LONGECITY

If cell division causes telomere shortening, then wouldn't having a high cellular turnover rate be a cause of aging? I heard that having a high turnover was a good thing? Would increasing the longevity of a cell be beneficial in reducing aging? Are there drugs aimed at modifying, or perhaps, modulating the cell turnover rate of an organ/cell type/organism?

We know today that ageing is a result of several things going on at once.  To name a few vectors:

• - Inflammation of the hypothalamus has been correlated to ageing, so we know good communication through all nervous systems (CNS/PSNS/SNS/ANS/PNS) is essential.
• - Therefore we know that chronic desensitization to, and/or reduction of, neurotransmitters, is also a vector for ageing since this vector would make all organs not work optimally.
• - Circadian rhythm that is not "calibrated" can cause chronic damage attributed to ageing (such as the liver doing different circadian operations other than the ones it's supposed to be doing while you're sleeping).
• - Running out of your pool of stem cells.
• - Running out of your telomeres which makes mitosis essentially come to a grinding halt (aka Hayflick limit).  This brings us to the next vector:
• - Threshold of senescent:non-senescent cell ratio in any particular organ or tissue is crossed towards being overwhelmingly senescent.
• - etc. etc.

So yes, a high cell turnover rate is one of the ways in which one's body can quickly deteriorate in theory.

Yes; in some circumstances a high turnover rate can be favourable in terms of a tissue or organ as a whole, through the effect of abundance: the younger/less senescent cells will proliferate more-so than senescent ones, and therefore you will remain with more youthful cells while the senescent ones die off without proliferating because all the protein/nutrients will be used up by the more active cells.

In terms of increasing "longevity" of a cell, the closest scientific insight we have for this is the observed/documented effect of "reprogramming" a cell into thinking it's new just like we see in newborn infants (usually by converting the cell back into a stem cell first).  So yes, it would be beneficial for sure, though it's still a phenomenon today because this "longevity clock" or "biological clock" mechanism is yet to be fully elucidated/characterized through research.

There are indeed all kinds of pharmaceuticals and nutraceuticals that affect rate of proliferation but without the indication that the drug is meant for anti-ageing; it'd be more of a side-effect.  Even food alone affects rates of proliferation.  You can search through pathway maps to find which does what.  For example: PPAR-delta signaling affects proliferation of skin cells, and arachidonic acid is one of the factors in the pathway map, so peanuts / peanut butter regulate(s) keratinocyte proliferation.  etc. etc...

> Threshold of senescent:non-senescent cell ratio in any particular organ or tissue is crossed towards being overwhelmingly senescent

Yes, at least in the short term the ratio may play a beneficial role. However, if the cost for this is a lower average or mean telomere length, then it's likely to be be associated with some long term risk. Hav had some interesting alternative thoughts on how this might be working.

> Threshold of senescent:non-senescent cell ratio in any particular organ or tissue is crossed towards being overwhelmingly senescent

 

Yes, at least in the short term the ratio may play a beneficial role. However, if the cost for this is a lower average or mean telomere length, then it's likely to be be associated with some long term risk. Hav had some interesting alternative thoughts on how this might be working.

In the post you referenced, hav seemed unsure as to how the benefits work out in the end.  Keep in mind that the telomeres are part of the chromosome itself, and they get copied during DNA replication when a cell divides.  A chromosome's highest weight density is at the centromere.  From that point, kinetic energy makes the q and p arms of both chromatids flail around.  The longer the telomere --> the longer the arm --> the more distance the telomere covers as it flails --> the higher the likelihood of binding to SIRT1 for adhesion to the nucleus wall and continue with successful mitosis.  (You will end up with many more cells that have copies of these chromosomes with longer telomeres.)  Therefore, the cells with shorter telomeres will take longer to multiply than cells with longer telomeres.  This goes on until all the cells with shorter telomeres die off due to apoptosis, oxidative stress, or whatever may end up terminating those cells' lives.  All that remains are cells with longer telomeres.  This is a natural effect.

That being said, nutrients such as lipoproteins are needed to be able to proliferate.  If the number of senescent cells are allowed to outnumber the number of non-senescent cells, then there will not be enough nutrients available for the non-senescent cells to follow through with the effect I described above for natural riddance of senescent cells.