Psychiatry & Psychotherapy Podcast - Dr. Chris Palmer: Ketogenic Diet for Mental Health

Episode Date: November 15, 2022

In today's episode of the podcast, we interview Dr. Chris Palmer, a psychiatrist, researcher, and expert in using the keto diet as a medical treatment for some treatment-resistant patients. Dr. Palmer is currently the director of the Department of Postgraduate and Continuing Education at McLean Hospital and is an assistant professor of psychiatry at Harvard Medical School. He also runs his private practice specializing in treatment-resistant mental health patients. By listening to this episode, you can earn 1.5 Psychiatry CME Credits. Link to blog. Link to YouTube video.

Hello and welcome to the Psychiatry and Psychotherapy Podcast. I'm here to talk about getting rid of burnout, increasing job satisfaction, and feeling like an expert in what you do. One thing that created a lot of burnout and angst for me was trying to get continued medical education right at the last minute. So why not join the CME membership and do CME while listening to this podcast? Go to Psychiatrypodcast.com, sign up, sign in, take the test, and the certification is emailed to you in seconds. Dr. Pudor and Dr. Palmer have no conflicts of interest to report. All right, welcome back to the podcast. I am joined today with Dr. Chris Palmer. He is a psychiatrist practicing at Harvard. He does research and he has part-time, it seems, clinical practice there. He has

recently written a book called Brain Energy. This is a book which talks about how the ketogenic diet can be used to treat different mental illnesses. He has published some case studies and reviews on this topic as well in scholarly journals, which we'll talk about. So I would like to start out by just kind of asking you maybe to give me the elevator pitch to the big picture of the book and then we'll zoom in and look at maybe individual aspects. Yeah, no, thanks for having me. The book is actually about so much more than just the ketogenic. The book for the first time actually presents a unifying theory of what causes all mental disorders. And I am making the bold and audacious

proposition that all mental disorders are, in fact, metabolic disorders of the brain. And that once we understand that, we can better understand mental illness. We can better understand the connections of mental and physical disorders that any mental health professional has long known. You know, our patients are more likely to die early deaths from heart attacks. Our patients are more likely to have gastrointestinal problems and migraine headaches and chronic pain syndromes and other conditions. And this theory for the first time helps us understand at the cellular level why and how that happens.

But more importantly, it leads to new treatments, treatments that come with the hope of long-term recovery and remission as opposed to just symptom reduction. And I know this sounds bold and audacious. The great news is that this book has been read and already publicly endorsed by leading psychiatrists and neuroscientists in the world. So it is not complete quackery. I'll stop there. Okay. So one of the articles that you kind of mentioned early on, or in the midbook is that you mentioned the 2017 article in JAMA on mitochondria dysfunction and how that seems to sort of link this idea of metabolic dysfunction in our patients with mental health issues to the metabolic world mitochondria.

Is that kind of one of the pivotal papers that started changing? in your mind, or how does that kind of fit into the big picture for you? No. That actually was not a pivotal paper, and unfortunately, that paper was quite disappointing because it missed the mark in so many ways, and that's why most people haven't heard of that paper or this concept. The connections between mental disorders and metabolic disorders have been known since the 1800s. It was well known and established that people with insanity, which usually would be diagnosed as bipolar disorder or psychotic depression or schizophrenia today, that people with insanity were much more likely to have diabetes, and people with diabetes were more likely

to develop insanity, and that these two disorders ran in the same families. That was well established in the 1800s before we had any medications to treat these illnesses for the most part. So a lot of people think that these connections like between diabetes or obesity and mental illness are due to the medications we're prescribing. And there's no doubt the medications we prescribe add insult to injury. But these connections were well established and well known before that. You know, the basic research evidence that people with mental disorders have metabolic abnormalities in their brains and bodies, it began accumulating in the 1940s. So in the 1940s, we had studies documenting differences in lactate levels in people with bipolar disorder and chronic depression.

You know, and by the 1990s, we began developing an enormous body of research. So we have all of these neuroimaging studies that most people have heard about. Pet scans, spec scans, functional MRI. Guess what those scans are all measuring? Every one of those functional imaging studies is measuring brain metabolism. By 2000, prominent neuroscientists and researchers were trying to understand what can these neuroimaging studies tell us. And all lines of evidence, basic science, neuroimaging research, clinical research, all lines of evidence were pointing to metabolic defects in the brain's.

cells of people with mental disorders. And more specifically, if you, if you ask the question, well, what does that mean to have a metabolic defect or a metabolic problem? You have to think about and talk about mitochondria because they are controlling metabolism. And so since the, essentially since the year 2000, numerous researchers and neuroscientists have all been in hot pursuit of the mitochondrial theory of a variety of mental disorders, including autism, bipolar, schizophrenia, depression, and other disorders. Okay. So when I think about the link between, you know, metabolic issues, health issues, and mental health issues, I think about the adverse childhood experiences studies, which you talk about in the book, and the link between,

you know, if you follow these kids for decades after they've had adverse childhood experiences, the more adverse childhood experiences they've had, the worse their mental health and their physical health in multiple categories. So how does that sort of fit into, to your paradigm where you have kind of like, it seems to me, trauma as kind of like a huge impact on mental and physical health. Like is the trauma influencing the metabolism or the metabolic functions? Yeah, I think one of the great things about this theory is that it unites the biological, psychological, and social theories of mental and physical health. So, trauma and adverse childhood experiences are absolutely related to metabolism and mitochondrial function.

We have direct evidence of that, both in humans and in animal studies. You know, animal studies allow us to get very granular about exactly which brain regions are impacted and what exactly is happening in neurons. We can't do those studies in humans. But there's more to metabolic health and mitochondrial function. than just adverse childhood events and trauma. So, you know, this theory looks at all of the known factors that we already know play a role in mental illness and connect them.

It connects the dots of mental illness. So, yes, stress, adversity, but of course, we know that some people with mental disorders had perfectly fine childhoods. They did not have adversity and stress. and some people could have vitamin B-12 deficiency and due to an autoimmune disorder or a poor diet. And that also can cause mitochondrial dysfunction and can result in a variety of both metabolic and mental disorders and neurological disorders as well. Okay. So one thing you talk about in the book is you're looking for that kind of like the one thing that links every thing.

thing. So help me understand, like, with the trauma, like if someone's been through a lot of trauma, in your mind is, and they've developed metabolic issues like fibromyalgia, herbal bowel, chronic fatigue, lower back pain, depression, anxiety, is the data that you're seeing, the randomized control trial supporting, like, the metabolic intervention as the cure, or is it, you know, like, so is the metabolic thing you would still always, go after as like this is what I'm going to treat or how I'm going to treat this person? Yes. If you once, I think once people understand the science, the granular science all the way down

to the cellular level, it's complicated. So the basic paradigm is this. There are many things that can adversely impact metabolism and mitochondrial function. And they are all the already known risk factors. for mental illness. They include things like stress and adversity and trauma, but they also include things like poor sleep, drug and alcohol use, you know, hormonal imbalances, vitamin deficiencies, and other things. And even genetics and epigenetics absolutely play into this. So there are lots of things that can lead to mitochondrial dysfunction. That is the center of understanding metabolic and

mental health. And then once somebody develops metabolic or mitochondrial dysfunction, the great news is that there are many ways to address it. And they include things like diet, exercise, management of sleep, minimizing or reducing substance use that is toxic to metabolism and mitochondrial function, et cetera. And so we can actually develop much more effective. and lasting treatments if we target mitochondria and metabolism as opposed to just shooting in the dark like we currently do, which is we're going to try one pill after another and see if anything works. Okay. So what about like psychotherapy? Because I think psychotherapy is kind of, it works for these people. You know, it takes time, sometimes 50 sessions, you know, but the effect size seems pretty profound.

