Today I'm very honored to introduce Dr. Dominic D'Agostino. Dr. Dominic D'Agostino, PhD, is an associate professor in the Department of Molecular Pharmacology and Physiology at the University of South Florida, Morsani College of Medicine, and a research scientist at the Institute for Human and Machine Cognition.
He earned his bachelor's in biological sciences and nutrition science from Rutgers University and his PhD in physiology and neuroscience from the University of Medicine and Dentistry of New Jersey.
His research focuses on metabolic-based therapies including ketogenic diets, exogenous ketones, and metabolic drugs with applications spanning seizure disorders, neurodegenerative diseases, brain cancer, rare metabolic disorders, and oxygen toxicity.
His work also includes research related to human performance, resilience, and extreme environments including NASA's NEEMO missions.
Dr. D'Agostino became particularly interested in ketogenic therapies through research into oxygen toxicity seizures and the challenges faced by Navy SEAL divers using closed-circuit rebreathers. His research subsequently explored how ketones can provide an alternative energy source for the brain and potentially support neurological function under metabolic stress. His work has expanded into the mechanisms through which ketones may influence brain energy metabolism, neurotransmission, inflammation, and cellular signaling. His laboratory continues to investigate these mechanisms across neurological and metabolic conditions.
He has been an early educational voice since the beginning of our journey and a hero of mine, and I'm very grateful for him to be here with us today. So, Dr. D'Agostino, thank you so much for being here. How are you?
Thank you, Ed. Yeah, I'm doing great and thank you for having me and for providing this educational outreach outlet to people. I really appreciate that because education really is key, and especially topics like this that are not necessarily formally taught at the graduate or medical school level.
Yeah, and I thank you. And to your point, that's why so much of the information that you've made available out there on the internet, on YouTube, all the interviews you've done over the years have been so helpful to people and families like mine because, like you said, the proper channels don't have this type of information, so it's not super accessible. And you've been one of those voices that for over a decade has really put some great and helpful information out there. So, you got to get us started with, you know, you have a background in nutrition, biology, neuroscience, physiology,
I mean, dentistry, right? What initially sparked your interest in metabolism and eventually led you toward ketogenic research?
Yeah, well, I said I was always interested in nutrition and probably why I majored in nutrition at a high school, right? I was more interested in it from a fitness perspective, I think.
So, as I started studying nutrition, I realized that it would probably be good to double major in bio if I was going to go to med school.
And it would also probably be good to get some research under my belt, you know, that looks good on a medical school application. And I was mentored by someone at UMDNJ. So, UMDNJ is a medical school and a dental school, but I was associated with a medical school and they had their own PhD program. And so I studied — she instilled in me basically — I studied how the brain controls our physiology. Physiology is very important when it comes to understanding how ketogenic diets work. So, I'm glad I had that background, as is neuroscience, you know, studying seizures.
So, after doing my PhD, I did a post-doctoral fellowship project and that was funded by the Department of Defense, which under the Department of Defense is the Office of Navy Research, and it was a very sizable post-doctoral fellowship that started in Ohio and then I moved to University of South Florida, Morsani College of Medicine. And my focus was really understanding why these oxygen toxicity seizures occur, and understanding the mechanism made me more interested in the idea of giving something that could enhance and preserve metabolism in the context of oxidative stress, in the context of metabolic stress.
And I was mostly focused on drugs and antioxidants, even things like melatonin I studied in the lab and published on that. But then, you know, I kind of discovered — I was not taught this as an undergrad — that the ketogenic diet was used originally for epilepsy, and then it was used for drug-refractory epilepsy, you know, very powerful tonic-clonic seizures that were drug-refractory.
And I kind of pivoted towards understanding the diet, and I connected with key people that steered me more towards ketones. And that was the late Dr. John Rowe, who recently passed away, Dr. Richard Veech at the NIH, Dr. Theodore Van Itallie — he passed away, almost lived to about 100 — Dr. Sammy Hashim, who recently passed away too, he was in his 90s, and a number of other people. But they were sort of some of the key people, and they were really like metabolic pioneers.
And ultimately I tested and vetted out different types of ketogenic diets and also different types of exogenous ketones. Interestingly, the ketone monoester developed by Dr. Veech did not work for oxygen toxicity, but the diester did.
