Bruce Bassi#FuturePsychiatryPodcast discusses novel technology and new ideas in the field of mental health. New episodes are released every Monday on YouTube, Apple Podcasts, etc.
Summary
Dr. Paul Putman is a psychiatrist and author of the book, Rational Psychopharmacology. Learn why you should not call illnesses “Treatment Resistant.”
Chapters / Key Moments
00:00 Intro
03:01 How History Informs the Future
06:56 Legalization of MDMA
09:12 Ketamine evidence
13:33 Genetic Testing
15:23 Approval process of medications
19:20 FDA Dose Max
23:07 Side effects not pharmacologically explained
25:48 Long term use of SSRIs
29:16 PSSD
36:46 Supplements Data
42:09 Immunomodulators for depression
43:53 Approach to treatment failure depression?
48:05 What about ECT for treatment failure depression?
54:03 Meta cognition
57:44 How do patients respond when they hear “treatment resistant?”
Transcript
[00:00:00] Paul Putman: The human brain is here to protect, is here to predict the future, to keep us safe. That’s basically what it does. And it doesn’t necessarily give us the right answer all the time. It just gives us a probability. So the more we’re aware of the shortcomings in our own cognitive processes as human beings, the more we can search for the results of those errors, trace them back, undo them, and come back with better answers for our patients.
That’s where my passion is right now. That’s why I’m writing these books, is to encourage us all to look at those processes, to not assume that we’re doing everything the correct way all the time, because we’re not.
[00:00:35] Bruce Bassi: So welcome to the Future Psychiatry podcast. Today we have Dr. Paul Putman, and he is a psychiatrist, an author of the book, Rational Psychopharmacology. Welcome, doctor.
[00:00:48] Paul Putman: Thank you.
[00:00:49] Bruce Bassi: So I love the title of the book, “Rational Psychopharmacology.”
Why did you feel that the profession needed a book on this sort of topic right now? What were you experiencing that was maybe the impetus of the book?
[00:01:04] Paul Putman: I was very fortunate in my training and education to be in the hands of very scholarly and caring clinicians who made sure that I began to assess patients and the data in the field from a scholarly perspective. And so that mentoring paid off very well for me and I hope for my patients.
I practiced over 30 years and over the years I’ve been asked to do second opinions and lectures and review difficult cases. And it’s just appeared to me that while many colleagues also do an excellent scholarly evidence-based job, not everyone else has had the same education. And so, in, in working with my colleagues and pointing out how I came up with different ideas and conclusions than they did it just struck me that it might be helpful to share some of what was passed on to me to the next generation.
So that’s, as I neared the end of my practice years, I thought that this would be a nice way to carry some of that useful information forward.
[00:02:00] Bruce Bassi: What would be a good elevator pitch of a summary of the book, essentially. I read a good portion of it, but I’d like to kind of know from you as an author a little bit about it?
[00:02:10] Paul Putman: The point is to create a meme from the evolutionary biology sense that can be imitated and passed on through the culture of practicing psychiatrists. And the essence of the meme is to be consistent and to be thorough and to be methodical when we evaluate data. When we evaluate our patients, when we think about treatment planning, and when we evaluate the results and effects of our treatment planning.
And so the hope is if I can get everybody to think about all of those three aspects consistency, thoroughness, and and being methodical, asking the exact same questions every time. Even if you think you know the answers, you’ll be surprised. The 50th time they say yes instead of no. If you can be consistent and you can be thorough, I think you’re going to find more solutions for your patients than if you’re making shortcuts.
[00:03:01] How History Informs the Future
[00:03:01] Bruce Bassi: And so you are very well versed in psychopharmacology the history of it, how it’s evolved over time. And one thing I find is really important is understanding from our past certain mistakes that have been made, how how things have progressed in psychopharmacology. And I think that can also inform us about where we’re going in the future.
And keeping with the theme of the podcast you know, talking about new and novel innovative ideas what is it about the prior history of psychopharmacology that can maybe inform us about where we might be going in the future?
[00:03:35] Paul Putman: That’s an excellent question. Thank you for asking it. You know, and a good example right now is with psilocybin coming back and talking about using hallucinogens in treatment. This is not. The first time this has come up. This is about the third time in my practice, that this has come up. We’ve been here before.
[00:03:50] Bruce Bassi: Really? I didn’t know that.
[00:03:51] Paul Putman: Yes. I’m finding that out from others. It, we, it was very of course people were very interested in the sixties and early seventies, and then in the eighties it came back as an aid to psychotherapy, and now it’s back again. And I’m not saying that we shouldn’t be investigating it, we should be investigating it.
We should be gathering data, but we shouldn’t be jumping to conclusions. And certainly, as you said, it’s not a new thing. When I was writing this book, rational psychopharmacology I talked a lot about process, how we think the metacognition, because that’s so important. Think about how you’re thinking in order to cut down on the errors that you might be making. And then I got to the point where do I include the medications themselves or do I not include the medications because this is not drug, you know, drug facts and comparisons where every fact you need to know about a medicine is in there. And as you were saying, I thought that the most important way to approach it would be historically.
I think it’s very important for practitioners to know where we’ve been so that we don’t repeat the past or we stumble along blindly. It really is important to know where antidepressants came from that antidepressants had to prove there as good as ECT in order to be approved. What were the different kinds of convulsive therapies, not just electroconvulsive therapy?
I think you’ve got to know the entire history so that when somebody says, here’s this brand new drug that affects one little ligand on the receptor site We don’t have any data on it, but theoretically it should be great. I think you should, you know, be very suspect. You should have an understanding of history to know, is this a me too drug?
Is this nothing like anything we’ve had before? Where does this fit? How interested am I in this new option? So I think you make a much better choice for your patients and can explain things to patients much better if you’re using the historical perspective.
[00:05:43] Bruce Bassi: One thing I heard over and over in your book is a call to prescribe in a cautious, judicious manner considering the evidence basis for medications and what’s out there for them. And I find often, you know, a lot of clinicians, myself included, we don’t have like that much time to, I do have a CME course that I go through.
But to evaluate all the studies out there is pretty time consuming. Obviously, you know, need to know the basics and this, the industry moves so quickly too, that there’s just so much time in the day to, to evaluate all the studies out there. And you know, I think the society and the public they want a treatment, they want an option and they’d rather have psilocybin available to them or some other sort of psychedelic medication option available.
And even without all of the data there, you look at marijuana, you know, marijuana is legalized before it’s even legally available for research purposes. So that’s kind of like the epitome of this push to move forward with treatments even before we have data on it.
[00:06:55] Paul Putman: Yes, very much.
[00:06:56] Legalization of MDMA
[00:06:56] Bruce Bassi: So what is your perspective on coming legalization of MDMA most likely?
