Yes, the main ones are that I take metformin (1500 mg daily), acarbose (with starch rich meals), high dose chromium, vinegar, cinnamon, and also a little bit of R-ALA. The only one of these that made an obvious difference in my blood glucose was the chromium, and it only made a difference when I increased the dose from a few hundred micrograms daily to 1000 mcg daily.
I haven’t researched SGLTi’s, but based on their mechanism of action I would think they are likely beneficial for most people, even those that are fit and healthy. However, people must be careful to make sure they don’t experience hypoglycemia when taking SGLTI’s. Hypoglycemic episodes can be harmful for the brain and they are not always easy to notice.
I see. Even if you were right (which I don’t necessarily think you are), lack of somatic renewal is still only a part of the causes of aging. There are lots of things that are of major importance for aging that cannot be renewed at all and therefore have other causes than somatic renewal problems. Glycation is one such problem.
I think this is very wrong. Yes, technically the process of glycation is the same in all species, since glycation is a stochastic process between molecules, and a such does not depend on the species and happens even in dead things. However, as far as being the same in all species, and therefore not effecting lifespan or healthspan, that’s not quite true. Longer lived species have evolved in ways to tolerate more glycation over their lifespan (and yes, improved renewal abilities would be a part of that) but I’m pretty sure most mammals end up having enough glycation damage at older ages that it contributes strongly to their aging and poor health. This is even more true for long lived mammals like humans because glycation damage accumulates slowly and poses more of a problem in long lived species.
As far as glycation effecting healthspan. The impact of glycation and AGE formation on healthspan is very obvious. You only have to look at how much stiffer all tissues in the body get with aging. A lot of that is most likely caused by glycation. For most of that damage, the body has no capacity to repair it, so even with cellular rejuvenation with epigenetic reprogramming the stiffness would remain. In fact, the stiffness makes cellular rejuvenation more difficult because it influences the programming of the cells.
A very clear example of the glycation damage, and the rejuvenation that can occur when you reverse that damage, is cataracts. As an example, you will see cataracts in old dogs as well as in old humans. It takes a lot more years to effect the healthspan of humans than dogs, because dogs live shorter and it occurs faster in them, but the effect is the same. Also while the body has no mechanisms to effectively reverse cataracts, it can be reversed partially with eyedrops containing n-acetyl-l-carnosine (NALC). This can be observed in various animals and even in lenses in vitro. Yellowish cataractic lenses become more clear in vitro after treatment with NALC, and regain some of their youthful flexibility. Also eyedrops containing NALC have been found to prevent and partially reverse cataracts in animals and humans. I think that’s just a glimpse of the rejuvenation that would occur if glycation damage could be reversed in the whole body. Also I’m almost certain that mitochondrial rejuvenation will not reverse glycation damage, although it would help slow it down. If you could replace all the mitochondria in your body of an old person with perfectly healthy young mitochondria, their cataracts would not disappear, neither would the glycation damage in most of the rest of their body. The body is fine with you getting cataracts at 80 years of age so it never needed to develop mechanisms to repair it. The same is true for all kinds of damages in the rest of the body. It doesn’t have mechanisms to repair them because it never needed it. Evolution only requires you to live to middle age to pass your genes along to the next generation.
