Ep. 57: Fighting Late-Onset Alzheimer’s with Prof. Francisco Gonzalez-Lima

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Most of the conventional wisdom about late-onset Alzheimer’s disease is wrong, according to Prof. Francisco Gonzalez-Lima of the University of Texas at Austin. In this conversation with Medcan Chief Medical Officer Dr. Peter Nord, Gonzalez-Lima (pictured above holding a donated brain) argues against the old hypothesis that amyloid plaques and tau tangles cause dementia in the aged. Instead, he says neurological problems arise due to vascular issues and the inhibition of an enzyme called cytochrome oxidase—which can be treated with infrared lasers and a substance called methylene blue.

Guest bio

Francisco Gonzalez-Lima, Ph.D., holds the George I. Sanchez Centennial Professorship at The University of Texas at Austin, where he is a professor in the departments of Psychology, Psychiatry, Pharmacology and Toxicology and the Institute for Neuroscience. Learn more.

Insights

The most common type of dementia is the one that is related to old age, says Prof. Francisco Gonzalez-Lima. That’s referred to as Alzheimer's disease—and he argues that it isn’t related to the early-onset variant. “My argument is that these are two very different diseases with different causes, and they affect different age populations,” says the University of Texas at Austin professor. “Most importantly, the amyloid plaques and the tau tangles are not the cause of this common type of dementia that we see in older people.” And further: “This is an important concept because a lot of the research [95%, he says] is aimed at understanding the early onset Alzheimer's, with the assumption that if we understand that, then we'll be able to treat the other common type of Alzheimer's that happens in older people. And these assumptions are not based on a clear scientific basis.” (Time code: 3:20)

“Old age is the number one risk factor for these late onset types of dementia that we're referring to as Alzheimer's disease,” says Prof. Francisco Gonzalez-Lima. “As a function of age, we have chronic deterioration in our vascular system, the circulatory system. And this compromises the blood flow to the brain, but most importantly, the oxygenation to the brain.” Central to this process is a mitochondrial enzyme called “cytochrome oxidase,” which catalyzes a cell reaction crucial to aerobic energy production. “And the important point is that as we grow older, the mitochondria… and cytochrome oxidase... are losing some of its enzymatic catalytic capacity.” (Time code: 6:15)

How the mechanism that causes age-related dementia is related to Soviet spies: “As long as you have about two thirds of the amount of the enzyme [cytochrome oxidase] working, you're still alive,” says Prof. Gonzalez-Lima. “But if you inhibit 40% of the enzyme, you're going to die from carbon monoxide intoxication. So every major classic poison that we can think of—it affects oxygen metabolism, it is likely doing that through cytochrome oxidase. For example, the most classic poison out there is cyanide. And from the early days, people committing suicide with cyanide or poisoning their enemies in the cold war with the Soviets. All the Soviet spies had cyanide in their rings… just consuming a small amount of cyanide inhibits enough cytochrome oxidase that you die within minutes.” (Time code: 9:00)

The other important cause of age-related dementia is the declining ability of blood vessels to oxygenate the brain tissue with blood, says Prof. Francisco Gonzalez-Lima. “So not only do we have enzymes in mitochondria, that are less effective at doing their energy production, we have less supply of oxygen, and all the issues like increased blood pressure, that are also damaging the flow through the arteries that supply the brain. And so the probing is compounded at several levels. It is naive to think that there is one cause of dementia in the elderly, When I'm talking about mitochondria and the vascular hypothesis, they are all operating in parallel.” (Time code: 10:45)

Links 

Dr. Peter Attia’s longer interview with Prof. Francisco Gonzalez-Lima clocks in at 150 minutes or so and will tell you pretty much everything you want to know about the science behind transcranial laser stimulation, the vascular hypothesis of Alzheimer’s, cytochrome oxidase and methylene blue. Check it out.