[00:07:03] Paul Putman: Well, MDMA was actually the drug that was being touted as therapeutic in the late eighties. Many psychotherapists were using it and, recommending that that it be the patients be taking it. Even though we could prescribe. And that there was a little bit, a handful of research in the late eighties about that, and then it largely fizzled mostly because of toxicity issues.
And then here we have it again. Granted we’re all busy and you can’t read every. Well, you can’t read every paper. Of course, it’s more useful once you have a patient to go and do focused research for that patient. But you can’t just read everything every day and know everything you need to know at your fingertips.
There are increasing number of resources like the Cochrane reviews where I think that’s very useful resource. I mentioned that in the book that they’ll do really good meta-analysis, the best meta-analysis that can be done and publish for free readily available on the internet.
All you have to do is use your favorite search engine and put in the topic and you’ll probably get a Cochrane review to come up. I think that’s an excellent data. They are very conservative, but very fair and I think that’s the kind of resources that I think can be very helpful for us and keep us focused on outcome studies rather than theories. I think we make a lot of errors when we just start talking theory and we don’t look at the outcome data
[00:08:21] Bruce Bassi: Keeping on the topic of psychedelics, I want to ask one follow up question about ketamine. In your book you mentioned the FDA mandated that it be given in the office by practitioner who must then monitor the patient for two hours after administration the patient may not take the medication and at home given concerns about abuse.
And I, I think there are startups that have found ways around that somehow, and I don’t know if it has something to do with the covid health emergency.
[00:08:48] Paul Putman: Preceded that, unfortunately. Like I say in the book, I, and there might be this enthusiastic zeal to help everybody as rapidly as possible. I certainly understand that. I’m sure that there’s some people who see a business opportunity in it the same way many of these clinics don’t involve psychiatric evaluation.
And so my guess is that they’re just ignoring the recommendations more than actually a legitimate way around them.
[00:09:12] Ketamine evidence
[00:09:12] Bruce Bassi: What is your thought on using ketamine? What’s your approach? Have you ever referred a patient to getting ketamine?
[00:09:17] Paul Putman: I haven’t yet, and the reasons I think it’s a very valuable research tool and I support it for research in terms of individual therapy. I don’t think it’s there yet in terms of safety or efficacy. I mean, yes, we can get an IV injection, I mean, I’m sorry IV infusion and have four hours of relief.
The question is, what are we going to do then? And that hasn’t been worked out yet. And some of the other similar agents that were on its heels have not fared well during phase two and phase three studies. So I think it’s an interesting research tool, but I don’t think it’s necessary.
The book, I’m just about to finish now is on treatment, the concept of treatment resistance. And, and I challenge the concept of treatment resistance. Treatment resistance used to be referred to used to refer to the treatment itself. Is this treatment effective or is this treatment refractory for that treatment?
Now we’ve turned it into an entity that this patient possesses a treatment resistant entity. And I really think that’s a cognitive conceptual error. I think it, the answer is you keep going until you get the right answer. We make lots of conceptual errors. Even as the brightest and best trained and best intention psychiatrists, we still make conceptual and cognitive errors.
If we can learn to minimize those to catch ourselves and reconceptualize, I think most of the time we’re not going to wind up with treatment resistant cases. So therefore leaping to a treatment that has many questionable elements just because we think that person might be treatment resistant, I think is premature.
[00:10:51] Bruce Bassi: The first time I ever heard of the word or phrase treatment resistant depression was to get t m s approved, and that was before I was even a medical student. I was working in a TMS lab, and I needed to know the definition of that by the FDA because the insurance companies then adopt the rules of the FDA to set their approvals process for TMS specifically, which was very expensive and still is very expensive. What do you think is the downstream implication of using that terminology to the patient and to the clinician? When we call somebody treatment resistant?
[00:11:27] Paul Putman: Oh yes. Like I’m just, like I said, I’ve been writing another book on that very topic for the last year to finish. So thank you for asking. You know, it’s funny because TMS is, to me the poster child of this entire issue, if is no standardized definition of treatment resistance for any diagnoses or any patient, every diagnoses has more commonly used definitions, but they’re never standardized.
And far TMS has the weakest TMS was approved for failure of one treatment. So if you didn’t respond to your first treatment and there’s nobody over viewing looking over the quality of that treatment.
[00:12:05] Bruce Bassi: Right.
[00:12:05] Paul Putman: you decide that it didn’t work, whereas hoping you did it correctly and that the patient actually took the medicine that that then you’re indicated to use tms.
It’s just a very watered down, meaningless term. It’s a conceptual error in my opinion. I think we ought to be calling it treatment failure. You have a treatment failure until you get treatment success and when you get a treatment failure, you need to back up, relook at the problem, reexamine your diagnosis, re-examine all your assumptions, make sure the patient understood what you were asking, that your information is the best it can be. Make sure that they understand what you’re asking of them and that they’re putting into place the way you need them to. And ask more and more questions. Gather more and more data until you get the right answer.
There’s just one of the reasons I’m writing this book is because Laura Roberts, who’s the publisher for American Psychiatric Association Publishing, when she was discussing Rational Psychopharmacology with me, said, well, do you have any examples of where this is reverse treatment failure failures?
Of course. I and my mentees and my colleagues all have these. She goes, great. Write a book on it. So that’s what I’ve done. I’ve included many clinical examples of how we thought it was one problem, it didn’t work, and it turned out to be another, and we found a solution. So I think
if just, instead of labeling something, “Treatment resistant,” which has no diagnostic or therapeutic value whatsoever.
just say it’s a treatment failure. We haven’t found the right solution yet, and we’re going to keep looking until we get there.
[00:13:33] Genetic Testing
[00:13:33] Bruce Bassi: Right, right. Yeah. In terms of cognitive distortions regarding a particular phrase, I noticed that when we talk about genetic testing my patients are always really hopeful that they’re going to unveil the holy grail of what they need for treatment. And there’s this disparity there between the way clinicians conceptualize genetic testing and what patients maybe understand from marketing from the those companies, marketing and advertisement.
What is your thoughts on genetic testing? How do you use it in your clinical practice?
[00:14:10] Paul Putman: Well, I usually don’t ask patients to purchase it because it’s terribly expensive and I don’t find it very helpful. There is a very small subchapter in rational psychopharmacology that addresses this basically, It can help us decide whether or not side effects are going to be more or less of a problem for some people and some medications, but that’s not what patients, as you said, think they think it’s going to tell you which medicine’s going to work for them.
And we are there. We are not there at all. So I don’t think it’s helpful for to them in that regard. And most of my patients don’t really want to spend upwards of $400 or more just to find out if there’s a 10% less chance of a side effect. We’re going to be discussing all the side effects anyway, and I just don’t ask them to do that.
Patients will often come to me very proud, proudly with the data that they went purchased for themselves, and we’ll go over it and we’ll read it and we’ll use it, but they’re often very disappointed in the data that it actually provides for us that we can use in treatment.
