Niacinamide, dexamethasone and others have also been shown to extend lifespan of human fibroblast in vitro, producing as much as 1.6-fold increase in the number of population doublings . Why take a staining compound with a short track record in life extension properties? Astragalus has not been shown to extend telomeres in humans. Cycloastregenol a stronger compound than Astragaloside IV has only been shown to delay telomere shortening is some immune system cells.
In my opinion, the difference is the fundamental mode of action. The more specific and direct a mode of action, the better, I feel, unlike with niacinamide and others, which can reek havoc on other pathways (such as downregulation of Sirt1 by niacinamide) that may matter more in vivo than in vitro. That is, we know niacinamide and other metabolic precursors may have several potentially adverse reactions that could become iteratively exacerbated in vivo. This dye, on the other hand, specifically interacts with the mitochondrial electron transport chain when in proportion to cytochrome c levels to give its effects (upregulation of complex IV and ROS defense enzymes, reversal of mitochondrial dysfunction and senescence, not just prolonging life span but also robustness; may also replace oxygen in accepting stray electrons from complexes I and/or III and thus prevent ROS production instead of scavenging, while keeping mitochondrial respiration at its max), and this only occurs at extremely low doses (~100 nano molar, or ~1mg per day), well below the threshold needed for interacting with the other pathways it can target as part of its medicinal use.
That's another difference, that we're dealing with something that's been around and used in humans for nearly a hundred years, and then decreasing the dose, instead of boosting to obscene levels like with niacinamide and others. Boosting doses increases the probability of adverse and unexpected side effects when molecules begin interacting in unexpected ways due to new and favorable thermodynamics caused by overabundance. That is true for all supplements. I believe everything has a U shaped dose response curve, and so proper levels are important.
At any rate, in my view from all the research out there, there seems to be three main modes of aging, which pretty much go in order: mitochondrial dysfunction leads to increased ROS -> increased ROS damage to DNA/proteins decreases Sirt1 regulation of genes resulting in aberrant gene expression in differentiated cells, potentially disrupting function, leading to cancer, and causing many of the phenotypic effects of aging -> telomere shortening in somatic cells leads to chromosomal break down and ultimate life span limit. The four I listed specifically address these issues, which is why they are so interesting to me, at least. After all, for the replication of any species, all for of those issues have to be circumvented in gametogenic cells, so it's possible or there wouldn't be life as we know it.
That is all just my opinion on the matter - and there's certainly no short supply of opinions in the world . Finally, we'll find out more about astragaloside IV here shortly from Anthony in February, with any luck, or maybe even earlier after this 3 week period he speaks of so suspiciously, heh heh. And besides, any controlled telomerase upregulation should be better than none.
Your opinion is much appreciated. Bruce Ames certainly believes in MB and thats worth a second and a third look. So I'm softening my stance I also found this patent application with B. Ames as an inventor. http://www.wipo.int/...mp;DISPLAY=DESC . It may be worthwile to start a thread on MB.
About Nicinamide; we have an interesting thread about that. It may not be a significan sirt1 inhibitor in humans after all. I invite you to read it and give your opinion, especially if it is a negative one. http://www.imminst.o...showtopic=25586