GLP-1 and Ketosis: Novel Mental Health Treatments

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.

Today, we’re continuing with our series discussing the use of GLP-1 receptor agonist medications, like Wegovy and Ozempic in a psychiatry population, specifically what effect they might have on mood disorders. How they fit into the whole paradigm of treatment. And I’m pleased to be joined by Dr. Roger McIntyre, who has been involved in the field of psychiatry for over about 30 years now, as he said.

And has been involved in every area from research to clinical practice, to advocacy to leadership. And he’s a very highly sought after speaker. So it’s a pleasure to have him on the show today to talk about his perspective of GLP-1 receptor agonists, how they can be used in psychiatry? How the research is going, and the analogies in comparisons to ketogenic therapy, and the same thing, how could that be used in psychiatric care?

Where does it fit into the overall picture? And also his hope and enthusiasm of new treatments, and new areas of research that are going to directly impact patient care. Now, Dr. McIntyre, he’s a Professor of Psychiatry and Pharmacology at the University of Toronto and Head of the Mood Disorders Psychopharmacology Unit at the University City Health Network in Toronto, Canada.

And he’s also the Executive Director of the Brain and Cognition Discovery Foundation in Toronto, and the Director and Co-chair of the Scientific Advisory Board of the Depression and Bipolar Support Alliance. He’s authored over 800 papers. So, you can see just by that introduction, he’s involved in the advocacy side. He’s involved in the research side. He’s involved in the leadership side. He’s truly one of the preeminent people in the field of psychiatry right now.

So it’s a pleasure to have him on to discuss this very, important topic. Now, remember as always, our channels for informational purposes only. We’re not providing direct healthcare advice or establishing a provider patient relationship. The things we discuss, whether it’s medications or changing your lifestyle, can have dramatic and dangerous effects if not done with proper clinical supervision. So please, take the information from this interview, learn from it, bring it back to your clinical team to discuss if it’s right for you.

So, any changes you have are done under clinical guidance. And also last thing, to find more about Dr. McIntyre, he is on Twitter or X, I’m still getting used to calling it X, at rogersmcintyre, M-C-I-N-T-Y-R-E. Okay, so with that as the introduction, please enjoy this interview with Dr. Roger McIntyre.

Dr. McIntyre, thank you so much for joining us today here at Metabolic Mind. 

Roger: 
So wonderful to be with you. 

Bret: 
So, as we heard in your intro, you have quite the accolades from academics and research and also clinical practice and leading different organizations. So, it seems like you’ve been involved in many different aspects of psychiatry and probably seen it change over time.

And one of the main areas that seems to be on the forefront now is the question of these GLP-1 agonist medications and what roles do they have in psychiatry? So, there’s the discussion of how they help in weight management, but now there’s also the discussion of how they help as a direct sort of psychotherapeutic medication.

So, give us your sort of overall thoughts on how this field is changing here. 

Roger: 
Look, you set that up so nice, Bret, and you’re absolutely correct. I would say that in my time in psychiatry, a surreal privilege I’ve been given to do this. I could tell you that by patients and families, is that we are really seeing a pivot towards a new frontier in how we think about what causes mental illness broadly, and how we can prevent and treat mental illness.

And we all share in common the wish to reduce the burden of mental illness to people. And when I started in the business, Bret, people talked about neurochemical imbalance in your brain. You didn’t have serotonin, take some SSRI, like Prozac, your depression gets better. Now, I’m obviously being overly simplistic. But that’s, it was sort of the mantra for a long time. The last decade or so, what’s happened is we’ve got technology that we didn’t have before that’s given us the opportunity to look under the hood.

In other words, look at the brain in ways we could not look at 20 years ago. When I started my career, this technology didn’t exist, and what we have now is a line of sight. We have a line of sight that is telling us, you know what, in the brain of people who are living with mental illness, again, mental illness is a big category but mental illnesses broadly, is that there’s something not quite right with how the brain cells are utilizing energy.

And we know that when the brain cells don’t utilize energy in a way that is considered normal, that could affect their survival and their function. Then we then did some detective work, and we’ve discovered that there’s a number of different reasons why this is the case. And one of the reasons why this is the case is that there’s something maybe a little not quite right with insulin or the GLP-1 system or both.

