How Ketones Support the Aging Brain & Psychiatric Meds disrupt brain energy – Dr. Stephen Cunnane

Stephen: 
What I want to do now is combine that with a reduced carb intake because Parkinson’s disease, like Alzheimer’s and like severe mental of illness, is associated with insulin resistance, and this is going to block ketone production endogenously. So, if we reduce carbs by to 30%, presumably we could reduce insulin resistance in this population as well.

Bret: 
Welcome to the Metabolic Mind Podcast. I’m your host, Dr. Bret Scher. Metabolic Mind is a nonprofit initiative of Baszucki Group where we’re providing information about the intersection of metabolic health and mental health and metabolic therapies such as nutritional ketosis as therapies for mental illness.

Thank you for joining us. Although our podcast is for informational purposes only and we aren’t giving medical advice, we hope you will learn from our content and it will help facilitate discussions with your healthcare providers to see if you could benefit from exploring the connection between metabolic and mental health.

Dr. Stephen Cunnane, a professor and researcher at the University of Sherbrooke is on the cutting edge of research for glucose and ketone metabolism in the brain and being able to actually measure it with imaging techniques. And he joins us today to talk about a number of different studies, in psychosis, in Parkinson’s disease, and also without imaging, just simply lowering glucose or lowering carbohydrate content for the meals in people living in retirement homes, and what type of impact that had over a short-term study.

So, some really interesting work by Dr. Cunnane, who really is committed to studying mechanisms but also drawing it back to interventions that can improve people’s lives. So. I hope you enjoy this interview with Dr. Steven Cunnane.

All right, Dr. Cunnane. Thank you so much for joining me here at Metabolic Mind again. 

Stephen: 
It’s a pleasure. 

Bret: 
Yeah. We had you on previously to talk more about sort of dementia, Alzheimer’s, the role of nutrition and ketosis, but you’ve got a lot of other stuff going on, and you’re in the midst of enrolling for a study about braining tone, metabolism, and first episode psychosis.

And you’ve recently published a study about carbohydrate reduction in retirement home, and the metabolic and cognitive changes. So, I want to discuss both of those. But before we get into those, just bring us up to speed. Tell us a little bit about who you are, where you are, what you’re doing, just so everybody’s on the same page when we get started.

Stephen: 
Sure. So my name is steven Cunnane. I’ve been in Sherbrooke for the past 21 years. It’s a moderately small city, provincial city, around 150,000 people, north of Boston and east of Montreal. Lots of snow this time of year. And I’m a professor in the Department of Medicine, and a researcher in the Research Center on Aging.

My primary interest and my reason for coming to Sherbrooke was because of the excellent imaging facilities they have here and wanting to learn more about the brain’s utilization of fuel as we get older. Glucose being a major fuel of the brain, and studied in many imaging centers with the PET technique and the tracer called FDG, fluorodeoxyglucose.

But no one had developed ketone PET Imaging until we started this in Sherbrooke. And, as we now know, the past 20 years or so, ketones play a significant role in the health of the brain. And we wanted to understand how they were used and where there were problems using them or not. 

Bret: 
Yeah, so let’s drill into that a little bit.

So, the technology existed for a while to measure glucose utilization in the brain, but as you’re saying, not really ketones. And so you’re one of the first to put those together to look at both glucose and ketone metabolism and energy utilization in the brain with this non-invasive imaging technique.

is that right? 

Stephen: 
The technology, there’s part of it is the hardware you need, the scanner, the instrument, and the other is the type of tracer molecule you put into the body. So, if you want to look at glucose, you put a glucose tracer in and it’s called fluorodeoxyglucose. And that’s been available for over 40 years.

And there’s probably in total 60, 70 different tracers that are used for all sorts of different purposes. The ketones have never really been developed for that purpose, and we wanted to compare them, and especially to study the two tracers as close together as possible in time so that the brain would be in the same physiological state.

And if there were differences, we wouldn’t be able to, we wouldn’t be confounded by the fact that maybe it was the next day or maybe something had happened and so on. It’s so we do them sequentially. We call it dual tracer. It’s sequential within two hours of time, and then you can compare these two and say, look, there are differences or there aren’t.

And you can develop interventions, which we use. So we do this at baseline, and then after an intervention has been been offered to the participants in certain cases. Not in all cases, but.. 