[00:15:05] Bruce Bassi: How far off do you think are we until we can get efficacy data from genetics?
[00:15:09] Paul Putman: Well, I wouldn’t say I’m the world expert on that, but I know Charlie Nimeroff recently talked about that and he thinks we’re significantly off to where we don’t need to be holding our breath just right now, it’ll be decades I think.
[00:15:23] Approval process of medications
[00:15:23] Bruce Bassi: I want to go back to the approval process with medications. You know, I was giving a lecture on the placebo effect because I was talking to some therapists recently about pharmacology what I would want a therapist to know.
And we were talking about the placebo effect and I was researching it. And one of the individuals who does a lot of studies on the placebo effect mentioned the studies that show no difference or no benefit com of the medication compared to placebo just don’t get submitted to the fda.
So they’re selecting out the studies that were of no efficacy of no significance. And I actually didn’t know that as a practicing clinician. and I feel like that’s super misleading. I feel like there should be a requirement there for people to submit all studies that makes sense on the medication that they’re going to approve, that we should know everything about it.
No?
[00:16:13] Paul Putman: Yes, absolutely.
[00:16:14] Bruce Bassi: What is your, how can we, can you kind of thought, walk me through your thought process of the fda approval process, weaknesses, and how it could be potentially approved, improved?
[00:16:25] Paul Putman: Yes, I’d be happy to. I also mentioned this in rational psychopharmacology and our patients think like, like you did initially, that the FDA is sifting through every bit of data that there is on a medication and then meeting with the top minds to decide based on all the information, what we should be– what they should be recommending about using a medication safely and effectively.
And nothing could be further from the truth. Basically they approve marketing. They don’t approve use of medications, they approve marketing. So a pharmaceutical company has to submit two positive phase two studies in order to have a valid application. And that’s it. You can, as you said, there can be eight phase two studies showing that it doesn’t work. You just need two that show that it does. Now, I’m not disparaging the people on the committees. I’m sure that they’re trying to do a very good job and that they are very knowledgeable and they understand the big picture. But you have to look at the way the actual policies and laws are written and it is possible to work around them, is what I’m saying.
I’m not saying that there won’t be people on the committee who know that there are eight negative studies, who want to send them back for more data, which is usually what happens. Acamprosate is a really good example. If anybody remembers that. It came from the uk, as you know, and the UK approved it based on self-report, patient diaries.
Okay, because it was fairly benign medication and safe, it mainly just caused some diarrhea. And there wasn’t anything else really great to recommend for for substance abuse alcohol use. Our FDA went ahead and said, okay, based on that, we’ll go ahead with the patient’s self-report diary, which isn’t usually up to our current standards.
That’s not a phase two study, but it’s all the data we have, we’ll go ahead and approve it. So things like that do happen. I sometimes I do feel like when the committees meet for the FDA that they don’t read the minutes of the last committee meeting. , sometimes you wonder because there’s a disconnect between the path that they were on and then what they decide.
But you’re right it, you just have to realize what the system is. The system is to get approval for marketing. That’s all it is because as you know, once something is approved by the FDA for the first indication, if we’ve got valid data to show it, we can use it for any indication we want.
We can use it any way we want. And the FDA doesn’t oversee that. They’re trying to get much better at post-marketing surveillance. And I really think in the last half decade to decade, they really have made good progress with that and going back and revising their initial assessments. But for the initial indication, it’s a marketing and all you need are two studies.
So yes, it’s very weak out as far as I’m concerned. It’s much better to do a a meta-analysis of all the available literature or read whatever Cochran did to do that, and you’ll get a much better guidance than you will from FDA indications. I don’t think FDA indications are really terribly useful in clinical practice.
[00:19:20] FDA Dose Max
[00:19:20] Bruce Bassi: Let’s talk about FDA approval dose maxes, the maximum dose theoretically that you can go up to until we don’t know what happens, you know, so most of the studies they do study up till dosage and then they submit it for approval and the FDA obviously can only approve up to that dose max.
And for a medication like escitalopram I’ve always heard that you can get additional benefit beyond the FDA-approved max of 20 milligrams. But when I tried to convince a patient to agree to go up above, beyond that, they ask me what are the potential ramifications? And I say, well, you can die suddenly, not like that. But Torsades, I explain Torsades and the risk of it and the potential for it, and how low of a chance of that it is, and if they, we go into cardiac history and whatnot. But even if it was a 1% chance I feel like because it doesn’t have the stamp of approval from the fda, it’s just very hard to to push those super therapeutic doses, so to speak.
What are your thoughts on the clinical pitfalls from having an FDA-approved max dose?
[00:20:24] Paul Putman: Yes. Good question. Well, I’ve done some of these studies for with and for pharmaceutical companies early in my career and I think it’s common knowledge that they designed the phase two and phase three studies in order to have the least amount of dropout possible and yet still be placebo.
So they’re trying to walk a very fine line. They want people to finish, they want them to have low side effects, and they want them to be placebo. And that’s the goal. Not treating as many people as effectively as possible. They just want to be placebo , so they do set the bar very low. They do not want to have dropouts and so it’s not at all surprising to see what many times with older medications you’d be horrified at what they think the dose range should be, it’s half of what you everybody uses and is well documented in the literature. So again I think it’s, it is perfectly valid and defensible and appropriate to know what the literature says because there will be other studies. There’ll be fixed dose and variable dose studies that you can find. What was the outcome?
What were the toxicities, what were the side effects when we went higher than the FDA recommended dose. A lot of those will be phase three studies. And many of them will be post-marketing studies. And I’m not talking about stray case reports. I’m talking about really well done studies, placebo controlled.
And so you should use that data with your patients and it’s another opportunity for education with your patients about what the FDA ratings really mean. And I just think explaining that to them and lending them help you make the final choice is correct. If they’re still uncomfortable going above that, then maybe you need to investigate a different medication, because if you’re not getting the outcome that you want and you’re feeling like this because you’ve got an unrealistic ceiling on the dose, you’re probably not going to get the outcome that you want.
[00:22:06] Bruce Bassi: So do you sometimes go above that FDA max for certain SSRIs? You do?
[00:22:13] Paul Putman: Yes. If I’ve got valid data backing it up.
I always want to see, published well done study showing me that it is safe and still, and there is some clinical value to going up. A lot of times you’ll see, oh, it’s much safer to go to 40 or 60 milligrams. It’s perfectly safe, but nobody got better when we went above 20 milligrams
Well then there’s no point in that, you know, but if I see that I have a certain response rate at 20, a certain response rate at 40 and a certain response rate at 60, and yet I still have safety for 40 and 60 maybe there is room to consider that. And I never found a whole lot of concern with my patients for doing that, and it might be because we’ve been discussing these kinds of issues all along with many different treatments.