The diester, instead of putting one ketone molecule on 1,3-butanediol, we put two acetoacetates on, and then that kicks off acetoacetate. And the 1,3-butanediol is an alcohol, but it can make beta-hydroxybutyrate, you know. When we drink ethanol, that makes acetate, and our brain gets addicted to the acetate.
1,3-butanediol goes through that same detoxification pathway in the liver, alcohol dehydrogenase and aldehyde dehydrogenase, but it kicks off beta-hydroxybutyrate. And then that becomes a fuel that we can use, and that elevating acetoacetate and beta-hydroxybutyrate in a 1:1 combination, that was very good for anti-seizure effects. And I do think that the acetoacetate can make a little bit of acetone, and that acetone has a sort of dampening of excitability effect.
And, you know, we've kind of vetted that out through a half dozen different seizure models. So, that's very real, relevant data. And that molecule then led to developing the ketone salts.
At first, there was just sodium beta-hydroxybutyrate, and then I was like, well, let me try potassium BHB, but you couldn't buy that, and it wasn't even in the CAS database, the database of all the different molecules that ever existed. I was like, oh, I got to make this. So, I was able to work with a chemist, the late — he also passed away — Patrick Arnold, and was able to synthesize the potassium BHB, calcium BHB, magnesium BHB. So, we put together various ketone salts.
Interestingly, like the formulation that I use now personally is basically the same electrolytes as another electrolyte supplement element. So, but the electrolytes are just bound to ketones, you know, instead. So, you take, you know, you consume it, it's like an electrolyte supplement, but you're also giving ketones. And we did find that the two different forms of ketones, there's D-beta-hydroxybutyrate and L.
And then D gets burned very efficiently for energy in the mitochondria. And now we know that L takes like four or five times longer to get metabolized because it's not metabolized by the ketolytic enzymes. But it has this really important signaling function. And yeah, I just came from a conference that showed that cardiovascular output was four to five times higher with the L-BHB. So, and that's through a mechanism that's not even energetic. So, it relaxes the vascular endothelium.
So, that results in this cardiac output, maybe a nitric oxide effect, we don't know. But what we do know is that the L-BHB hits the signaling, the NLRP3 inflammasome, the cardiac effects, and then the epigenetic effects. So, it's like a timed release. So, the two together tend to be, you know, Dr. Veech was of the opinion that the D was superior. And I think from an energetic standpoint it was, but at that time, and he did not know that ketones were a signaling molecule.
So, that came later, and then it was work done in Europe and published in a number of American Heart Association journals that really I was like, "Whoa, okay, I got to look back at this." And it maybe explains why we had, you know, sort of this blood flow effect, you know, when we administer the DL-BHB.
So, yeah, out of that work, you know, oxygen toxicity, but then it went to cancer, and Dr. Thomas Seyfried, who's not too far from you, I've worked and published extensively with him, and we studied Alzheimer's disease. Dr. Mary Newport kind of turned me on to that, and we studied a whole host of rare genetic and metabolic diseases, with the and also muscle-sparing effects with cancer and also exercise. So, it has become a very interesting field to be in.
Yeah, absolutely. All your great work is so important now that, like you listed off all these great science minds that are no longer with us. You definitely — they've passed the torch to you, and we need that torch to continue.
Take us back and just to reinforce. I mean, this to a lot of our audience, this is probably just revision, but it's important really to reinforce here that the ketogenic diet or ketogenesis as a therapy is not new, right?
Yeah, I mean, you could — there are different ways to implement ketogenesis therapeutically. That could be through fasting, of course, and then time-restricted feeding, and then carbohydrate restriction, caloric restriction. There's about seven different types of ketogenic diets, and then we have exogenous ketones.
Well, let's talk about the precursors, could be MCT or 1,3-butanediol. And then exogenous ketones would be — there's about six different types of ketone esters, and there's over 20 different types of ketone salts, and then there's a whole bunch of other molecules being made. So, we have many different ways, and they're not mutually exclusive. So, you could do kind of what I do, you could do like time-restricted intermittent feeding with a ketogenic diet and ketone supplementation,
you know, and MCT. So, you could do all these things kind of together, but no one really studies that. But I do think it needs to be studied, but we need to understand the benefits of things in isolation, you know, scientifically.
