Holistic Neuropsychiatric Care with Dr. Arnie Mech

Arnie: I always joke that I know what your diagnosis is after seeing somebody for a minute or so, and then they’ll say wow, what’s my diagnosis?

And I’ll just, say their name and say, yeah, John Brown, that’s your diagnosis. And they go Well, I said well, I thought I, you’re not bipolar disorder, you’re not alcohol dependence, these are things that are going on right now at this scene in the movie, but you know, you’re moving along, and that journey should be characterized by better understanding and returning a locus of control back to a person, rather than just ceding all this to other people around the professionals, and then I’m just a consumer.

Bruce: welcome to the Future of Psychiatry podcast, where we explore novel technology and new innovations in mental health. I’m your host, Dr. Bassi, an addiction physician and biomedical engineer. Today we’re going to be talking about those with chronic and complex illnesses in psychiatry.

Now I’m with Dr. Arnie Mech. He’s a psychiatrist in Texas. He provides neuropsychiatric care with a unique and holistic approach. He acknowledges the crucial interplay between mind and body, leading to a comprehensive and patient centered treatment plan. Dr. Mech’s practice thoroughly investigates the potential factors that influence symptoms, including vitamin and neurotransmitter cofactors, hormone levels, sleep patterns, ambulatory EEGs, and genetic testing.

This all comprehensive approach enables Dr. Mech to offer personalized treatments that support brain health and overall wellness. With a particular focus on addiction and attention deficit disorders, Dr. Mech is a specialist in dealing with complex mental health issues. His approach invites patients on a journey of wellness that spans their lifetime, grounded in understanding of their individuality.

Welcome Dr. Mech.

Arnie: Thank you. Great to be here.

Bruce: Tell us a little bit about Dr. Arnie Mech and how he got here today with this approach to treating patients.

Arnie: Thank you. Yes. I was very interested in medicine as a child. And I was interested in neurosurgery. You know, There was a program on television that focused all the medical drama, and it was all this excitement about being able to help people. When I got to medical school, I did a rotation in neurosurgery and it wasn’t very inspiring.

I did a rotation then in neurology, kind of shift over to something else, and it’s yes, the brain, excited about the brain but they didn’t seem to have a lot of great solutions. Like there are progressive, chronic illnesses that will, sprinkle a little steroids and maybe we’ll see what happens.

Then I got a chance to do psychiatry as a student and I thought this is great. And this is an opportunity to really treat the whole person. And a lot of times that person that you have in front of you is of course a member of a family. And they have family members that have similar issues.

And so it got to be really like a family. Kind of family approach and then a holistic psychosocial, biopsychosocial approach. And the idea of focusing on wellness, I remember riding my bicycle back and forth to the health food store when I was a kid, to get the latest healthy foods.

And looking at that in medical school, there was not a lot of focus on wellness and nutrition. So I’ve always had that as a strong interest. And it turns out that’s really very helpful. Other than just selecting, medication. 

Arnie: Medication is very important. Somebody comes with very difficult symptoms.

Getting that right medication. I’ve done clinical trial research for decades. That’s a great benefit for people. But then, that’s the beginning. What do you do for the next part and the next part? What’s your exit strategy? So when I was in training, we would say how long do you keep somebody on an antidepressant? They go well, you know, a year or so. And so then what happens? Then you taper them off and see if they, get better, stay better. And if they get worse you put them back on. Then what?

Well, Leave them on for maybe two years and then stop. I go this doesn’t seem like a very hopeful, scientific approach. Doing clinical trial research using outcome measures I thought was very helpful, getting information, listening to a patient, and then taking that and systematizing that into an inquiry that can be looked at with a pre interventional kind of state, and then in follow up to see are the things that we’re doing together helping or not? How are they helping? How much are they helping? And there are a lot of co occurring things, right? A lot of moving parts. I always joke that I know what your diagnosis is after seeing somebody for a minute or so, and then they’ll say wow, what’s my diagnosis?

And I’ll just, say their name and say, yeah, John Brown, that’s your diagnosis. And they go I said I thought I, you’re not bipolar disorder, you’re not alcohol dependence, these are things that are going on right now at this scene in the movie, but you’re moving along, and that journey should be characterized by better understanding and returning a locus of control back to a person, rather than just ceding all this to other people around the professionals, and then I’m just a consumer.

So that’s always been my interest and I set up the eating disorders program at the Menninger Clinic when I was there. And there was a lot of interest about nutrition again and so forth. At the same time, developed a program to help patients look at their nutrition. So we completely revamped the dining room at the Menninger Clinic.

We looked at fitness kinds of things that can be done. We had a prominent spa owner from California come and set up that part of the program. So this health opportunities program was then a clinical trial. That was the experimental condition. The control was another unit that was exact same range of patients.

At the end of the year, the incidence of difficulty critical incidents and so forth completely disappeared. It was low to begin with anyway, but the the difference being that looking what a person ate the kind of activity that they had made a huge difference about their wellness.

They felt better. They really embraced then some of the things that, that we were otherwise trying to do. So rather than doing something to somebody, we were working with somebody in partnership and then being able to say, yes, of course, who wouldn’t want to raise your level of wellness? So that isn’t necessarily always The approach in psychiatry, it’s a lot more about, here’s the medication and in addiction medicine, I’ve been boarded in addiction medicine, addiction psychiatry there’s a lot of opportunities to help the whole person, but again, it can be some programs, and training about more therapy and some are lean towards more psychopharmacology.

You want all of those tools in your tool chest And including TMS which I think I was one of the first psychiatrists in Texas to embrace that when it became available in the mid 2000s. So that’s all helpful, and but being able to try to identify what are the factors that are predisposing and perpetuating in a person, and then trying to get at those functional aspects not just, all right, we’ve got a kind of a standoff between the depression and the antidepressant.

We’re done. No. We’re just beginning, and so the idea of what was going on before? I always tell people, look, you weren’t always taking five medications. What’s going on with this? And and try to understand. So, The whole nutritional aspect and getting the pharmacogenetic testing has been very helpful.

The pharmacokinetic testing when that became available outside of research, we used that in research to see, Non responders characterize them and see perhaps they were rapid metabolizers of a pathway for a medication. And that’s all helpful when that became available outside of clinical trial research.

That’s what was genetic testing. So that’s fine. That’s helpful. But what’s what’s more interesting to me is the Pharmaco dynamic testing, in other words, looking at things such as MTHFR. So whether a person is able to prepare to methylate B vitamins and to have them be brain ready, that’s a huge thing.

I’ve done a lot of clinical trial research over the decades, but we, a lot of this has been investigator initiated. We did a study with people who had MTHFR polymorphism, so they had difficulty with utilizing B vitamins. and had major depressive disorders. So they got randomized to a placebo or to a methylated B vitamin.