But if you help them understand our perspective of what the FDA’s mission is, what they’re trying to do, and how they try to do it then I think that they’re more than willing to hear your advice.
[00:23:07] Side effects not pharmacologically explained
[00:23:07] Bruce Bassi: When you have a patient who has a side effect that seems antithetical to that medication, how do you describe or explain that to the patient? Say they have weight gain on Abilify or they feel fatigued on Bupropion or they have sexual side effects to bupropion. Things that are, they’re not typically known to cause those or insomnia with Mirtazapine, does the psychopharmacology side of you come out and say, you know, this is extremely unlikely, just try to work through it it might be something else going on. Or do you honor what they say and say, let’s try a different medication option. And it sounds like you had a bad side effect, bad experience with this one.
[00:23:48] Paul Putman: Yeah, and you’re right. I mean, we all have those times where Wellbutrin causes weight gain or, you know, something you’re just not expecting. And like I say, mirtazapine, you know, never adds weight gain or sedation when you want it. , that kind of thing.
So, so yes. Well first I go back and I re I retake the history.
And is there some over-the-counter supplement you’re taking that I don’t know about? Did you change bioavailability because you’re on a new generic brand? I go through all of the things. My, my mantra is nothing quits working for no reason. So, I just like, if something quit working, if there’s an unexpected side effect, I would be taking history.
What else are you taking? invariably somebody has a rash two years into taking a medication. It’s not very likely to be your medication, but everybody always points to the psychotropic drug, you know, you know, my family practitioner thinks it’s this one. Then again, your OBGYN just added an antibiotic, you know, that week, maybe was it.
So I, again, I think you cannot be at a comprehensive, thorough history. So the first thing I would do would be re, you know, repeat the history, ask more and more questions, get as much data that as you possibly can, and then if you’re still, as you see, seeing a side effect that doesn’t make any sense. And if it’s particularly bothersome to the patient and and they would like to give up any potential benefit of the medication because it’s so bothersome, then of course we make a change and try to find another an alternative.
I have had patients many times over the year where it’s a minor side effect, they don’t mind it that much. They might prefer it wasn’t there, but they are so happy with the benefit of the medication, they do not want to change. In fact, one of the vignettes I’m putting in the new book is about that someone with a very serious chronic mental illness that we improve but could never get completely rid of we reached a point where they were so much happier than they thought they would ever get, that they didn’t want to take any risks to go further, even though we had some possible opportunities for that.
But they and their family were delighted. With the significant progress that they’d had, and maybe some people will call that a treatment failure. My patient certainly didn’t.
[00:25:48] Long term use of SSRIs
[00:25:48] Bruce Bassi: Yeah. I want to talk about long-term use of SSRIs. I know there was a study recently that showed that there was a correlation, not causation with all cause an increase in all cause mortality and cardiovascular events when people take SSRIs for more than 10 years. I believe the study was looking at.
If you can give me your thoughts on that and if you’ve had clients who are on medications long-term or have just started them and had concerns about long-term use of SSRIs and how you would explain those findings of a study like that, them wanting to stay on the medication longer.
[00:26:23] Paul Putman: I think an even better example might be the benzodiazepines and dementia that we went through about 10 years ago, and because you’re right, many of the illnesses that we’re helping our patients with are chronic illnesses and we can expect that if medication is a part of your treatment, it’s not going to be surprising that you’re going to be on medications long term.
And so we had to be prepared for what those risks are, and we try to tell them in the first session of discussing treatment what we know about that. And of course, as new data evolves, we’ve got to update them about that and discuss that with them. That being said, I think you have to be particularly careful about these long-term studies because so many of them are observational.
They are not they are not even meta-analysis, they’re not studies. They’re observational and there are lots of limitations to the conclusions that you can draw from it. One of the ones that drove me nuts about the benzodiazepine one was, of course we know that there’s some possibility of cognitive impairment from taking benzodiazepines.
There also is some possibility in anxious patients that their cognition improves. That’s actually one of my old papers. But yes, of course if somebody’s on a benzodiazepine, you might see some measurable cognitive impairment. So it’s very difficult in fact, I have yet to find any good studies that will show you taking apart the acute use and separating it from the chronic use.
There was an observational study in a retirement home in France that came in the British Journal of Psychiatry, for heaven’s sakes, I used to say this must be the Brits way of laughing at the French because it’s such a terrible study. It’s just horrible. I mean, they, you can tell they didn’t control for, of course you can’t control for things in those kinds of studies, but they didn’t acknowledge, they hadn’t control for it, and they didn’t make any distinction between people taking them acutely and people developing dementia years later. And yet they drew the conclusion that because they had taken it at one time in their life, that resulted in people with dementia where they did not show that at all, not even close. And this was one, this was a course of study that got lots of famous press and that was cited by other studies.
And so yes you need to discuss, you need to be thoroughly familiar with those because your patients are going to bring that up. And at times you need bring it up with your patients. You know, you may encounter this because when Aunt Betty says, oh, quit taking that because you’re going to get dementia. They’re not necessarily going to call you before they do that. And of course, stopping a benzodiazepine is dangerous. Stopping an SSRI is going to have side effects and consequences. So I think you need to bring it up as you’re aware of these things so that your patients will continually look to you as their best source of information.
And always tell people, you know, if for heaven’s sake, stay out of chatrooms. But if you ever hear anything that you’re, that doesn’t fit with what we’ve discussed, please discuss it with me first before you change call me. We’ve got to, we’ve got to work through this. We’ll discuss whatever the data is and we’ll go through it together.
And that always, I think is the best.
[00:29:16] PSSD
[00:29:16] Bruce Bassi: Yeah. Speaking of certain side effects, getting a lot of bad press, PSSD is making the rounds lately on social media, post SSRI sexual dysfunction. I did a video on this a couple weeks ago and it was by far the most popular video that I’ve probably done in the last year. And I did not anticipate it.
It is not because of my special productive qualities came out that day. It was because of the topic is one that I think a lot of patients they place a high degree of value on sexual functioning, especially when it comes to psychiatric medications. And notoriously physicians are known to downplay or undervalue sexual functioning and dysfunction from the medications. So I think this is where it hits a nerve among the public, and for the listener, all physicians and most psychiatrists, all psychiatrists will they would admit that there’s potential for sexual side effects from SSRIs.
But the where the medical community diverges from a very vocal group of individuals is where they believe that the sexual dysfunctioning and cognitive flattening persists for more than three months after stopping the SSRI. So most of the time, vast majority of patients the cognitive flattening and sexual dysphoria lack of ability to orgasm, diminished satisfaction and orgasm, that usually returns after stopping the medication. But for some people it can persist long-term. And obviously this is another topic I think that has a lot of confounding variables. You know, sexual history. I mean, it could be related to hormone levels, time of day, your partner, your mood, any other medical illnesses like vascular illnesses. So I don’t know. I’m, I haven’t talked to another psychiatrist about this topic yet. I feel like it’s just on the bursting on the scenes, even though a lot of people have been talking about it for 10 years, it’s finally getting this momentum among the community. What are your thoughts on it all?