for a lot of trauma or a lot of these patients with mental health issues. Now, I know in some of the patients that you're treating, you're treating them, when they have bipolar or schizophrenia, those are classically, you know, patients that need medications and you're treating them with the ketogenic diet. Or, you know, it seems like that's, you know, you have some case studies that support that that has been helpful. But I'm thinking, like, how do you fit in how psychotherapy would help someone's metabolic function? Yeah, so it's a great question. And I have a whole chapter on that in the book. So psychotherapy is well

known to play a role in both metabolic and mental health. And as you said, I mean, this theory isn't going, is not trying to replace what we already know works. This theory is helping us better understand mental health and coming up with additional treatment options that I think can restore long-term health. So psychotherapy has many different roles, and it depends on how we're using the psychotherapy and what the intervention is. So for some people, psychotherapy can simply reduce stress levels. And we know that stress in and of itself is harmful to metabolism and mitochondrial function. So if we can help people reduce stress levels through whatever techniques the psychotherapist is using, that can improve both metabolic and mental health.

Some psychotherapies instead are focused on behaviors. So if somebody has alcohol use disorder or opioid use disorder, those psychotherapies, which might include even 12-step programs and others, are going to be a very different type of psychotherapy, but it is talk therapy, and it's going to be focused on reducing behaviors that we know impair mitochondrial function, and if people are successful in reducing those behaviors, they will improve their mental and medical and physical health, basically. Okay. Okay.

So, you know, when I was looking at your work on the mitochondria, it reminded me of a in a prior episode, I talked with this guy on exercise. And like, specifically there was a study looking at people with metabolic syndrome, normal people who exercise somewhat and extreme athletes, and they looked at the amount of watts that these different people were able to use at specific levels of lactic acid. Are you familiar with this one? I could pull up the very nice figure if you want to take a look at this. But what they found was that the mitochondria function was very connected with the amount of

watts that they were able to produce at given levels of lactic acid. And, you know, the professional cyclists, of course, were able to produce quite a bit more watts per like, you know, at the 2-millomol of lactic acid, they were able to produce somewhere like 350, whereas the person with metabolic syndrome was producing maybe 100, normal person, somewhere around like 150, 200, right? So does this kind of play into your thought process of like, you know, if you improve muscle metabolic function, mitochondrial function and the muscles, that has impacts on brain metabolic function and brain mitochondrial function? Like, is there a link between improving one and improving the other? Absolutely. And we have robust evidence on this in both animal studies and in human studies.

So we know the exercise itself improves brain health. And if you get really granular about, well, what exactly does that mean? How does that work? A lot of people have heard of BDNF, brain-derived neurotropic factor that is associated with neuroplasticity and learning and everything. And exercise increases BDNF. Well, if you ask the question, well, what exactly is BDNF doing in the brain? BDNF is increasing the number and the health of mitochondria in your brain cells.

That allows your brain cells to be more neuroplastic, which means your brain cells will grow and thrive and adapt. So we have an abundance of evidence that exercise overall stimulates neurogenesis, stimulates neuroplasticity, stimulates overall brain health, is associated with decreased risk for all sorts of mental disorders. So a large population study looked at exercise as a prevention strategy for mental disorders. And across the board, yes, exercise is helpful at preventing mental illness. It's also helpful for preventing neurodegenerative disorders like Alzheimer's disease and Parkinson's.

And if we look, again, if you get really granular about exactly how is that working, it comes down to mitochondria. You have to understand mitochondria and the impact of exercise on mitochondria in order to understand exactly how it's working. But whether somebody wants to understand that level of detail or not is neither here or there. But the good news is that we know that exercise can be an effective treatment for mental disorders. Is exercise on its own going to stamp out depression, schizophrenia, bipolar disorder, absolutely, positively, no. No way. We've already got more than enough studies telling us that's not the way it works. So you have to understand why would that be? Why wouldn't exercise help somebody with schizophrenia? Why wouldn't exercise cure

depression in everyone who tries it? And once you understand the science, you can actually come up with a multifaceted treatment plan to really allow people to heal and recover. I want to show you this specific study that I'm referring to, or this graph. It looked at absolute workload watts and blood lactic acid and showed the three groups. So this bottom group here is the cyclists. The middle group is the sort of the average athlete, and then this is the person with metabolic syndrome.

So there was this study that was pretty groundbreaking to me. And another one that looked at all-cause mortality in different groups of athletes. I don't know if you've seen this one. But the all-cause mortality, they took a group of like 122,000 patients. So this is not a small study. And they gave them a treadmill test and then they followed them for like eight years. And they looked at all-cause mortality. So the bottom 25% group, all cause mortality, 23% died.

Whereas the elite group, the top 3%, 2.6% died. That's a 10-fold difference. I've never seen any medication that can cause a 10-fold difference. I was looking at statins. It's like a, in a high-risk group, it's like a 20% difference. And that's probably relative risk 20%. That's not the absolute risk. Right, right, right.

So this is an absolute tenfold. Yes. In the same study, they looked at smoking was only a 30% reduction in all-cause mortality. Whereas this exercise was after controlling all the variables was a five-fold difference between the low and the high group. So 30% or verse fivefold. You know, it's like 0.3% versus fivefold to put them in the same like thing. So, you know, we've talked about strength training. We've talked about endurance training.

It's really important for mental health. I've had Drew Ramsey on. We've talked about diet twice. And so I think the piece that you're a little bit different is you talk about the ketogenic diet. So I'd like you to talk about that. Interestingly, I was. at, so I run a program, an IOP program for people with medical and psychiatric issues. We have about 50 people in the program, and it's been going for about 10 years. It used to be

about 10 people in the program. It's grown. And so I see a lot of people with like psychogenic seizures, real seizure, you know, epilepsy, fibromyalgia, irritable bowel, chronic fatigue, all the, all the different issues that kind of like, where the body gets stressed and the mind gets stressed, and then they have depression and these things. And so I was at a, a, seizure conference co-presenting on this kind of like work that we've been doing. And ketogenic diet was like, boom, front and center. I think they were even putting on the conference. And I was like, what? Like, how could, like, how could getting people into ketosis help people with seizure disorder? Like, it was like, what? And then I had a close friend who had a kid, really bad epilepsy. And

and I think it was sometime after that, I was like, man, you should just try this ketogenic diet. He had tried multiple meds and they did like a ketogenic diet and the kids stopped having seizures. Wow. So it's like a known treatment for treatment resistant epilepsy. And I think it's so hard to get someone on the ketogenic diet. It's so hard that it's like they kind of push, you know, if you're a neurologist, it's like, here, take a pill. This is easy. Take this pill.