Bret: 
Yeah, so you’ve done a lot, you’ve done work with this with dementia, cognitive impairment. What’s the high level of what you’ve seen in both glucose and ketone utilization for those who are suffering from cognitive impairment and dementia? 

Stephen: 
It’s quite clear that there is a problem, especially in the above the ears, an area called the parietal cortex, which is quite a large processing area of the brain in utilizing glucose, as dementia develops, even at the early, early signs, subjective signs often.

And then that problem gets worse over time and it spreads across the brain in the same individual on the same study day. We have seen no difference in ketone uptake. In fact, in some of them, there’s an increase. It’s as if there’s a starvation in that region of the brain because it’s not getting enough fuel and the capacity to use the alternate fuel, the ketones is actually improved.

Supply hasn’t changed, but at least the ability to transport those ketones appears to go up in some of those individuals. 

Bret: 
Yeah, which is a really important finding for a potential mechanism of cognitive decline and then leading to a potential therapeutic intervention with providing ketones either with a ketogenic diet or exogenous ketones or other means to provide that fuel.

So, have you also taken that next step for the therapeutic intervention? 

Stephen: 
Absolutely, yeah. Medium, good old fashioned, MCT, it was what we started with when we got funded by the Alzheimer’s Association of the USA in 2015. We did a six month study. We didn’t even know how to provide the MCT at the time.

We simply said we’re going to give people 30 grams a day, and we hadn’t really thought through what it involves. It’s simpler than a ketogenic diet. But still, you want to have a placebo. And these are older people, how often do they need to come to the lab to pick up stuff and so on?

But we got over those sort of logistical issues. And we had some quite positive results on memory learning, language processing, speed and attention, which are the five main cognitive domains. And that product has actually been launched in Europe, as available to the public. And it’s also part of a major multicenter trial in Europe and the USA that’s just gotten started.

It’s about halfway through recruitment now. So, we did the sort of proof of principle. And we showed with the imaging that the more you got ketones into the brain, the more you improved the memory and problem solving issues that these people were starting to develop. Yeah, so there’s a direct link between the brain energetics and function. 

Bret: 
That’s why it’s such an important point that you started with the mechanistic imaging study.

And then were able to turn it into the clinical therapeutic study, which I think is just such a critical bridge. But now you’re moving from dementia and cognitive impairment to psychosis, and you’re going to do a study or you’re currently enrolling for a study to measure brain ketone metabolism in first episode psychosis.

So tell us a little bit about what motivated you to make that the change to psychosis and do a similar study there. 

Stephen: 
So there’s two. It comes from two sides. One is that there are a lot of common risk factors between cognitive issues in older people and mental health issues in at all age, in all ages.

And insulin resistance type II diabetes are under underlying that metabolic problem that seems to be present and exacerbated by some pharmaceutical treatments as well. So, we were aware that if you’ve got type II diabetes or insulin resistance, your chances of being able to correct the glucose problem in the brain with ketones is going to be quite impaired because the insulin levels are a little higher and they block ketone production endogenously.

So, we were thinking about it at that level. And then I was fortunate to be invited by Jan Ellison to the first Metabolic Roadmap Meeting in 2022 in Santa Barbara. I guess I’m sure in part because we were doing this metabolic brain imaging. And I didn’t know much about, I didn’t know anything about metabolic psychiatry at the time so that was an eyeopener.

And I said, if these problems confront younger individuals with severe mental illness, I think we could apply this technique to them and see what is the state of the brain in terms of these two major fuels. How much does it get worse with the antipsychotic treatment? And what can we do if there are ketogenic treatments that are being developed and we can collaborate with people doing that sort of work? What is the state of the brain in those individuals, and their overall quality of life, of course, once they’re on that treatment in and in relation to the change in brain fuel utilization? Like how important is the brain fuel utilization story to their mental health? And that’s what this tool offers. 

Bret: 
Yeah, so tell us a little bit about the study. I think you alluded to it, that you’re going to, you’re going to measure people when they’re first diagnosed, before they’ve been started on medication and then again after they’ve been started on antipsychotic medication.

Is that, is that right? 

Stephen: 
That’s right. So we had some discussions with Jan before that workshop got started, and she knew she, that we were looking for a research chair position here in Sherbrooke to develop this. And in the end, she provided us with a donation to get started. We hadn’t identified a potential chairholder at the time, and we still haven’t, in fact.