And again, we didn’t even have this technology that, you know, 15, 20 years ago. But in many ways, as you know Bret, history repeats itself. And going way, way back, like a hundred years ago, even in the 1800s, more than a hundred years ago, the writers at the time observed that people who had diabetes were more prone to mental illness and vice versa.

There was some type of connection, and people tried different ways of manipulating it. But it never really took off. There wasn’t really the traction, so to speak, but now there is. So in short, the prevailing view in psychiatry, broadly, is that mental illnesses are a result of an abnormal function in the brain cells.

One of the reasons, not the only reason, why these brain cells are not performing normally is because something wrong with energy utilization and that might be related to inflammation, might be related to other aspects .And that then invited an opportunity, maybe we can reset that energy homeostasis in this brain cell to provide not just treatment, but maybe a protection against mental illness. 

Bret: 
Yeah, so interesting just to how you laid that out. How it evolved over time, and as new theories pop up, that opens up new areas of research and potential new therapeutics. So, whether it’s a medication, whether it’s a lifestyle that we’ll get to.

So, this medication, these medications, the class of medications, the GLP-1s. People hear those and they think, Wegovy or Ozempic, they think weight loss. They think, works in the gut, decreases your appetite. So, how does that then translate to mood improvements? Is it the improvement in metabolic health, which then leads to better metabolism in the brain?

Is it a direct brain effect? What’s the underlying theory right now? 

Roger: 
Underlying theory right now, Bret, is that there’s two pathways wherein we think that GLP-1 agonism, in other words, activating the GLP-1 receptors may be beneficial.

First is indirectly by virtue of the fact that someone is losing a lot of excess weight and, or the person’s diabetes is coming under better control. That, in and of itself, is good for brain health because I coined this phrase a few years ago, the metastasis of obesity and diabetes to the brain.

And what I was trying to capture with that notion is that, when I went to medical school, we heard so much about how bad obesity and diabetes is for your heart, for many organs and so on. No one talked about the brain. And I had noticed early in my career when people had obesity or diabetes, they were more likely to have problems with their cognitive functions to be able to think clearly.

They often complained of low energy and motivational deficits. Long story short, we now know that’s latent. And so, that’s one possible pathway because GLP-1 agonism can result in significant weight loss and improve your diabetes. And that would be a nice, easy to understand story. And there’s a second way as well.

This is the part we didn’t know about until fairly recently. GLP-1 is actually produced not only in the bowel, that’s what’s mimicked by the medication, but it’s also in the brain. What’s interesting is that they always say location, location. The location tells you a lot. Wherever you see a 7-11, that usually means there’s lots of people living nearby.

And when you have, in fact, GLP-1 receptors in regions of the brain, it can often tell you a bit about what its job description is. And GLP-1 receptors and GLP-1 in the brain, whereas locally manufactured, is in areas of the brain critical for us to be able to think clearly and for us to be able to feel emotion, feel ourselves, feel a sense of well-being.

And it not only does it directly, but does it through other neurotransmitters, like dopamine, which is the pleasure hormone. And so we’ve discovered in our animal work and other folks have shown this, and we’ve done this also in our human studies, that by giving a GLP-1 agonist, yes, you could lose weight, and by that, could help the brain.

Also, it can directly go into the brain, and it can actually affect the brain and that might be able to reset the circuits in the brain. I always talk about Bret, CNN: circuits, nodes, and networks. So, in the brain, you’ve got these circuits and these networks and these nodes and all keep it together.

It’s just like your motherboard on your PC. 

Bret: 
Yeah.

Roger: 
And when we look at the circuitry and the networks in the brain with MRI scanning, something’s a little off in many mental illnesses. When you give the GLP-1, it might reset that. So again, these are not mutually exclusive, the direct route, the indirect route, but we’ll take whatever we can get. Anything that’s going to help the brain, I’m signing up for.

So, this has been of interest to us. And it’s provided the impetus now for us to say, heck, why don’t we just study these medicines as direct therapeutics for mental disorders, like Alzheimer’s disease or mild cognitive impairment or depression or what have you? But something I know about you, you and I talked about before, is that at the end of the day, the way I always want to encourage people to think about not just medication, but also dietary interventions or psychotherapy, exercise, sleep.

