A link to the paper covering details of membrane pacemaker theory of aging

 

More than 100 years ago, Max Rubner combined the fact that both metabolic rate and longevity of mammals varies with body size to calculate that "life energy potential" (lifetime energy turnover per kilogram) was relatively constant. This calculation linked longevity to aerobic metabolism which in turn led to the "rate-of-living" and ultimately the "oxidative stress" theories of aging. However, the link between metabolic rate and longevity is imperfect. Although unknown in Rubner's time, one aspect of body composition of mammals also varies with body size, namely the fatty acid composition of membranes. Fatty acids vary dramatically in their susceptibility to peroxidation and the products of lipid peroxidation are very powerful reactive molecules that damage other cellular molecules. The "membrane pacemaker" modification of the "oxidative stress" theory of aging proposes that fatty acid composition of membranes, via its influence on peroxidation of lipids, is an important determinant of lifespan (and a link between metabolism and longevity). The relationship between membrane fatty acid composition and longevity is discussed for (1) mammals of different body size, (2) birds of different body size, (3) mammals and birds that are exceptionally long-living for their size, (4) strains of mice that vary in longevity, (5) calorie-restriction extension of longevity in rodents, (6) differences in longevity between queen and worker honeybees, and (7) variation in longevity among humans. Most of these comparisons support an important role for membrane fatty acid composition in the determination of longevity. It is apparent that membrane composition is regulated for each species. Provided the diet is not deficient in polyunsaturated fat, it has minimal influence on a species' membrane fatty acid composition and likely also on it's maximum longevity. The exceptional longevity of Homo sapiens combined with the limited knowledge of the fatty acid composition of human tissues support the potential importance of mitochondrial membranes in determination of longevity.

https://www.researchgate.net/publication/51113341_Metabolism_and_longevity_Is_there_a_role_for_membrane_fatty_acids

IS AGING PROGRAMMED? Aubrey de Grey vs. Yuri Deigin debate at Vitalist B...

comment: one thing is that parasites, diseases, germline mutations accumulate with age, fighting all of these is easiest by killing organism, that is in addition to increased evolvability. Also, the exceptions to the free radical theory of aging were explained away with the membrane pacemaker theory of aging, wherein membrane resilience determines rate of damage accumulation. Evolution determines membrane composition, during Calorie Restriction and similar interventions organism even alters membrane composition in a controlled manner increasing lifespan drastically.

In organisms like insects same genome different epigenetic regulation allows 10x--100x lifespan difference between queen and workers. But even here, it was believed queens of some species might be immortal, but for whatever reason it was found that sequential replacement with clones was easier for nature than actual immortality, the longest lasting queens last like 30 years ageless iirc, with extreme reproduction.

Few snippets on aging

 Compared to other elderly, membranes from centenarians (> 100 yrs) showed:
1) decreased lipid peroxide levels and reduced susceptibility to peroxidation
2) increased unsaturated/saturated fatty acid ratio
3) higher levels of EPA and DHA, reduced LA and AA
4) higher fluidity 
Membranes from centenarians show some distinct features in comparison with elderly subjects that might act in a protective way against injuries
 -http://www.waiworld.com/waitalk/phpBB3/viewtopic.php?f=20&t=3385

The above is from a thread where the topic of membrane composition, peroxidation and lifespan is covered

I was reading the book Neurons and the DHA Principle, and it seems that neuron's have substantial polyunsaturated fat content in membranes but can overcome this by antioxidant defenses.   Given these are the longest lived cells in the body and can function for over 120 years(oldest human is said to've been free from dementia), it suggests to me that if some lipid soluble antioxidant was found that didn't turn pro-oxidant nor significantly interfered with ROS signalling it could be an overall positive.

The accumulation of lipofuscin-like material may be the result of an imbalance between formation and disposal mechanisms: Such accumulation can be induced in rats by administering a protease inhibitor (leupeptin); after a period of three months, the levels of the lipofuscin-like material return to normal, indicating the action of a significant disposal mechanism.^[3] However, this result is controversial, as it is questionable if the leupeptin-induced material is true lipofuscin.^[4][5] There exists evidence that "true lipofuscin" is not degradable in vitro;^[6][7][8] whether this holds in vivoover longer time periods is not clear.-link

Assuming the cells can't actually digest it, all that would be necessary is some mechanism to export the waste and discard it elsewhere.   Whether such a mechanism exists is a good question, but I think it is likely. 

We report that long-term overexpression of
Parkin can eliminate mitochondria with deleterious COXI mutations
in heteroplasmic cybrid cells, thereby enriching cells for wild-type
mtDNA and restoring cytochrome coxidase activity.-link

Emerging data indicate that selective mitochondrial degradation through autophagy (mitophagy) plays a critical role in mitochondrial quality control. Inhibition of mammalian target of rapamycin (mTOR) kinase activity can activate mitophagy. To test the hypothesis that enhancing mitophagy would drive selection against dysfunctional mitochondria harboring higher levels of mutations, thereby decreasing mutation levels over time-link

The mitochondria has its own dna, it codes for vital functions not redundantly covered in the nucleus.  It is subject to direct exposure to damaging reactive species, so it can become dysfunctional much more easily than the dna in the nucleus.   An obvious question was how can such an organelle subject to far more mutational damage not lead to extinction of most any species.   A method of quality control has been found in female reproductive systems, iirc at the level of discarding cells, again iirc.   But it opened the question as to whether an intracellular method of quality control might also exist(after all neurons last for over a century of high metabolic activity and they don't divide).  As the above two links show it seems very likely there is a method of quality control that can preserve mitochondrial quality.