come back. If you're having seizures, take a little bit more. It's not working. Take a different pill. That's not working. And then it's like you get to the end and you're like, okay, what do I do now? Okay, there's this thing called the ketogenic diet, which is like super hard to get a kid to do, right? Be like life changing. Parents have to put in a ton of effort and yet it can work. So that's how I got introduced to it. And I'm curious, how did you get introduced to it? And then how did you start to see it? impact and like how big like is this like 25% of the work is 50% exercise or like where do you how do you fit this into the whole like all the hammers that you used to change someone's metabolic function it's um that is an important question so the the way that i got into this is i actually

you know i actually noticed it in myself first it so when i was in my 20s and during my residency training, I was already diagnosed with metabolic syndrome. And so blood pressure was up, cholesterol, lipids were, you know, triglycerides were through the roof, and already pre-diabetic. And I had been on a very low-fat diet and I exercised regularly. I was not technically overweight, even, let alone obese. And yet I had metabolic syndrome. And kept doing everything that the doctor was telling me low-fat diet exercise, and it did not work. And I finally decided, he finally decided, you know, was like, you got to take medicine. I said, I'm going to give this low-carb diet thing that I've heard about a chance. And I went on a low-carb diet. Not only, in three months,

not only did I reverse my metabolic syndrome, but I noticed remarkable and dramatic changes in my mood, energy-level sleep, and other metrics. And so I began recommending this treatment to other friends, family, saw equal results in many of them. And so within a couple of years, started using it in patients with treatment-resistant depression. And lo and behold, it worked for a lot of people

with treatment-resistant depression. And these are people, yeah, I have a pretty hard population of patients. I see patients after they have been hospitalized numerous times, usually after they've tried dozens or more of medications.

They've often had ECT. They've often had death. decades of psychotherapy, and then they come to me. And so it's pretty powerful that a diet change could heal these people when all of our standard treatments failed to. So to be clear, this is post-residency? This is post-residency now. And how many hours a week were you splitting between research and clinical practice at that time? So depending on what year we're looking at, for a long time I was about half-time research, neuroscience research, and about half-time clinical, and then I transitioned to administrative

educational work. And slowly but surely, by surely, over the last five, ten years, I have taken on more of an administrative role. I'm the director of continuing ed at McLean Hospital. So, but always maintaining a private practice through all of this. And, you know, everything really changed for me. You know, a diet helping depression was kind of interesting and it was nice. And I was glad to offer it because these patients had exhausted every other option. And almost all of them were disabled by their illness. So I don't mean to minimize the effectiveness of it for chronic debilitating depression.

But for me, the thing that was life changing or career changing was when I used the diet and a patient with schizoaffective disorder to help him lose weight. And at that point, I had no expectation that this would do anything for his mental symptoms because schizophrenia or schizoaffective disorder is totally different than depression. And, you know, within two weeks, not only did he begin losing weight, but I began to notice this powerful antidepressant effect in him, and it was quite remarkable and striking, most astonishingly, within six to eight weeks, he spontaneously reports to me

that his long-standing auditory hallucinations are going away and that his long-standing paranoid delusions are also going away. He begins to realize that they weren't, they're not true and they never really had been. That man went on to lose 160 pounds and keep it off to this day. So in terms of people who say,

this diet's too hard, it's not sustainable, Well, guess what? I can get people with schizophrenia to do this diet and sustain it and lose 160 pounds and keep it off. So I take anyone on who says this diet's too difficult to do. And he was able to do things that he had not been able to do since the time of his diagnosis. He was able to go out in public and not be terrified. He was able to complete a certificate program and actually perform improv in front of a live audience. And that case sent me on a journey. I have now used this treatment in dozens of patients.

I've collaborated with researchers from around the world. There are dozens and dozens of patients with chronic mental disorders, schizophrenia bipolar, who are in full and complete remission off psychiatric medications by using this dietary strategy. Okay. So, you know, we have a lot of mental health professionals who listen to this. And I bet one thing they're going to ask is like, when is the randomized control trial coming out to test this? You know, with that population, with bipolar patients, with schizophrenia patients, like, is there a study in the pathway? Is there funding for that type of study? You know, I know having run some, you know, been a PI in my own research, it's like, I know how difficult it can be to do.

this type of work, but I'm curious from your perspective, like, what's on the horizon there? So the great news is that we have a major philanthropist. The Bazuki Brain Research Fund has put over, I think over $60 million or so toward this research. We have a group of international neuroscientists, psychiatrists, and others who are working on this. We have at least five controlled trials underway now of the ketogenic diet for serious mental disorders. But we are not alone. We are joined by numerous people. National Institute of Alcohol Abuse and Alcoholism recently did a study of the ketogenic diet for alcohol use disorder. And guess what? It was positive. It worked. It decreased brain inflammation, improved brain metabolism. And that was a lot. And that was,

a randomized controlled trial. What was the effect size on that or what was the, like, how big of a impact was it? It was pretty remarkable. So the patients, patients were admitted to a detox unit at NIA, they were all given a regular detox protocol. Half of the patients got standard American diet. The other half of patients got ketogenic diet. Patients on the ketogenic diet had fewer withdrawal symptoms and nonetheless required lower doses or fewer benzodiazepines as part of their detox protocol. They reported lower cravings for alcohol. More importantly, they did brain scans and they showed that the ketogenic diet was

improving brain metabolism in critical areas known to play a role in alcohol use disorder and it also decreased brain inflammation. Okay. So what would, what do you think like in terms of like the randomized control trials that are coming out? Like is there one like how big are they like what are they using as the control? And then how are you actually measuring that someone's in ketosis? So the, the randomized controlled trials are varying in size and length and metrics that they're studying, which is obviously a good thing because we want to use different methods. We want to use different methods. We want to. We want to. We want to. to, we want to see which research groups can actually get compliance and finish these studies. You know, if you've been a PI, you already know, a lot of research studies that get started never get finished. And for a variety of reasons. The PI just can't recruit subjects. They thought they would be able to recruit them. And this goes for medication studies. It goes for exercise studies. It goes for all sorts of interventions. So it's great that we've got all those.

Measuring ketosis is, that's one of the great things about doing research on this intervention is, you know, this diet above every other dietary intervention. Like if you do the Mediterranean diet with someone, you have no idea whether they're really on the Mediterranean diet when they come in to see you. There's no way to objectively measure. whether they were compliant 100% of the time with the Mediterranean diet. This diet is the one and only one exception, because you can actually measure ketones through blood, breath, and urine. So there are urine sticks that you can use to measure the presence of ketones.

There are blood monitors that's just like a finger stick glucose, glucometer. We can measure ketone levels that way. And there are actually breath meters. You just have somebody breathe into this meter, and it will tell you the level of ketones that they have in their system. Okay, so having tried ketosis myself, you know, checking your blood, pinprick, and your finger, looking at your ketone levels, it takes a couple days to weeks, right, to get the ketone level.

to get the ketone level to go up, which is part of the adjustment phase that people go through. So I'm surprised when people were detoxing, because detox can be like, what, five days, seven days? I'm surprised in that study that they actually found that result because doesn't it take longer to get into ketosis? It does take longer to get into ketosis, and that study was a three-week study. Okay. So, yeah, they admitted the patients to the unit for three weeks. Okay, that makes sense. With your own patients and the outpatient, like, how are you monitoring if they get into ketosis?