It is like a game of rugby. And there’s, for those who know the game of rugby, when you run down the field, you hand the ball off to the next person who throws the ball to the next person. You keep running down the field as a team. The first step is where the drug binds to, and then that’s the football.

You hand it off to the next person. And so, the downstream effects in the brain the cells of the brain, they’re probably overlapping. So, when you give a GLP-1, it’s possible that some of the downstream effects of doing that is not dissimilar from dietary modification. Maybe it overlaps with ketogenic, maybe it overlaps with sleep normalization, maybe mindfulness-based therapy, maybe exercise?

In other words, there’s many ways that you can take the interstate to go to a city. There’s many routes of entry, but you end up in a similar place. So, it was interesting. 

Bret: 
Yeah, it’s a very interesting analogy. And I definitely want to talk more about lifestyle and the comparisons. So now, with these GLP-1s, there’s a lot of excitement about doing research on them, and that makes a lot of sense.

And there’s some clinical experience. But if we were to, in broad strokes, say they’re antidepressant medications, they’re mood stabilizing medications, they’re antipsychotic medications with some overlap there. Where would the GLP-1s fit? Would they fit into any sort of generic category like that?

Like how do you think about them in a psychiatry practice? 

Roger: 
That’s such a great question. And you know something, they say that names matter. Names do matter. I think what we’re going to be talking about with these medications is to be determined. For now they’re called GLP-1s. But for me, I’m going to call them brain protective medications.

How’s that? That’s just being somewhat extemporaneous. In other words, we really believe that these interventions targeting metabolics in the brain. We’re focusing on GLP-1 right now, but we could also extend this to insulin and other ways to affect cellular metabolism. We think this cuts across from the nursery to the nursing home.

What I mean by that metaphor, conditions of childhood, like autism, maybe ADHD, all the way through diseases of adulthood, like depression, bipolar and so on and on, all the way to the elderly, like Alzheimer’s disease and so on. So, I don’t think we’re going to be held ransom to one single disorder. I think we’re looking at, they are broadly effective and therapeutic for the brain. And that will have, what we call transdiagnostic, to simply meaning it applies a different diagnosis.

What’s been so interesting to me is that when we talk about mental illness, what we tend to talk about is risk. This person has a risk of mental illness by virtue of having this molecule not quite right or that receptor not quite right. This person has risk for this, risk for that. We don’t see enough about resiliency.

In other words, what’s protecting the brain from all those daily insults and so on? And what’s cool about the GLP-1 system is the GLP-1 system ignites at the cell, a set of molecules that protect the brain and also ignites a set of molecules that reduce the risk. So, just like a seesaw, risk and resiliency.

Risk and resiliency, once risk is starting to take a heavier load, then that’s where you get into trouble. Your resiliency should balance it off. And so, they’re targeting two aspects. They’re boosting some of the molecular systems that we implicate, for example, reducing inflammation. But they also, in fact, reduce some of the risk in the brain.

That is, they eliminate certain proteins in the brain that are bad customers. One of them is called amyloid, which is implicated, of course everyone knows it, in Alzheimer’s disease. But it’s implicated a whole bunch of other problems, and it’s a bad customer. GLP-1 seems to reduce and get that, export it out of the brain.

So, it does a lot of really interesting things. Academics love really unnecessarily complicated words. One they love is pleiotropic, which just means it does a bunch of things. And so it does a bunch of things. 

Bret: 
Yeah, and I really like that talk about resiliency and brain protection. Now, so they’re saying there’s no free lunch. So these medications come with risks of nausea and gastroparesis and intestinal blockage and pancreatitis. Any drug has a laundry list of side effects. So one question is, what else can we do to achieve similar results?

And the way we talk about ketogenic therapy is often very similar. It can help with the weight loss from antipsychotic medications. It can help with metabolic health. It can reduce neuroinflammation. And it can be a brain protection, whether it’s from mild cognitive impairment or Alzheimer’s disease or potential treatment for psychiatric symptoms.

So, how do you see that analogy or how does ketogenic therapy fit in light of the enthusiasm around GLP-1s? 

Roger: 
Such a great question. I think that, in fact, when it comes to ketogenic diet, I think that the evidence is really getting us more and more interested in this modality. In the sense that we know that when the diet is shifted towards a consumption of nutrient that creates a ketogenic diet state, that there are, in fact, mechanisms that are ignited, like anti-inflammatory antioxidant.