So, with that pilot funding that she provided to us last year, we said that we’re going to focus on this particular issue because no one’s addressing it at the moment. No, most people don’t have the tools for one thing. I’m sure other people would do it if they had the tools. And so we said, and Maggie Han, by the way, is a co-investigator in this study along with the psychiatrist that I work with in Sherbrook, Kevin Zemur.

So Maggie was insistent, if I can put it that way, that we look at the patients before they start the antipsychotics because most people, I think, who work in this field recognize that the antipsychotics tend to make the metabolic state worse. The question is, how bad is it? To start with, is it already, is that signal already there or is it only really there after the start of the antipsychotics?

And this is one way to address this question. So, we are specifically looking at individuals who are not in an urgent need to start the antipsychotic and can wait maybe 10 days from diagnosis to starting and that gives us the window to do the baseline scans. Anyone who absolutely needs to start, there’s no question that they will be put on the appropriate treatment.

But if they are able to give us a short window, then we’ll get the baseline. They’ll go on the antipsychotic that appears to be the most appropriate for their needs, and then four to six weeks later, we’ll do the scan again along with continuous glucose monitoring so that we can see the state of their peripheral glucose utilization as well, and try to see if, is the peripheral state of glucose metabolism actually a good proxy for what’s going on in the brain.

So, it makes it much more accessible to everyone because the imaging technique is still expensive and it’s, there’s not many, there’s no one else doing it. 

Bret: 
Yeah, great point to try and find an easily accessible for everybody, a proxy for that. So what if you find that the glucose utilization is impaired at baseline, and then when you start the medication, it worsens?

And what would you expect the ketone utilization to do as well? What can you, what do you hypothesize would happen and what do you expect to potentially do with the findings? 

Stephen: 
I think it’s reasonable to speculate that ketone metabolism is not as impaired and is perhaps not impaired at all.

Because we have evidence now, both from retrospective and prospective studies that have just been published in the past couple of years, that people with severe mental illness will benefit from metabolic improvement that involves raising ketone levels. So, there must be some way that the brain can use those ketones, and we don’t know whether there might be some deficit compared to normal, but there’s certainly a residual capacity to use those ketones that can help the brain.

So my, I would speculate that we will find that with the imaging. What areas of the brain are touched is to me is unknown. There’s very little actually on the brain glucose utilization. There are systematic reviews, and they suggest that some relatively small centers in the brain are affected by glucose, impaired glucose metabolism in severe mental illness in schizophrenia, a bipolar disorder.

So we won’t be, we’ll be starting at the early stage, and not when full-blown bipolar or schizophrenia has developed. By the way, I’m a physiologist, I’m not a clinician, so I may be a little bit vague about some of the terminology because it’s not my firsthand experience.

Bret: 
Yeah, and that’s why it’s, building teams is so important. That’s why you have a team with psychiatrists on board, clinicians on board, too, so you round out the team. Yeah, so important. And then that can really open the door for further research in terms of ketone therapeutics and seeing how that also changes fuel utilization in the brain with imaging as, down the road.

So, do you see that as a natural sort of progression? 

Stephen: 
Absolutely. the psychiatrist that I work with, and Maggie for that matter, are clamoring to start ketogenic interventions in patients they already have who are succeeding, more or less, shall we say, with their antipsychotic treatment.

But there’s some symptoms that are not responding. It’s typical. And the question is would the ketogenic interventions help reduce the dose of antipsychotic required or the one, or allow some improvements, an optimization, shall we say, of the whole process?

And how with a pharmaceutical, like a GLP-1 inhibitor or some other pharmaceutical, actually be a nice compliment to an exogenous ketone or to the ketogenic diet if we can get people to stay on that diet long enough to benefit from it?

Bret: 
Yeah, and I think it’s so powerful. We talk so much about brain energy utilization, but the power of actually being able to see it and measure as a mechanism and then measure that with treatment is so important. So that’s fantastic work that your lab is doing to be able to image that. So, I assume, since there’s so much imaging involved, people have to be local. They’re probably diagnosed in one of your local clinics and then referred to you for the study?

Stephen: 
Yeah, my collaborator is responsible for the first episode of Psychosis Clinic. So there’s a sort of a hotline from people directly to him. And it’s, so he will have to make the judgment as to whether someone is appropriate for the study or not, but we’re on standby to mobilize the team and open an imaging slot so that person can be seen as quickly as feasible.

