Food First, Pharma Last: Part Two of our Interview with Chris Masterjohn

Welcome to the Madden America Podcast, your source for science, psychiatry, and social justice. Welcome to the Madden America Podcast. My name is Brooke Seam and I am the author of the award-winning memoir on Interdepressant withdrawal, May Cause Side Effects. Today I am back with Chris Masterjohn at PhD. This is Part 2. Chris is a nutritional scientist, former professor and founder of Mytom. With a PhD in nutritional sciences and years of research in mitochondrial biology, his work focuses on translating peer-reviewed science into practical tools for human health. At Mytom, Dr. Masterjohn pioneered the first analysis designed to measure mitochondrial respiratory chain function directly, identifying individual energy bottlenecks and guiding personalized science-back protocols to optimize the system responsible for over 90% of cellular energy production. His mission is to bring mitochondrial testing out of the rare disease space and into everyday health. If you haven't listened to Part 1, I would recommend that you go back and give it a listen. We do get into a lot of the more nitty-gritty science of Chris's work and its connection to serotonin antidepressants. And we are going to do a little bit more of that here before getting into more practical strategies and how we can take Chris's work and apply it to the day-to-day life of people who are recovering from withdrawal and psychiatric drugs. So, Chris, thank you for taking the time to come back and talk with me. Thank you for having me. All right, we're just going to jump right into it because last time we were talking, we ran out of time just as we started to talk about the Sigma 1 receptor. And the reason why this is important is because when it comes to antidepressants, we spend a lot of time talking about serotonin and serotonin receptors and serotonin system. But you have hypothesized that another receptor called the Sigma 1 receptor is quite involved when it comes to antidepressants and it may help explain a little bit of why withdrawal can be so difficult for some people. So, if you wouldn't mind explaining a little bit about what the Sigma 1 receptor is and why it matters in this context, I really appreciate it. The Sigma 1 receptor is still poorly understood in terms of its overall function, but we at least know that it appears to be involved in the stress response because it is necessary for the response to cortisol. And so, we can at least say that it sounds like something that should be activated cyclically and rhythmically, although irregularly, according to how stresses go up and down in a person's life. Now, we can look at what its function is in a number of different angles. So, for example, if you just knock it out in mice, meaning you delete the gene for it so they don't possess a Sigma 1 receptor, they have a pretty interesting response. So, on the one hand, they are less likely to despair when put into restraint stress. So, they're less likely to give up, and they seem to fight back more effectively. But, on the other hand, they seem to have, you know, other signs of a disregulated stress response. So, for example, they are more likely to be depressed, and they have a more chronically activated hypothalamic pituitary adrenal axis. These are big words for our audience. Can you come that down for me, especially? So, okay. So, cortisol, you could think of as your main stress hormone, and it is considered a glucocorticoid, because it's made in the adrenal cortex, which is part of the adrenal gland, and gluco, because its main purpose throughout the body is to increase the amount of blood sugar you have, so that you can drive more fuel to feed your brain during acute stress. And so, if the signal one receptor is involved in the response to cortisol, or the response to stress, that would explain why if animals don't have it, they have a more chronically elevated stress response, because their cells are not responding to the stress hormones, so they're trying to compensate for that by making more stress hormones, and whether that leads to them being in a more stressed state or not, it's kind of unclear what that means, but it looks like they have various personality-like changes, some of which are good, but which are largely irregular and negative. But anyway, so this simplest high-level way to explain that is that the signal one receptor is essential to the stress response. You want it to be intermittently activated by signals that are natural to the stress response. You don't want it chronically activated, and you don't want it chronically underactivated either. Now, if you look molecularly and cellularly, what is it doing inside the cell? What is it trying to do? It appears to do a whole host of things that are natural to certain types of cellular stress, so one of the things it does is it improves mitochondrial energy production in general, and that makes sense because when you're under stress, your body perceives that there's an acute need to use energy quickly to fulfill the demands of the flight response. However, another thing it does is it helps the cell in a very similar way to how I described serotonin in the last podcast that we did. It helps the cell respond to oxygen, a relative deficit of