This might scare some of us straight! I'll have to summon this from my memory next time I walk into carb-hell (work kitchen lately).

http://www.drperlmutter.com/dietary...-new-frontiers/

Well, it sure scared me. No more thinking that an occasional 'carb up' day won't hurt. Apparently, it hurts a lot.

Ooooh... if only I'd reread this before last night. Oh well! Thanks for bumping it. Better a late reminder than none.

Pottenger already established the epigenetic effect of diet on cats, though maybe he didn't see it that way back then. What he really found out was that the current generation's diet had an effect on future generations, right up to the point of infertility at the fourth generation. Pottenger's work was with chronic dietary deficiency. I think what we see here is acute dietary poisoning, i.e. excess of a thing rather than lack of a thing.

There's a few things going on. First is the damage from oxidative stress. That's probably plain old atherosclerosis. Then there's the epigenetic changes, but I have no idea what those specific genes do, don't do, or do different once they're flipped by the acute glucose bolus. I'm gonna say it's either a genetic adaptation involved in the repair of oxidative damage caused by the acute glucose bolus, repair which takes time and explains why the epigenetic effect lasts several days, or it's outright detrimental and this means nothing good in the end but I have a hard time figuring this part out. I mean, if the epigenetic effect of an acute glucose bolus is outright detrimental, then there's no more ambiguity about what dietary glucose really is.

And then we have genomic aging, the shortening of telomeres. I know pretty much nothing about this, but I suspect telomeres don't just get shorter, I bet they can also get longer with the appropriate stimulus. Genes are maintained by enzymes, so it's possible some enzyme takes care of telomeres too. If that's possible, then it's also possible telomeres could be lengthened by some other enzyme. I'm gonna say a healthy cell does all this without explicit external stimuli. I mean, it's not like cells are programmed to kill themselves that way when they're healthy and working properly. So maybe if we just avoid the acute glucose bolus for long enough, cells will eventually repair all the damage, including the damage done to telomeres.

Then there's the question of amplitude. Just how acute must the glucose bolus be in humans for this effect to show itself? Depending on the answer, we could be looking at the withdrawal of the OGTT as standard medical practice, cuz you know, that's an acute glucose bolus if I've ever seen one.

Finally, the whole thing supports my paradigm, which says dietary carbohydrates disrupt normal metabolism of all fuel substrates. But here, instead of this mysterious and vague metabolism, we have tangible evidence of the effect in the form of epigenetic changes. It's good to know.

I think it's important to put this into the proper context. It's not like carbs are the only thing that do something like that. I'm sure alcohol, tobacco, and a slew of other substances we commonly consume also do this to different degree. Also, the effect could be dose-dependent, such that say, a 50g glucose bolus affects only some cells mostly near the primary site of intake into the blood, a 100g bolus affect more cells and further away, and a 200g bolus affects pretty much all cells everywhere, etc.

I'm gonna say most of us on this forum don't eat our entire daily carbs quota in a single sitting, so we're safe for the most part. But if we do, then we now have more info to allow us to organize our indulgences in a less harmful way. Also, one of the papers says the epigenetic effect lasts at least 6 days, but I suspect the effect duration is dependent on post-bolus diet as well. We eat mostly low-carb and this could affect post-bolus duration.

Some research shows exercise can activate telomerase and help protect telomeres.

http://cardiobrief.org/2009/11/30/c...ting-telomeres/

There is also research on how telomeres can be protected and even lengthened through supplementation. One study that showed telomeres actually getting longer used omega-3 supplementation, particularly improving the omega-6 to omega-3 ratio

http://www.sciencedirect.com/scienc...88915911200431X

But only a fraction of the cells in the body even have telomeres. So elongating them may make absolutely no difference.

I read the first link, and a question popped up that I didn't find the answer to in there. It's like this, isn't it possible telomere lengthening is an adaptation to the greater oxidative stress induced by exercise itself, so that longevity remains the same? But as opposed to the oxidative stress of an acute glucose bolus, we're much better adapted to the effects of exercise. Incidentally, exercise causes BG to rise, so the telomere stuff going on with exercise could just be a parallel effect to compensate for this otherwise normal BG rise. This means if BG rises without all the other stuff that comes from exercise, it's probably not a good idea. Now that I think about it, I wonder if the epigenetic effect of a dietary glucose bolus also occurs with exercise, since BG rises there too. I remember Taubes explaining how exercise has a lasting effect on insulin sensitivity, something like a couple days.

I will be celebrating with pickles, pistachios, and pepperoni from now on. (Not that I indulge any more.)