Peter Attia is negative on SS-31 saying that its potential for targeting mitochondria “only does this in people that have a very, very serious genetic condition” (Barth syndrome).
He has missed the noted trial showing increased ATP in healthy elderly 60-85 years In vivo mitochondrial ATP production is improved in older adult skeletal muscle after a single dose of elamipretide in a randomized trial - PMC.
It is this study that makes me consider SS-31. However, 47 persons were excluded from the trial because they had too high mitochondrial function compared to the 39 below the cut-off point who were included. Are the positive effects on ATP likely to be valid for a person like myself, with an age within the target group but likely too high mitochondrial function to have been included in the study?
I asked Perplexity, after giving it my VO2 max and other numbers. Snippets from Its reply:
“At 78, the probability that you have no damaged mitochondria is essentially zero; aging inevitably produces: mtDNA mutations, cardiolipin peroxidation, accumulated ROS damage and heterogeneous mitochondrial quality across fibers and tissues.
You almost certainly have a non trivial fraction of damaged/dysfunctional mitochondria, simply as a function of being 78, even though you have excellent fitness for your age.
It’s plausible that in some muscle regions or other tissues (e.g., cardiac, kidney, brain, or less trained muscle groups), there is more mitochondrial impairment than your cycling metrics reveal; VO₂max is heavily influenced by heart + trained muscle, not all tissues.
So the answer to “Am I likely to have a fair amount of damaged mitochondria?” is “yes, but probably less than typical for 78, and your functional tests indicate that the integrated system is performing at a high level despite that.”
Key Takeaways
- Some mitochondrial damage at 78 is virtually guaranteed, but your excellent VO2 and lactate profiles indicate that your overall mitochondrial and cardiorespiratory function is high for your age.
- You probably have less severe mitochondrial impairment than most 78 year olds, especially in your trained cycling muscles, though other tissues may still harbor more dysfunction.
- If we’re considering interventions like SS 31, your data support the view that there is some room for mitochondrial “normalization,” but not a huge deficit, so any drug effect would likely be modest on top of already good function”
Given that mitochondrial health may be the top longevity issue, a modest effect is enough to make me consider SS-31.