Augmentation of cognitive brain functions with transcranial lasers. Front. Syst. Neurosci. 8:36. doi: 10.3389/fnsys.2014.00036

Protection against neurodegeneration with low-dose methylene blue and near-infrared light. Front. Cell. Neurosci. 9:179. doi: 10.3389/fncel.2015.00179

Cognitive Enhancement by Transcranial Photobiomodulation Is Associated With Cerebrovascular Oxygenation of the Prefrontal Cortex. Front. Neurosci. 13:1129. doi: 10.3389/fnins.2019.01129

Methylene Blue Preserves Cytochrome Oxidase Activity and Prevents Neurodegeneration and Memory Impairment in Rats With Chronic Cerebral Hypoperfusion. Front. Cell. Neurosci. 14:130. doi: 10.3389/fncel.2020.00130

Using Lasers to Fight Late-Onset Alzheimer’s with Prof. Francisco Gonzalez-Lima final web transcript

Christopher Shulgan: This is episode 57 of Eat Move Think, and I'm Christopher Shulgan. If you ask most people about the scariest and most worrying elements of getting old, most of them will mention Alzheimer's. There's the comparatively rare, early onset form, with symptoms manifesting before the age of 65, and then the much more common version that happens later. If you break it into very rough percentage terms, the early onset is around 10 percent, with late onset up around 90 percent.

Christopher Shulgan: And according to one of the world's leading researchers into Alzheimer's and dementia, the early onset and late onset forms are two very different creatures, with different causes, which lead to very different ways to prevent and treat them.

Christopher Shulgan: That researcher is Professor Francisco Gonzalez-Lima of the University of Texas at Austin. In this conversation with Medcan Chief Medical Officer Dr. Peter Nord, Gonzalez-Lima argues against the old hypothesis that amyloid plaques and tau tangles cause dementia in the aged. Instead, he says neurological problems arise due to the interaction of two factors: impaired blood flow to the brain, and the inhibition of an enzyme called cytochrome oxidase—which can be treated with infrared lasers and a substance called methylene blue.

Christopher Shulgan: During their conversation, Dr. Nord walks Prof. Gonzalez-Lima through the vascular hypothesis of late-onset Alzheimer's. They discuss key ways to prevent impaired blood flow, and to promote the action of cytochrome oxidase that everyone can do. They also discuss the future of Alzheimer's therapy, which one day could see those who wish to preserve cognitive function walking around with devices that shine light through the skull and into the prefrontal cortex. Sounds fascinating, right? So let's get right to it. Here's Dr. Peter Nord's conversation with late-onset Alzheimer's expert Prof. Francisco Gonzalez-Lima.

Peter Nord: So Dr. Gonzalez-Lima, thank you for being here. Your work is absolutely fascinating. You question historically some of the conventional wisdom on Alzheimer's disease and dementia. What's wrong with the way people today understand dementia and Alzheimer's disease?

Francisco Gonzalez-Lima: Yes, thank you for the question. I think the major problem with Alzheimer's research and our understanding of how to diagnose dementia is that they have developed in a way that strayed from the reality of what's happening, and some of these ideas actually ended up to be wrong. So for example, the most common type of dementia is the one that is related to old age, elderly, having dementia. And this is usually referred to as Alzheimer's disease. However, it's not related to the other rare type of dementia that you can see in younger people, the one that is referred to as early-onset Alzheimer's disease. And my argument is that these are two very different diseases with different causes, and that affect different age populations.

Francisco Gonzalez-Lima: And most importantly, that the amyloid plaques and the tau tangles are not the cause of this common type of dementia that we see in older people. I like to refer to it as geriatric dementia, even though the most common type is the one that we call Alzheimer's. There are, of course, other types of dementia. So this is an important concept because a lot of the research—I would say 95 percent, if one can estimate a number—is aimed at understanding the early onset Alzheimer's, with the assumption that if we understand that, then we'll be able to treat the other common type of Alzheimer's that happens in older people. And this assumption is not based on a clear scientific basis. They're really two diseases. And even Alzheimer himself never claimed that the original disease that he described in that younger patient was the same thing that was happening in the geriatric population. These were claims that were made afterwards, in particular by his department head, who wanted to give the impression that they had already worked out what was wrong with these older people that resulted in what was called senile dementia.

