Cancer, Diabetes, Cynthia Kenyon discussed on The Peter Attia Drive


We know 'em tour which and i'll go back to rapamycin in part because you know it's again something i think a lot about but it actually. It's a really good. I think example in specific case. Because we know that. Mtr which is the target of rapamycin right. The protein that rapamycin inhibits plays this fundamental role in regulating cell division and cell cycle. Right so if you inhibit in a in a noncancerous i'll if you inhibit tour enough you will stop the cell cycle. The cell will stop dividing right but there are mutations that can happen that lead to cancer that caused the cell to no longer pay attention to the tour break right and so once. That's happened if that's the type of cancer you have that no longer responds to. Mtr inhibition. rapamycin won't do anything to sell cycle and in that case so that's a really specific example that you can point to their. They're sort of an infinite number of other examples that we could use. But that's a really nice one because they're rapamycin will be quite effective at preventing cancer before that mutation happens but after that mutation happens in the cells not responding to rapamycin anymore. because it doesn't sit sense the tour break it's completely ineffective right. So that that. I think is is a case where the mechanisms have changed the mechanisms that are important for preventing cancer before that mutation occurred are different from the mechanism that my deal with that cancer after that mutation has occurred. Yeah it's funny. This is a little off topic. But i've often contemplated this question in the context of nutrition because inasmuch as there's an optimal nutrition to prevent a condition. It might not be the same as the optimal nutritional strategy to treat the disease. Once its present. An example of an extreme sense might be a ketogenic diet. I happen to believe a ketogenic diet is probably the best treatment for someone with type two diabetes because of course type two diabetes by its very definition is a carbohydrate intolerance disorders. A once a person has it. You pull out the carbohydrates completely and you let them. He'll right you basically let them recover and regain their ability. You know and again. We've seen that people who have been on a ketogenic die for a long period of time can resume some amount of carbohydrate consumption provided there other factors are changing such as exercise. Does that mean one needs to be on a ketogenic diet to prevent diabetes. No i don't think so so. It's a little bit of the same idea though. It's still something that's unclear. One thing i want to go back to on the disease front is and i believe it. Was cynthia kenyon who who spoke about this once. I think i read it in a paper. Something to the effect of using a disease based definition for aging is she didn't use the word tautology but she effectively said it is a bit of a topology because at what point is a disease a disease. It's only a disease when some people have in some people don't if everybody has cancer by a certain age than its normative aging to your point. It's no longer a disease and then we get into. What does it mean that something like. Why do you know point. Zero zero zero. Four percent of the population lived to be one hundred. They've managed to not succumb to a disease by the age of one hundred. And what does that tell us about their normative aging versus everybody else. All of this is to say. I literally still don't think i understand what age which is unfortunate. Given my line of work we have to just accept that. It's extremely complicated right. And so you're never say never. I don't think i will ever understand aging fully. And i don't think the field will at least in any timeframe that i can expect to experience right but i also believe that we don't have to understand it fully to be able to have an impact on the biology of aging through interventions and. That's kind of where i'm at. I feel like i've got a conceptual flavor for what aging is. And i have a some information about what the molecular mechanisms are. It's enough information. That i can come up with rational. Approaches to target those mechanisms with the prediction that those approaches should have an impact on health and longevity as animals and people get get older and then we have to test those predictions. That's kind of the way i think about it. I do want to come back to one point. Though which i also think is often under appreciated in this relationship between disease and the biology of aging. Sometimes people get into this debate about whether or not. The biology of aging causes diseases of aging rights does the biology of aging cause alzheimer's disease cancer cardiovascular disease right people get in debates about that and i personally think the date are pretty good that these that what i think of is the biology of aging the molecular mechanisms the hallmarks whatever. You wanna call them. Contribute in a causal way to your risk of developing diseases. But i also think it doesn't matter in this i think is really important. From the perspective of what is the best strategy to keep people healthier longer. It just doesn't matter whether aging causes disease or it creates a permissive physiological state for disease. You can't argue. That biological age is the single greatest risk factor for every major cause of death and disability developed countries. That is just a fact and whether or not biological age causes those diseases or creates a physiological state that allows diseases to manifest themselves doesn't matter from the perspective of what is the most effective way to prevent those diseases and i think that's where this debate is counterproductive right. Should we call aging disease. Does aging caused disease. I think those are. Those are not the right questions to be asking in my view. Yeah let me see if you would agree with my assessment. I think you would but it. I'll tell you how. I think about this problem clinically. So let us atherosclerosis. As an example. And i want to highlight what you just said. In case the person watching this or listening to this missed it in any way shape or form. When i used to give talks. I had always lead with a question like this. What is the greatest. Risk factor for atherosclerosis. Handle go up yes smoking now handle. Go up high blood pressure now. Hand will go up if it's an especially area date audience. Ab or ldl. See now and they'll just keep rattling inflammation. Nope nope nope nope. The number one thing is age hands down. You take a seventy year old person. Who has everything perfect about them. And you compare them to a twenty year old trainwreck. Who has not a single thing that is in their favor. There is no comparison about their ten year mortality prediction. That the seventy year old is enhanced down in worse shape. So you can't do that now. Here's how i think about this problem. Clinically atherosclerosis is a great example. Because it's the disease that we understand the most of the big right which is not to say we understand it completely but we have a far better understanding of what it's drivers are and how to prevent it than we do cancer. Alzheimer's disease lowering ape. Ob pharmacologically nutritionally etc is arguably the most important strategy. You have to reduce it along with probably improving metabolic health. So those two things rights regulating glucose. Insulin lowering apo. All of these things can be done through lifestyle through drugs..

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