oxygen. So it's activating something that's poorly understood in the mitochondria that is allowing the mitochondria to do what it usually does with oxygen when there's not enough available. And in that sense, it shares a lot with serotonin. When you take SSRIs, you get too much extracellular serotonin. You block the ability to transport inside the cell. So those responses are really going haywire on SSRIs. When your body is perceiving that you have less oxygen than you need in the moment, more serotonin is released. Serotonin helps the mitochondria adapt to that state and helps them rise to the occasion and helps distribute oxygen to them. And so, Signal 1 Receptor is doing something very similar to that. Part of that might actually be by increasing the amount of interest cellular serotonin, both by increasing the synthesis of serotonin and also by increasing the transport of serotonin. So the cell has two ways of getting serotonin inside of it. One is to transport it from outside the cell to inside the cell, which is blocked by SSRIs. And the other is to make new serotonin from the amino acid tryptophan, which comes from the dietary protein that you eat inside the cell. So there's two ways for serotonin to get inside the cell. It has to be inside the cell to have the full spectrum of its beneficial effects on mitochondrial function. Signal 1 Receptor is at least in part acting by making more of the serotonin transportor, although that's blocked by the SSRIs and also making more new synthesis of serotonin inside the cell. And that's at least part of why it's playing a role in helping mitochondria respond to the oxygen deficit. Now, as to what is supposed to bind to the signal 1 Receptor, there's been a search for the endogenous ligand. The ligand is something that binds to something. And endogenous means, you know, not a drug, but something that normally exists in your body without you having to put it there. And there's a there's a bunch of candidates, but no one really knows exactly what is usually the thing that binds to the signal 1 Receptor. Now, we know that SSRIs go inside the cell after they block serotonin from getting into the cell, they go into the cell instead. And once they're there, some of them activate the signal 1 Receptor quite strongly and others don't. So there's a 52 fold variation between the different SSRIs. And so I think that is a big part of what causes heterogeneity, meaning variation, not everyone's the same between people's different experiences in SSRIs continuation, as well as what works to help different people. And I think that's also why the animal experiments on what do SSRIs do to brain serotonin levels is so discrepant. I mentioned this last time, but, you know, people who make claims about what SSRIs do to brain serotonin are not, they don't have good evidence at their disposal. So there's there it's it's just unfathomable to me that there's only a handful of animal studies that even address this topic and they find opposite results between them. I think the reason that the animal experiments conflict is because they're done with different SSRIs and the effects of different SSRIs on brain serotonin are different. And that's why I think that's one of the reasons why I think that the the field, I mean, they're not exactly if there's a field actually researching SSRI discontinuations at drop, but the people that have published some papers on animal experiments that they've done are just making the assumption that the SSRIs all do some same thing to brain serotonin and they will just use different SSRIs interchangeably in different animal experiments and they get different results so they can't explain the details of what they're seeing because they're not recognizing that these two SSRIs are doing totally different things doing the opposite thing to brain serotonin syndrome as a huge problem because all the hypotheses to try to deal with it are conceptualizing it as if it's rebound effects from removing the impact on brain serotonin, but they don't do the same thing to brain serotonin. And so I don't think the I don't think the rebounding of serotonin or secondary neurotransmitter systems acting on the levers of personality and cognition, I don't think that's where the answers lie. Part of the reason is just the massive differences between the different SSRIs and how they impact those systems. Psychiatry is all about emotions and mood and, you know, acting in ways that are unpleasant to society. And so I think a lot of the withdrawal world, even in the language that patients use, is just all about how you're feeling. And what I'm gathering from your work is that I think it would be really interesting if we started maybe focusing less on the emotion and more on the physical, physical side effects, physical symptoms because I've really seen in the hundreds of folks I've talked to at this point over the years, kind of clusters of different kinds of symptoms that tend to affect people. And I think if we almost started looking at it from that perspective, we might start to see patterns that might reflect on everything you're talking about. It's interesting that you bring that up. And another kind of what I suspect as a false lead is to make arguments about the half-lifes of the different drugs and try to explain them