LONGECITY

In a recent study published in The EMBO Journal, mitochondria were shown to trigger cell aging. Elimination of the mitochondria from aging cells rejuvenated the cells and enabled them to take on characteristics of younger cells. Furthermore, the levels of inflammatory molecules, oxygen free radicals and gene expression associated with aging dropped to the level characteristic of younger cells when the mitochondria were removed.

What do you make of this? Also, how does this bode with supplements such as PQQ which have been shown to trigger mitochondrial biogenesis?

References:

https://www.scienced...60204084958.htm

https://www.ncbi.nlm...pubmed/26848154

Bodes well for Auwerx and others who are pushing mitophagy.

Another way of eliminating mitochondria (eg, dysfunctional mitochondria) is to do take NAD+ enhancers over a period of some days. Nicotinamide will do this, and is both cheap and effective--

 

Dysfunctional mitochondria are a major source of the high level of ROS in aging cells in vivo and in vitro...Nicotinamide (NAM) treatment causes a decrease in mitochondrial respiration and reactive oxygen species production in primary human fibroblasts and extends their replicative lifespan. In the current study, it is reported that NAM treatment induces a decrease in mitochondrial mass and an increase in membrane potential (ΔΨm) by accelerating autophagic degradation of mitochondria.

 

http://onlinelibrary...09.00487.x/full

 

Note that it is not just the elimination of mitochondria, but the elimination of defective mitochondria and an improvement in the average membrane potential that provides the benefits. See Fafner55's post here. He experimented with nicotinamide riboside (NR) instead of nicotinamide (NAM), but given the figures showing a dramatic "decrease of mitochondrial mass in the NAM-treated human fibroblasts," there is no reason to believe that NAM is not sufficient to do the job.

See also Nicotinamide-induced Mitophagy.

Another way of eliminating mitochondria (eg, dysfunctional mitochondria) is to do take NAD+ enhancers over a period of some days. Nicotinamide will do this, and is both cheap and effective--

 

 

Dysfunctional mitochondria are a major source of the high level of ROS in aging cells in vivo and in vitro...Nicotinamide (NAM) treatment causes a decrease in mitochondrial respiration and reactive oxygen species production in primary human fibroblasts and extends their replicative lifespan. In the current study, it is reported that NAM treatment induces a decrease in mitochondrial mass and an increase in membrane potential (ΔΨm) by accelerating autophagic degradation of mitochondria.

 

http://onlinelibrary...09.00487.x/full

 

 

Note that it is not just the elimination of mitochondria, but the elimination of defective mitochondria and an improvement in the average membrane potential that provides the benefits. See Fafner55's post here. He experimented with nicotinamide riboside (NR) instead of nicotinamide (NAM), but given the figures showing a dramatic "decrease of mitochondrial mass in the NAM-treated human fibroblasts," there is no reason to believe that NAM is not sufficient to do the job.

 

See also Nicotinamide-induced Mitophagy.

Or nicotinic acid, right?

 

Or nicotinic acid, right?

 

Nicotinic acid has a half life of around an hour, compared to around 4 hours for nicotinamide. The latter vitamin also has the advantage of not causing skin flushing. So nicotinamide at a one to two gram dosage every four to eight hours for a couple of days should be inexpensive, tolerable and effective.