[00:31:17] Paul Putman: Well, you know, it’s funny because I almost brought this up as an example earlier in our talk. I have several thoughts on it. One, one is it’s a really good illustration of one, how unique, very good initial data on your patients. You should be finding out if they have sexual dysfunction before you prescribe anything as a baseline. And you should, of course, put that in your notes so you can refer to it later. The other thing is, it talks about is the design of controlled studies.
In the nineties is when this really started to come out. And we’d all gone through the SSRIs in the early nineties. By the late part of that decade and into the next decade, our patients were coming to us and saying, I’m having all this sexual dysfunction.
And we were looking at the data that we had been given from studies showing that there was a very small rate of sexual dysfunction. And again not not erectile dysfunction, but but libido particularly, or as you said, anorgasmia and and we’re just looking at the data and saying I hear you and we’ll try to figure out what the problem is, but I’m looking at the data and the numbers are very small.
Well, what turned out is that in the studies they were not specifically asking patients about sexual dysfunction, and so they were getting maximum of a 6% incidence rate, which if you compare to placebo, probably was a 3%. So you’ve got a 3% measurement, which is a very small chance of a side effect.
So, what we learned is that if you ask patients, are you having any of these particular sexual dysfunctions while they’re on SSRIs, you get about a 25% yes rate. So then it became, in evaluating studies, it became very careful to look at did the manufacturer and the the key investigators include this questioning in their initial data.
And for most of the old data, it wasn’t. And then it became the FDA did start saying, you need to start including these studies these questions in your studies. And then we started to realize that yes, these patients are right. This is a very, you know, a quarter of our patients are having, this is side effects.
Now you’re also correct, we are now viewing these as temporary reversible side effects. Now, I wouldn’t say that anyone has particularly done the exhaustive study to prove that beyond the shadow of a doubt. But nevertheless, there are studies that show that they do go away. I think you’ve got to go back to your basic pharmacology and look at half-lives.
If a patient’s on fluoxetine. We have to remember that the half-life of nor fluoxetine, the primary metabolite is very long. If we’re thinking five half-lifes, it’s going to take at least six weeks to get Prozac out of your system once you’ve been on it for at least six weeks. And so for somebody to say, all right, I stopped my Prozac, and then, you know, two months into this, I’m still having that.
Well, yeah, of course, because it’s still in your body. So I think you’ve got to, you’ve got to take that into account as you’re exploring the possibilities with your patients. And then, as you said, very wisely, it could always be another factor. You can have more than one cause for every problem.
And–
[00:34:14] Bruce Bassi: Mm-hmm.
[00:34:15] Paul Putman: investigating those and considering those as well.
[00:34:17] Bruce Bassi: Yeah. Why? I mean, certain side effects like tardive dyskinesia they can persist long term. Is it possible? We just don’t know everything there is to know about certain side effects from SSRIs.
[00:34:30] Paul Putman: Well, I was hoping that, yeah, that’s what I was illustrating here. We were using them for 10, 15 years and we didn’t realize because of inadequate data collection that yes, this really was a common side effect and one that really distressed our patients. So we did not serve them well in that regard.
And yes, I am certain there are other issues that we’re in, in very well meaning and caring fashion, yet unaware of, and and we always want to listen to our patients because if it had not been for them pushing and pushing back in the mid to late nineties, I don’t know that it would’ve been reinvestigated.
But that really did come from our patients insisting that something was up and we had missed something. And we had.
[00:35:09] Bruce Bassi: In your book I think you also alluded to some of the newer SSRIs having not had that question asked. I think it was Trix and vibrant. , can you clarify, was it in the nineties or was that something that was a more recent phenomena?
[00:35:24] Paul Putman: Well, they, we became aware of the side effect really in the nineties. And then at the turn of the century, that’s when they began to open the d the vault and start looking at the data again. And I would say probably it was another decade before they started looking. Again I appreciate our friends in the pharmaceutical industry for giving us tools, and many of them are wonderful, caring people who really want to do a good job in every field.
There are some people who are more interested in the business opportunities, and there are, despite the fact that they started asking these questions and getting 25% rates, there have been studies that still don’t ask and that the drug rep will still show up and show you a 6% SSRI effect. And if you go back and look at the methods in the study, no, they did not ask that question. So yes, you still see that. That was the point I was making. Yeah.
[00:36:15] Bruce Bassi: Yeah. Maybe for the non-physician listeners do we have any disclosures to mention about pharmaceutical? Because I, I feel like there’s a common knee jerk reaction when psychiatrists talk about meds that a viewer who doesn’t know us is going to think we’re affiliated somehow with corporate profits.
[00:36:33] Paul Putman: Oh no. Happy to say not at all. I have no relationships with them whatsoever. My only relationship is with American Psychiatric Association Publishing, and that’s it.
[00:36:44] Bruce Bassi: And same here. And same here for the record.
[00:36:46] Supplements Data
[00:36:46] Bruce Bassi: I’d like to talk a little bit about supplements. Again, it’s another topic that , we have this disparity where there’s not enough data, no companies really incentivized to, to spend the money on a good study that gets a supplement approved. And nonetheless patients really want, there’s this desire to have a non-prescription option.
I think. They’ve tried exercise, they’ve tried therapy, they’ve tried good sleep hygiene. They just don’t feel ready for a SSRI yet. What, where, I know the book that you wrote kind of, it was a very good perspective on the, basically there’s nothing that really truly stands out for depression.
Let’s take depression as an example for a sub using a supplement. But if you had to pick, is there one that has the most amount of data?
[00:37:36] Paul Putman: There really isn’t any good data to be perfectly honest.
[00:37:39] Bruce Bassi: Not even a front runner?
[00:37:40] Paul Putman: I hesitate to say this, I really hesitate to say this. There is legitimacy to the claim that in a tiny percentage of the population might respond to SAM-e.
[00:37:52] Bruce Bassi: I thought you were going to say Deplin.
[00:37:54] Paul Putman: No . There data for, there is some data for deplin. The problem is that most of the people that, that that are low don’t respond when you replace it. So that’s the main problem.
[00:38:08] Bruce Bassi: Okay.
[00:38:08] Paul Putman: mean, you can, you have a correlation with the low levels, but then when you replace it in controlled studies, they don’t get better.
You know, there are many inherited metabolic disorders that can affect the outcomes of our patients. These are, of course tiny percentages of the population. But nevertheless, if that’s you, it’s a hundred percent okay. So it’s very important and we learn about those. The more we learn about those, the more we know to look and to ask.