Peter Nord: That's fascinating. You know, when we think about dementia as sort of that overarching term, and over the last couple of decades, we've increasingly realized that there's a vascular component, so the blood vessels can cause some issues, and also there's a nerve component. And so when I'm teaching students, I often just start with that. Like, that's how things start. But you've taken it to that next level, and looking at that early-onset versus late-onset dementia. Maybe you can describe what's happening there, and how does your research that you're doing right now have implications for each of these populations, this early onset and the late onset dementia?

Francisco Gonzalez-Lima: Let me start out with the late onset, which is the most common one and the one that affects the overwhelming majority of the population, maybe more than nine out of 10 cases of dementia. And the key to approach that is that aging and old age is the number one risk factor for these late onset types of dementia that we're referring to as Alzheimer's disease. So this cognitive decline doesn't happen overnight. It's a process that's linked to the aging process. And one of the problems with this is that, as a function of age, we have chronic deterioration in our vascular system, the circulatory system. And this compromises the blood flow to the brain, but most importantly, the oxygenation to the brain. And in addition to this, the longer we live in our modern world, the more we are exposed to environmental toxins that have impact on especially energy metabolism to the brain.

Francisco Gonzalez-Lima: And this is where we focus our work on how that energy metabolism is affected in this common type of Alzheimer's. And that's where we made the discovery that the mitochondrial enzyme called cytochrome oxidase, which originally was referred to as the respiratory enzyme, the one that is able to bind to the oxygen that is brought by hemoglobin in the blood, and then catalyze a reaction that results in chemical energy production. However, the other type, the early onset, I think most of the work that I do, doesn't speak to that one, where the lesions are produced by a different mechanism that involves genetic abnormalities and even entire chromosomes, chromosomal abnormalities. So the two are very different from that point of view.

Peter Nord: And as you said, you're focusing on the 90 percent and less on the 10 percent. So that's where the priority has to be, when so many of our population participants are really feeling the effects of that, for sure. And even in cytochrome oxidase, things like carbon monoxide even has an effect on that cytochrome, doesn't it?

Francisco Gonzalez-Lima: Oh, yes. Cytochrome oxidase is completely inhibited by carbon monoxide. Of course, we don't get to that point. As long as you have about two-thirds of the amount of the enzyme working, you're still alive. But if you inhibit 40 percent of the enzyme, you're going to die from carbon monoxide intoxication. So every major classic poison that we can think of, if it affects oxygen metabolism, it is likely doing that through cytochrome oxidase. For example, the most classic poison out there is cyanide. And from the early days, people committing suicide with cyanide or poisoning their enemies in the Cold War with the Soviets, all the Soviet spies had cyanide in their rings.

Francisco Gonzalez-Lima: So just consuming a small amount of cyanide inhibits enough cytochrome oxidase that you die within minutes. So cytochrome oxidase is vital to life. And the important point is that, as we grow older, the mitochondria, generally speaking, and cytochrome oxidase in particular, are losing some of its enzymatic catalytic capacity, so the enzyme is less efficient. When the oxygen is fully reduced to water, all of that exchange can be used to generate this oxidative phosphorylation for more ATP production. But if the enzyme cannot fully reduce oxygen to water, then some of that oxygen becomes superoxide, which is the first of this cascade of reactive oxygen species.

Francisco Gonzalez-Lima: What happens during aging is that we have a constant diminution of this that is happening over time. And in addition to this mitochondrial problem, we have in parallel a problem with the vascular supply to the brain. So not only do we have enzymes in mitochondria that is less effective at doing their energy production, we have less supply of oxygen and other issues like increased blood pressure that are also damaging the flow through the arteries that supply the brain. And so the problem is compounded at several levels. It is naive to think that there is one cause of dementia in the elderly. When I'm talking about mitochondria and vascular hypotheses, they are all operating in parallel. They interact with each other.