At the end of eight weeks breaking the blinding, those people that were on the placebo, no change people that were on the methylated B vitamin had their mood improve. In fact, the effect size was better than a lot of clinical trials with antidepressants. And all they were getting was a methylated B vitamin.

Okay, that’s important. Otherwise, that was used methylated B vitamins one or two that first came out were used as an adjunct treatment. Well, If you tried, six or ten different medications and a person doesn’t respond, maybe add this to them. I looked at that the other way around to say why did they develop this in the first place?

Perhaps they’re elevated homocysteine because homocysteine can’t be converted to SAMe to all the neurotransmitters. Perhaps that was a predisposing factor. This elevated homocysteine… got to show up on the radar for cardiologists to say, okay if the inflammation is there for the heart, we want to get that lower.

So getting it to less than 11 was great, but we found that really for the brain, getting it to 4, 5, or 6 by using the methylated B vitamins and by looking at some other measures, that was a huge contributing factor to them improving and being able to discontinue sometimes some of the medication.

So, you know, The medication and tow truck pulling you out of the ditch, that’s great, you don’t necessarily want to stop with that. What’s wrong with my vehicle? What’s wrong with my driving? Where am I? And those are all important questions really when a person is looking at this. And so we can have that perspective, again, be something that is understandable and able to be utilized by each person.

So again, raising that level of wellness instead of pin holding and then somebody, okay, there they are, you’ve got this disorder and this now becomes your identity. And you have all the direct consumer pharma ads on TV. Ask your doctor if our drug might be right for you. Maybe you fit into our categories.

Oh, yeah, I fit in. Okay, now I’ve got four or five pharma. Maybe I’ll get another one. 150 vaccines, what do I do? It’s okay, so there’s a different focus, and that’s one of wellness. And that’s true, whether it’s, the physical, psychological, spiritual aspects. All these things are… better than, to me, just treating somebody as, you meet this criteria, inclusion criteria, you have this disorder, and now I’m going to treat that disorder, and now it’s better, and that’s all we have to do with each other.

To me, that’s pretty one dimensional, right? The person’s really wanting to say, how can I… I just talked with someone earlier in the week and they said, before looking at at some of these things, I had a tendency to get really upset at family members and just really just spoil the evening and just rage and so forth.

How much sleep are you getting? I sleep pretty good. What time do you go to sleep? Four in the morning. What time do you get up? About seven. Okay, so you’re getting three hours of sleep. It’s that’s not a lot of sleep. And no, I’m fine. I can get up. I just push myself. I get some coffee and…

Okay well, how’s that working for you? is there a different approach that could be done? We talked about some of that. He made some changes and I initially got him some medication that helped him with some of that short fuse, getting his fuse longer. But then doing the testing, the pharmacodynamic testing and seeing, yes, he did have MTHFR issues.

Getting methylated B vitamin was something that allowed that homocysteine level to go down. Homocysteine is a pro inflammatory amino acid and… In the brain, inflammation is really excitation. Too much excitation, all of this going on is overwhelming. And sometimes the other things that we see co occurring with that, might be somebody who really responds poorly to having a deficiency in omega 3 fatty acids.

Maybe they’re not sleeping well. Maybe they tend to look for some way to calm their brain down. And so that could be seeking all kinds of Self medication, other things that may be going on, but having the opportunity to say what could I be doing differently that might really be able to help me prepare my brain for the next day.

Arnie: So looking at sleep architecture is something else that I became very interested in. A lot of medications affect the ability for the brain to get into REM sleep or get into Delta slow wave sleep, N3 sleep in the beginning of the night. And those all have crucial functions. And so when somebody has symptoms. Why wouldn’t it be important to look at that, just like we would somebody coming in for a general physical exam. You’d want to check their blood pressure, their pulse, look at some general laboratory studies. Looking at somebody’s sleep architecture would be great. We even looked at fitness bands to see, okay could we find something that would closely correspond to the data we’d get in a polysomnogram.

So. Going to sleep, getting the full data collection in a sleep study. And then looking at how did that show up on the fitness band? Better than nothing, but difficult to distinguish between REM sleep and slow wave sleep. And they’re different things. People that abuse alcohol increase slow wave sleep.

That’s great. But then you inhibit REM sleep, and it fragments sleep all the way through the night, so you’re not getting that fortified periods of REM sleep with increasing length which is preparing you for the next day. Also increasing serotonin and crashing it then, along with that, so you’ve got multiple pathways that are going in the wrong direction.

Being able to know a person’s sleep architecture is important. So this fellow I was talking about said, I had no idea that this affected, how I was doing. I’ve been doing this for a long time. I’m cheating because I’ve seen thousands and thousands of patients tell me this, but it was really important information for him.

Just as it was for a family that came in. With a seven year old and said he’s just having trouble. He’s all over the place. He’s easily upset He just has no ability to tolerate anything. And so going through some different things Information and what about sleep? What time is it good asleep? He goes to sleep about 2 in the morning He goes to sleep at 2 in the morning?

Yeah, his dad doesn’t get home until 1 o’clock. So he likes to play with him . Do you have dogs or something else that you couldn’t stand in maybe? But being able to have enough sleep, not something I thought about. I said, okay, here’s what you’re going to do. Please, if you want this to look better, then why not do something, arrange a schedule differently so he gets his sleep.

So we did it, I came back in two weeks and said, he’s like a different kid. iN fact, we just realized that before his dad had that change in his work schedule, that’s what was going on. Okay, you have to ask about sleep, and it would be very easy to give him some medication and just to do that only.

Not that medication is wrong, but that if you look at more of a functional medicine perspective, why did that happen? And that involves circumstances family relationships stressors on the job at school, other things that may be going on. But then also that underlying biology if there’s some… genetic aspects that need to be supported. We’d like to know that. Okay, somebody who has extra excitation in the prefrontal cortex and has trouble managing stress, that increased anxiety is often converted to anger, secondary emotion, and then they have all this anger trouble. Well, they must have bipolar disorder. Well, maybe. But if you look at then those people who have that those kinds of symptoms and when you see that they have some of these genetic factors and you support that genetic biodiversity, then now that reduces the tendency to have symptoms develop, and now you have a better way of now working to integrate some other aspects.

Kind of hardware and software analogy with a computer, that’s great to have different programs, but if there’s a hardware issue, you want to be able to address that, maybe first. That’s the idea of looking at the wellness aspects of sleep, nutrition, and trying to incorporate that into a plan that involves more than just what medication should I stay on for the rest of my life, or how many medications should I stay on for the rest of my life.

Oh, by the way, the medication’s 1400 dollars per month, and that’s with insurance. Probably not a good plan. 