based on the rates of discontinuation. And I thought what was interesting about one of the, or probably the only major investigation of brainzaps was that the drugs that had a longer half-life just caused a proportionally longer number of days to onset of the brainzaps, but they didn't have any impact on the incidence of brainzaps. So I thought that was interesting. I do think that symptoms are often important clues to things, but I also think that symptoms can be incredibly misleading in terms of trying to signal something about the underlying pathology. And I do think that most people and most doctors generally put too much emphasis on analyzing symptoms to the detriment of them figuring out what they are. If your primary problem is an energetic deficit, then whatever that's going to manifest in is going to be your weakest links that have nothing to do with energy metabolism. So for example, if I have some kind of latent vulnerability because of my genetics or my nutritional history or my trauma history or whatever goes into who I am today, if I have some kind of latent predisposition to dizziness, in an energetic deficit, I'm going to be more likely to get dizzy. But if I have some kind of predisposition to muscle pain, in an energetic deficit, I'm going to experience muscle pain. And if I have a genetic, genetic, or not just genetic, but if I have a predisposition to anxiety, in an energetic deficit, I'm going to get anxiety. And so I, I don't at all want to throw out symptoms as guidelines or as rules of thumb or as potential clues to what's going on. But I do think it's important not to get stuck in overemphasizing them because you could have heterogeneic or highly variable manifestations of something. But you could have a very homogenous or, you know, very sort of universal underlying feature of what's driving all of it. So the fact that one person got brain zaps and, you know, not restlessness and another person got restlessness and not brain zaps, it's not, I don't think that's telling you that those two people are suffering from two totally different things. And I think that's why we just, we need a ton of research on this because I think what we're going to find is that there's going to be some common themes of how the underlying metabolism is dysregulated. But the most universal thing is going to be that the underlying metabolism is dysregulated. That's really interesting because again, if we look at the physical versus mental and emotional side of this, when it comes to the mental and emotional side, often people, often it seems to reveal the weak link or just the old issues, whatever the reason why someone was medicated. In the first place, those things tend to come roaring back and withdrawal. And it's like it just puts a magnifying glass on it. And it never really occurred to me that that could be happening from a physical standpoint to where we are sort of revealing the weak link. If you want to call it that or where a person's most likely to, if their body's most likely to struggle, it could reveal that too. But this makes a lot of sense to me when we're talking about full body, full cellular chaos, basically. I think that this is not a fruitful place to make progress with people who are skeptical from the medical establishment because they're going to say, well, yeah, of course it's returning because you took them off the medication that was helping them. The way I look at it is I say, well, yeah, because you had an energetic problem in the first place, that's why that predisposition manifested into what it was. And we could go back to stuff I mentioned the last episode, like why is depression threefold higher at high levels of high altitude? Why is it, you know, why are people with insomnia twice getting twice the risk of having depression in the future? And I think those things come down to energetic deficit is driving the predisposition. So you can convince me about that, but for sure to do the research that's going to convince the establishment, we really need to focus on the things that are obviously not a return of the original thing the person was medicated for. And I think that's why the science on this is so compelling is because there is so many, there are so many things to point to that are obviously not a return of depression. When you started talking about the sigma-1 receptor, I started digging around a little bit too. And one of the more fascinating things that I came up with was the sigma-1 receptor and its connection to neurodegenerative diseases, like ALS or Parkinson's. And so the reason why I'm asking this and we're really going into the world of theory hypothesis and just brainstorming here, which I cannot overstress enough because neither you nor I are medical doctors and I don't even have a master's degree. So let's start there. But when we're talking about symptoms that show up that didn't exist before, right? One of the most devastating and difficult for people to endure is acathesia. And acathesia, when it's more serious, can look a lot like Parkinson's or something where there's this shaking, there's this, there's this, there's this tremoring. And I just couldn't help but wonder if maybe there's some connection between SSRIs activating or not activating sigma-1 interfering with it. Let's put it