So with my patients, I routinely, so before the pandemic, when everything was in person still, I would, I actually have a glucose monitor and a ketone monitor right in my office. I also have a scale. So I would weigh them, and I would measure both glucose and ketone levels. And all of those metrics are interrelated, but they are separate ways to kind of measure outcomes. And if it's an obese or overweight patient who is on a ketogenic diet, I typically expect them to be losing weight. So that's one of the metrics that I'm looking at. The interesting thing is that, you know, for weight loss, you know, when people do a weight loss version of this diet, any level of ketosis is probably fine. because it just signifies that your body is burning fat as a fuel source.

And that means you're going through at least some fat stores, probably. When I'm using this diet as a brain intervention, and certainly when neurologists are using this to treat epilepsy, it's a different story. It's a different version of the diet. It really is a medical intervention that should be done by a competent, licensed, medical professional, whether that's a dietitian or a physician who really knows what they're doing. But this is not, tell your patients to go out and try that keto diet thing on the internet and everything will be fine. That, you don't tell a seizing patient to just go out and look on the

internet and, you know, figure it out and just do something. We don't do that. We shouldn't be doing that for schizophrenia and bipolar disorder or severe chronic debilitating depression either. So the first thing is that professionals need to understand what they're doing and they need to know that there is a medical version of this diet. It's very rigorous. And it comes with some risks that need to be monitored and managed safely. So that means checking blood levels of different biomarkers that you really want to stay on top of. What are the biomarkers that you're like most worried about? So there's a whole range of them, but obviously just for medical legal liability, we're going to measure cholesterol and triglycerides and all that, because everybody's going to get worked up about that. We're going to measure insulin and glucose levels, but it can get as granular as I'm going to measure something called carnitine, and I'm going to measure something called selenium. And the reason is carnation is a molecule that has been highly associated with chronic depression and mitochondrial impairment.

But carnation is required in order to get fat into mitochondria. And if the levels are low, it means that the people's mitochondria may not be able to use fat or ketones effectively. So I'd want to measure carnitine. Selenium deficiency has been associated with chronicle. ketogenic diets, and in some rare cases, has been fatal. It can result in cardiovascular complications, which can result in death. So that is very rare. We use medications all the time that also come with rare side, you know, potentially fatal side effects. So what I'm saying is that this is a medical

intervention that should be managed by a medical professional. Who knows what they're doing? Okay, so go back to the carnitine real quick, because I mean, this is your chance to educate medical professionals who are going to get their first sort of glimpse at, like, how to do this, right? And, you know, we're putting this out there as medical information. This does not replace the doctor-patient relationship. But the carnitine specifically, do you measure it before you start the ketogenic diet, or do you measure this selenium before the ketogenic diet or after, like, when do you measure that? I'm going to measure all of these things beforehand. And then I'm going to do them at routine intervals along the way. So the best resource that I would give, because there's no way, even if we spend the entire rest of this podcast talking about it, there's no way I'm going to be able to provide all of the information on the medical ketogenic diet. So two recommendations. One, find a licensed ketogenic dietitian who knows what she or he is doing. and partner with that person.

That person knows all of this stuff already, and that person will tell you as the physician, here are the labs that I need you to order before we go the next step. Or here are the vitamin supplements that I'm recommending to the patient because I'm worried that patient might be deficient in this vitamin or this whatever.

So partnering with a licensed ketogenic dietitian is the easiest way for you as a medical professional to implement this treatment. The other way to do it, if you really want to learn it and get granular, is there is a book called Ketogenic Therapies. Lead author is Eric Kosoff, K-O-S-S-O-F. He is a neurologist at Johns Hopkins. He and others wrote this book.

It's actually written for healthcare professionals, but also patients and families who are doing this medical version of the diet. And this book will actually has a list of all the labs that you might consider checking how frequently they should be monitored. But it also comes with meal plans and recipes and a lot of practical hands-on advice. So it's an invaluable book if you actually seriously want to think about using this dietary intervention. That's good.

We had a psychiatrist in our program at Loma Linda Darcy Temple. and she was really into this ketogenic diet and she would talk to the residents and she got me into it for a while and I did it and I'm a lifter so I was doing some power lifting and I would get these horrible spasms after I would lift

and she said drink some bone broth to get my electrolytes way down right? What is it about the ketogenic diet like going into it that changes your electrolytes and changes the electrolytes So the waste salt, how much salt you have, how much fluid you have. Any thoughts on that briefly?

Yeah. So I think the big point is exactly that. The ketogenic diet causes major shifts in fluids and electrolytes, and those need to be understood and managed safely. So one thing is that you're getting rid of, you know, especially in the keto adaptation phase, the first week or so, you're actually getting rid of a lot of glyphys. And that takes with it water. So glycogen is one of the molecules that's helping to hydrate your muscles.

And so when you lose glycogen from muscles, your muscles will actually look smaller. You're not necessarily losing muscle tissue, but they are kind of dehydrated, relatively speaking, muscles. But when you're losing water, you can also lose electrolytes with it. And so usually I recommend that people use a light salt, which is a combination of sodium and potassium chloride. And I really want the combination. I want the 50-50 split. Because if you just have people take potassium chloride, they can actually overdose on that.

I think for any of you in medical school, if you did dog labs or anything like that way back in the day when I did, that's actually how you euthanize a dog is give them massive boluses of potassium. So potassium can be fatal on its own in large doses. But if you combine it with sodium, they balance out and you'll just urinate out whatever you don't need. I also have people take magnesium, a magnesium supplement initially. But there are some other things. Some people will add calcium to the mix. So again, all of that would be covered in the book or a ketogenic dietitian will be able to kind of guide you how to do this all safe.

this podcast is not going to be enough that fully educate you on this medical therapy. Right. Since I have you here and I'm just curious, like if you were working out in this diet, and let's say you were three weeks in, so you were already, you know, your blood was showing some ketones two to three,

you know, as a level. But you were getting like lightheaded and you feel kind of hypoglycemic. Your glucose is around maybe 60 after during towards the end of the workout like any thoughts on what you would do for that type of situation so I would I guess I would want to know just a little bit more information I would want to know why is this person on the ketogenic diet to begin with and what are their goals just trying it out you know medical experimentation let's say that just just for kicks um because again I mean

this is a medical treatment. And so if I'm working with somebody who's got treatment-resistant epilepsy and this diet is stopping their seizures, I recognize this is essential for their brain health. This may be the one and only one treatment that stops their seizures and allows them to not be disabled by epilepsy, in which case I am going to be bending over backwards to figure out how can we accommodate all of the other goals that this person has, whether it's, it's lifting, whether it's competing in athletic events, whether it's losing weight, whether it's gaining weight. You can gain weight on this diet.