Bruce: We have an interesting backstory about how you got interested in psychiatry. Something similar happened to me with my background. And I started off in emergency medicine and when I would present a patient, I would, for example, say this patient ran out of their medications. They can’t get to the bus station because of their caregiver is no longer there. They’re like, Hold on. Hold on. Is are they breathing? What are the A. B. C’s it’s like they didn’t care about the actual reason. They just wanted to know all of the most important life threatening issues at hand. And if we had labs done, if we had a chest X ray if we ruled out aortic dissection and like the things that are going to kill the patient and I’m like yeah, those are normal, but this patient can’t get their medications and that’s why they came in.

And it just seemed like there was definitely a disconnect there between treating the patient and their social psychosocial issues as well as the medical issues. And I had pretty similar experience as you. For a clinician who is interested in maybe incorporating more integrative medicine into their practice, what would you suggest to them? Are there any sort of new, novel, exciting approaches there that they can incorporate that you’ve heard of recently? Or is it just the bread and butter? History and physical exam type of approach.

Arnie: Fortunately, there’s more than that, and I share that perspective there’s so many complex things that go on with people, and we, in medicine, tend to simplify things for the sake of trying to understand, but we can oversimplify very easily and lose focus on , the entire patient.

If there are, somebody is coming in, and if you don’t know anything about how they’re metabolizing medicine, you don’t know anything about nutritional factors, and you’re going to intervene without doing that would be like someone in the emergency department saying, We don’t need chest x rays. We don’t need CBCs.

They’re H and H. I don’t, care about that. We’re just, we’re interested in something else. Obviously, these things are very important to know. To me, the sequence of if you can do the little buccal swab and get back data within a week or so you can temporize in the meantime with medication to be able to help, reduced suffering, reduced symptoms, and so forth. But then, the next step ought to be to look at that, present that information, discuss that, and develop a plan to address anything that seems like an obvious opportunity for improvement. And that would then also be accompanied by then looking at sleep aspects that could improve sleep.

Arnie: For example, I have people I just saw somebody yesterday who incorporated Omega 3 fatty acids into their supplement plan. Before that, they took a multiple vitamin. I’ll get to multiple vitamins in a second. But they just had no idea that they needed Omega 3s. We 35 percent dry weight of the brain is docosahexaenoic acid Omega 3s, and but the other Omega 3 subgroup, the EPA, the eicosapentaenoic acid is a very calming effect in the brain, so when people can, if they can get a supplement that is a 4 to 1 ratio of EPA to DHA, take that, and do that in a therapeutic intervention that can a lot of times reduce some of the difficulty with sleep onset latency sleep discontinuity, and then that can help them have a better opportunity to respond to whatever else we’re going to think about. And then looking at some of that, I said, okay perhaps we need to get some blood studies. And so I looked at for one trial we did, we had people that had the MTH of our polymorphism. And so we treated that, but they also had difficulty with sleep.

So on the fatigue assessment scale inventory development mid 2000 , out of 6 different inventories only those things they had to do with … mental fatigue make the cut so in this people would have 2 or 3 times as many symptoms of fatigue also we look at being able to measure the RBC membrane component made up by omega 3. If somebody’s low in their the amount of Omega 3s in the RBC membrane. That probably corresponds to other organ systems.

Like, what about the neurons? We’re not, doing any brain biopsies, but I’m being able to look at, okay if they’re low in that, let’s supplement them with the EPA to DHA high ratio Omega 3s. And sure enough, then, that led to an increase in the RBC Omega 3 membrane component and led to a dramatic decrease in their fatigue.

On the fatigue assessment scale, they look normal. What did they have? They had methylated B vitamin, and then they had the omega 3 EPA DHA high ratio. That’s great. Okay, then, so we want to look after those things. What if somebody’s low in magnesium, they have trouble, calming down, going to sleep?

Okay, then supplementing magnesium can be a benefit. You can’t do the same thing for everybody, You can’t take uh, one approach, well this is good for this symptom. Two people could have the exact same symptom set, but have arrived at those symptoms in very different ways.

Even though they look the same they have other things that are underpinning that we need to understand individually. And that’s really the importance of functional medicine and individualizing that approach. We don’t treat people as diagnosis, we treat people as people seeking a higher level of wellness.

Bruce: Yeah, you mentioned a number of concerns there for people to investigate and check out. What would you tell a patient who has seen numerous doctors and they can’t come to A diagnosis, I know there’s more to a person than a diagnosis, but they don’t know what’s causing any of their symptoms, they’ve been bounced around, they have maybe a variety of different issues that are all contributing to their fatigue and malaise and body aches, maybe chronic pain issues.

What do you think our healthcare system needs to do better at treating these types of individuals who have these issues?

Arnie: That’s a great question because a lot of times the easy things don’t come to us as specialists. Obviously, we see complex situations where people haven’t been able to get a diagnostic understanding. And there’s nothing wrong with the diagnosis. You just don’t want to use that diagnosis and replace the understanding opportunity to understand the patient with that diagnosis.

But not being able to ask the right questions leads to maybe a smaller chance of being able to understand that etiology, that evolution of the symptoms. Being able to, in the emergency department, okay, you’d get some blood work, you get a chest x ray, maybe some other things, depending on what’s going on.

If we never look at genetic biomarkers. If we never look at or ask questions about or measure the quality of a person’s sleep if we just miss those things, then we’re going to miss opportunities for improvement and probably aspects that have been contributing to developing those symptoms right along.

To me, The diagnosis we’re trying to reach was preceded by several steps of things that were going off. So you get off kind of the, the GPS kind of coordinates. You’re going off the wrong direction, wrong direction. You don’t necessarily end up way off right away, but over time there are things that maybe if they could have been known it would lead to something other than just the gradual development of a full blown… Illness that has to be diagnosed. So of course we want to diagnose it. But we need to ask the right questions, sleep quality, look at genetic biomarkers look at blood work. So in psychiatry, most psychiatrists don’t get blood work. They might get a level, I mean I remember having discussions with the managed care review person I remember with they didn’t want to approve sertraline at a level of 300 milligrams a day because we’ll be… on label dosing that was done in 1990 or so was up to 200 milligrams and shown it was safe and effective and that was it. And for six year olds, up to 200 milligrams. I said, this person was a rapid cytochrome P450 2C19 metabolizer and their level was low, their sertraline level was low, and we looked for that because, of course, they weren’t responding.

We had this genetic, consideration we could look at and then we measured their sertraline level and it was like… Crickets and the farm D working for the insurance company said, you can do that. I said, yes, we can do that. And that’s not always done, but yes, we can measure blood levels of medications because everybody’s different.

Of course, there’s a difference between what’s on label. And if you’re, a pharma company, you can only talk about. What you’ve demonstrated in clinical trial research to be safe and effective and have FDA approval for same and that’s great and it should be the way it is.