When SAM-e came out, the thing was, this is so rare. Don’t even test for it. You know, it’s that rare. Don’t waste your patient’s money, you know, so there is a legitimacy. If you’ve got that rare inherited metabolic disorder, yes, SAM-e might work for you there. At the same time there, somebody went to the store and bought SAM-e a variety of pharmacies and grocery stores, and analyzed it to see if there was any SAM-e in what they were buying. And of course, found that most of the time there was no SAM-e in it at all. So that’s the other problem you’ve got what are you buying? Am I even buying the thing that I think I’m getting?
So, I’m not a huge Deplin fan from what you, as you can imagine certainly no St. John’s Wort. Please, no St. John’s Wort. And as I used to tell my patients, because there was a– in the eighties, you know, Germany came out with like 70 different studies. I read every single study. Every single one of them is what on earth has happened to the German reputation for science?
I mean, this is really bad. This is not science, you know? And yet it was being published in a volume for patients to read, to treat themselves. So, again, supplements you need to know about, sometimes they’re harmful. Like Ginkgo Biloba can be very harmful and very dangerous and does not work. So you need to know that your patients are taking these things.
You’re trying to treat your patients for anxiety and they’ve been having fatigue, and so they’re taking gensing well, that’s going to make them more anxious and occasionally manic. So, you’ve got to know what they’re on. And again if you know as much as you can about these supplements, your patients are going to work with you and trust you and listen to you.
If you just completely poo poo them and say, oh, nah that’s trash I, well we don’t know anything about that. They’re going to ignore you and they’re going to go do what they want to do and talk to Aunt Maud who it’s working for. There’s a whole chapter in the book on supplements because you’ve got to know what you’re talking about with that.
We do have data, sadly not of, not a lot of it’s encouraging.
[00:40:29] Bruce Bassi: I send them over to examine.com. I love that website that has it all tabulated pretty well. that’s what they’re interested in. So I’m interested in what they’re interested in, let’s put it that way.
[00:40:42] Paul Putman: Same thing, I’m in austin. Every patient wants to cure themselves with exercise. I mean, , I understand that and I have the data, which is in the book on what do you do for exercise, how can it be helpful? And certainly we’ll work with whatever they’re willing to work with, but we have to realize that there might be some limitations of what we can get out of it.
And then again, I think the other lifestyle issues are important, is caffeine ruining your treatment plan? Is that two, two to three drinks of alcohol a week ruining your treatment plan? Is that occasional marijuana? One of the vignettes in book is– Yes, or heavy, is a very typical young man comes in, he is at work, his first job, he’s not concentrating well. A buddy tells him he has ADHD goes to family practitioner who thankfully referred him to me. We do the history smoking marijuana every day and has been for years. And you say, well, did you tell your primary care physician that you were smoking marijuana? Oh, no, I couldn’t do that, he’s been my doctor since I was a little kid, you know. And say, okay, well, fortunately as a stranger, he told me. I said, well, why don’t we have you go off of it for a few months and then reassess. And then of course, three months later, he has no cognitive impairment whatsoever. So, I mean, this happens a lot.
So, being aware of how they can lead to treatment failure as well as lack of treatment efficacy is very important. I think if my patients would just scream if I asked them one more time about caffeine, but, we’ve all got stories about how stopping caffeine made a huge difference for them, so.
[00:42:09] Immunomodulators for depression
[00:42:09] Bruce Bassi: Like we can talk about the marijuana topic for a while. it’s an interesting topic and dilemma as a clinician who grapples with this like legality on warp speed, you know, with lack of data. And then we see the problematic side of it. And when we try to voice our concerns about it, it just, it looks like we just don’t get it.
I do get that it was initially helpful for some people and then it turns out to not be helpful over time. But it’s hard to tell where it changed from the thing for them to being something that was a hobby, to now being something that’s causing them more anxiety and amotivation and impaired cognition, concentration, et cetera.
The ketamine, NMDA receptor modulators don’t excite you very much, but what about immunomodulators? There’s a lot of data to show that there’s in some subsets of patients an immune com autoimmune component or a autoinflammatory process particular with IL-6 and TNF alpha and there’s not really much data on that.
Is that something that, that you’re interested in, that excites you?
[00:43:19] Paul Putman: Data excites me. That’s what I’m excited about. well I’m of those very interesting and fascinating theories. I hope that it brings us very useful information. I’m waiting for the data. I mean we need good controlled studies. We need good outcome data. And if we’ve got that and we know how to use it safely, then I’m all for it.
But I don’t think we should be offering things in the office that we don’t have outcome and safety data for. Again I think we make all kinds of mistakes when we start assuming that theory is going to guide our instead of outcome.
[00:43:53] Approach to treatment failure depression?
[00:43:53] Bruce Bassi: you give us your treatment resistant depression treatment failure, depression algorithm in a nutshell? People have exhausted atypicals, of course, SSRIs, SNRIs, maybe a few tricyclics. what do you do next?
[00:44:08] Paul Putman: I keep digging. I keep digging. I go back to the data, I go back, I I take very detailed notes and because I need to go back and reread them constantly, you know, occasionally the patient will say, well, let’s go back and try Depakote again. I think that helped. Okay. We go back, we look at the notes together.
No, Depakote didn’t help at all. I go back I re-examined the history, you know, as in doing research for the new book. There’s a lot of data on on how clinicians, expert clinicians make mistakes because we make diagnoses too quickly, and then we ignore the data that doesn’t fit with that diagnosis.
And that’s been replicated and shown time and time again, and all experts in all fields, including medicine. And in fact, if you, if some data that fits with your diagnosis appears later, that didn’t show in the initial assessment. Clinicians will even remember that as being part of the initial assessment when it wasn’t.
So we really distort the picture. We completely distort how we make So one of, if I’ve been a patient, has been through everything for a treatment for depression and they’re not better, I really need to begin to doubt that they’ve got depression. I maybe I’ve got a different diagnosis here.
Maybe it’s another medical diagnosis. in the new book I’m writing on frequently missed categories, of course, endocrine, of course under evaluated head trauma. And I decided, you know, I’m going to put infectious disease in there too. Because, you know, we all know neuro syphilis and all that.
[00:45:35] Bruce Bassi: Lyme.
[00:45:36] Paul Putman: it Yes, Lyme is the chapter I’m actually writing right now.
And, and it’s amazing. It’s a much longer chapter than I thought it was going be mean. So there’s all kinds of diagnostic errors that we might have made in good faith and that we need to go back and redo the history with the patients. We need to look for other answers the information I really believe in.
Backing up un chunking your thoughts and reevaluating your initial assessments. And then of course you’ve got to make sure that the patient has understood how you want them to use the medication. You’ve got to make sure that if it’s psychotherapy that that you have repaired any ruptures in your therapeutic alliance, because that’s going to make a huge difference.
And then of course, you’ve have to be looking for things that they’re taking that they thought were innocent, that that you didn’t.