that way. And then withdrawal, people having acathesia. I just thought it was very interesting even though obviously the pathology of acathesia is not the same as Parkinson's or ALS or whatnot. Well, I think Parkinson's is really easy to make a super clean story about ALS is I think a little sloppier. But in in animals, the one of the primary Parkinson's models is to just give them the fish boys and rotonone, which is a specific inhibitor of complex one of the mitochondrial respiratory chain. If the mitochondria, the powerhouse, the cell, the respiratory chain is the engine cylinders and they drive the production of energy and they're named after their different complexes. And so if you look at the sigma-1 receptor, one of the primary, one of the most specific things it does in the mitochondria is it activates complex one. So it does the opposite of rotonone. So I think you could make an argument there. I do think that the actual pathology of Parkinson's is not so simple. But if you just look at those couple of things, it looks like the main driver of Parkinson's is how inhibited or activated or complex one is. Parkinson's is a great example of how you should think of your total energy production as if the majority of it is just used to produce stuff and maintain repair stuff. But the last 10 or 20% of the energy you produce is used to control the distribution of all the rest of the energy. I guess what I'm saying is that Parkinson's and acathesia and anxiety are all manifestations of not distributing your energy in a productive way. And they're just variants on that theme. And if we go beyond this enormous significance of complex one of the mitochondrial respiratory chain for Parkinson's and just look at what is the main theory about how it happens in the first place. It's a degeneration of the dopamine based neurons in the basal ganglia that are controlling movement. But what do they control about movement? Dopamine in the basal ganglia is signaling a subconscious calculation of value of investing energy in something. It's like, you know, you anxieties over here and Parkinson's over here and acathesia is kind of in here somewhere. But it's just another manifestation of not controlling where that energy is going. Anyway, in terms of the sigma one activation, I think that that might indicate that there's a specific complex one relevance kind of like there is for Parkinson's. I think a lot more research is going to have to be done on that. But I definitely think that dysregulation of the sigma one system should be highly suspect for discontinuation problems from SSRIs, especially if they if you're if what you're withdrawing from is a powerful sigma one activator. That's all the more reason to suspect it in that case. Can you just quickly list the more powerful sigma one activators versus the ones that don't do all that much just quickly for the audience. So there's a 52 fold variation between them. And you could generally say that peroxetine is trivial. Sitalopram and esketalopram are kind of weak. Fluoxetine is in the middle and fluvoxamine and sirtulin are the high the powerful activators. Sirtulin is a incredible gray area because there are some studies where they looked at models of what does sirtulin versus fluvoxamine do. And even though they're both powerful regulators of the sigma one receptor in some end points that are thought to be sigma one related, they do opposite things. And that might indicate that sirtulin is actually a very powerful inhibitor of it. We're very much into the gray area when trying to separate fluvoxamine from sirtulin. But you can at least say that, for example, peroxetine, super weak, probably not relevant. Sitalopram and esketalopram, pretty weak, probably not relevant. And then for the the other ones, I think you could you could posit some relevance. Great. Thank you. I think, you know, if nothing else, I think what this does is that it just proves how much more complicated this all is than even most doctors understand. And anytime I can make a doctor start to question things I like it. So it's what I asked. Well, I don't think almost anyone who's prescribing SSRI has even has heard of this sigma one receptor. So let's move on a little bit. I want to again, let's try and focus on more practical things that folks can do for the last 25 minutes or so of our time together. One of the things we talked about in part one was that at any point certain cells in our body can be in a hypoxic state, which means they don't have enough oxygen. And that there's a correlation between high altitude, which means there's less oxygen in the air and depression. And so that starts to make me wonder about breathing exercises and could breath work in some way or some sort of hypoxic training, perhaps be beneficial to folks who are in withdrawal. Well, let me just say at the outset that I'm sure you've covered this with other guests, but I do think the extended parabolic taper should be the kind of basal, how am I going to get off this with with minimal problems? But but that said, I do think that everyone should practice breathing exercises because almost none of us breathe that well. James Nester has a great book, breathe that covers all kinds of breathing exercises. So first of all, you should exhale fully. And in general, that means