But if you are treating somebody, if they’re not responding, you don’t want to give up too early. Perhaps there’s a reason why that medication is not working. Are they getting an adequate level? If we just… Throw out all the people that aren’t responding without asking any questions. Then maybe we miss the opportunity to use something.

It would be very helpful. But we have to ask more questions. Asking the right questions leads to a better understanding diagnostically. And then say, all right, now what do we do for an intervention and treatment approach? We can do that better by knowing who that person is. And, all right, they ended up getting out of that 200 milligrams.

When they’re metabolizing it five times more rapidly as an ultra rapid metabolizer they’re getting one fifth the blood level, right? 40 milligrams is not usually the effective dose for so often. That’s that’s a an approach. And in primary care clinicians will, of course, start with a medication that they’re familiar with.

For, I’m talking about for psychiatric say depression or anxiety. And then they’ll start with a starting dose, and maybe they’ll go a little bit more, but they’re, That’s not their area. They’ve got to do all kinds of other things at the same time. They then typically refer, right? So refer to a specialist and the specialist is typically used to seeing people that don’t respond to the starting dose.

I rarely see people who are slow metabolizers who responded great at just the starting baby dose, if you will. And that’s great. You want to individualize treatment. That’s perfect. That’s why you would start at a low dose because you’re going to find some of those people. But there’s a lot of people who have these kinds of contributing factors that MTHFR difficulty. Activating B vitamins is something that 80 percent of people we see have, 80%. That’s higher than the general population. But the kind of homocysteine theory of contributing to depression not that everything is all one approach, but if there are 80 percent of people that have trouble methylating B vitamins, and they end up having high homocysteine levels, And you don’t even look at that and don’t ask the question, but you just do one serial trial after another of antidepressant medicine.

Maybe then there are people that don’t respond, and maybe those people have something else going on, a question that needs to be asked that hadn’t been asked. And that’s the idea of trying to… Characterize somebody better, but doing that earlier, I always joke that when parents leave the hospital with their newborn, they should, here’s your owner’s manual, right?

You should have all these things. We’ve done this by this genetic characterization. You want to, and these are not the things that people are afraid of. There’s a lot of fear about genetic testing. I don’t want to find out I’m going to die three days after, the full moon or something. No, no, no, no.

These are things that have to do with knowing that if you have someone who has, and this is a family issue MTHFR. You look at a family that has somebody who’s depressed. Okay you get the testing, that they have the say C677T, the Allele that problem with being able to utilize B vitamins, you only get not 100 percent of, say, a perfect, we used to get B12 and folic acid levels, of course, that’s great, but what if they can’t utilize what’s there?

They may only be able to utilize 70%, or 50%, or 35%, or 5 percent if they’re heterozygous for those two alleles. That is something that should be asked, because it’s so prevalent, right? Once you know something, it’s hard to go back to not doing it, right? Once you know that you need to have clean drinking water, you don’t go back and say, Oh, I want to care about the sewage.

No, you want to be able to make sure that you utilize all those things. Then you build on that and you get better. What’s the best practice you build on the information that you’ve gleaned from others. And I’ve learned most of what I’ve learned from listening to patients. Patients will tell you.

This is what my story is. And then my job is to think with them. So from a medical perspective, what are some things that we could understand? Or questions that we could ask maybe. to be able to then have a better approach at getting some answers that’ll make a difference for them. Again, give them more of an internal locus of control about their wellness.

Bruce: Let’s talk about the concept of a diagnosis for a second. We know that a diagnosis has a purpose depending on who’s considering it. An insurance company, they need it for billing issues. The clinician, they might need it for making sure that we’re treating the patient appropriately for that diagnosis.

And the patient themselves might find it useful for validation, for clarity. for understanding more about themselves. But, a nosological category for a particular set of symptoms, obviously, has some drawbacks to it. There are people who we all know that bipolar exists on a spectrum, as does numerous other psychiatric disorders.

We also know that certain medications for the treatment of one disorder can also help treat another disorder. Even though they’re not FDA approved and so we can use them off label. What is your perspective on the dilemma of a diagnosis and what do you tell patients about the purpose of a diagnosis for your patients?

Arnie: that’s a great question. To understand what’s happening, we certainly want to utilize our medical experience, expertise, training to come up with a diagnosis and that’s, it’s just not the end. That’s important, that’s the beginning looking at that and so in clinical trial work we use outcome measures and we’re looking at the, does a person have symptoms of depression?

As measured on a Hamilton Depression Inventory or a PHQ 9 or whatever you may look at however complex that may be, but That helps them to be able to say when we see new people, we use about a dozen inventories. So we’re having these inventories and we’ll go over that with people and say, okay, so you have this, tell me more about that, tell me more about that.

So you get, it’s like having a a structured interview before you ever see the person. So they’re being able to wax lyrical on all of the things that are going on that they’ve experienced and then My job is to integrate all that information and say you’ve got elevated scores here and here, so it looks like you have co occurring episodes of major depressive disorder based on the history and here are these inventories supporting that but you also have co occurring anxiety, you have an elevated anxiety and by the way, then you have an elevated fatigue score.

So what about your sleep? Ah, I sleep okay. What is that like? do you feel rested? Do you feel like you have restorative benefit when you wake up in the morning? No, I never have that. Okay a lot of times people have given up for, the quest to try to say, I would like to jump out of bed in the morning like I’m eight years old and go, Yay, it’s great, what a great day.

Maybe there’s some things standing in the way that we can understand so that we could get people, closer to to something that is, is attainable, but we have to ask the right questions. I like clinical inventories to help then guide my… Inquiry, when I’m talking with people, listening to their story, but then at the same time I’m formulating, an understanding in terms of So that, they have this theory that’s related to this, I wonder about this, I wonder about that.

Then I’m going to pursue some investigation by looking at the genetic testing, looking at some blood levels of things, perhaps. And and then be able to ask the right question, and then have more information. And then be able to say whatever levels there are of those things to be able to over time.

I like using a a graphic so that you can see somebody’s mood is down here and is depressed. Every time, the first visit, and the next visit, next visit, next visit. Now they’re, you know, in a normal range based on what they were doing. So they get some kind of sense of how am I doing?

That’s how you’re doing because it’s hard to say, Hey, how you doing? I’m fine. That’s, there’s so many complex things going on, you have to really have a chance to understand that more and break that down. And that’s what inventories can do. And most psychiatrists don’t use inventories. I’ve traveled all around the country talking with physicians about the use of inventories. It can be helpful not just in clinical trial research, it can be helpful just in clinical medicine. And having that kind of partnership between the patient and the clinician to ask those questions, to understand more, gives a better way to to get that complexity, that more finer grid understanding.

Other than, oh, you’re depressed, you have anti, you have major depress disorder, here’s an antidepressant. We’re just going to throw things against the wall and see what sticks. Okay, that’s so 1970s, right? We want to be able to have something that’s a little more nuanced, something that’s 2023. So being able to have those ways to characterize people, with getting their history, getting those symptoms, coming up with a diagnosis based on evidence and inclusion criteria.