So the Baszucki funding has, is going to allow us to get our foot in the door and establish whether or not we, at least in principle, we in, maybe up to 10 people, I don’t think we’ll be able to do many more than that, but whether we have a story to tell that’s based on the two types of brained imaging.

And if so, I think it’s going to give more credibility to look for funding to combine this in treatments of people who are already on an antipsychotic. What’s the state of their brain after one year, for instance? And to what extent can we make some improvements as they go along? 

Bret: 
Yeah, such important questions. I really look forward to having you back on in the future to talk about the results of that study.

Before we continue, I want to take a brief moment to let our practitioners know about a couple of fantastic free CME courses developed in partnership with Baszucki Group by Dr. Georgia Ede and Dr. Chris Palmer. Both of these free CME sessions provide excellent insight on incorporating metabolic therapies for mental illness into your practice. They’re approved for a MA category one credits, CNE nursing credit hours, and continuing education credits for psychologists, and they’re completely free of charge on mycme.com. There’s a link in the description. I highly recommend you check them both out. Now, back to the video.

But speaking of results, you have another study that you have published and have results on, and this was interesting, where you took individuals in a retirement home who had some evidence of insulin resistance and lowered their carbohydrate intake, not quite to a full ketogenic diet, down to about 33% of their calories from carbohydrates and saw some significant metabolic improvement.

So, tell us a little bit about that study, the motivation behind that, and how that was structured. 

Stephen: 
So, as I mentioned when we started, I’ve been working in a research center on aging, and we’ve mainly had people that come to the lab to be tested and so on. But I realized early on that retirement involves moving into a home often, and that the economics of running these types of homes means that they’ll try to economize on the cost of food as much as possible.

Which generally means that the carbohydrate intake will remain relatively high because rice, potatoes, and bread, and so on, a pasta, is less expensive than meat, fish, eggs and cheese and veggies for that matter. And we knew that older people have a higher incidence of insulin resistance and a tendency to drift towards type II diabetes.

And so we said, what would it take? We’ve got a captive population in residence here. We got, they’re all eating from the same kitchen. So in technically speaking, they’re all eating the same thing. Isn’t that’s perfect? And for a certain scientific design of a study so what would it take to change the way the meals are prepared over a two month period?

And we had this discussion with the kitchen staff and the director and the part and the residents. We did a 10 day trial to start with. We also used continuous glucose monitoring. In the 10 day period, we looked at what their normal excursions in glucose were over 10 days.

Then we did the 10 day trial. It was a bit of a stress for everyone because it was new and it was short-term. The thing about the two months period is, yes, it’s longer, but then if you extend it beyond, that was their menu cycle was two months. So we simply can restart and there’s, they don’t have to reinvent the wheel when we start the third month.

So the study was, what are the metabolic benefits in, over this period? And what is the achievable goal? What’s realistic if we go too far? I think people will start to drop out in terms of reducing carbs, and we made it clear the residents from the beginning that they get two desserts a day and they want to continue getting two desserts a day.

So we said, okay, we have a dietician who’s quite versed in low carb. and she, it made it her challenge, to figure out how to accommodate that goal because we wanted to keep them motivated to keep doing it. And we figured 30%, we weren’t expecting it to be ketogenic.

We knew this is technically not a ketogenic diet at all, but maybe it’s beneficial for insulin because it’s beneficial we’re reducing the carb stress on insulin. So it does it help? And the answer is yes. It brings down insulin. It brings down glucose. It brings down hemoglobin A1C. And you can see this over the 10 day monitoring period.

In fact, it comes down within days of starting it. It’s not something that takes two months to get started there. The body is reacting to lower carbon intake very quickly. The acceptability was quite good, the metabolic improvements. There was no red flags in terms of cardiometabolic risk. LDL went down, triglycerides went down. Body fat and body weight didn’t change.

And nobody went into hypoglycemia, which was the flip side of our, of the risk, we’re going to reduce carbs too much. We didn’t reduce carbs too much. And that’s what the continuous glucose monitoring was really helpful to catch anyone who might. if you measure it once a week, that’s most of the time you’re going to miss whether they’re in hypoglycemia or not.

But the continuous glucose monitoring allows you to see that every five minutes over 10 days. 

Bret: 
Yeah, so from feasibility and safety, absolutely shown to be incredibly positive. But then also the next point is the metabolic benefits without significant weight loss.