Not that we've always — I mean, we combined ketogenic diets with the supplements and hyperbaric oxygen for cancer. And that was — but you don't typically publish that in Science or Nature. It got published, you know, like a mid-tier journal. But yeah, I think for the listeners out there, it's important to know that there are different ways to achieve and maintain that, and that will depend on the individual, their tolerance to the diet, their tolerance to fasting, and their interest in using something like MCT or exogenous ketones.
But there are options out there, and that's important. And when you elevate ketones, you get very real benefits from a fueling effect and then a signaling effect. And we can talk more about the mechanisms there if you want to.
Yeah, definitely. We'll definitely get into those mechanisms. And just so people know, I mean, the ketogenic diet just as a standalone therapy, I mean, this is over a century old, right? Therapeutically.
Yeah. 1921, Wilder at the Mayo Clinic, you know, kind of published a short clinical report on it. And then prior to that, you know, fasting has been used for millennia, from Hippocrates to scripture, you know, in Mark it was made in the Bible. So, it's like, you know, there's a long history of fasting. And they didn't know about ketones back then. They just knew that it was therapeutic for certain disorders, you know.
And then I think that was the impetus or the motivation behind creating the ketogenic diet for epilepsy at the Mayo Clinic, that you could do a macronutrient ratio and formulation that when the person ate it and you looked at their blood, it would look like they were fasting because their insulin would be low, and then their glucose would be low, and the ketones would be high. So, it would mimic the physiology of fasting.
And when we change metabolic physiology, we change brain energy metabolism, and we change the neuropharmacology of the brain in a way that prevents seizures. And we're still trying to understand all the mechanisms associated with that neuroprotective anti-seizure effect.
Wow. Wow. Yeah, that's powerful. Yeah, in simple terms, like what happens to the brain when it starts to use ketones as an important fuel source preferentially over glucose?
Yeah, I don't — you know, I think the brain is very opportunistic, right? It'll use whatever fuel is available. And ketones represent an alternative fuel for the brain.
And the ketones can travel through the blood, enter the brain, and be converted in the mitochondria to energy, and it bypasses the rate-limiting bottlenecks of glycolysis. And I think that's really important to kind of understand.
So, there's like four different kind of mechanisms at play here when you get into ketosis. So, the energy supply to the brain is much higher, and that's through an increase in cerebral blood flow because ketones have a vasodilation effect, and some studies up even 20 to 30%. So, a lot of people don't like talk about that, but I think that's probably a big factor in like the cognitive — we always talk about just the energy effect, and that's true.
But I think like, for example, you know, beta-hydroxybutyrate, especially the L-beta-hydroxybutyrate, can cause a big boost in cardiac output. So, there's cardiac output, cerebral blood flow, and our cardiac output does not always correlate with cerebral blood flow.
There's like — there's a brain autoregulation. That's like your sympathetic nervous system, parasympathetic. When you're in ketosis, it tends to dampen sympathetic tone and even activate more of the parasympathetic, and that can influence the autoregulatory mechanisms of cerebral blood flow.
It's a little bit too technical to go into, but I do think that that's an area that I want to explore more because no one's really studying it. But then you have an increase in transport of energy to the brain and an increase in metabolic flux.
So as we age, even with epilepsy or neurodegenerative diseases and even psychiatric diseases, there's typically like — there's enzymes that are not as active as they should be, and one of them is pyruvate dehydrogenase complex. The PDH complex is in the brain, and that's like your major gate for the brain's ability to use glucose.
So in Alzheimer's disease, for example, if we take that example, you know, pretty much all Alzheimer's disease brains have a deficiency in PDH and also the catalytic activity, which means just the activity of that enzyme is decreased. So that will decrease — that makes glucose hypometabolism a hallmark characteristic of Alzheimer's disease. And then so there's a function of like supply and demand.
And then through the neurodegenerative process of amyloid and tau plaques, the demand for energy is also down too. So the big discussion in the field is the, you know, the chicken or the egg kind of thing. It's like, you know, many most investigators think the accumulation of tau and amyloid then results in this phenomenon of glucose hypometabolism, but if we have neuroinflammation and we have mitochondrial dysfunction, that will cause — we think the accumulation of tau and amyloid is a downstream epiphenomenon of neuroinflammation and also mitochondrial dysregulation.
And I think at mitochondrial health. And the ketones do tend to have an effect on the NLRP3 inflammasome complex. And that complex gets activated like if we have like a viral infection like herpes simplex or COVID or something. So, it can help dampen systemic inflammation which often leads to neuroinflammation, especially if for example an infection or microbe gets into the brain, which does happen.