So whether it’s DSM 5 or ICD 10, being able to look at those things that characterize, okay, this is a diagnosis. The question is, why do they have that diagnosis? We never know, it’s just family history. It’s a genetic, it’s genetic. There’s genetic predisposition, but there’s also epigenetic interventions, things that can be done to help mitigate that risk or help improve the opportunity for somebody to really have a fully developed capacity that’s something positive.

That’s, that comes from me asking the right questions. And I, sitting down with a legal pad saying, tell me about your mother is a, that’s one way, but it’s not a very efficient way. It’s just a it doesn’t really help the person be able to give the right information that could then be used to say it looks like we’re ruling this and this up, but they do have this and this area, so let’s look at that more.

And then perhaps look at an EEG, an ambulatory EEG, somebody that has. Periods of time where they have mood changes and sometimes they have maybe history of absence seizures, petit mal seizures or something as a child in school. And then looking in at a EEG can give us some, a clue that there’s something else going on there.

Bruce: tell us more about an ambulatory EEG. I would say vast majority of psychiatrists don’t order that. If they suspect a neurologic issue, they’ll refer to neurologist who would order, an in-lab, EEG. Tell us more about an ambulatory EG. How do you order that kind of referral? Would you give, and what kind of data does that give back and who would you order it on?

Arnie: Yes, great question. well, You’re right. If somebody has a neurologic problem, it makes sense to send them to a neurologist. The trouble is this is the integrative medicine aspects. So this is the, the American Board of Psychiatry and Neurology for a reason, right? So these are very related specialties.

If it’s a neurology problem, okay, they’re maybe they have had a stroke or something. Okay clearly that’s a neurology issue. If somebody’s having depression, okay that’s clearly a psychiatric issue. What if somebody’s having, irritability or having outbursts? and so forth. If you send them to a neurologist, they’re going to do a neurologic exam and say, okay, it’s normal and may, order some, a few biomarkers to see if they have any elevated issues and say, no they’re okay. But they still have the symptoms. So that didn’t get them anywhere in terms of any, gaining any understanding.

So integrated medicine would have to do with, in this situation, what is an EEG going to show? It can have 8 on the Richter scale and having a, an ictal event and that’s an obvious thing, that’s a neurology opportunity for improvement and understanding why they have the seizure of course but what if they have more subtle findings?

If they have 8 seconds here and there between say N3 sleep and then getting into stage 2 sleep or so, and you see this left frontal temporal sharp wave activity going along and a couple of sharp deflections. That doesn’t show up as any kind of generalized seizure or motor seizure or something.

That’s just interesting finding. Oh, a lot of people have that. Yes, but do those people also have these other symptoms that we’re looking at more? Because again, neurology is looking at a different frame of reference. So it’s like, how do you understand something? You want multiple frames of reference.

You want to be able to characterize that as best you can from a lot of different perspectives of understanding. All valuable, potentially. But in this instance, I use that when people have… They have mood swings. What are the mood swings? They just get really frustrated and they just, just lose it.

Okay. When does it happen? Did they have a history of head injury? Yeah, they had a couple concussions. In fact, they had eight concussions in high school playing football. Okay, that’s a clue. Did they do any studies at the time? Yeah, they did a CT scan to see if there was any bleeding and there wasn’t a cortical bleed, so they just was the end of it

Okay, but then the person since then maybe has had difficulty regulating their emotional response to frustration. Doing the ambulatory EEG looks at 72 hours. 20 leads. It looked at 200 times a second. And if there’s all normal, there’s nothing there, that’s a very fine… grid fine tooth comb to look for something, but oftentimes we see with those histories something that’s there, those little, that sharp wave activity.

Then treating somebody, of course, with an antigen bolts, and there’s nothing else there. The neurologist says, I don’t, they don’t have a seizure disorder. Oh, those are just epileptiform discharges. There’s nothing there. Okay. There’s nothing there for you as a neurologist, but there’s something there for me as a neuropsychiatrist.

So that’s the kind of way in which we would use that and refer that to a neurologist maybe to get that done or we’ve done that ourselves in the in the practice. And then the key is reading it so that you see everything. You don’t just look for the, the 10 out of 10 kind of events.

You want to look at the entire thing and make sure that each. Those opportunities to consider if they’re there and then treating somebody and now they’re better and you look at the EEG and now it’s normal, I think that’s helpful information.

Bruce: So, for the individual who has irritability after a concussion, what do you do with that information next? What kind of treatment might you suggest for them?

Arnie: It’s a great question and that happens a lot of times. People can have concussions and have, again, same thing, have identical sets of symptoms but got there in a different way. Before the and I’m thinking of an adolescent that had a concussion and before that. Everything was fine. That was the initial history, but everything wasn’t really fine. There was some other trouble there with short fuse, trouble with frustration tolerance. After the concussion, that magnified. So then that became that this is what’s gone on after the… But there was something else there to begin with.

So then looking at the MTHFR, okay, the person is heterozygous for the C677T and the A1298C. mutations together, dropping the most severe genotype, dropping the availability of B vitamins, and homocysteine way, way, way elevated. So that was there before the concussion. So then now the concussion’s here, and so what do you do?

Treat them with the methylated B vitamins, and then utilizing the EPA, DHA high ratio omega 3s, that’s helpful. And then looking at their sleep. Do they have enough delta slow wave sleep where the body is sending out stem cells to do reparative work. I’ve seen people who’ve had, one patient who’s had a persistent coma for weeks and weeks, and after a motor vehicle accident, she actually fell out of a vehicle.

And so then after that, she was not herself, was irritable angry, family members just, ugh, that’s just the way she is. Looking at those symptoms, doing an EEG, seeing that she had that sharp wave activity, And then treating her with Omega 3 fatty acids and also with an antidepressant.

Serotonin, dopamine, and reuptake inhibitor, which is… Sertraline is the only one that does that. You have to get the right level though, the right blood level to get the secondary binding affinity for dopamine to come in. And her symptoms dramatically resolved. In fact, they said we have her back. She’s the old, Mary.

And so that’s that’s great. It’s wow, okay. What do you think about that? I think we should do more of that, right? We should look for opportunities. When people give up and say there’s nothing you can do. Now, I, I think we need to look for something, other things that we could do, and then that’s the idea

Bruce: You mentioned when we were first talking about the importance of coming off of a medication. I don’t think that’s something that’s emphasized very much in training and mentorship and it’s probably one of the key. Important factors on a patient’s mind when they’re starting a medication, and I think it could lead to polypharmacy, it could lead to med, drug interactions, they can also build tolerance to that medication, and before you know it, they are on 10 medications and they don’t really know what the purpose of any of them is for the individual who has found benefit to a medication, they’re not having any issue with it necessarily, no side effects. What would you suggest for patients and clinicians about when they should think about coming off of medication? Let’s take SSRIs, for example, since they’re so commonly utilized by our audience.