And I think that’s a really important point to drill down on because a lot of people say, oh, it’s not really reducing the carbs. It’s just losing the weight. But this study seems to suggest something a little different, doesn’t it? 

Stephen: 
It’s not dependent on weight loss, that’s for sure. In this case, I’m not saying that weight loss wouldn’t help or weight loss couldn’t compensate or give you the same result, but this suggests you don’t have to lose weight.

And some of them, we even excluded some who had low BMI and we didn’t want to put them at risk.

And the average age was 84 years old. So, at that age, someone who’s underweight, it could precipitate issues that, chronic issues that we would, didn’t want to induce. So, it was, it was definitely a preoccupation to not induce weight loss unless it was, if they had excess weight, then obviously it would be beneficial.

So, that was encouraging in terms of feasibility and in terms of safety and metabolically. And the icing on the cake, if you will, was that the ketones actually tripled, which they started low and they went up to a relatively low number still, but they still went up. And so now you’ve got more effective insulin signaling.

Glucose is coming down because there’s less pressure on insulin. You got a little bit more ketones so they can help even if there’s a glucose problem in the brain, which in, statistically and most of them, there would already be reduced glucose uptake in the brain of someone at 84 years old.

You’ve got your alternate fuel that’s coming in 24/7 because there, these are the three meals that they’re eating. So the sustainability, I think for those that are saying keto is great, but I can’t stand it anymore, thing or the cost is still an issue in this sort of approach.

But it seemed to be an intermediate step that was feasible and acceptable to quite to all of them. 

Bret: 
And were you able to measure functional or cognitive outcomes as well? Or was this study not geared towards that? 

Stephen: 
It wasn’t powered for that at all. We, and we saw a couple of things in relation to reaction time that were positive, but overall, there’s no really dramatic effect on cognition.

But they were also mostly a relatively normal cognition for age. I think three of them had mild cognitive impairment, but that’s not a basis by which you can judge whether you’ve made an impact on cognition, especially over two months. Cognitive changes take a while to deteriorate and they take a while, if ever, to improve.

I think so, the right kind of study needs to be done to address that. 

Bret: 
Yeah, very good point. And the timing of this was really interesting. We had a recent interview with how Cranmer, who runs assisted living facilities and retirement homes, specifically feeds them ketogenic diets and even carnivore diets, and has seen some incredible benefits from it.

And now people are specifically searching out his facilities for that type of diet to get those benefits, and so to have some research to back it up. Now this is, maybe, I guess you could say the early stage research and more can follow for longer term and other outcomes.

Focusing on people with cognitive impairment and so forth. it opens up a whole world of potential treatments, and we talked about how the nutrition guidelines would say, no, this isn’t really the appropriate treatment or the appropriate diet to feed individuals. It should be a low fat, high carb-type of diet and say, maybe not, where we actually are starting to see evidence that maybe contrary to the guidelines is where we should be focusing.

So did you feel any of that controversy from nutritionists or dieticians or medical community that you’re going against the grain here, so to speak? 

Stephen: 
We knew we were going against dogma, that’s for sure.

But we felt it was worth trying. We went to real, and the residents themselves were worried about starting higher fat intake. The dogma was been ingrained for long enough that everyone was a little bit sensitive about this. But we did the 10 day study at first, and no one was too worried about anything dramatic happening in 10 days.

These guidelines have developed over time, and they’re based on certain types of evidence. But maybe they’re more extreme than can be justified, and I don’t think there’s any indication from our study this vulnerable population was put at any sort of risk whatsoever by reducing carbs to 30%.

There’s still plenty of carbs, and the basic parameters of health at that age were unchanged, cardiometabolic and weight and so on. I think we need to have a little bit more openness to this type of approach.

Bret: 
Yeah. 

Stephen: 
For sure. 

Bret: 
And with the carbs going down, the fat went up and also the protein went up a little bit from 16% to 21%. So, all of those factors could have been having a roll in addition to the carbohydrates. 

Stephen: 
Yes, absolutely. I’m not, I can’t say exactly, what, which part of that change was responsible.

Bret: 
Yeah. but that type of change seems to be consistent with improved metabolic health and often improved strength and less frailty. But I’ll, I’m not in the study that wasn’t necessarily measured, but often those go hand in hand. So, that would be interesting to see as well. 

Stephen: 
But I, coming back to the point I didn’t, I missed the name of the person who you said has now developed some centers like this and you’ve had an interview with that person. But it’s something I realized as well that some people will be looking for this type of menu plan, and it could become a feature that is, in fact, draws a certain type of clientele, if you will, a retiree anyway to stay because they want to.