it should take like six to six and a half seconds to exhale. And then you should inhale fully, which should take a similar amount of time. And none of us are going to breathe like this all the time. But if you set aside 10 or 20 minutes a day where you are paying attention to your breath, these are some things that you could try to pay attention to. And then you build better habits as time goes on. And then I do think that you should be trying to utilize your entire chest cavity in a three-dimensional structure without letting your belly hang out and without and while also maintaining your shoulders relaxed. But you should be able, for example, to breathe into your upper back, your middle back, you should be able to lower your diaphragm to breathe into your deep belly. And most of us are missing something like that. Like for me, it's super easy for me to breathe with my gut hanging out. And it's, if I try to breathe into my upper or especially my upper back, but into my mid back too, I just get this incredibly powerful stretch. So I do 50 deep breaths every morning to try to work on that. Although for me, it's less about trying to manage a health problem and more about trying to restructure my body. But I think most people are missing some of the big things that they should, low-hanging fruit they should be doing for their health. And everyone should be doing those things before they're trying to work on idiosyncratic stuff. And I do have an article on my website, what everyone should be doing for their health. And so there's a checklist there. But, you know, but breathing through your nose and breathing fully is one of the items on that checklist. I don't know if it's, if it has specific relevance to SSRI stuff, but it is, it has energetic relevance to everyone. And so therefore, everyone should be doing it. And I'm sure most people who are suffering from SSRI just get deduations that are we're not doing it. And then hypoxic stress is a flip side of that coin. So training yourself to be more hypoxia tolerant. I, you know, I'm very bullish on this, even though the only thing that shows that it helps with depression was the animal study that shows that it's 20 times more, 25 times more robust than antidepressants. I think that's a big signal. And I think when you look at the fact that depression is so strongly correlated to altitude, I think that's a big signal and just a role of serotonin in handling hypoxia. I think those are all big signals that we need some type of hypoxic stress. In the new year, I'm going to be doing some biochemistry experiments on myself. I'm going to be looking at, in fact, I'm going to take the mydome test and I'm going to retest that various intervals spending different times in the mountains. But I'm also going to be running a bunch of blood tests on hypoxia response and hormonal changes. And I'm very interested in the idea that we can take the randomized controlled trials that have been done in athletes showing increases into testosterone that we can use that as kind of a dosing amount for how much hypoxia is good in general for people. And in those studies, they got the max benefit from doing 10 to 12 hours a night for three nights a week and continuing it indefinitely. I'm really hoping that you can condense those 36 hours a week into five days in the mountains per month. If this is true, if I can show this is true in the study, I think I think we could, you know, do we could use it in the corporate world to leverage some, you know, universal five days in the mountains for the five day retreat once a month. But anyway, there's a lot to know about this, but they're, first of all, if you do live at altitude, you probably are not getting enough oxygen. So the deep breathing thing, go to an oxygen bar, get an oxygen machine, take a vacation somewhere that's at sea level, see if any of those things help. But if you're at sea level in your depressed, you might need more hypoxic stress training. And I know this, people are so confused. They need to listen to this like 15 times to get this. Hypoxia is always relevant to everyone. In every breath you take, when you get up in the morning, when you exercise, it's not something that's conditional on you living at altitude, we're having a lung disease or being strangled or drowned. And you know, every time I say something about hypoxia, there are, I get so many people that are misunderstanding what I'm saying. If you live at sea level, you probably are not getting enough hypoxic stress. If you live at altitude, you're probably getting too much. And both of those things play a role in energetic dysfunctions that could contribute to depression or to problems getting off SSRIs. And trying to get into the happy medium, the middle ground that seems to be associated with maximal health is something like 80% of your time at sea level and 20% of your time at 6500 feet. Obviously to say that everyone needs to do that is a little crazy. So to figure out exactly how to apply that to everyone, we're going to need a ton more research. But it's something you can play around with. When I was in withdrawal and I was recovering, I started getting in a lot into the breathwork world through XPT, which is extreme performance training with Laird Hamilton and Gabby Reese. And then I also came