Arnie: Sure, and so SSRIs, are helpful. Before SSRIs, people were getting tricyclic antidepressants, and if you take the entire bottle, then you have a widening QRS complex, have an arrhythmia and die. That’s bad, and so now you could take a whole bottle of fluoxetine and be okay. That was a safety thing, people got, all right, we do SSRIs. The trouble though is that when you have the unopposed increase in serotonin, the raffinucleus has input into the ventral tegmental area that’s inhibitory. A lot of times what you’ll get is this is great, okay, now they have improvement, but then what you’re noticing over time is maybe they start to have some other things that are developing.

Lack of initiative, motivation, drive libido task initiation, task completion. So you’re almost inducing some of the… Executive function deficits that people would have with adult attention deficit symptoms. And that’s because you’re causing this kind of this depletion. The other thing is, again, it’s not just somebody who’s depressed and getting an SSRI.

Who are they? I mean, What’s the best treatment for me? People will ask me, they’ll go, wait, dude, who are you? We want to be able to know what is there that we can characterize about that person. And if we if we just give the the medication only and we don’t really look for these other kinds of symptoms, we might miss the opportunity to to do something else.

So I like the idea of balancing. And this was called when this increases and decreasing Doping was Prozac poop out. Okay, Prozac poop out was described as, people do great on Prozac, then after a while, they’re not doing so well. Yeah, because you just, you suppress their dopamine activity into the basement.

It’s really not not just what goes on initially, but, and it may be fine initially. Yeah, it’s okay. initial intervention, perhaps, for some people, but what if they break down dopamine more rapidly? So their COMT genotype is really important. If you look at people who 50 percent of the population are looking at alleles characterized by methionine and valine, they’re Valmet, so they have that pairing, and that, let’s say, is 100% dopamine level.

People that end up being Valmet end up being a Val Val, they break down dopamine more rapidly they end up having only 60 percent of the amount of dopamine potentially. And let’s say they get depressed, and they get put on an SSRI, and that works for a while, but they’re already potentially set up to have a deficiency in dopamine activity.

Not always, but they could be. That’s something you’d want to think about, and not necessarily just let that go too long without… looking for what’s the next thing that can be done. So that’s the idea of looking at a more integrative health functional medicine approach, what are some things we can do to increase wellness that perhaps would now allow a person to be able to get off of some of those pharma interventions.

And then the flip side, there’s 25 percent of people who are at MedMeds. So they have… Increased levels of dopamine, so you don’t necessarily want those people to drink a lot of coffee. So the methylxanthines caffeine, theophylline, thebromine will cause them to be more tremor or have migraines or other kinds of things.

So they’re vulnerable differently because they have a different genotype for regulating catecholamines. So it’s important to know that. Once you know that, then that can be something that can be utilized. We also have done some studies with vitamin D. And looking at vitamin D is a cofactor for the synthesis of dopamine, for tyrosine hydroxylase and the rate limiting step of dopamine synthesis.

So if a person is low in vitamin D, really low in vitamin D, stays there, okay, you get rickets. 1920, you figure out, okay, let’s put vitamin D in the milk, vitamin D milk, and let’s get it up above a 20 nanograms per milliliter 25 hydroxy vitamin D level. The brain is a kind of high maintenance organ.

It needs a lot more. Being able to supplement that when we had people low, they did better with their depression. In fact, we measured depression scores, keeping everything else constant, and then giving them 10, 000 IUs of vitamin D. 10, 000? Yeah, that’s what you get if you’re in the sun for half an hour, lightly pigmented skin.

Or, darker and darker pigmented skin, it may take as long as six times longer, three hours. It just depends on who you are, the kind of treatment you get. Looking at the incidence of colon cancer in people at higher risk, African Americans, other high risk groups. If you got the level above a, not just a 20, but a 30 or 40 and higher dramatically reduces the risk of colon cancer in those people in that population.

So that’s good but what about the brain? The brain is more high maintenance and you need to get that up higher. So being able to get that up to 60 makes a huge difference. So a lot of times people can at that point get off of their initial SSRI intervention because That was a contributing factor for them.

Not necessarily everyone, but it’s for a lot of people. So same thing with the, winter blues and, seasonal affective disorder symptoms, people in Anchorage or Minneapolis or what have you, a vitamin D. So that’s a huge thing. And then we did, swallowing, the old vitamin D2, 50, 000 units orally once a week to then D3.

And then how, okay, using 10, 000 as a swallowing, as a PO. Oral form of the medicine, or of the supplement rather and then comparing that to an oral dissolving tablet. The tablet actually did better for people in terms of their depression. So we looked at that and go to that. And then we looked at vitamin D liquid versus the oral dissolving tablet and stay in the mouth longer, make full access to the oral mucosa and not have to go through first pass metabolism through the liver. Those people did even better. We presented that in European Congress on Neurosurgical Pharmacology. And in Europe there’s a lot of interest in these kinds of things, right? Looking at things that are perhaps not just pharma interventions but things that could be dietary supplements and other things that would be helping certain people.

It’s all about who, you can’t give something to everybody vitamin E you might, but you can give targeted interventions really a very better, A much better approach if you know who you’re treating, and that’s the idea. So SSRIs are great maybe to start with but you need to make sure that you’re getting enough of it. And then make sure they’re not starting to develop symptoms of dopamine deficiency.

Bruce: On the topic of SSRIs, let’s talk a little bit about PSSD or post SSRI sexual dysfunction. What are your thoughts on that? Do you have any integrative suggestions for an individual who continues to have sexual dysfunction after stopping the SSRI? Most typically anorgasmia, low libido difficulty having any sensation during intercourse.

Um, What are your thoughts on PSSD?

Arnie: Yeah, I think it’s a, it’s an interesting symptom that is, fairly common. And then getting, having the intervention of the serotonin enhancing drug. Okay, that’s what’s going on, so let’s get off of that. But it doesn’t necessarily, these are systems in the brain that are changed by whatever you’re doing.

So it doesn’t, it’s, the intended effect isn’t the last effect, so there are other things that go on, so taking that out of the way can still leave residual effects, and so looking at that and doing things that would enhance dopamine so for example, getting a 25 hydroxyvitamin D level, and if that person is low push the dose up higher.

What will that do? That will tend to increase some of the opportunities for improvement in people that have post SSRI sexual dysfunction and then having that be now something that’s maybe in their daily regimen for what they can can do. So that’s an example. And then getting enough sleep, again, repleting sleep.