Peter Nord: And to simplify a lot of that, in previous episodes on these podcasts, we've actually delved into some detail in terms of the physiology of the endothelium, and what happens with NO and oxide. Maybe you can just take a minute and connect the dots around vascularity, what's happening with the endothelium, especially with regards to inflammation.

Francisco Gonzalez-Lima: Yes. It is hard to know where to start because all of these processes connect to each other. But let's get started with something that happens we know in healthy aging. In healthy aging, at least in every decade, you have a measurable decrease in the perfusion to the brain. So there is a reduction in the perfusion to the brain, so we can refer to that reduction as hyperperfusion. So every decade of life, we can quantify this. So when this is happening, the enzyme is not getting the amount of oxygen that it's supposed to get, and this results in down regulation of the enzyme. Once this happens, as soon as you try to do anything that increases metabolic demand, you're going to produce more reactive oxygen species. For example, you mentioned nitric oxide. The walls of the arteries, they become smaller as they break down into arterioles and capillaries. Well, as they become smaller and smaller, you have now a small diameter for this so-called laminar flow, and you have issues of elasticity.

Francisco Gonzalez-Lima: One of the most common findings that anybody knows that happens in aging is that we lose elasticity in all of the tissues that have elastic fibres. That is why we have wrinkles. And it is the same with the arteries. The arteries are no longer responding with the same level of elasticity. That's where we start them building up chronically an increase in blood pressure and hypertension as we're getting older. Of course, as we grow older, and the endothelial walls have been damaged and lost elasticity of the muscle fibres that surround them, this vasodilation also is compromised. It's not as effective. For example, in our own research, one paper that is just in press right now in a journal called Brain Stimulation, we show in the aging brain when we do laser treatment to the forehead, that you can get a good response of increasing what is called the photo-oxidation of cytochrome oxidase from their baseline in these older patients.

Peter Nord: Yeah, so you mentioned the transcranial laser stimulation. Why don't we just dig into that a little bit? A lot of your work has been focused on the transcranial infrared laser stimulation and methylene blue. Two very different things. But maybe you could dive into a little more detail about how that actually works. How do we get lasers from the outside of the cranium to affect something that's inside the cranium, namely the brain? Whether that's the vasculature or the nerves. How does that actually work?

Francisco Gonzalez-Lima: Excellent question. To tell you the truth, at the beginning we didn't know whether this was going to work. There were a lot of people claiming, and some were writing about this, but most of the work was in vitro work or with cell cultures. In other words, there were no real barriers to the light. So that was important work because we found out that this light produces this—they now call it photobiomodulation, but the primary process, it was already fully understood from the physics point of view by the 1920s. Albert Einstein was the one who worked out this from a scientific theoretical point of view. It was called the photoelectric effect. Essentially, when photons from light hit a metal—this is what it was originally discovered—then they can produce the electrons that are on the outer orbits of that metal to come out from this. The process of electrons going out from a metal is called oxidation. So this is a type of photo-oxidation.

Francisco Gonzalez-Lima: However, we didn't know whether we could act on a living animal. And this is where I got into the picture. We first verified that, for example, we would have brain homogenates, and we could get an increase in cytochrome oxidase activity. And the reason is that cytochrome oxidase activity becomes oxidized when you hit it with these photons. And, in fact, cytochrome oxidase—the name cyto means "cell," chrome means "color." It is the primary and largest intracellular photo asector. And that's because it has six photons that are a particular wavelength, and it reflects some other wavelengths. It gives the color to the inside of the cell. So all of the cytochrome systems that we have in the body have that characteristic. So this was very useful information. It seems mitochondria are related to chloroplasts in plants, so they still have the ability to use this photon, normally derived from the sun—a form of energy—and transform that into something else. In the case of just having the electrons out, this photoelectric effect, this photo oxidation phenomenon.