So different people are going to need different things. If I'm working with somebody who's grossly underweight, obviously we've got to get them to gain weight, even if they're in ketosis. But, you know, if somebody's obese, we want to be thinking about losing weight. So for power lifting in particular, if it's just somebody. who is fairly athletic already, and their goal is simply to lose a few fat pounds. They don't even care what the scale says

because they kind of ideally might like to be even bigger and have more muscle, and that means weigh even more. If that's their goal and they're just looking to lean down and just get cut more, then I would actually advise that person to eat more meat, eat a lot more protein, eat more protein, basically. I shouldn't necessarily say meat because there are other ways to get your protein, but eat more protein.

Protein will decrease the level of ketosis, and it will increase your blood sugar a little bit for in most people, especially if you use like a protein shake, that will stimulate insulin secretion, will stimulate gluconeogenesis. even if it's a zero-carb protein shake, it will stimulate insulin and gluconeogenesis, which will probably be helpful to the athlete. If it's an athlete really doing long-distance running or something, then I'm actually going to advise that person to actually introduce some degree of carbohydrates during that run.

So there's a man named Zach Bitter, who is the world record holder for the fastest 100-mile run. He is typically on a ketogenic diet, but when he does 100-mile runs, he actually consumes some carbohydrates. That's really essential to his game plan. And so you got a, you know, it's a little more nuanced. They get, they get, it's like, it's like your body then is really used to burning fat

to run. And then all of a sudden it has sugar. so it all of a sudden it has like a second energy source, right? That's kind of the... Well, and you, yeah, that, but you also want to keep up with the, you know, you want to keep up with the basal glucose requirement. So you need a glucose of about 60 in order to remain not lightheaded, healthy, you know, all, everything functioning well.

And so when you're running that much, and doing kind of that kind of exertion, you're more likely to get hypoglycemic. And so you do want to, you do want to consider supplementing with carbohydrates in that situation. Okay. I do want to get a little bit into the science, because it seems like the rats, the animal studies are a little bit further along in terms of the models for like schizophrenia or bipolar and how it may help.

What have those studies shown and how is that problem? almost seen for this field in your mind. In terms of the ketogenic diet? Yeah, in terms of the ketogenic diet specifically. So the ketogenic diet, what's probably shocking to many of your listeners is that we actually have decades of neuroscience research, both in animals and humans, documenting what impact this diet is having on the brain. And that's really surprising to most people.

We actually know more about what the ketogenic diet does to the brain. than we do about any other dietary intervention. And this includes Mediterranean diet or vegetarian diet or anything else. And the reason is because the ketogenic diet is a 100-year-old evidence-based treatment for seizures. And so neurologists, biotech companies, neuroscientists, and others have been studying this diet for decades, trying to figure out, how the hell does this work? Like, why would a diet stop seizures when our great pills? don't. And so they've been studying this diet trying to understand as mechanisms of action.

So we know that the ketogenic diet changes neurotransmitter systems, including glutamate, GABA, adenosine. It better regulates calcium channel or calcium regulation, which many of you probably know is essential to brain function and brain health. It decreases inflammation, including neuroinflammation, it changes the gut microbiome. It improves insulin signaling. And although insulin plays a role in diabetes, insulin we now know plays a powerful role in brain function itself. And it is separate from its role in diabetes.

And this is kind of a new cutting-edge field, and there's a lot we don't know about this field. But insulin plays a powerful role in brain function and ketogenic diet can normalize insulin signaling. And then the thing that I am most excited about is that the ketogenic diet actually does two things. It stimulates two processes, mitophagy and mitochondrial biogenesis. And what that means is that after people have been on the ketogenic diet for a while,

their cells have more mitochondria, and those mitochondria are healthier. and that allows those cells to function normally and to repair themselves. Cells mitochondria are instrumental in kind of directing resources, both energy and also the kind of building blocks used to maintain and repair cells. And so if mitochondria are dysfunctional cells fall into a state of disrepair, and they can begin to malfunction. Yeah, see, I think my listeners would want to go neurotransmitter by neurotransmitter. But what you're, what it kind of in summary, it's a whole host of things going on. Like there's like, it's not just one little neurotransmitter that's being modulated. And you know, as you look through that list, glutamate, gaba, dynocene, calcium channel

regulation, like you can think of the different medications like Depico that influence those or the different things that help with seizures. I guess one of my thoughts, like, it makes sense to me why I would help for something like bipolar, because the overlap between like Deppicoad and seizure medications and bipolar. Schizophrenia seems a little bit like more confusing why I would help with someone with schizophrenia. Can you, I know we're talking like we haven't done any randomized controlled trials,

so I don't like to lead my audience further than the evidence shows, but what are the potential mechanisms on why it might be helpful for someone with schizophrenia? So the most important thing to just point out is that we use epilepsy treatments in psychiatry for every single diagnostic category in DSM. Epilepsy treatments include depocotechytagetal, lomotin, nirontin, or gabapentin, Valium, Clonopin, Xanax. Those are all seizure treatments. we use them in hundreds of millions of people throughout the world, and we use those medications

in people with schizophrenia. Most patients with schizophrenia have been on at least one or more of those medications. So now that's off-label, of course. So we don't have randomized controlled trials showing that they're efficacious, but we in psychiatry use epilepsy treatments off-label all the time. And so what I've been advocating for is using an evidence-based dietary epilepsy treatment off-label in the exact same way that we would use neurontin, which is actually not indicated for any mental disorder whatsoever, or Valium or Clonopin, or Limitil or Topamax, or any of the other ones that we're throwing at our patients right and left. The evidence that bipolar disorder and schizophrenia are unique diseases doesn't exist actually. The National Institutes of Health

for the last 20 years has been hot on the trail of trying to understand what makes schizophrenia different from bipolar disorder. And the largest multi-site, multi-million dollar trial that we have, the B-Snip trial, B-S-NIP, if you don't know it, over two thousand. patients with schizophrenia, schizoaffective disorder, and bipolar disorder, their first-degree relatives who were not impacted and normal healthy controls. They did a variety of metrics on these patients and controls. They looked at blood biomarkers, brain imaging, EEGs, neuroinflammatory biomarkers. They did, you know, all sorts of cognitive testing and questionnaires and everything. the end of that study, the conclusion was that the researchers could find no difference, none,

no difference between patients with bipolar disorder, schizoaffective disorder, and schizophrenia. I mean, I hear that and I say to myself, well, we don't have biomarkers to make diagnosis. You know, we don't have neuroimaging to make diagnosis at this point, which is probably why patients won't benefit from like a PET scan, you know, to like help. their psychiatric management. Like, we just don't have that. But there was no biomarker, even if you look at the genetic studies,

Disk one. Huge overlap. Dysk one. Disordered in schizophrenia, one. What does that confer risk for both bipolar disorder, schizophrenia,

major depression? So one root cause, one genetic problem, or one genetic allele confers risk for multiple psychiatric disorders. Right. What the conclusion is that our psychiatric diagnoses, in fact, are not distinct disorders unto themselves. And although many people still cling to DSM-5 as though it is the Bible and it must be

truth, the National Institute of Health abandoned DSM-5 over a decade ago because they looked at all of the science. and they came to the conclusion that DSM-5 diagnoses are not valid constructs. They're just not. And I think we as a field are going to have to wake up to that if we're ever going to make progress. Right. Well, and they also said, which you quoted in the book, that all the money that they poured into it didn't move the dial very much in terms of treatment in terms of reducing suffering.

