Dr. Brad’s take on Glycine. He takes it.
Short video on benefits below.
I just learned I should take it in the evening… thank you.
Weight loss drugs help against dementia.
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Dr. Brad weighs in on protein intake.
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@A_User you might have already found what you were looking for, but I remembered you asked where I saw Attia mention his protein advice of 2.2kg per kg. There is a quick snippet of him saying this in the short YouTube Destrider just posted.
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Related to Stanfield, weren’t the results of that Rapamycin with old people exercising study supposed to be out by now? He had the results back in June or July.
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It takes a while. However the results were positive as Dr. Brad is going to get his PhD in Rapamycin.
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Positive how? He sort of alluded to there being a significant difference between groups, but the groups weren’t unblinded yet. However, if the study was about exercise and Rapamycin, a difference means Rapamycin was detrimental vs control, or was beneficial vs control. If Rapamycin doesn’t affect exercise, there’s no significant difference to report.
I can’t see how a literal growth pathway inhibitor could be beneficial during exercise, so I’d have to assume it was detrimental. (Though I will of course love to be wrong)
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He says the results from the Rapamycin trial are available and anyone who is at the conference could talk to him and he’d tell them the results. Not sure why he didn’t talk about it in the video.
His top interventions:
- SGLT2IS
- Rapamycin
- GLP-1s
- PCSK9 drugs
Then he goes into skin aging at 13:30.
Also Matt Kaeberlein also probably knows the results. Can anyone reach out to either of these guys to get the results? @mkaeberlein care to share here or by DM?
Dr. Brad’s state of the union address on longevity. The first part is about criticizing resveratrol, so just skip that. He also criticizes Fisetin.
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The paper is under review right now and I don’t think Brad wants to talk publicly about the results until it’s in press. It’s his call, and I’m going ot respect his wishes. I will of course give my interpretation of the results once the paper is out. Brad and I sat down for a longer interview at the same conference, which should be out on the Optispan Podcast page soon. Podcast — Optispan
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Thanks, Matt! Truly appreciate your opinion and stance. We’ll all just have to wait patiently and of course watch your videos! 
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Odd presentation. How do glp-1RA and pcsk9i fit into being longevity drugs? As far as I know neither have been tested as such. And the literature on pleiotropic effects of pcsk9i is pretty sparse. Apart from the generally salutary effects of lowering LDL, what’s the longevity benefit for non-CVD people?
A lot of work went into the drawn out rocket analogy for a modest payoff and Dr. Brad seemed very nervous. I confess I couldn’t get up any curiosity to watch the skin care fragment, so maybe that was stellar.
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I would think generally keeping glucose levels down has benefits. Not such an obvious case of pcsk9i. I am personally, however, not persuaded by glp 1 agonists for myself. However, my HbA1c tends to be under 5.
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Preventing CVD is one of the most important ways of improving longevity as most people die of a circulatory disease caused by arteriosclerosis. You can take all the Rapamycin you want but it won’t help if you die of a heart attack. Preventing this is what PCSK9Is do best. That’s why he mentioned it. Also probably goes over better than talking about stations and Ezetemibe.
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Well, sure, but those are preventative or curative drugs, not longevity. If I cure or prevent a disease, it’s not a life extending drug, it’s just an anti-life shortening, an antibiotic can prevent an infection, but that’s not life extension, it can prevent you dying from an infection, but that again is not life extension. That’s why a statin, simvastatin failed in the ITP. For a pcsk9i to be a longevity drug, it would have to have a good ITP result. So let’s see it - I doubt it would. And until it does, you cannot make a longevity claim for it as is understood as a “longevity intervention” at a longevity conference - drugs that address CVD belong at a medical conference, a completely different animal.
PCSK9I, statins and all other CVD targeting drugs will fail in the ITP because mice die of cancer not heart attacks. However, 1 in 3 people globally do. Anti-death is as valuable as purely longevity IMHO.
Anything that works in the ITP is probably something that prevents cancer which is why the mouse model is flawed and why the marmoset study was so important.
The most common causes for marmosets to die are gastrointestinal issues, nephritis and trauma. Everything dies of something. Even when you die of natural causes in old age, it is usually heart failure. So every longevity treatment is also anti-death.
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An additional complication with any studies and particularly mouse studies is that a proportion of the animals are euthanised when they seem to be suffering. I am not criticising this, but there should be a distinction in the analysis between those that die naturally and those that die from human intervention as the latter is less objective. Hence a mouse may not die because of a tumour, but may have been euthanised because it has a tumour.
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Thanks Matt… keep up those fantastic interviews on Optispan. Looking forward to this one.
Optispan is playing on all my frequent trips around the state.
The one with Dr. Greg Fahy was an all time favorite and got me very interested in HGH. I play it often… you drilled on the details and delivered excellent information.
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Well when you dramatically reduce cardiovascular risk by virtue of reduced insulin levels and ApoB, you cut your risk of death, meaning your odds of living longer increase.
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Agreed that it wasn’t the best presentation. However, I think he was intending to tailor it towards the “investor conference”, rather than a biology/geroscience audience.
And I’m sure you know why he mentioned PCSK9is and GLP1RAs. Whether you “count” than as longevity drugs or not just depends on how you define longevity. But, in the context of the conference, they are recent examples of profitable drugs which are preventative/slowing-death in nature. (I agree that him framing them after explicitly mentioning the ITP was confusing though). And FWIW, I reckon GLP1RAs might achieve similar results to acarbose in the ITP, when they’re eventually tested.
IMO, Rapamycin was the odd one on his list out since it has very little commercial/investor value at this point. But obviously mentioned because of his own research interests.
Second FWIW: I heard Joe Hill (Editor of Circulation, former AHA president) speak recently and he said GLP1RAs have been transformative, and the biggest and most impactful new intervention he’s seen in his career. He described how you can take a cardiovascular patient with pre-diabetes, obesity, fatty liver, terrible lipids etc - and 9 months later they don’t have any of those things. You can also take patients and make them lose weight by diet and exercise vs GLP1RAs, and the latter group actually turn out healthier. Presumably that means there are other benefits than just the weight loss.