across Patrick McCown's book, The Oxygen Advantage. And I was doing some private work as well. And what I realized through all of that is that if you start doing some basic breathwork protocols with people, they kind of tell you where their issue is. If they can't breathe through their nose and take a walk, they're probably pretty CO2 intolerant and definitely would benefit from some hypoxic training. Or they just never go for walks. Or they just never go through walks. And then you can go the other direction too. There are people who you ask them to try and slow down their breathing and they get really uncomfortable. And so you can kind of tell if you start working on it a little bit, but I did want to mention the Oxygen Advantage because it's a fantastic book from a protocol standpoint of things you can do at home just to learn. Whereas breath is a really damn good story with a lot of great information. It's a really entertaining read as well as being just filled with incredible information about breathing. It does have an appendix with a bunch of different breathing exercises in it. Let's move a little bit more into nutrition. I would want to caution on any sort of blanket supplementation recommendations because a lot of times people in withdrawal are hypersensitive to supplements. And so what I'm curious about is from your nutritional background. Let's go back to the low hanging fruit thing. Like what should people be eating to support their mitochondrial health and therefore hopefully help them through withdrawal? I believe in a food first pharma last approach. And the food first part of that doesn't just mean food before pharma. It also means food before supplements. Supplements are meant to supplement a good diet not not stand in the place of one. And most supplements are dosed way too high. And they're dosed way too high for two reasons. One is that there's a widespread belief that taking more vitamins than you need just gives you expensive urine meaning you paid for the supplement and you just peed it out. That's total nonsense. Supplementing with high doses of a vitamin can cause some pretty massive problems from imbalancing with other nutrients. And you're not maybe not going to wind up with toxicity but you might wind up with you know high blood glucose or anxiety or jitters or sleeplessness or whatever. And so I generally advocate if you have a specific need to increase riboflavin for example. I would do a very slow titration up with riboflavin rich foods which are things like liver, heart, kidney to a lesser extent milk, red meat and salmon. And then microdose the riboflavin and go up at six milligrams at a time. And there's two ways to microdose supplements. One is to see if there's a liquid version on Amazon in which case the dose is probably measured as the whole dropper. And you can get 140 of it by using a drop providing you don't have any digestive problems with whatever it's dissolved in which is usually glycerin. And then the other is to empty out capsules. You can get a milligram scale if you want to be precise so you can you know there's various ways to do that. I think that even people who think that they that there's nothing no negative effect to a supplement they're taking. Often there isn't any negative effect over the first one month, but you know seven to twelve months down the road you've become like just massively imbalanced in your nutritional profile. So I actually I've come to the belief that most people should just act like they're very sensitive to nutritional supplements. And they're you know it might seem like real overkill in the short term. But over a one to three year time horizon you're going to be so happy that you didn't wind up on some bag full of things that were you know giving you 37 imbalances and trying to figure out what what they were on the back end of that. In terms of you know the mitochondria depend on all the nutrients and the easiest ways to get all your nutrients in are to work in a small handful of major super foods and then follow some basic benchmarks for the rest of the diet. So I would say to the extent you eat animals try to eat nose to tail which means try to eat all the organs try to eat the bones but at least work in liver and bone broth and if you have to you know if you're looking for the next organ meat to work in I would say heart. But you would be surprised at a lot of people are you know pinching their nose right now but you would be surprised if you blend in a bunch of organs into ground beef. Yeah you don't even notice it. And yeah so there are there's various companies like US Wellness, North Star Bison, white oak pear pastures is a bunch of different ones where they produce a organ blend that you can just buy as ground product you just cook it with taco seasoning or something into crumbles and put in a taco and you're not not even know the difference. I think nutritional yeast a lot of nutritional yeast is fortified with vitamins but sorry nutritional yeast is one example of an unfortified nutritional yeast where it is naturally very high in B vitamins but not anywhere near as high as the supplements you get on the market and then oysters would be a would be the you know one or two oysters a day could be a nutritional miracle for a lot of people and then just more