Francisco Gonzalez-Lima: So then I had an MD who was doing his PhD in my lab, and his name was Julio Rojas. And I give him a lot of credit to convince me to start trying to use light in the lab. So we decided for his dissertation work, let's do this with the eye, because in the eye, we have the retina. We can use the eye as a model for the brain. But more importantly, we know the light is going to get there to the retina. We're not going to have any barriers. And so we did it. We created an animal model, first with mice and then with rats, in which we compromised cytochrome oxidase activity inside the retina by micro-injections of mitochondrial toxins into the eye. And then what we found out is that we could prevent the atrophy and neurodegeneration of the retina by stimulating the eye with essentially what was red to near infrared light. And not only did we prevent the anatomical and histological changes, the animals we would test them functionally and you could demonstrate that they could see, they could see in behavioural tasks where they had to do discriminations. They could see in more sensitive tasks of perception when you will have threshold changes in illumination and you can create curves in terms of the responses. So we could prevent the anatomical damage. So this encouraged us to say, "Well, this is a real phenomenon. It can happen in vivo in an animal. Can this happen in the brain trans-cranially?"

Francisco Gonzalez-Lima: Again, Dr. Rojas in my lab, we were the first to demonstrate this in the brain of an animal. And there we could be invasive. In other words, we could put a probe inside the prefrontal cortex that would measure the oxygen consumption. And then we go to stimulate trans-cranially and see how that oxygen consumption would be changing over time, and do different doses and do dose responses. And these were the first experiments. I would say the first prevocations was in the Journal of Neuroscience in 2008. And by 2012, we'd done the animal. And then we also did some behavioural testing like memory testing that related to prefrontal function, that we could demonstrate that we could increase cytochrome oxidase activity.

Francisco Gonzalez-Lima: We had an advantage over older labs that I had developed years earlier, a quantitative histochemical method to measure cytochrome oxidase activity in the brain. And we could then monitor these changes. And from there, we moved to humans. And so we provided the first control that could demonstrate an increase in prefrontal base cognitive functions. We estimated this based on what we learned from the animal models and some tests we did with cadavers. With the transcranial laser or light stimulation, you're tapping on a mechanism that generates more energy for the brain, and generates more oxygenated blood getting into the region.

Peter Nord: And you were looking at functional MRI as well to prove that.

Francisco Gonzalez-Lima: Yes. We did an analysis with functional MRI, which is sort of a standard in the field. However, the technique that was best suited was called near-infrared spectroscopy. However, we wanted to demonstrate in people, what we saw in the animals, that we could see this cytochrome oxidase effect, that we could see that we were increasing the oxidized cytochrome oxidase so that there could be more oxygen use. And this is where I started collaborating with bioengineers and physicists primarily at the University of Texas at Arlington, but also some at Austin. And we were able to put together a custom-made device that we called the broadband near-infrared spectroscopy device that was designed to measure the changes in oxidized cytochrome oxidase at the same time.

Francisco Gonzalez-Lima: And it took several years, but we were the first to demonstrate that transcranial infrared laser stimulation indeed can increase cytochrome oxidase concentrations, and can increase also the oxygenated hemoglobin concentrations. In other words, if you want to stimulate the circulation, the best place to stimulate, the best organ is the brain because the brain is full of capillaries. And it has a very high level of blood flow and blood volume at any given time. So if you want to increase circulation overall ...

Peter Nord: The brain is the place.

Francisco Gonzalez-Lima: The brain is the place to stimulate.

Peter Nord: Great. And you've done some work with—you mentioned colour and cytochrome, "chrome" being Latin for "colour." What about this methylene blue? How does methylene blue fit into this?