Yes. So, well, but here's my thought, okay, coming back to schizophrenia. So we know that depicoat, for example, in studies, shows that it decreases days of hospitalization in acute episode of schizophrenia by like one, very, very small decrease. Maybe, you know, maybe that's important. I've seen some attendants throw on depocote to every schizophrenic patient that comes into the psychiatric hospital. for me it's like okay but then you're also you know dooming them to all the side effects of depa code so it's like is so for my in my mind when I'm treating someone to schizophrenia I don't want to use depocode if I don't need to I don't want to use like more medications that I need to you know

you use it you use an antipsychotic if it's not working you get a blood level you increase the dose to the highest therapeutic range, if not, if it doesn't work, maybe use a second one or maybe you go on to clozapine. And I've had, I have a number of patients that are on closopine and doing awesome, like much, much more effective for treatment-resistant schizophrenia than anything else we have. So, you know, I guess, I guess my thought is like, okay, if Depicoot reduces like hospitalization like one day, and we know that ketogenic diet is like a mood stabilizing, has a mood-stabilizing effect. And we use these things off-label because often we don't really know what we're treating.

But, you know, I can tell the difference between someone who has like auditory hallucinations, delusions of grandeur, responding to internal stimuli, and someone who lives a pretty normal life and then gets manic for a discrete period of time, you know, to the point of psychosis maybe. Like those seem like very different diseases in my mind, at least. So maybe I'm not completely coming along to where you're at. But if you look at the root cause, look at any root cause, any specific gene, childhood trauma, alcohol substance abuse, sleep deprivation, stress, any one, is there any one risk factor that you can identify that separates that person with bipolar disorder from somebody else? who exposed to the exact same risk factor might develop the symptoms of schizophrenia. Well, I mean, the answer is like risk factors, you know, in the biopsychosocial model,

you know, you have someone who has some biological, epigenetic, genetic sort of wiring, and then you throw on a bunch of stress. And if you keep throwing on stress, you're likely to have some medical, issue or psychiatric issue, people would present with different things depending on their unique biology, their unique genetics. But I don't necessarily think that you can diagnose someone with schizophrenia or bipolar or any mental illness with biomarkers or neuroimaging. And so that's where I'm pushing back against this study that you showed that, you know, like, oh, we couldn't find anything to diagnose someone differently between bipolar and schizophrenia. And therefore, they don't

exist. It's like, well, maybe we haven't found... It's not that they don't exist, is that they're not different from each other. They're not... Therefore, they're not different from each other. I am a psychiatrist and make no mistake. Mental illness is real. It ruins people's lives. It causes tremendous suffering. I know that. I know that 100%. I am not a psychiatry denier and I am not a denier of science. But what we know, like we've had the human genome mapped for 20 years.

The expectation was that the human genome would give us clues about what makes bipolar disorder different than schizophrenia. And we have had artificial intelligence on the human genome. And the conclusion is that there is no difference. Well, there is no difference in the genes. That predispose one person to develop bipolar and an... another person developed schizophrenia. The exact same genetic pattern can result in depression in one person or schizophrenia and another or bipolar in another. Right. But I mean, epigenetics plays

an obvious role. I mean, have they done all the studies looking at the different epigenetic manifestations between these two things? Or like, I mean, just because we haven't found it doesn't mean it doesn't exist, right? Or are you just thinking that they're one of the same thing? Because they look very different to me. The way, you know, the analogy that I used in the book is that we have many diseases that we call one thing. So is diabetes a real disease? Type 2 diabetes.

Is that real? It's very real for a lot of my patients, you know? It's like, it's a lot of suffering. And what exactly, what symptoms does type 2 diabetes cause exactly? Right. So it's kind of like the, what is the, what is the HIV? HIV versus what is the AIDS, right? Well, what symptoms does type 2 diabetes cause in most people?

It depends on how it's manifesting. A lot of people just feel awful. And others get amputations because their limbs are infected. Nerve damage and others are having brain problems. Others are having liver problems. Others are having GI problems. Others are having kidney problems. Right.

So what's going to hit first? We don't know what's going to hit first, but we know that if they have uncontrolled diabetes, 20 years later, they're going to have issues. So, but I guess my point is that type 2 diabetes is a metabolic disorder, and it can result in a wide variety of signs and symptoms affecting every organ in the body. And what I'm arguing is that mental disorders are metabolic disorders of the brain. And yes, they can affect different regions of the brain, which result in different symptoms and different people, but they are all metabolic disorders. And this matters, because if you have

somebody with type two diabetes, there are some basic common sense lifestyle interventions that you can implement with that patient to help them reverse all of the consequences of diabetes. You can help them prevent the brain problems, the liver problems, the kidney problems, the GI problems, the cancer, all of it, if you get the diabetes under appropriate control. And I'm arguing that a similar, if you understand that mental disorders or metabolic disorders, we can actually begin using similar approaches with psychiatric patients. Okay. Well, I hope that you feel like I'm not being too adversarial because I actually,

I welcome the challenge. I actually do really prescribe diet and exercise and therapy and, you know, treat the obstructive sleep apnea. Like, these are profound things and, you know, minimize polypharmacy. Like, this is how I practice psychiatry as a full-time psychiatrist and what I advocate. I think where I'm trying to sort of see where. where this can potentially integrate into this sort of holistic paradigm, like which patients would you say you might consider something like ketosis?

So in your current practice, you're full-time doing continued medical education at Harvard, and then you have like a private practice on the side. What, like, how do you decide which of the patients you're going to try what interventions on? So the most important thing is I'm going to do, you know, a basic common sense assessment that, you know, many in the mental health field already know. I'm going to ask about sleep, stress, substance use. I'm going to look at the different medications that they're using. But I'm actually going to take a very different perspective on the medications people are using. I'm looking for which medications enhance metabolism and mitochondrial function and which medications. and which medications might be impairing metabolism and mitochondrial function.

And that's really important to information that might change. So that can result in a radical change from the current field and the current recommendations in terms of how we think about these diagnostic categories and treatments. But I'm going to look at all those things and then I'm going to prioritize what's most important. So if somebody comes to me and they have out of control alcohol use disorder and opioid use disorder, I'm not prescribing the ketogenic diet right away. I'm going to be sending this person for detox. And that's probably the most powerful intervention to improve their mental and metabolic health.

Right. Okay. So you said something there. Like imagine they come in on like Syracquil 100. night and zyprexa 10 at night, right? Because they have schizoaffective disorder and they come in with Depakot 1,000 twice a day. So as someone who's thinking about their metabolic health, how are you going to potentially switch the medications or treat them differently to optimize their metabolic health? So the first question I'm going to have is how is the patient doing? If the patient is symptom-free and

functioning fully in life. That means they are employed. They have good relationships. They have purpose in their life. And they are a productive member of society. I'm not going to touch a damn thing. I'm going to say, wow, good for you. You're doing great. Even if I believe they're metabolism impaired, and they've gained 20 pounds from that treatment. If their mental health is perfect, I'm not going to touch that regimen because I'm going to say, well, you know, 20 pounds, oh, well, big deal, no big deal. However, as you probably know, the patients, or at least the patients that I see who come in on those regimens are coming in telling me, oh, I'm taking these pills, and I'm still tormented by hallucinations every day.