I had– famous vignette of mine is the patient who I treated for years with for bipolar disorder, that we went through everything and every combination and every, and could not get stability.
And and of course we’re going through stimulants. Are you taking cold medications? Are you taking caffeine? Are you taking this, are you taking alcohol? Are you taking it? No. Until one day she was sitting at her kitchen counter, staring at a box of her her diet product, I’m forgetting what the name of it, SlimFast and realized it was chocolate, which has caffeine. She went off of it and she stabilized. Now, you know, these almost sound like bedtime stories, but this is a real case. This really happened. And this happened a lot. And you can see it in the literature, it’s reported. So, again, it’s just digging and digging. I don’t “always do” anything, is my answer.
I don’t have an A-B-C of I start with this, then I go to this, then I go to that. Because you might say, all right, I want to start with venlafaxine for major depression. Because if you really look at faces data, it’s more likely to work than anything else. Everything being equal. Okay? And I love face C does wonderful data.
And then you say, oh, well, but I had a twin brother who took it and didn’t get well with venlafaxine. Well, there, there goes my list, you know, I just don’t think regular have any value. You might as well start by individualizing your treatment, which is one of my points in the book.
I think you’ve got to. To do what makes the most sense for that patient? We’re la layering probabilities. Every time we’re treating we’re using Bayesian inference to alter our treatment models. When something goes wrong you’ve got to use the probabilities you’ve got to use all the possibilities.
You can’t just use a fixed list. So I don’t always do anything. I try to go where the data, takes me.
[00:48:05] What about ECT for treatment failure depression?
[00:48:05] Bruce Bassi: About you didn’t mention ECT in there. What is your thought on ECT?
[00:48:12] Paul Putman: Oh, it’s a very safe and a very valuable tool for the right person at the right time. I’m not anti ECT at all. And again, in the book, when I discussed the somatic treatments because I thought you, everyone needs a familiarity with those as well. And to compare them to the pharmacology options remember that it’s convulsive therapies.
It’s not electroconvulsive convult. If there’d electric, convulsive therapy was the new, safe, modern way of doing convulsive therapies. They used to be chemically induced. So, and then insulin induced. And so, and then the electricity is the safe. And it’s interesting that around I haven’t looked at the numbers in the last few years, but it used to be that 17% of patients year in and year.
With major depression would be treated with ECT no matter what they were doing in Berkeley, no matter what they were doing with new medications, it was all going to be the same amount because those were the people that were not getting well and that were agreeable to doing the treatment.
I, I am much, much more likely to recommend ECT than I am tms. I do think the data for TMS is weak. I just don’t think we’re out there yet. I don’t think they found the right paradigms. They may. You know, I was in residency with Mark George. I have a lot of respect for him. He’s done wonderful work and he’ll be the first to tell you, I, we just don’t know exactly what to do yet.
again, it’s a terribly expensive treatment. I think it’s very iffy. I think the indications are very iffy. I do not feel that way about ECT. The problem with ECT is, of course, doing it safely and doing it enough when Feen, and a lot of other people in the late nineties started updating the treatment paradigms and recommendations for ECT.
It really took us further because it used to be you’d give a series of treatments and then you just wait to see if the depression came back. Well, usually it did. So then would you treat again? Yes. You treat again. Well, what were the, what’s the algorithm? We didn’t have a good algorithm but with those guys at mostly up at in Albert Einstein in New York in the late nineties, they came up with really good algorithms.
Now we have continuation in maintenance, ECT, and we have valid indications for that. I once had a patient who remained on medication. And I swear every single time she went let over three weeks between single ECT treatments she relapsed for depression every single time. Now you could say, oh, that’s just, you know, observer error.
Well, I had to completely review her chart this thick for her insurance company twice during the five years that I treated her and going over every visit, every note, every symptom, and I can give, I can show you on the graph that every single time she went out of town and missed her ECT treatment or for some reason wasn’t able to get it in three weeks, she showed a decline.
Every time we stayed on that schedule, she did well. Now I very much believe in it. I think for the right person at the right tool it’s very valuable. It just, to many patients, it seems distasteful. You know, the media has not always been fairly portraying it. and so it, it takes a lot of education even in the last few years.
You know, I would recommend that as one option and patients would listen to me but not really even want to go further with it.
[00:51:15] Bruce Bassi: Interesting. Yeah. It seems like when an individual gets hurt by something, they’re very motivated to help protect other people from that thing and can’t really see how not everybody has the same side effects that they have had, and some people, in fact, can greatly benefit from a medication and if it, if their voice is preventing certain people from receiving appropriate treatment, it’s actually hurting a subset of individuals out there because they’re falsely planting this narrative something is extremely harmful when in fact it may only be just a small percentage of people having that side effect.
[00:51:52] Paul Putman: think that’s well said. You know, I think about myself. You know, when I, before I went to medical school, if you would’ve asked me about ECT, I’d seen one flew over the Cuckoo’s Nest, you know, which of course is psychosurgery, not ECT it’s not fairly depicted. But anyway I, you’ve asked me, I would’ve said, oh no, I’m not for that at all. That sounds horrible. That sounds barbaric.
And I go in a student to watch my first treatment, and I said, when are we going to start? They said, we just finished. I said,
[00:52:15] Bruce Bassi: Right.
[00:52:16] Paul Putman: didn’t realize you did it. That was before the EEG monitoring. And and then you see people get better and you’re just you understand that for the right person, this is lifesaving.
And, and who are we to not mention that option? I think it’s it’s a treatment that I think has definitely got the outcome studies behind them. Unlike some of the newer somatic treatments that need to be worked out better
[00:52:40] Bruce Bassi: you mentioned when you were talking about your chart review, looking at a graph, it sounds like you do some standardized testing or rating scales for patients. Is that a standard practice in your practice, or is that for certain individuals and which?
[00:52:55] Paul Putman: That’s a good question. I don’t use standard rating skills. And the reason I don’t is because technically that’s not what they’re for. They’re for research and they’re to help with interrater reliability and standardization of outcome. And if you really look, say, look at the Hamilton Depression Scale, Or the Beck Anxiety or depression scale, all they are numbers attached to the same symptoms you should be asking about. So ask about all the neuro vegetative symptoms and estimate them myself. What I’ll often ask patients to do, say particularly bipolar patients, is to give a mood chart. And I want it as simple as possible. I don’t want lots of detailed data.
Just give me a number. And we go over interrater reliability of what do I mean by 10 and what do I mean by one? You know, 10 is high, one is low. Sometimes people don’t clarify that first. And I just want something that I can, we can discuss in the session together. I just use that as a tool to get going with them.
I don’t find that patient rated scales are at all helpful. Again, there’s no interrater reliability for that. They’re often not filled out in the way that you’re expecting or find useful. And now, so I just use the underlying data. I don’t try to convert it to numbers, because for me that’s just for research.