Francisco Gonzalez-Lima: Yes, methylene blue is what we actually used first, because methylene blue is more conventional in the sense of being a drug, a pharmacological agent. And I have been doing work with pharmacology and toxicology, so that was the first thing that we tried. We understood that the reason methylene blue was being effective, for example, in animals to allow them to have better memories. We were the first ones to demonstrate that in living animals, and years later in humans. So it turns out that methylene blue is really unique in its property to cycle electrons from its immediate surrounds, and then donate those electrons. Of course, the advantage with methylene blue is then when you inject methylene blue into the circulation, it goes and concentrates inside mitochondria, and then it reaches an equilibrium because methylene blue asects and donates electrons. It oscillates into being oxidized or reduced. So at a low concentration you get an equilibrium where it's constantly grabbing electrons from the surrounding molecules, and donating to whom? Well, to the friendliest electrical sectors that are the electron transport proteins inside mitochondria.

Francisco Gonzalez-Lima: And they become a bypass to the regular supply of electrons from the electron donors that we derive from our nutrients. And also, if there is a mitochondrial toxin that affects any one of these complexes—and we tested all of them—we can still maintain electron flow going, cellular respiration, energy production, in spite of these mitochondrial toxins. So we will demonstrate, for example, these mitochondrial toxins will result in neurodegeneration. We could do that with the retina, with the brain. And if we use methylene blue, we created this alternate route that kept the electrons flowing and maintained cellular energy production, and then we didn't have this atrophy and neurodegeneration happening. So the one who first injected methylene blue in living animals was Paul Ehrlich. He was working in Berlin, and like many other people there, he also won a Nobel Prize for this work. And he was impressed when he injected in living rats systemically in the circulation, that he concentrated in nerve tissue: peripheral nerves, brains, retina. And he used the term "magic bullet."

Peter Nord: For the first time. That was the source of that. Just to bring this to a bit of a head, because fascinating work, really interesting, but there's the "so what" question, right? So, you know, the research continues, so great results. And if we think and we look out into the future, how will our listeners benefit from some of these interventions that you're working on? You know, what can we do to preserve our cognition as long as possible? That's the real takeaway. So what do you see the future of this work? It's obviously building to something. What does that look like in the future for the listener?

Francisco Gonzalez-Lima: There are things that one can do immediately that are around the principles that are behind the work. And they're the same thing that you recommend to do: aerobic exercise, where you are using oxygen in greater demand, builds up the amount of cytochrome oxidase, not only in the brain, but also in all the tissues, especially the muscles, the—what we call the aerobic type of muscle fibres, the dark red muscle fibres. And the effects of exercise in those fibres are the same as the light. Our group was the first one to demonstrate you can convert the so-called intermediate muscle fibres that have the potential to become red or white. That is, aerobic using oxygen, or not using oxygen to transform them into oxygen consuming, so increase your endurance, your aerobic capacity.

Francisco Gonzalez-Lima: Unfortunately, most people don't do enough aerobic exercise. It's very difficult to convince, but I will encourage people to do that. Something else is synergistic with this approach. We can do this with the light, especially people who cannot, like older people who may be fragile, may not be able to do enough aerobic activity, we can compensate that at least at the level of the brain with this phenomenon. But you have to avoid mitochondrial toxins. Toxins affect this energy, metabolic machinery, and these things are found primarily in pesticides, lots of mitochondrial toxins there.

Francisco Gonzalez-Lima: So aerobic activity, but also avoiding mitochondrial toxins is fundamental. So it is all related to brain energy metabolism. And so what can you do about that? You can, for example, try to eat alternative sources of energy. Even though the preferred substrate is glucose, we can still use things that are called fatty acids that produce in the liver. Other compounds are called ketones. We can use these also as a source of energy. They can go into the mitochondria and end up with forming these electron donors. So the most common one out there is coconut oil. In particular, it has so-called medium chain triglycerides that are good sources for this. And we use them every night. If you sleep for many hours, fasting, your brain still needs energy. So early in the morning, when you wake up, if you slept enough hours, especially like a 14-hour usual interval between your last meal and your breakfast, then you are getting into this so-called ketogenesis.