So, I think there's a lot of things going on there that I just described, but I think it's important to acknowledge that like, you know, some of the drugs now just target the amyloid as an antibody and kind of clears it, and that leaves like damage in the brain that could cause like micro hemorrhages that could be problematic. Whereas it's targeting very specifically a specific thing.
Whereas therapeutic ketosis is changing the physiology of our entire body, and that's altering in a way that has less side effects of course, but in a way that's more gradual and working with your body's natural capacity to heal itself — it could be a term — but also to preserve homeostasis, right?
And I think, you know, and it doesn't necessarily have to be done continuously. I think you could do cycles of ketogenesis that could produce some benefits too. The bottom line is that there are cardiometabolic biomarkers that correlate with brain health. And whatever dietary intervention or metabolic therapy you're doing, and that could be a GLP-1, if that, you know, causes a constellation of effects that improve that whole profile.
And I don't like to use the term cardiometabolic. I like to use the term neurocardioimmunometabolic biomarkers because they're all interrelated. So, any intervention, and exercise is huge too, and we don't talk about that enough. But exercise is a form of metabolic therapy, probably better for your brain than anything we're talking about here.
But I do think that a diet plus supplement and then plus exercise is kind of like if you're just doing your metabolic therapy and exercise, like one and one equals three. I think there's a synergistic effect between the dietary and supplement intervention combining that with exercise.
So, that's really important for the older individual that can — I don't like to use the word exercise. I like to use the word physical activity. Because just getting out and going for a walk, gardening, being outside, things like that is really important, that physical activity.
Yeah, definitely. Definitely. Yeah, this is great. So, if I could just sum this up for people viewing and listening,
if I'm hearing you correctly, the glucose hypometabolism in the brain is a hallmark of Alzheimer's. Many of us know this. And there's some research that's showing or hypothesizing that maybe the hypometabolism is an effect of the amyloid and the tau aggregation.
And then there's another camp that's looking at this and saying, "Well, actually the amyloid and the tau aggregation accumulation is downstream to the hypometabolism that's going on, and that inflammation —" which by the way, I'm in that camp just based — I'm not a scientist, I'm not a doctor, but just based off of listening to the great minds like yourself, it seems more intuitive to me that there seems to be some sort of inflammatory triggers in the brain that can cause a hypometabolism, like infections seems to be a big one that's kind of proving out. And then the amyloid and the tau are downstream to that. Is that what I'm hearing?
Yeah, the chronology, I guess, and the sequence of events are not fully worked out. But we do know, for example, that, you know, for example, if you take mice and give them something called lipopolysaccharide or LPS, that LPS, that inflammation, will then quickly cause an accumulation of, you know, tau and amyloid.
So, you know, and I think if we look at the data as a whole and we try to undo our bias towards amyloid and tau driving Alzheimer's, I think that we would come up with, you know, the general consensus would be that there are many things happening in tandem or at the same time, and that the initiating — and this kind of falls back into what Thomas Seyfried with cancer as a metabolic disease — that the initial hit to the organ and the cells would be, you know, metabolic dysregulation.
The cells would be starved of glucose. If the cells are in an energetic crisis, they can't clear proteins well, protein folding is impaired, and also many viruses can hit the nucleus, but many viruses actually cause their damage by specifically impairing mitochondrial function.
And the mitochondrial DNA do not have the repair capacity that the nuclear DNA has. They just don't have the robust repair mechanisms. So, progressive mitochondrial dysfunction will lead to sort of like the pseudo sort of energetic crisis, and that can lead to — and this is sort of it happening in the background of inflammation and oxidative stress.
And, you know, the things that I'm mentioning here are all — and it's super — I just simplified it way too much, but there's a lot of other growth factors going on and there's a lot of other signaling mechanisms that are not mentioned here. And also, there's also the genetic vulnerability. If you're APOE4 positive, especially homozygous, then you have the sort of inability to cope with this and your brain is kind of less resilient.
We could say you have a greater capacity for that. And then our cardiovascular health as we age, with there's less elasticity of the vascular endothelium, and we have less cardiac output, so less blood flow, less oxygen, less energy to the brain. All these things contribute to the amyloid and tau. It's not like the amyloid and tau — so that's, you know, that's a very controversial opinion, but everybody would have laughed at that 10, 50, 20 years ago. Everybody would definitely have laughed.