We see a boosting of the performance of different, what we call organelles or sub components of cells. We also see something I’ve been interested in a long time, a boosting of insulin sensitivity. The very first patient in the world, Bret, that received insulin for the treatment of diabetes was a young boy, in 1922, at my hospital in Toronto at the Banting and Best Institute.

So, maybe it’s something about Toronto, about insulin, maybe it’s in the air here? We all take an interest in, at least I did early in my career, but insulin’s so interesting because insulin in the brain is not so much there to help with your sugar or glucose control.

It’s there as a protein to support the brain cells, to help them grow, to help them protect against injury. And also, they’re there to help us form new synapses or connections. And ketogenic diet seems to also boost the insulin signaling system. So, we talked about pleiotropic, which means does a bunch of things.

Ketogenic diet is certainly touching on some of these sweet zones. And what would be really interesting, Bret, here would be an interesting and cool study, something we’ve been marinating. And that is to compare, to look at what’s the effect in the brain of GLP-1 and ketogenic diet to see if that in the brain, some of the effect is overlapping.

That’s something we’ve been marinating internally. It’s something we’re going to explore. 

Bret: 
Yeah. That does sound exciting. Now, as we’ve talked about in the beginning of your career, you have the clinical, the research and the advocacy. You’re really in all of those areas. And when it comes to something, whether it’s GLP-1, whether it’s ketogenic therapy, there’s a bit of a disconnect, right?

The research is trying to catch up with some of the enthusiasm, some of the clinical experience and anecdotal reports. But then from the advocacy standpoint, we have patients looking for treatments now, struggling to find treatments now. So ,how do you see the recommendations for using ketogenic therapy to treat, serious mental illness or the clinical use of GLP-1s?

How do you connect the dots from the research to the clinical practice to the advocacy? 

Roger: 
You touched on the elephant in the room, Bret, and that is that, quite tragically the unmet need. The problem that we have with mental health treatment, not just in rich countries, like US and Canada. But around the world, is that people don’t have sufficient access to the treatments in a timely way overseen by a coordinated, high-quality healthcare system.

And that’s been a major problem. I also think a second point is that just recently, the Nobel Prize in Medicine, just a week or two ago, was awarded to two outstanding researchers to say the least, who discovered the mRNA vaccine. And vaccines, according to the World Health Organization, have done more to help human’s health than any other invention.

Where I’m going with this line of thought is prevention. Prevention and more prevention. In other words, it’s always easier to prevent than it is to treat. And I see dietary manipulation broadly as an opportunity to prevent mental illness. We know from many lines of research that dietary nutrient composition can protect you, or put you at risk of mental illness.

It’s not the only thing. There’s never one simple explanation. I wish there was, but it’s one suspect in the suspect line of the police station committing this crime. In other words, we know that Mediterranean diets, which are very high in oils or high fish diets, again, higher in oils with low carb intake, protect the population in these observational studies against depression, bipolar disorder, as an example.

So, there’s opportunities for prevention. The major problem, as in North America, we got too many food deserts and too many food swamps. Food deserts meaning there’s no local store that can offer good food.

We’ve got swamps of low-quality, high glycemic foods that are fast food and in the orientation. So that aside for a moment with respect to people who enter the healthcare ecosystem, who have access to care. What is in 2023, what is the state of the union as it relates to using these medicines, using a ketogenic diet, dietary manipulation?

Now, I have the utmost of sensitivity to social and economic issues. And I know that to eat healthy is a heck of a lot more expensive than eating a pizza. Okay, I got that. And I understand that. I’m very sensitive to that. But that aside for a moment, what I would say is that GLP-1 medicines have specific FDA indications. And it depends on which one.

There’s about a half a dozen of these drugs for diabetes and or obesity. So, I think that the use of those medications should stay within their indication. Some of you saying, hang on, you’ve just been spending the last time talking about how they could help the brain for maybe depression and bipolar, et cetera.

I’d say yes, but let’s just hold on. We got to make sure this is true. These are hypothesis. This is still a work in progress. I wouldn’t be treating depression or schizophrenia or autism or Alzheimer’s with the GLP-1. I would say that’s a research hypothesis that we are currently pursuing. But that’s something I thought people would be interested in with respect to ketogenic diet.