It’s not because they’re forced to change to that style, but because they want to. and certainly because there’s benefits of doing so. So yeah, I hope there’s going to be a market for this type of approach as well in retirement homes. 

Bret: 
Yeah, I hope so as well. The interview with how Cranmer was really inspiring and he talked about the financial aspect of it. You have to; it’s a business. You have to run a business and make it financially viable, and be able to provide this menu in a financially sustain, sustainable way. So, he talked about that part and he talked about the results he’s having, and he’s talked about the demand that is being driven.

So, I think it’s going to continue to grow and I think this will be of, maybe now a small niche, hopefully in the future, a big niche for people who are seeking this out. 

Stephen: 
Yeah. 

Bret: 
Such important steps. Very fascinating always to speak to you and hear about all the work you’re doing.

Do you have other studies you’re working on and where can people go to find you if they want to learn more about your work? 

Stephen: 
We have a website here, which I could send to you, Bret. Then you could post it wherever it’s appropriate. But I guess the study that I’m working on that I’m most encouraged about that combines what we’ve just been talking about, both imaging and reduced carb, is in Parkinson’s disease. And now I haven’t done low carb or reduced carb in Parkinson’s disease yet, but through a personal experience with a friend of mine who decided to try this, the effects were remarkable and we have just been studying spring ketone and glucose utilization in Parkinson’s patients with a ketone supplement and exercise because exercise has been recommended in Parkinson’s disease for some time.

It’s not been ,not that long, but shadow boxing, dancing, running and so on. And we knew from earlier work that in Alzheimer’s disease, exercise increases brain ketone uptake. It doesn’t increase much, at least the modest type of exercise that we’re able to convince our Alzheimer patients to do, was not sufficient to raise ketones.

Intense exercise will raise blood ketones, but modest exercise will increase the transport. So, if we combined the exogenous ketone plus the exercise, we thought we might get a benefit for the Parkinson brain. We also didn’t know much about problems with glucose metabolism in Parkinson’s disease and nothing about ketones.

So, the long and the short of it is that the combined intervention gives a 50% in increase in brain ketone uptake in Parkinson’s disease over either alone. But clinically, we only had 10 people, so we didn’t even look at major clinical outcomes in terms of tremor and so on.

But what I want to do now is combine that with a reduced carb intake because Parkinson’s disease, like Alzheimer’s and like severe mental of illness, is associated with insulin resistance, and this is going to block ketone production endogenously. So if we reduce carbs by to 30%, presumably we could reduce insulin resistance in this population as well.

And there are people who practice this already. So in my, if I on my wishlist, is to get funding to do a project where we combine exercise exogenous ketone and reduce carb intake in Parkinson’s patients. And logistically speaking, the results are more obvious in a Parkinson’s patient more rapidly than they are in an Alzheimer patient who’s, where you’re trying to follow variable memory performance and other cognitive measures.

The Parkinson’s patients will know. I could tell by his voice and by several other parameters that things were going better for some reason, and he was absolutely stunned at the improvement. It didn’t change medications at this point, so what we’re trying to find out is whether the part of the brain that’s really affected with produces dopamine in Parkinson’s disease, it’s called the substantial nigra.

We actually got an improvement in in fuel utilization in that part of the brain. And so I’m hoping we can resuscitate that and help that part of the brain actually produce more dopamine and that will help improve the general situation. But that’s looking ahead, we just built the large, the most high, highest resolution PET scanner in the world, actually has been just been built in Sherbrooke and for these small regions of the brain. That tool is going to be invaluable in looking at Parkinson’s patients. So we’ve got permission to scan them as soon as the instrument is available, and that’s the first thing we’re going to do.

Bret: 
Wow, that sounds fascinating and could be just revolutionary in terms of treatment for a disease where the treatment has not been so great. But when you’re a trailblazer, that’s the way you do it. You do the small study that to show proof of concept and then build upon it with bigger studies. And that’s what you are, definitely a trailblazer.

I look forward to, seeing those studies as well. And thank you for all your work, and we’ll definitely link your website so people can follow all that you’re doing. So, thank you very much. 

Stephen: 
I’ll send it to you then, Bret. Thanks very much. Take care. 

Bret: 
Thanks for listening to the Metabolic Mind podcast.

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