10 years ago, they would say, "Oh, there might be something to it." But now, we're at the point now where we're like, "Oh, yeah, that's probably true." Like even the amyloid and tau researchers are kind of like, "Okay, yeah, there's something here. We need to look at neuroinflammation. We need to look at brain energy." So, the tides have kind of shifted. I knew there would be a tipping point, but I thought it would happen faster, but it's happening now, so.
Yeah, it is happening now. And that's great. And yeah, you know, of course, there's some people that will laugh at that, but on this channel, nobody's a stranger to — you know, we really see amyloid and tau as the firefighters and not the arsonists, and there seems to be a lot of root cause triggers upstream that lead to the amyloid and the tau, and metabolic dysfunction is a massive factor in all of that. So, if I'm hearing you correctly —
I'd also like to point out that I do think that therapies that target amyloid and tau have potential, but they also have more for harm. So, I think we have to explore that scenario much more cautiously than what I'm talking about here, which is kind of a do-no-harm approach, which is like, you know, just improve your general health and brain function through, you know, some easy lifestyle things and then some things that are a little bit more technical, right?
Like achieving and maintaining therapeutic ketosis is a level of complexity that's, you know, that's a whole another talking point. We could discuss that too, how to do that. And that could even involve some drugs. Even GLP-1s can be a good way to spark ketogenesis and maintain it that I've seen.
That's kind of new for me to even say that, but I've just been looking at the data and getting feedback from patients who could not implement the approach and then they can implement it with microdosing GLP-1s, and that's, you know, that's interesting data coming out of a number, like dozens of clinicians that I have contact with.
Including Dr. Annette Bosworth, which I did a couple podcasts with her recently. I mean, she's got hundreds of patients and she doesn't use the full prescription dose GLP-1, but she can microdose it like a tenth or like a quarter and then getting the same or better results. Better results because you're not getting the side effects.
Wow. Wow. That's really interesting. Yeah, you know, it sounds like for everybody a blanket principle that everyone can apply into their life without a ton of complexity is just work on improving metabolic health. If we want to prevent dementia, if we want to give ourselves the highest probability of preventing dementia and Alzheimer's, work on metabolic health.
Can you expand on that? Like what — you know, you talked about exercise, you talked about GLP-1s. Can you kind of list out what are the best ways from your research that we can improve our metabolic health and we can improve our ability to just even generate ketones? Because I feel like so many of us in the United States who have either come from the standard American diet or are still in that don't generate ketones at all or, you know, very negligible levels. So, could you kind of list those out?
Yeah, I think you need to start where the patient's at, and that could be if someone's already exercising, right? It could be like running an extra mile above the 6 miles you're already running. Or for some patients who may be overweight and highly insulin resistant, it could be just, you know, getting out and walking a quarter mile every day as a start, you know, and tracking your steps too.
I think, you know, we have these devices, we have our phones, we have different things, and I do think what gets measured gets managed, you know, that saying. And I do think that if we can set small goals, incremental goals for ourselves, those incremental goals over time reap very big return on investment, I guess.
So, my advice would be, I think with metabolic health that is defined by your metabolic biomarkers, and everybody should be getting yearly, at the very least yearly, comprehensive metabolic panel, CBC, you know, CMP. And in addition to that, they want to ask their doctor to measure fasting insulin, hemoglobin A1C, hs-CRP, and do a lipid profile test.
Probably the most important would be just apoB. LDL is informative to some extent, but apoB is more informative. LP(a) too, that's, you know, unless you're going to PCSK9 inhibitor, you know, you can maybe budge the needle on that a little bit, and triglycerides.
So, if you can kind of convince the doctor just to, you know, and that you may not remember all these things, but I think if you just search like, "What are the five best cardiometabolic biomarkers?" you know, that they would come up there. I might have mentioned six to add on. And most insurance will cover that. And doctors can be talked into that, especially if the patient says, "Oh, you know, we have type 2 diabetes in the family or obesity or metabolic issues." So, that's first and foremost is that yearly checkup.
And I also recommend doing a DEXA scan, especially if you're like 40 or 50. I started doing it when I was 40, but I did one I think when I was a little bit earlier too. It's interesting to compare my body composition from like, you know, when I was at my peak, maybe like at 30, to in my 50s now, you know, it's like kind of alarming seeing something that changes.