I also think that’s where we’re at. We’ve got plenty of evidence now to show this is really starting to help some people, not just in depression of bipolar, but some other, many other conditions as well. That’s why I don’t think it’s held ransom to one diagnosis, right? But I would say that for now, what I would say is we need to have, and they’re starting right now, Bret, you know it well, some larger randomized control trials that are what’s called adequate.

Just simply means really rigorous and controlling for all the confounding variables and all that stuff. But that can really, in fact, answer the question, is this the way to go? And I am a very open-minded person, and I’m a curious person. The science has to always guide this. The science has taken us in a direction that we have a believable and viable hypothesis, that maybe it could be used for certain conditions.

Some might be saying, isn’t it already used for pediatric epilepsy? Yeah, it already is. You’re right, and that’s already a proof of concept that it can help a suffering population. The question now is, can we extrapolate that into other patient populations? And I’ve been a research scientist for a long, long time. And what I’ve learned is that, I’ll say it this way quite humbly, Bret, that a lot of my hypothesis haven’t quite turned out.

But I keep going. and sometimes they turn out. You have to be really humble in this business. And so let’s see where it lands. Let’s make sure it’s safe. And let’s make sure it works, and I think so. It’s an exciting time. 

Bret: 
Yeah, and, do you think the burden of proof, though, is different from a medication that needs FDA-approval and is expensive and whatnot, and you need a physician to give it to you versus just changing how you eat?

You can simplify it that much. Although, I would argue that in this realm, ketogenic intervention is a medical intervention as well. But do you think the research burden of proof is different or would you hold them on the same level? 

Roger: 
The way I would approach it is, I would approach it with nothing but respect.

Nothing but respect for the seriousness, the hazards, the agony and the immeasurable suffering that mental illness causes. And as I think about it, in my experience, and I’ve witnessed first hand, I’ve been providing care for people with depression and bipolar for a long time, and they’ve given me a privilege.

And I think that people who are suffering in that kind of agony, I think that they deserve to know that the treatments that are recommended are safe and are supported by an evidence base that’s compelling. Now, the question then is, what’s compelling? The FDA defines compelling, you have to have a couple of studies.

You can’t just have one, one fluke or one mulligan. You have to have a couple of replicated studies. The scientific community, generally speaking, has guardrails on what’s considered a rigorous way to do this. And it can’t be done, and it is being done. And I think that before we say to somebody, because whenever I say to somebody, I think you should try treatment X or treatment Y, that person’s trusting my professional judgment.

They’re trusting my ethics. They’re trusting my advocacy. And when I go to a car mechanic, I don’t know anything about car mechanics. I’m trusting what the person’s going to tell me. And when it’s your health, what can be more important? And so, I think we have to respect the seriousness of the mental illness that people will suffer from and say, okay, I’m going to respect that by saying we’re only going to recommend the highest quality of evidence.

Now again, I’m a researcher. I appreciate first hand, it’s a little tricky to do some of these studies. You can’t just, taking a pill or placebo is pretty easy. Changing diets not quite as easy. I’ve done a lot of, we’ve done some of this work, et cetera, so there are obviously some challenges with the method, how you do this. But there are ways to do it ,then again, that’d be considered compelling.

One of the challenges, as you know, Bret, is that in order for research to flourish or to be adequately interrogated, it has to be supported financially. Research doesn’t just happen. There’s a cost to doing research, right? And part of this is the streetlight effect. Where’s the streetlight shining?

That tends to get the money, so to speak. But I think, now, I think we’ve been flirting with the opportunity that might be provided by ketogenic diet for decades. But I think what we’re now seeing for the first time, is really top-notch researchers leading people around the world in research, who are taking this question on and testing it.

So, I think it’s going to be very enlightening over the next three to five years. I got to put my bias, everyone has biases, some that you’re aware of. Most of our biases, we’re not even aware of. But my bias is that I strongly believe what you eat does affect your brain. And whether it does it directly or does it through other mechanisms, like the gut biome, we can discuss that for hours. But I’m a big believer in the energetic model of mental illness.

And so anything that’s affecting energy homeostasis in the brain and body has implications for that organ called the brain. So, to me, it’s just so intuitive, and I think this is going to be a very exciting time. 