[00:54:03] Meta cognition in prescribing
[00:54:03] Bruce Bassi: It’s very interesting. One, one thing you mentioned way back at the beginning of the interview was being aware of how we think as prescribers, and this is taught often and talked about often in the context of doing therapy, you know, counter transference and how we feel towards certain patients. And also mindful meditation too.
I don’t hear of it often as a clinician talking about prescribing. And can you go into that a little bit more? What you mean by that?
[00:54:36] Paul Putman: Yes, thank you because this is part of what my passion is, is to try to pass this on and change the future, as you said. We’re not as, we’re not fully aware of all the mistakes that we make. Even as very well educated, well-intentioned, very bright people we are very prone to learning just as many incorrect facts about science as we are the correct ones all through our education.
When we finally learn the correct information, the incorrect information does not disappear from our brains. It’s measurable how much effort it takes and time it takes to suppress the incorrect information in order to then refer to the correct information. This is measurable. We know that we tend to lean on teleology all the time.
You know, giraffes develop long necks so that they could reach the food in the trees instead of that the animals, the, when the food was in the trees, the animals with long necks survived and the others didn’t. You know, so we, we tend to want to have a narrative. We tend to misunderstand, emergence from different levels of complexity.
We always want to be teleological and narrative about about any scales that we see, and we want it to be scales that are familiar to us. So we often make cognitive errors and conceptual errors. So I think we need to begin with just accepting that we do that, that’s human. That’s the way the human brain works.
The human brain is here to protect, is here to predict the future, to keep us safe. That’s basically what it does. And it doesn’t necessarily give us the right answer all the time. It just gives us a probability. So the more we’re aware of the shortcomings in our own cognitive processes as human beings, the more we can search for the results of those errors, trace them back, undo them, and come back with better answers for our patients.
That’s where my passion is right now. That’s why I’m writing these books, is to encourage us all to look at those processes, to not assume that we’re doing everything the correct way all the time, because we’re not.
So thank you for the opportunity to stress that point, I really appreciate it.
[00:56:35] Bruce Bassi: Is there something that you find your trainees often learn, like SNRIs are more activating, that you’re trying to correct the narrative that they had learned from some, maybe some other colleague or website or something that now we’re having to undo and suppress that, that falsehood?
[00:56:58] Paul Putman: Well, the big fad right now is treatment resistance. As we were discussing, and which blows me away, and you’ll see this on social media, people will say, what do you use to treat treatment resistant PTSD? and you’re thinking, let me think through that. Logically, if there’s a treatment, it’s obviously not treatment resistant.
You can go to poster sessions. I was at the APA last year and I enjoy going to the poster sessions because I just like talking to people. You know, I know it’s sign necessarily, but I really enjoy finding out how they were thinking and what they were doing and why they came up with this study.
And there’s, you know, this is what we use to treat treatment resistance and I’m going then it’s not treatment resistance.
[00:57:34] Bruce Bassi: You have the new treatment.
Yeah. It is a little bit of a thought circle.
[00:57:38] Paul Putman: that’s the current battle that I’m against. It’s, let’s get rid of the word treatment resistant. It’s taking a life of its own.
[00:57:44] How do patients respond when they hear “treatment resistant?”
[00:57:44] Bruce Bassi: And I think patients too, I feel like when they hear that word, I maybe, you know, maybe you can also give your thoughts on this too. I would feel more broken and like, there’s something unique about me that the medical professionals, mental health professionals don’t get.
And I am a more hopeless case, like, because they’re calling me treatment resistant and I feel like, you know, when you were going back to saying, well, think about what the diagnosis is. Maybe, there’s somewhat of a depressive personality there, or persistent long-lasting depressant depression that psychodynamically they’ve become so attached to because of all these names and labels and terminology that they’ve now become to over-identify with.
And somehow, in some way, the depression serves a purpose now because it’s labeled as treatment resistant. And kind of nurture it as, you know, maybe it gives them some sort of meaning or they get some attention or they get some sort of different change from the depression itself.
[00:58:47] Paul Putman: That’s a very good point. It could well be iatrogenic as you’re saying, and with some patients that might be the answer. you know, it’s probably not the right answer for everyone, but it’s certainly, it a possibility that needs to be explored. Absolutely. I, that’s exactly what I’m talking about. Going back and breaking it down and putting it together in a different way.
Very much. And there is data showing how demoralizing it is for a patient to be labeled treatment resistant. I know that there’s, some people might feel that if we label a treatment resistance that’s showing there’s certain features that causes us to want to study it or to go in this direction.
But think about when your patient hears that, you know, that I’m treatment resistant. I mean, how hopeful is that? I mean, what does do to your therapeutic alliance and your relationship and their relationship to themselves and others and their hope? We never give unrealistic hopes, but obviously we’re working with patients because we do hope that they will get better.
We’re still in it, we’re still in the fight. We’re still here with you side by side on the same side of the table, looking at the data, trying to find the solution. You know, when you start using terms like treatment resistance, you’re implying that you’re giving up and think it’s anti therapeutic.
And the case you mentioned, of course, could be iatrogenic.
[00:59:58] Bruce Bassi: Right. Dr. Putman, so nice to have you on the show to talk to you. I think this is a really enlightening conversation. One, I enjoyed very much talking about psychopharmacology. Thank you so much.
[01:00:11] Paul Putman: Thank you so much. It’s been a pleasure. I’ve really enjoyed it myself. It’s been a, you’re a wonderful colleague. I really enjoyed discussing it, these cases with you and these ideas, and I appreciate the invitation very much.
[01:00:22] Bruce Bassi: What’s the name of your new book for our listeners going to be
[01:00:26] Paul Putman: It’ll probably come out in about a year. It’s encountering treatment resistance: success through reconceptualization. Thank you.
[01:00:33] Bruce Bassi: That’s going to be really helpful for people. absolutely because I think as the rate of depression increases, there’s probably also. rates of treatment. I wonder if it looks like a bacteriogram over time where, you know, how we develop increased resistance to antibiotics, I wonder if that’s also increasing. Is there any data for that?
[01:00:52] Paul Putman: No, not specifically. You know, there’s not even really good, there’s not even really good data on tachyphylaxis and the treatment burnout. There’s no data for that. No data.
[01:01:03] Bruce Bassi: Another thing we have to undo in our mind.
[01:01:05] Paul Putman: Right, exactly. So again, as I say, instead of just saying, oh, it’s, it pooped out, go back and figure out why did it quit working.
There is always an answer, you need to find, and there might be more than one. You just need to find out what the answers are.
[01:01:18] Bruce Bassi: Interesting. Uh, well, thank you. I appreciate it.
[01:01:22] Paul Putman: Thank you.
[01:01:22] Bruce Bassi: As a reminder, if you’d like to support this show, one way you can help us is by subscribing to the channel on YouTube and leave a comment if you’d like.
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