“Alzheimer's disease. One is called metformin, which is a diabetes pill. And the other is actually an ADHD drug called Stratera. And this is a trial of about 1,000 people.”
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“Alzheimer's disease. One is called metformin, which is a diabetes pill. And the other is actually an ADHD drug called Stratera. And this is a trial of about 1,000 people.”
“dementia. That said, the reason I bring it up is metformin is a metabolic drug. It's a diabetes drug. Think about that. They've moved away from targeting beta-amyloid to finally recognizing that metabolism is a central player here.”
“to the drug that's now being used in the Alzheimer's trial right here in England. Think about that. That metformin. Metformin does many things that exercise does.”
“But again, upstream of all of this is the energetics. It's the mitochondrial fun. And this is what is so sensitive to our metabolism, to insulin, to exercise on the positive side, to metformin on the medication side. We're damaging our mitochondria, and that's causing it to malfunction and then change from the M1 to the evil twin.”
“our ability to get rid of defective mitochondria. Exercise does it. And metformin does it as well. This drug that is being used right here in England now is part of a treatment protocol for Alzheimer's. Metformin? Is that what metformin is?”
“The question was asked: how many of you are taking metformin? This is about eight years ago. And I think 80% of the scientists raised their hands. What you're not hearing from me right now is that we should all jump on board and take metformin.”
“It's, I think, about a $70 million project. He can't get funding because metformin has gone off patent, so nobody's going to get the brass ring at the end of the day. But it's looking at the intervention of taking this drug, metformin, to see what effect it has on longevity and dementia for that matter.”
“Exercise is the single most validated reproducible longevity intervention available. Multiple randomized control trials have demonstrated that metformin actively interferes with exercise's adaptations. Number two is risk of masking lifestyle fundamentals in long-form clinical data.”
“And metformin was described and rapamycin was described. What led the list, and you know, and he's a big NAD guy, as you know, what led the list was exercise in terms of these aging clocks.”
“all of the things are getting better, even cancer markers. But we don't know if it's like metformin where it works really well in individuals that are overweight, but it can be detrimental in those people that are at a healthy weight.”
“Some are trying to manage blood glucose using metformin or berberine, neither of which I do, I should be clear. Some are taking even more aggressive measures. And now there's the discussion about the GLPs.”
“the DRTRCR framework. Why I stopped taking metformin for longevity and my shifting position on rapamycin. Whole body MRI and liquid biopsies for cancer screening, including why I think whole body MRI data quality has actually gotten worse”
“So metformin, we think of as fairly safe in pregnancy and potentially helpful. But really, insulin is most effective and we have good safety data, and it has the best influence on improving the neonatal outcomes.”
“What about metformin? What about red light therapy? What about hyperbarics? We can talk about those things, but the broad strokes are what we've just mentioned. And do them. You've got to do them.”
“There's a future there. Even the drug metformin has a mitochondrial play. So there's not just from its glucophage. It is glucophage. But there's much more than simply the activation of the AMP kinase that it looks like metformin glucophage is doing.”
“taking metformin are gaining, if they're gaining anything, and I think they will, based upon this way of targeting their mitochondria. But guess what? You've got incredibly powerful tools for targeting your mitochondria right now.”
“That's only about 3% of FDA-approved drugs do not have a clear mechanism of action. Yeah, metformin doesn't, is it? Right. Tylenol. Right. We have other examples of where the MOA is not known. So when you and I embarked on, okay, how are we going to get this to humans?”
“That's what you can do and you should do on a daily basis. It's what I do. Then there's drugs, which some of which may work. So that's metformin, rapamycin, some senolytics, and probably GLP1, receptor agonists would fall into that bucket.”
“In terms of like something that's hugely important. Yeah, I'm going to do it. And I mean, he's into science. He's been taking NMN resveratrol, Metformin, exercising. He goes to the gym two or three times a week.”
“I see a lot of metabolic syndrome, and obviously one of the leading causes is insulin resistance and high blood sugar. And looking at some comparative studies between like GLP1s and Metformin and a 15-minute walk immediately after a meal post-prandial. It's so exciting. I mean, that's why. That's unbelievable. Like, that should be the first prescription.”
“So animal-derived versus plant-derived medicines is the way to think about it. You think about aspirin, you think about metformin, the statins, those were all discovered in, you know, plant tissues. Statins are more so fungi, but you get the point. Now we've been looking into animal tissues to find cures, medicines, treatments.”
“Yeah. There's an interesting study, a trim trial from Dr. Greg Fahey. He's doing a study where he's giving a cocktail of growth hormone, metformin, and DHEA. Gave that for 12 months and had the thymic size increase on imaging. The amount of CD4 or CD8 T cells increased and the ratio of which improved.”