broadly I think you want to eat most of your food not at restaurants eat mostly unrefined foods not junk food try to diversify across the proteins that you tolerate try to diversify across the carbohydrates that you tolerate so for example don't eat all your carbs as bread try to work in legumes like lentils peas and beans try to work in tubers such as potatoes diversification is a great protection against ignorance you don't have to eat a diversified diet but if you don't want to develop an expertise in nutrition and you don't want to do dietary vitamin and mineral tracking although I recommend people do at least for a few representative days chronometers great out for that if you have an allergy or an ethical restriction or whatever you know put a box around that but otherwise try to be it try to diversify your nutritional portfolio make sure you're eating foods that you digest eat things that help your digestion with every meal like fermented foods or ginger or bitters and you know things like that um make sure you're getting some fresh minimally cooked or raw fruits and vegetables strawberries and bell peppers are really great examples of where you can get enough vitamin C from um and then that's going to take care of most things salt your food to taste is going to take care of the salt probably the one thing you need to think about after that is calcium and you should have three servings of a calcium rich food that could be dairy or it could be bones but if you're doing just plants you have to be pretty selective uh so bok choy and napa cabbage are pretty good sources of calcium but when you get into like broccoli and kale those are your top greens for the typical American grocery store but even those you need to eat a lot of that to get enough calcium so I do think that the but it's so much easier to get your calcium in if you're doing either dairy or bones you do when you're doing bones you do want to look for a clean source because uh bones can be contaminated with lead so do you know opt for pasture based when you can if you're using a bone meal powder try to get a uh you know one that has a certificate of analysis showing it's lead-free um things like that but I think those cover the nutritional bases for most people and is an excellent starting place if people aren't there yet all right I have one more question for you just based on everything I've learned about your work and talking you over these past couple episodes uh what would you say to child psychiatrists who are putting kids on antidepressants well I would I would say something to psychiatrist in general first so there was a randomized controlled trial uh a few years ago that randomized psychiatrists to either answer the question um what would you do for yourself if you were depressed what what what what what should I do if I'm depressed and what would you do if you were me and 80% of the psychiatrist said that they would put the patient on an antidepressant but only 40% of psychiatrists said that they would put themselves on an antidepressant but 80% of the psychiatrist told the patient that if they were them they would go on an antidepressant I think the most generous way to interpret that is that the psychiatrist is thinking in their head I can handle depression without a drug but you can't so if I were you I would be like you unable to handle depression without a drug so therefore I'm going to tell you that if I were you I would take the antidepressant there are more cynical interpretations than that but I think that says that there's a huge problem in psychiatry of not having confidence in their patients but anyway in terms of the the children I mean uh if you don't know what SSRI's are doing at the molecular and cellular level which I know you don't um you shouldn't be putting them in kids you know because that's uh we have no idea what that does the process of development but in a well-formed adult you can be wrong about something and you can you have a much better chance of erasing the error um you have a much less chance of erasing the error when you when you make a big mistake in a kid so I I think that um in general we need way more metabolic study of what these things are doing on the whole I don't think most people who are prescribed them should take them but I think that it's you know a worse malfeasance to be putting kids on them yeah I agree I mean I'm having been in kid who was putting on them I'm constantly trying to untangle what of this was my development being interrupted and the more I learn about how they're affecting ourselves and not star emotions it's just like infuriating to me that this is this is continuing all right Chris thank you so much do you have any final uh things for our audience and where can they find you I've written an um uh an incredible volume of stuff about this so go to chrismasterjohnph.substack.com and put an SSRI and um or just put in prozac is in performance enhancing drug that's the beginning of the series and then you can just click the bottom of it and read the whole thing um and the mitochondrial testing I have is that mighto.me and um look forward to to seeing people on both thank you so much for having me thank you thank you for listening to the madden america podcast or more news views and updates visit maddenamerica.com