Some medications will inhibit REM sleep and afterwards they’ll still have REM sleep inhibition and SSRIs will do that. So being able to have enough time for REM sleep to restore, doing things that can improve On that for example, alcohol, people drinking alcohol, say, okay it’s fine, I’ve always been drinking some.

But you’re always inhibiting REM sleep, and now you’ve got these symptoms, that had to do in the aftermath of the SSRI treatment. Lose the alcohol certainly lose the alcohol later in the evening, so that, if you’re doing that at lunchtime, it’s probably not affecting the sleep architecture as much as if you’re doing it at 11 o’clock at night, and then, going off to the bedroom.

So that’s those are things that, it can make a difference trying to characterize the individual predisposing factors. Again, thinking what happened before the symptom

Bruce: you mentioned the importance of genetic testing and you drew the distinction between pharmacokinetic testing versus pharmacodynamic testing. And I think a lot of patients think that when they do genetic testing, generally speaking, they’re going to know which medication they should be on in terms of effectiveness.

And from my understanding, other than the MTHFR. Genetic tests. I don’t know if there’s many other pharmacodynamic tests that get done. Unless maybe you can educate us if there’s any others that are tested for that help draw a conclusion about efficacy.

Arnie: Great question. So yes, there are and So the MTHFR we talked about that’s obvious and that’s a huge effect So again 80 percent of people we see in our setting I have MTHFR polymorphism. So Okay, that’s one thing. What about what other than that? Exercise affects the brain a lot.

People have known this for a long time. Looking at the effect of of exercise on mood. And that’s great. But exercise also has effects on on sleep. And it also has effects with certain people differently. Differentially, it’s good for everybody. However, there’s a certain slice of people BDF, Brain Derived Neurotrophic Factor the gene that has to do with this question.

If you have somebody that shows they’re either hetero or homo for this this defect or variation, if you will, then if they don’t exercise and they do everything else right, they’ll have some benefit. But if you’re heterozygous or homozygous for that variation for the brain derived neurotrophic factor gene.

Doing exercise, doing cardiovascular exercise and strength training exercise can make a huge difference. There was a study, back a few decades ago with women looking at strength training increasing bone density. Okay, so that was shown to be helpful. But a secondary outcome with that was that women who were depressed got better.

It’s oh, okay so exercise makes a difference for those, and this was strength training exercise doing cardiovascular exercise and doing strength training exercise for people with that BDNF, either heterozygous or homozygous variation makes a huge difference. And so sometimes they can get off of some of their medicine because this is now what they’re doing.

Ah, I feel great with this. And they get that excitement that comes from recognizing they can do something and have control over something that can restore. The way things used to be when they were, before developing the symptoms. So that’s another psycho dynamic gene to look at. So brain derived neurotrophic factor, BDNF.

Another one is uh, CACNA1C. So this has to do with prefrontal cortex calcium channel activation. So there are people who have a higher level of stimulation, activation, excitatory activity in the prefrontal cortex. Those people, if they’re deficient in omega 3s, are really predisposed towards anxiety, difficulty sleeping, and maybe irritability, poor frustration tolerance, and pulse control.

Giving those people omega 3 fatty acids that are high in that icosapentaenoic acid so that 4 to 1 ratio, that makes a huge difference in being able to do well. We did a study in with kids that had ADHD and looked at fatigue. Kids don’t have trouble sleeping. Kids do have trouble sleeping.

Some of them have trouble getting restorative sleep. And looking at those kids with ADHD and giving them omega 3 fatty acids with that high EPA to DHA made a difference over just regular fatty acid, just a kind of one to one ratio. And that was something that I presented that at the adolescent psychiatric scientific meaning.

So that’s something that looks at There’s always maybe more complexity than we can appreciate, right? We only know a little bit. It’s the tip of the iceberg that we have as understanding, but so that’s another gene that has to do a lot with predisposing people to Anxiety, trouble sleeping, depression, irritability.

So if they have that increased excitation and they have MTHFR polymorphism Now they have two things going on. Now they have more homocysteine. Now they have a lot of excitation going on And then they’re not sleeping, and so they’re not getting that restorative benefit of sleep. So now they have a lot more difficulty during the day. 

SLC6A4 is another serotonin receptor gene that if you have a certain genotype like that, someone will likely do well with SSRIs. If you don’t, then maybe not so much. If you know that to begin with, you can then choose a medicine that’s more likely to work. But also at the same time again, somebody’s not just one gene, just like they’re not one diagnosis.

So we have to look at all this together. And so it can be very interesting if they, or a met genotype, and they have all this dopamine going on, and yet they’re not sleeping, they’re going to be short fused, irritable, because you have all the stimulations, like having your accelerator stuck, and you’re trying to navigate down a side street, and almost side swiping the cars as you’re going by, that has to be offset with, again, the omega 3 fatty acids. Huge difference from met, COMT genotypes if you are able to use that omega 3, the EPA omega 3. And there are many more like that, but there’s, so that’s the benefit of looking at that and starting to study that, because we have begun that process.

There’s so much more to do. But there are a lot of those kinds of things. These are like the keys to wellness. What are some things this person maybe can do? Let’s… help them in that way. Let’s address that one factor and see if that improves things. Great. Now, what else can we find? There’s a, it’s, you’re never wanting to rest on one gene.

Are there this genotype there for where you got the answer? No, there’s no gene for depression. There’s no gene for This, that, or the other thing, there’s a combination interplay, a complex interplay between genetic predisposition and epigenetic factors which either make some of those genes more likely to be expressed or some not to be expressed.

And that could be either for positive outcome or for negative outcome. That phenotypic event is underscored by that what, what got there? How did they get there? Understanding that the predisposition and then having the epigenetic interventions. And that’s what we do as physicians, really.

We’re doing epigenetic interventions all the time. We just don’t think about it that way. We look for people that respond to increasing serotonin. We look for people who respond to something else. People who have obstructive sleep apnea. A small percentage of the population. It’s a great benefit to… Treat that, to do that with CPAP or whether it’s elevated or oral appliance or stimulating the hypoglossal nerve with a stimulator. But there’s 63% of people that have disturbed sleep architecture every night, and that’s not because of obstructive sleep apnea. So what about 63% of people that need improved sleep? We need to be looking for these kind of factors, and that’s what I’m thinking would help reduce the incidents ultimately of some of the psychiatric disorders.

Bruce: Let’s talk about diet for a little bit because you mentioned the importance of supplements. I think if we go upstream, it’s probably important to talk about what is a good healthy diet to, to have. And we grew up with thinking about the food pyramid and since then, there’s been just so many studies about what your diet should be and what is the best diet to lose weight and the Atkins diet, the Mediterranean diet, the paleo diet, there’s just a million of them.

I think it leads to a bit of confusion and frustration and also patients are probably like, well, they don’t really know what they’re talking about, because there’s just so many diets that are all competing for the public’s attention. But what do you recommend to patients? Is there any new data there that we can help use to guide them? About proper diet.