But I could tell you that as with age, you tend to lose a lot of lean body mass and muscle and strength. So, I think it's important to make an effort to do that, to get a baseline. And that could be — you could also do like an InBody, you know, device, and that's the bioelectrical impedance, but I like the DEXA scan, especially for women, because it gives you the bone density.
You know, it's a little bit. And nowadays, I mean, when I was in college, they were like $1,000, $2,000, but nowadays you can get it for under 100 bucks if you shop around. And you know, gyms can offer it. So, I would do that like once a year.
And so, you have that, and then try to beat that every year. Try to beat your body composition. And that's done, you know, you do that through two ways, right? With a dietary — I don't like to call it intervention — you do it with a nutritional protocol, I guess, if you want to call it that. And then you do it with a structured progressive exercise program. That could just be incremental changes over time to increase the, you know, in regards to muscle resistance. And that could be with body weight exercises or —
Incrementally increasing the weight on the bar or dumbbells or whatever you're using over time. And there are so many different, you know, nowadays, so many different platforms that you can just go online and say for AI, right? And then, you know, here's where my starting point and I want to achieve this and write me out a progressive resistance exercise program that's three days per week. You could probably even get results with two days per week. But the more you do it, I think the more benefits you'll derive from it and that'll probably get you more interested in doing it more. I could say that I only really work out a total of like an hour per week. And that can maintain strength. But it's also I've also worked up the ability to train very, very, very heavy and very, very intense during my session. So, yesterday's session was only 15 minutes.
But it was, you know, warm up and very heavy for, you know, two or three sets. And that applies the stimulus for the adaptations to preserve and maintain muscle and even build muscle. You know, I'd probably have to step it up. But I think for people starting out, the message is that you got to get the fundamentals down. And that could be, you know, 30 to 40 minutes, upwards to an hour, three times per week to build that to build your central nervous system. Because when you first start lifting, it's like the central nervous system needs to adapt to be able to like move the weight to the point that and then your muscles have an incredible ability to adapt. And then once you train the nervous system for a particular movement and to do it in a way that's not going to cause injury and it's good to work with a personal trainer, you get the basics down and, you know, I favor more like, you know, heavy pressing, deadlifts, squats, things like that. Like these are the big muscle groups that are going to put muscle on your body and actually that muscle is a metabolic currency. So the more muscle you have, the less potential you have for getting injured, the more your metabolism's going to be higher, you can eat more, you'll be stronger, you'll be more, you know, energetic over time.
So, and that's important too, the diet should be able to support your muscle and muscle growth. So you want to ensure that you're getting, you know, if you need to put on muscle, I would go as high as 1 g of protein per ideal body weight. So, you know, if you're 300 lb and overweight, you don't want to get 300 lb of or 300 g of protein. But you would be, you know, if you're 5'10", 300 lb and you're overweight, whatever your ideal body weight is, like 180, 160, 180 or whatever. So you would get like that many grams of protein if your goal is to like, you know, that you don't need to go any higher than that. But that should be like the upward limit to your protein. So yeah, high protein, low carb, Mediterranean style diet, you could do that or a keto diet if you really want to, you know, lose some body weight and then a progressive resistance training program. And then I hate doing cardio, but I always do like at least one or two walks every day and try to get in, you know, typically I try to get in always over 5,000 steps and on some days I get, you know, 10 or 15,000 steps, but 8,000 is kind of what I shoot for and that seems to be good for me, you know, and I sleep better. And then yeah, we're not talking about it, but sleep is really important too. So, get early morning sun exposure and then try to get off all your devices by 9:00 p.m. So, there was a study that was done that 60% of people with insomnia is associated with being on your device after like 9:00 or 10:00. So, just simply doing that can cure most people's insomnia. And you sleep better, your metabolic health is better, and your brain health is better, too.
Alcohol, too. So, moderation. I tend to do, I will do a glass of wine every day on some weeks. But it's, you know, like super low carb, you know, wine. But I never do more than one glass. And, you know, and I tend to just do it around certain occasions. So, but if you're drinking more than one glass per day, definitely try to cut back to that. Like, there's a lot of people out there listening that are probably drinking. And if you just cut back on that, that would be a good thing to do for your brain health. So, the data is like you can't argue with the data on that.