Bret: 
Yeah. I like how you talked about the streetlight analogy. That the streetlight was shining brightly on serotonin, on neurotransmitters, and that’s where the drug development was.

Roger: 
Absolutely. 

Bret: 
And now we are starting to see that streetlight move towards brain energy. Now, like me, I’m deep into brain energy. That’s what I focus on, and ketosis for it. But so, you’re in the broader field of psychiatry though. So, do you see that streetlight starting to move in the broader field of psychiatry as well?

Roger: 
I absolutely do. And I really do, in fact. And I think part of this is a consequence of our technology, and the ways that we can look at brain cells in the microscope. And what we are discovering, for example, in the brain is that the brain is, the brain is comprised of two types of brain cells.

They’re called neurons, or brain cells, and also the glia, the white matter. The gray matter and the white matter, respectively. And when we really sharpen the focus and look into these cells, what we find is that the way wherein that the cell is able to produce, able to allocate, able to utilize and dispose of energy’s abnormal.

And it stands to reason that if we can reset that, we could have a corrective therapeutic. And what’s interesting is that when I look across the medications that we have in psychiatry, some of the medications that we have also affect these systems.

So, the streetlight, you’re right, has shined on serotonin. We’ve been worshiping at the altar of serotonin for decades, quite frankly. And no doubt it is a critical neurotransmitter, but it’s not the only one that’s relevant. And when we look at conventional treatments, not all of them, but some of them, we see effects.

We see effects on cellular energetics. So, here’s an example, lithium. Now, lithium’s not a treatment for everybody, but lithium is a treatment for many people who live with bipolar disorder. It’s been a game changing treatment. It reduces suicide in bipolar. In fact, the global bipolar community, which I’m very privileged be part of, would say that’s one of the gold standard treatments still today.

Now, lithium’s mechanism of action on the brain is not fully known. But it is known, it has a very potent effect on resetting cellular energy. And then, so that’s one example of a therapeutic affecting energy that can really be lifesaving for people. Turn it the other way around. People who have diabetes, I think everybody knows diabetes.

You got too much sugar. Your body’s not able to use the sugar. And consequently, the cells, because they can’t get the sugar, the cells actually begin to frankly starve. They can’t get the sugar, and there’s something wrong with the energy system inside the cell. And just to put a couple of percentages on this, that the rate of depression and other mental illnesses increased two to five fold in people with type II diabetes.

I always mention that in people living with Alzheimer’s disease, 80%, 8-0, have brain insulin resistance. There’s something wrong with the insulin system. So, the pathway of perturbing or disrupting the energy system is putting the brain at risk. And when we correct the energy system, it seems to protect the brain.

And we’ve known that, and I think that’s really cool. The other thing I find really interesting is it’s not just about the pills. I’m a pharmacologist. And that’s, for me, is more of a probe. I’m also trained as a psychotherapist. In the past, I actually was in psychoanalysis for six and a half years.

People go, you’re a pharmacologist. Why were you in psychoanalysis? I’m like, where did this come from? But I’m, so I think that mindfulness-based therapy, exercise ,aerobic treatment, I think those are still waiting for someone to hold onto those horns and really research it. I’m a big believer, that I think that the exercise component could help cellular energetics.

And I do think one final part, just to finish that off, Bret, we don’t say enough about is sleep. Sleep affects every single mental illness, and sleep is a big problem. We know that we’ve got a sleep deprived society. And sleep affects every single system in your brain, and one of them is cellular energetics.

You want to know something that’s really cool is that one of the treatments we have for sleep, for Insomnia, is a group of medications, called orexins. Orexins? That sounds orexigenic. That’s right. These are drugs that were developed initially, they were discovered to be involved in the appetite system and the energy system.

We have these medications. They go by the trade names Belsomra, QUVIVIQ, Dayvigo. These are drugs prescribed in US and Canada to help people with their sleep. But these are drugs that help the brain, help cognition. And guess what they are? Resetting the energy homeostasis of the brain cell. So, we have energy modulating drugs right now to help you sleep.

So, I think we’ve got lots of leads. This is why I really think we’ve got to take this bull by the horns, and we’ve got to really test ketogenic diets. it’s a different topic for another day. But there’s a lot of hype in psychedelics right now. And I always say that the only thing more hyped than psychedelics is the Eras Tour from Taylor Swift.