Arnie: Yes. And I’m going to sound the same alarm that by not knowing a person’s genetic makeup, it makes it difficult to make recommendations. For example, if someone needs Omega threes, it’s not just getting Nordic natural Omega threes and swallowing the supplements as good as they are. But those people really need to have more Omega threes. What should they do? They should be able to consider that if somebody has an overbalance of pro inflammatory omega 6 and under representation of anti inflammatory omega 3s, perhaps getting it back into balance would be An important intervention that that could be done, so it really has to be more complexly thought of in that way so there are there’s just a lot of of interplay, I think, that that can be helpful, and we have to ask the right questions, and to me, it’s, , we can’t stop, but, We have to always look at, is there something else, I wonder about these other people that there was nothing else to be done for.

So for example, when people have been diagnosed with bipolar disorder, okay, they have bipolar disorder. And there’s a family history, so they’re going to always have bipolar disorder. And the thing that characterizes them is bipolar disorder. What do you call when people have mood instability and then you identify some of the genetic factors and treat that and Eventually tapered to a lower and lower and lower doses of medicine, which were very helpful to begin with But now they no longer have those symptoms.

A spontaneous remission? Not bipolar disorder?. So people develop syndromes and disorders But they do that gradually so again thinking of that long process There are things that could be thought of that are dietary interventions that might be better. So the standard American diet, for example with all carbohydrates, that’s not a good thing.

We’re made to be flexibly metabolic. The brain uses glucose, yes, but the brain also uses beta hydroxybutyrate. So BHB is very helpful, but you never get any because why? We don’t break down fat, we store fat because we always, like a hybrid vehicle, we always have carbohydrates available, right? So we never switch over to that other circuit of of utilizing beta hydroxybutyrate, but that’s something that causes a change with people that that diet helps, so having, the whole, now this is, I think, in vogue somewhat, intermittent fasting there’s always some kind of new thing that’s as you’re saying, that’s, eat this way, eat that way, but for thousands of years, cultures have used fasting, intermittent fasting.

Having certain days of the week that they would fast, right? Why did they do that? It’s just some kind of genetic, or… No, wait, they would never say that. They’d say some kind of religious something. And what if it’s both? But yeah, so that’s that’s another factor is being able to think about food. As supporting certain genotypes, why do people do certain things? It may be a cultural aspect to it, but there may be some biologic underpinnings, right?

And so certain things that certain people do, maybe that’s good for a certain group of people, but maybe something else is needed over here, or this factor isn’t important for these people. And it is over here. So for example the genus Allium some people have trouble with that.

Some people have trouble with FODMAP, high FODMAP foods. And so being able to identify that, and being able to eat in a way that support one’s genotype is important. But you can’t do that if you don’t know, right? I’ve had patients who have had abdominal pain depression, and other things going on, but…

We can put somebody on antidepressant, but what about these other, oh, let me just send them to a gastroenterologist. We can do that, but what if you also, make a person aware of certain foods maybe they should control for, to eat a low FODMAP diet, and then reintroduce some foods, and different foods for different people maybe can be tolerated and not be so much of an issue.

But that’s, that requires asking something about myself. How do I respond to different things versus I’m supposed to do this, or this is what everybody should do. Cholesterol is bad. There’s some data that pursuing low cholesterol may increase risk of certain cancers. Then you want to maybe do something different, right?

In the back probably in the fifties or so, you know, I started having margarine. Margarine’s healthy. Butter’s bad. Now we know, of course, it’s the other way around, right? But if you’re just hearing this again and again, that may be excuse me, hard to sort out. So that’s a a way that you have to ask those questions and then individualize the approach, but be open to making a change.

Somebody who eats high glycemic carbohydrates the lots of reliance on carbohydrates and never has a chance to get away from carbohydrates because they’re not eating any for 16 hours, doesn’t have an experience of using the beta hydroxybutyrate. In that situation, it really makes a huge difference to be able to experience that, and that can, for a lot of patients, make a difference.

I’ve had patients come back and go, Why didn’t anyone tell me this? I said I’ve been eating this way for my whole life. Welcome to America. You’ve been eating whatever all the rest of us have been doing. You can do something different and uh, have a different outcome. 

Bruce: Are there any novel treatments within psychiatry that excite you? That are particularly interesting that have come out recently? What are your thoughts?

Arnie: I would say TMS is what that is for me. Transcranial mandibular stimulation has to do with Doing a reset really in the brain and having that somebody’s on medication, they have a little bit of response but not all the way. Try another medicine, try another medicine, and then they have the opportunity to get TMS.

That does a reset and often times people can then start to get off of some of the medicines that they were on. That’s pretty exciting. No medicine, no medicine side effects, and something that is really of significant benefit in terms of reducing the risk of relapse. And then doing that along with the genetic characterization I was saying, then improves their outcome.

In other words, if you did a reset, and now you’re not experiencing those symptoms, if you could also do some of the genetic informed interventions with supplements, maybe then you reduce the same contributing factors of developing that depression. So they stay on and a year later ninety percent of our patients are doing very well and haven’t had to get back on medicine or haven’t had some other kind of treatment for depression.

So that’s a real benefit. It’s exciting to me and it was looked at as just another treatment for depression but you want to treat the whole person. If they need to be following a low FODMAP diet, if they need to be having Methylated vitamins. These are all things you want to do after the reset, otherwise you’re likely to fall off track again.

So TMS is really exciting. That’s something that I think is is more than just a treatment for depression. It’s an opportunity to change the direction of things moving forward in a person’s life who’s had depression because it can really make for the opportunity of incorporating these other changes and not having to have that weight of symptom burden. Be hanging over them. Maybe they’re not there now, but it’s gonna come back. It did with all of my medicines it’s different with TMS. So I think that’s a very exciting.

Bruce: Thank you, Dr. Arnie Mech, and I appreciate you joining me today and talking more about integrative psychiatry. We talked about a lot of different, really important topics, patients issues with chronic illness, complex patients, struggle with the diagnosis, when to stop medications, the importance of diet and genetic testing, TMS. Polypharmacy, there’s just so much here and I really appreciate you giving us your insight into these topics on the future of psychiatry.

Arnie: My pleasure. I’m excited about what we have now for patients And I thank you for the opportunity of discussing it

Bruce: Thank you so much. Appreciate it.

I’d appreciate it if you please like and share the podcast with your colleagues. It would be especially helpful for us. And if you’d like, please leave us a rating on your favorite podcatcher. If you’re a clinician, I developed a course on how to start a private practice. And for patients, I’ve also developed a course on ACT and CBT based lessons for treating and helping anxiety.

And you can find those all on our website as well. Thank you so much. And I’ll see you in the next episode.