Francisco Gonzalez-Lima: And this is really good for your brain, because then your brain starts off-regulating enzymes that can use the fat, not only the fat from these fatty acids like the coconut oil, it can start using your own body fats. Because if you keep consuming other sources of energy, you're not going to be able to lose your fat, and you don't have the enzymes to take advantage of it. So I personally, at least once a week, like from Friday to Saturday, I make sure that I have a long fasting period to facilitate those enzymes. Hopefully there will be a day when we can come out—and we're working on it. We have a team of engineers now working on it at UT-Austin, to come up with a small sized, inexpensive device that we can put on the forehead to facilitate light stimulation. So we're gonna figure this out.

Peter Nord: So let me see if I can simplify it in one word: we want to have in the next couple of years, a laser headband, where the laser is pointing in, as opposed to pointing out.

Francisco Gonzalez-Lima: But not even with lasers. With LEDs, that are as close to what we call—the lasers are monochromatic, one wavelength. We want to have a quasi-monochromatic LED, that is high efficiency, doesn't produce heat. And we can have enough of them without occupying a lot of space that will simulate the power levels that we need for the laser.

Peter Nord: Well I'm glad you said that, because that's where I was going with the next piece. Because after all that discussion about photostimulation, there has to be some sort of practical application of that. So let's see if I get this right. So aerobic activity, improving the efficiency of the whole system, avoiding toxins like obviously pesticides and pollutants, the genomic factors that are critical, and maybe some upregulation that might happen with that. Antioxidant foods, so high-pigmented foods, antioxidant foods. And on these podcasts, we have talked about the MIND diet and specific diets that lead to the same sort of end result. And then as you said, glucose transport decreases with age. So, you know, coconut oil and even leading to intermittent fasting. And that's all stuff that we can do right now, before we have any sort of appliance that we can apply to upregulate and stimulate the cytochrome. So that we again, our prefrontal cortex has the optimal function as much as possible. So this is probably a great way to wrap up because that's the "so what," I think. That's what you're really working on, is that endgame where we can end up pushing off dementia, stave it off for as long as possible.

Francisco Gonzalez-Lima: And the only thing I will add from that is you can do it yourself. But from a medical point of view, you want your physician to take control of your vascular health, because you want that blood flow to be as efficient as possible. So that is something that your family physician can do. Do not go to the neurologist for that. They're not going to be able to fix that. Unfortunately, most of the problems with the brain in otherwise healthy people have to do with the circulation to the brain.

Peter Nord: That's right. So keep the blood pressure down, watch the cholesterol, watch your lipids, watch your sugars, obviously. You know, manage diabetes if you have that, and don't smoke. Those are all the big four or five things. And probably the fifth one is stress. You know, all those things can be bad for your circulation. And we've talked about that in the past as well. So it's a great place to connect a lot of these dots. So thank you so much for your time today. This has been fascinating. Congratulations on your work. You've done an unbelievable amount of work. And you certainly had a historical push. You've been standing on the shoulders of greatness – many Nobel Prize winners. And we'll wait to see your name amongst those next Nobel Prize winners. So again, thanks so much for your time today. It's been great speaking with you, and congratulations on the work.

Francisco Gonzalez-Lima: Thank you.

Christopher Shulgan: And that's it for this conversation between Medcan chief medical officer Dr. Peter Nord and the University of Texas at Austin professor Francisco Gonzalez-Lima. I'm executive producer Christopher Shulgan. For those seeking to learn more about the professor's fascinating research, we'll post links to some of Prof. Gonzalez-Lima's key studies in the show notes, as well as a link to an interview that podcaster Peter Attia MD did with Gonzalez-Lima that spans two and a half hours.

Christopher Shulgan: Eat Move Think is produced by Ghost Bureau. Senior producer is Russell Gragg. Editorial and social media support from Chantel Guertin, Emily Mannella and Tiffany Lewis.

Christopher Shulgan: Remember to rate and subscribe to Eat Move Think on your favourite podcast platform. Follow our host Shaun Francis on Twitter and Instagram @shauncfrancis—that's Shaun with a U—and Medcan @medcanlivewell. We'll be back soon with a new episode examining the latest in health and wellness.