Interesting, since mitochondria ATP production is the main cause of ageing, because of generated oxidative stress, do you believe supplementing exogenous ATP would reduce mitochondria energy generation and therefore oxides gen? If so is having locally an excess of ATP toxic? What is the ATP half life in a cell, in blood? since ATP is not bioavailable orally studies should have tested it e.g. sublingually but they are far too mediocre to do so..

Also if you really want an intellectual challenge and to help me on a problem I fail to understand, is the debate on mildronate vs ALCAR effect on health. Mildronate: The main cardioprotective effects of meldonium are mediated by the inhibition of GBB. By subsequently inhibiting carnitine biosynthesis, fatty acid transport is reduced and the accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues to produce energy is prevented, therefore blocking this highly oxygen-consuming process.[4] Treatment with meldonium therefore shifts the myocardial energy metabolism from fatty acid oxidation to the more favorable oxidation of glucose, or glycolysis, under conditions where oxygen is limited. It also reduces the formation of trimethylamine N-oxide (TMAO), a product of carnitine breakdown that has been implicated in the pathogenesis of atherosclerosis and congestive heart failure. https://en.wikipedia.org/wiki/Meldonium#Physio-pharmacology

https://en.wikipedia.org/wiki/Acetylcarnitine#Biochemical_pr... ALCAR has many many studies showing a potent improvement of health/metabolism and especially a reduction of oxidative stress. Despite this, ALCAR supposedly do the opposite of mildronate, it shift the mitochondria bioenergetics to an increase in beta oxidation and reduce glucose consumption. Beta oxidation is oxidative stress but I believed glucose oxidation leads to more oxidative stress?

How to make sense of those contradicting both positive narratives ?? Also weird detail: Excess acetyl-CoA causes more carbohydrates to be used for energy at the expense of fatty acids. This occurs by different mechanisms inside and outside the mitochondria. ALCAR transport decreases acetyl-CoA inside the mitochondria, but increases it outside.[4][5] plz halp