I'm still, I can't function in life. I am using substances in, you know, ways that are probably not helpful. And I'm smoking cigarettes and I'm doing this and I binge eat and my life is miserable. And don't you have a pill to help me? If that person has already tried 30 other pills, as is common in the patients that I see, I am going to say, you know what? I don't think there's a high probability that another pill is going to do the trick because you've already been down that road.

You are treatment resistant. You've already tried more than enough standard therapies. I would never use the treatment that I'm going to describe on a first episode patient because I am a licensed, evidence-based physician, and I am going to practice. but once somebody develops treatment-resistant disorders, I absolutely start resorting to off-label use. So I use neurontin or gabapentin in lots of patients. That's an off-label use of a neurological epilepsy treatment, and I use it commonly in patients, but I don't use it first line.

So at that point, then I would talk with this patient about whether that patient might be interested in a metabolic treatment plan. I would look at whether this person is exercising at all. I still want to know if this person is sleeping. I want to know stress levels. I want to know about abuse. I want to know about substance use. I want to know all these other things.

Assuming there are no problems in any of those areas, and any mental health clinician is probably laughing because you know that there are going to be problems in all those areas. But assuming there are no problems in any of those areas, then I might consider the ketogenic diet as a treatment. And the first step would not be to change any of those meds. The first step would be to implement the ketogenic diet, try to get them into ketosis.

I usually tell people we're going to try it for at least three months before we give up on it. It doesn't always take three months to work, but for some people, it does take up to three months to work, just like it might take clozapine three months to work. So we're going to give it an adequate amount of time. if I see a signal that it is clearly helping, and oftentimes I do see signals that it's having a profound beneficial effect, then at that point I'm probably am going to work with the patient to devise a plan to very, very slowly and safely see if we can taper some of the medication. And the reason I'm going to want to taper some of the medication is because those medications that you listed are actually all counteracting the effects of the ketogenic diet.

They are increasing insulin levels, increasing glucose levels. They are causing metabolic impairment and mitochondrial dysfunction. And so I'm going to want to try to minimize those pills so that we can give the ketogenic diet the maximum chance of a benefit. okay that's good that's good that's good some good practical some good practical stuff so three months and then okay so like let's say you're one month like at what point do you start to try to pull off some of the medications gently and carefully how how closely are you monitoring them like are you seeing them once a week or once a month like let's say they were on an antipsychotic, would you potentially try to get them off of that? Like how, like over what amount of

time would you try to get them off that? There are, there are really important questions and there's no one size fits all recipe. So a lot of it's going to depend on who's the patient in front of me, how dangerous are their symptoms. So is this a person who has a history of assault? Is this a person who if they get two hours few sleep one night, they're manic and psychotic and in the hospital or the police are getting called? Or is this somebody who is quite stable, safe, has not been hospitalized in 20 years, but is chronically ill with schizophrenia or bipolar. So all of that is going to play in. but the real answer is that I, at some point, once stabilized, usually that's at least three months into the diet,

once stabilized, because I need to make sure the patient is capable of maintaining this treatment. Right. If they're going to stop the diet, that's like they're going to stop the clozapine, too. It's the equivalent of me prescribing a pill that they are about to stop. and that's not an effective treatment. It's not like somebody goes into ketosis and then poof, their brain is fixed and everything's, their illness is in remission. That's not the way this works.

This is, I would want people, clinicians, to think about this as a medication. This is comparable to taking a medicine. It means there are no cheat days. They can't cheat on the weekend. Yes, with every other diet, you can encourage people to cheat. Not with this. Not when you're using this for a serious brain disorder. like seizures or psychosis.

No cheat days allowed. No cheat days. No cheat days. No cheat weekends. No cheat weekends. Because when people cheat, I can just tell you firsthand, they come in floridly psychotic. And it's not pretty. It's as though they stopped their antipsychotic treatment.

And in fact, that's what I think they've done. So, but at the three months mark, if all is going well, I might slowly start to taper some of their meds one at a time, very, very slowly and gingerly, some of how much, how fast is going to depend on how long have they been on this medicine. If it's somebody who's been on the medicine for four months, I might be able to get that person off that medication pretty quickly because four months isn't that long in the grand scheme of a psychiatric patient. If this is somebody who's been on that same medication at high dose for 20 years, I'm going to need to do a gradual slow taper. It might take me three years

to get that patient off the medication. If this all sounds far fetched, I have published, so I know of dozens of patients who are in full remission from chronic mental disorders, including schizophrenia and bipolar, off medication. I've published two of these reports in schizophrenia research, peer-reviewed journal. So this is not Chris Palmer just sharing anecdotes. This is not Chris Palmer making stuff up. This is actually legitimate kind of medical research. You've published some good case reports, and I believe you've had a couple of patients with huge amounts of success. Have ever seen this study that looked at a psychiatrist effect and the impact on treatment of depression, specifically that some psychiatrists were more effective at treating

depression than other psychiatrists. There's just one paper in particular, if you haven't seen it. For depression, I'm not surprised. And I think that may have to do with therapeutic alliance. And we've long known that depression and anxiety disorders, even personality disorders, lot of eating disorders, lots of those disorders have a strong, you know, therapeutic alliance plays a powerful role in those disorders. I think most psychiatrists understand that therapeutic alliance does not play as powerful a role in schizophrenia and bipolar disorder. Patients are not able to control those symptoms as well,

regardless of whether the psychiatrist is nice to them or not. And when we look at the long-term outcomes of patients with those diagnostic labels, the outcomes are pretty poor. I mean, one longitudinal study, 6,000 patients with schizophrenia, only 4% got a recovery. Yeah, I think, I mean, if you look at the Katie study, the compliance was pretty horrible across the board as well. you know 30% compliance or something with like antipsychotic regimens so yeah it's it's it's a tough population to treat part of part of the aspect of schizophrenia is a low insight right that's like baked into the cluster of things that we see but even when people are compliant like if I look at patients in long-term residential treatment programs a nurse is giving them their pills every single day and watching them swallow the pills, the overwhelming majority of those

patients are not going into remission from their schizophrenia. Yeah, there's a lot of treatment resistant schizophrenia. It's a topic near and dear to my heart. So instead of thinking about chlozapine, if someone was on an antipsychotic, and instead of thinking about checking their blood level, increasing the drug to get to that max level, blood level of the antipsychotic, you would start to think, let's try this ketogenic diet, let's see how it goes, three months in, let's see if their symptoms have reduced. No, not instead of, because again, you're talking about an evidence-based treatment. So do I think patients deserve a trial of evidence-based psychiatry? I do. And again, that's what the most licensing laws require. So I'm talking about the

patients who have had their six trials of antipsychotics plus their clozapine trial, they've been on four antipsychotics at the same time, and they are still not better. We have millions of those patients in the world to choose from, and I'm saying those patients deserve a chance at an off-label treatment for a serious brain disorder. Yep. That's fair. No, I like it. No, and actually, I'll have you back on at some point, and we'll, I'm going to try this on two of my patients. So I've selected these treatment resistant people. Let me put you in touch with a licensed ketogenic dietician because I want to make sure they get it done.

