Latest insights on Alzheimer's disease, cancer, exercise, nutrition, and fasting | Rhonda Patrick, Ph.D.

**Peter Attia** (0:11)
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Now, without further delay, here's today's episode.
My guest this week is Rhonda Patrick. Some of you may recall that Rhonda was one of the original guests on the pilot series of The Drive back in July 2018 when we were trying to figure out if we really wanted to do a podcast. Well, of course we did, and it is awesome to have Rhonda back. Rhonda also hosts her own podcast called Found My Fitness.
In this episode, we focus the conversation around a few important concepts, and we talk about Rhonda's current interests along with areas where her perspective has either shifted or evolved over the years. We start the conversation with a deep dive into Alzheimer's disease. We talk about the possibility of a vascular hypothesis for Alzheimer's disease. And we also talk about the different factors that can affect Alzheimer's disease, including type 2 diabetes, omega supplementation, blood pressure, exercise, sauna, and more. We then go on to talk about the relationship between exercise and cancer, and also the relationship between alcohol and cancer. And then finally, we talk about protein and aging, and we talk about fasting, time-restricted feeding. These are two areas where Rhonda and I have had different points of views over times, and both of our views have evolved. I think in some ways, we're actually converging at about the same place now. So this is a really interesting discussion. It was really exciting to sit down with Rhonda. It had been far too long. And so I hope you enjoy this discussion half as much as I did.
Rhonda, it is so great to see you, especially on that awesome remote setup that I almost shouldn't have said to people was remote, because it really feels like we are in person, about as close to in person as we've been in a few years.

**Rhonda Patrick** (2:25)
It's really great to see you, Peter. It's been a minute.

**Peter Attia** (2:28)
We'll meet together soon in a couple of months. So I'm looking forward to that. There's a lot to catch up on. Over the past few years, we've obviously exchanged a bunch of emails about things that we each find interesting.
And I think in the last couple of years, well, let's just pause it in the last five years, was the last time we did a podcast. Just going back to that point, I think both of us have evolved a lot in our thinking. And I think we've done so unapologetically. That's the nature of science. That's the nature of what we do and we're trying to learn. So in thinking about our discussion today, I think we both agreed it would be most enjoyable to at least spend some time talking about areas where your thinking has evolved.
But I think first, we wanted to start with, I don't want to put words in your mouth, but maybe that which you're thinking about the most right now, would that be a safe assessment if we were to start to talk about dementia, specifically Alzheimer's disease, and maybe the change in how you think about that?

**Rhonda Patrick** (3:19)
It would. For me personally, I have neurodegenerative disease on my mind quite a lot because Alzheimer's disease and Parkinson's disease both run in my family.
And I have a genetic predisposition.
So for me understanding everything I can do with my diet, with my lifestyle, exposure to, or limiting exposure to certain things, et cetera, becomes paramount because I don't want to get Alzheimer's disease and Parkinson's disease.
Like as you know, Peter, the Alzheimer's disease field has been, it's been quite a roller coaster in a way. Like we've had this dominating hypothesis, this amyloid hypothesis as it's called. So there's, you know, one of the major pathologies of Alzheimer's disease are amyloid plaques in the brain.
And there are other pathologies, tall tangles, also glucose hypometabolism. So glucose uptake into the brain is impaired and also perhaps even the utilization of glucose as well. These are like three major pathologies of Alzheimer's disease. And it seems as though the majority of targeting how science and scientists have decided to target Alzheimer's disease is through this amyloid, anti-amyloid hypothesis. And as you know, we've had quite a few failed trials, although of recent a little bit more, I would say, possible success maybe. But generally speaking, it's been, are we just trying to treat a symptom here or are we too far downstream? Like what's the deal? And I started reading some studies by Barisov Slovovich at USC and Dr. Axel Montaigne, who was trained with Dr. Slovovich and now has his own lab at the University of Edinburgh in Scotland. I recently did a podcast with him on my podcast and it was really like when I started to read some of this literature and I'm going to talk about like what this sort of new, it's not even necessarily new, but like it's not a new way of understanding it, but it is in a way because in the public opinion, in the public mind, it's a new way. This is sort of like, okay, well, what are the underlying causes of dementia? So there's three major types of dementia, Alzheimer's disease being the most common, there's small vessel disease, cerebral small vessel disease, and then vascular dementia. Those are the three most common forms of dementia. But like is there a common underlying denominator between those? On top of that, what sort of lifestyle factors and genetic factors do we know really increase the risk of Alzheimer's disease and dementia? Well, we know having an APOE-4 allele, so this is a version of a gene that is known to increase the risk of Alzheimer's disease. If you have one of them, it increases the risk twofold. If you have two, if you got one from mom and one from dad, it could be up to tenfold. And this isn't like an early onset Alzheimer's disease. It's more of what's called late onset, which is the normal sort of age-related aggression of Alzheimer's disease. But that gene really does play a role in someone's risk.