apoptosis you refer to is very much in busy-business from our drugs. I suppose ageing is hastened by the damage our drugs cause (I only gave here few examples) but ALL drugs without exception modify protein(s) and/or DNA (ours or mitochondrial DNA) causing increased chaos. Not sure how this fits into the thermal explanation though I assume that a protein that is being squished into a different shape releases heat from the pressure so it may add to the thermal devastation. I also can see that a mitochondria ordered to commit apoptosis would release all its electrons to be oxidized (free radicals) creating thermal energy in the process. I find your article very thought provoking. You sure got my wheels rolling! Angela " [1]

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" But I think that Medawar's argument was that all animals are subject to random accidents, predation, disease, etc. This will produce an exponential distribution of lifetimes. As a consequence, beyond a few half-lifes, there will be exponentially few members of the species. So if there is some mutation in the DNA which causes the animal to die beyond that time, there will be so few members of the species around to exhibit it that there will be effectively no selection pressure to keep this mutation out of the population. As a consequence, even if you started out with a population that could in theory live forever, it will very quickly become riddled with mutations which start to kill the animals after a couple of half-lifes. From the outside, it would appear as though the animals were "programmed" to die at a certain time.

George Williams presented a similar argument, but also claimed that some mutations can increase an animal's fitness early in life at the expense of decreased fitness much later in life. If the animal will likely have died of some accident by that time anyway, this trait effectively has no downside and will be selected for. " -- antognini