I want to make sure they get it done right. I don't want you winging it. Not that I'm disparaging you, but. No, no, no. I actually really appreciate that advice. And I think having tried to wing this myself with little support, you know, I could see how that would be valuable. And plus, I think I think you're right. Like if someone is going to really try this, they need to try it completely.

Because in my own experience, you know, I could eat an avocado or too much avocado. Maybe I should say too much avocado and push myself out of ketosis. You know, so there's like, there's like a. there's only so many carbs that you can eat before you get out of ketosis. And so one of my critiques of diet studies in general is when you read diet studies, you have to look at the level of compliance to the diet because often it's like 70%. Okay, so I'm 70% compliant on a vegan diet. So what are you not?

You're not. Exactly. No, you're not. And so when I read these ketosis studies, I specifically look for how are they measuring if they're actually in ketosis? Are they measuring blood levels? because that seems to me pretty straightforward, were they actually in ketosis the time to get?

So if you have patients that you're thinking about doing this, are your patients actually in ketosis? You know, it's like they're not, it's not like they can try it just a little bit, right? It's like you have to really 100% dive into this, yeah. Absolutely 100% agree. I couldn't agree more. And again, the good news with the ketogenic diet

is we do have easy, accessible biomarkers, blood, breath, and urine that we can measure ketones in, so we can measure their compliance. But I think you're absolutely right. It's as though if you give clozapine to a patient and they only take it half the time, it might work, but there's a reasonable chance it may not work. and they might actually be kind of going through withdrawal every now and then when they're skipping it and making matters worse. So for better or worse, that's the way I think about the ketogenic diet. This is like a pill.

This is like a medication or a therapeutic treatment. And we need to at least shoot for 100% compliance. If they're intermittently noncompliant, it's not the end of the world. Just like if they forget their pill one or two days, it may not be the end of the world. but yeah. Okay, so coming back, and this would be kind of our last question, and then we'll do a little wrap up, if someone was on potentially like an antipsychotic and depicoat,

which I know messes with metabolic function, right, you made a comment that maybe the ketogenic diet would be working against, these medications would be working against the ketogenic diet really being functional. So would you ever consider, switching them to other medications like first-generation antipsychotics to get them out of the metabolic side effects of some of the second-generation antipsychotics, for example. Your face says no.

My face says no only because you sound like a seasoned clinician as I am, and switching antipsychotics is dangerous in and of itself. If somebody is stable on a medication for many years, Switching, stopping that medication and introducing a new medication that may or may not work, that may or may not involve new side effects is dangerous on its own. And so I certainly would not want people trying to do that at the same time they're trying to try the ketogenic diet and see if it works. Because then in my mind, I'm a pretty conservative clinician in terms of trials. Like I like to try something, assess, see if it works.

And in that scenario, you're discontinuing one medicine, starting a new medicine and starting the ketogenic diet. So you're actually making three major changes to their brain physiology all at the same time. And you're going to have no idea what's what. Okay. Let's say, okay, so I heard, though, you hint at you're assessing which medications are potentially hurting their metabolic function. Yeah. So at what point in your sort of work with patients, are you utilizing that information to make changes?

So I would, so I'm definitely going to use it if I'm implementing the ketogenic diet. So if you're, so for instance, you said you might try this on two patients. I would, I would encourage you to maybe think about trying it on two patients who have not had massive amounts of weight gain or who are not yet pre-diabetic or diabetic. because if they're already pre-diabetic and diabetic, and that's because of the medications they're on, or you think the medications contributed to that, we already know those medications are having profound impact

on their insulin and glucose signaling. And that the biggest problem isn't that the ketogenic diet can't work, but it's that those patients may really struggle to even get into ketogenic. ketosis. So they could come in, you're going to measure them for ketones, and it's going to be negative, and you're going to be like, well, you're not doing the diet, and they're going to be like, yeah, I am, and I am doing it. I'm doing everything you told me to, and they may very well be telling you the truth. They really might be doing everything you're telling them to do, but the medications are preventing them from getting into ketosis. It doesn't, it doesn't

or break. So one, you know, that index patient that I described, who lost 160 pounds, was on 30 milligrams of Zyprexa. I think he was on like 800 milligrams of Seraquel on top of it. And he was also on, I think, like 20 milligrams of Abilify. That doesn't make sense. And, well, that's, that's, I inherited, I inherited them that way. And he was on lots of other medicines. Poor guy. He was able to do it.

He was able to do. He was able to do it. I eventually got him off most of those other meds, but he was still on the xyprexa, and we very slowly over years reduced the dose. And so he, you know, for full disclosure, he is not off all his meds. we're still trying because when we get him off even a little bit and then he stays on the

ketogenic diet, his symptoms get even better. So this man is functioning at a much better level in life than he ever was prior to starting the diet. But I'm, I and he, more he, are really struggling to still get him off meds because getting off meds is challenging and difficult and comes with possible increase in symptoms just as the withdrawal. And so it's not that you can't try the ketogenic diet and someone on Zyprexo, but you can. But if they're not getting into ketosis, just kind of be mindful that the medication might actually be the problem or might at least be the problem in terms of their ability

to get into ketosis instead of like, wagging your finger at them and saying they're not doing it right. No, don't, don't wag any fingers. Moral of the story. Never wag fingers. Don't wag fingers. That doesn't help any. Our patients are suffering enough.

They don't need a psychiatrist wagging a finger at them. If you're wagging fingers at patients, get help yourself. That's like, okay, I may be burned out. I need to get some help. Hey, last minute, like any final thoughts, any like that are still floating in your mind? like I really want to get this information out. Any final thoughts to kind of wrap this up? I think that, you know, so we've spent a lot of time on the ketogenic diet,

and I'm really obviously passionate about it, and I think it can be a powerful treatment for some patients. I don't think it's the end-all be-all. My biggest message is that if people can understand the connections between mental health and metabolic health, and that specifically means mitochondrial health or mitochondrial function, And I actually think this is an opportunity to move our field forward in potentially profound ways. And again, it supports and reinforces a lot of our current treatments, but it just gives people a new lens to think about our current treatments under.

But at the same time, it also offers entirely new tools and treatments that mental health clinicians might consider using in their patients. Good. Yeah. Awesome. Well, hey, thank you so much Christopher Palmer for coming on. And if you would like to learn more about Christopher Palmer, in the show notes, I will put a link to his website. I think it's like what, Christopher Palmer.com or something like that. Chris Palmer MD.com. Chris PalmerMD.com. And you are also on Instagram. And this book, Brain Energy, will be coming out. I think we'll try to release this episode. on the day it comes out, so you could go check that on Amazon. And yeah, I'm looking forward to having you back on when the first randomized control trial comes out. I will have you back on. So email me when that's happening, and we'll get you in for that, and we'll leave it there for today.

Awesome. Thank you so much for having me.