But there’s so much hype. And look, with hype, hype is good. I’m all for hype. \But we also have to be measured. There’s some really exciting leads with some of these psychedelics, whether it be ecstasy or ketamine or psilocybin. And guess what? These drugs do affect energy systems in the brain.

So all my, all I’m getting at is, whether smoke, there’s fire. And we’ve had the smoke for a long time around energetics. And I think dietary manipulation, we talk about ketogenic in other ways, are coherent, viable. Let’s get them really forcefully and thoroughly studied. 

Bret: 
Yeah. Wow. What a great way to tie that in, tie all those different therapeutic options into brain energy, and the way the brain uses energy more efficiently. And so, you hinted in the beginning that psychiatric care is not where we would want it. That there’s a lot of room for an improvement. So now, that the spotlight is different.

Now, there are all these other options that you just mentioned. Do you think, is the future pretty bright for the improvement of psychiatric care to really help people get back to their full-functioning lives?

Roger: 
A huge yes, Bret. A huge yes. And I remember about five years ago, maybe longer, maybe seven, the pandemic has messed up all my time, sort of anchor points. But five to seven years ago, I wrote a paper, and I mentioned that psychiatry’s in a cul-de-sac. Psychiatry is in a kind of a stagnation of innovation.

And look, science. What happens in science is we have this incremental evolution going on. Things are getting more and more better and so on. And then, every 10, 20, 30, 50 years, we get this leap forward, okay? A leap forward and that’s just how a lot of things in life work, including medicine. And psychiatry entered into a remarkable time in the 1950s, which was called the Psychopharmacological Revolution.

Prior to 1950, we didn’t have any drugs for any mental illness, period. Full stop. People were getting all kinds of things done to them in asylums back in the day. Then, what happened in the fifties, we had the introduction of drugs, like benzodiazepines, the valium-type drugs. We have antipsychotics, the lithium, anti-epileptic drugs, antidepressants. As they say, the rest is his.

There’s no doubt, there’s no doubt that many lives have been saved by these medications. We’ve seen deinstitutionalization. We’ve seen many good things happen. That’s the good news. The bad news is that they’re not perfect, and the great majority of people living with all kinds of mental illnesses are not having their needs adequately addressed by status quo.

So, we’re not throwing the baby out with the bath water. I don’t, we’re not throwing SSRIs out the door. They’ve saved people’s lives, but out of a hundred people who take those medications, at least 70 to 75, are not really getting the goals met. So, what we do is we don’t throw the baby out with the bath water.

We say, okay, let’s hang onto the baby. But let’s actually add to our arsenal other treatments that take on this enemy, called mental illness. And it has to be guided by, we could be as passionate as we want. I always say that passion should not be the mediator, it should be the moderator. That’s what gets us out of bed in the morning.

We have to be measured in our science. And I do think that this is incredible because in my time, I’ve been in this for 30 years now. I can’t believe that I still feel like i’m 18. But anyhow, this is like an incredibly interesting time. We got new medications, we got new ways to do TMS. There’s new psychotherapies, all kinds of science around nutrition and diet.

Sleep science has just taken off. It really is an exciting time, and I think we’re going to have a larger percentage of people have treatments that are scalable. They can access it, that don’t give them all kinds of horrible side effects and all that stuff.

Everything has side effects, but not too many problems. it really is a hopeful time. You want to know what, Bret? I’ve had tens and tens of thousands of people come through my program since I started it. And as I’ve sat and I’ve met tens of thousands of people suffering from depression, what I would say is that we’ve had a real lack of hope. And what we need is more hope. And I think hope comes in the form of having viable treatments. And so this is a wonderful, hopeful time for the field. And the next 5 to 10 years, you’re going to see paradigm shifts in how psychiatric is going to be treated, without question. 

Bret: 
I really admire your passion and appreciate your passion and your enthusiasm, and your approach from a research standpoint, and for all you do from an advocacy standpoint, and all you do to help the field of psychiatry move forward with a message of hope, like you just said.

Roger: 
Thank you so much. 

Bret: 
Thank you for that. Thank you for all you do. Thank you for joining us today, and I look forward to hearing more from you in the future. 

Roger: 
Thanks for having me, Bret. I really appreciate it. Warm regards. 

Bret: 
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