madinamerica
Joanna Moncrieff, MD October 12, 2018
A few months ago I was surprised to receive a request from an obscure journal of consciousness studies to review a paper. I was surprised because, although it was not immediately obvious from the title, the paper contained the first reports of the primary outcome measure of the massive and notorious STAR-D study, 14 years after the study was finished.
What in the world were the main findings of the world’s largest ever antidepressant trial doing being presented now in a little known journal? The answer may lie in the fact that they show how miserably poor the results of standard medical treatment for depression really are!
With 4041 participants, the STAR-D study is by far the largest and most expensive study of antidepressants ever conducted. The intention of the study was to see how antidepressant treatment combined with high quality care performed in usual clinical conditions. It did not involve a placebo or any sort of control. All treatment was provided free for the duration of the study to maximise engagement.
The paper I was asked to review, which is now published in Psychology of Consciousness: Theory, Research and Practice, is written by a group led by Irving Kirsch and based on the original data obtained through the NIMH.1 Shannon Peters describes its findings in detail.
Kirsch’s group point out that the paper that describes the design of the STAR-D trial clearly identifies the Hamilton Rating Scale for Depression (HRSD) as the primary outcome.2 This makes sense since the HRSD is one of the most commonly used rating scales in trials of treatment of depression, especially trials of antidepressants. As the STAR-D authors note in the study protocol “the HAM-D17 (HRSD), the primary outcome, allows comparison to the vast RCT literature” (cited in (1)).
Yet the outcome that was presented in almost all the study papers was the QIDS (Quick Inventory of Depressive Symptomatology), a measure made up especially for the STAR-D study, with no prior or subsequent credentials. In fact, as the authors of the present paper point out, this measure was devised not as an outcome measure, but as a way of tracking symptoms during the course of treatment, and the original study protocol explicitly stated that it should not be used as an outcome measure.
The analysis found that over the first 12 weeks of antidepressant treatment, people in the STAR-D study showed an improvement of 6.6 points on the HRSD. This level of change fails to reach the threshold required to indicate a ‘minimal improvement’ according to the Clinical Global Impressions scale (a global rating scale), which would be 7 points. It is also below average placebo improvement in placebo-controlled trials of antidepressants. A meta-analysis of paroxetine trials, for example, found that the average improvement in placebo-treated patients was 8.4 points on the HRSD.3 A meta-analysis of trials of fluoxetine and venlafaxine reported average levels of improvement on placebo of 9.3 points over just 6 weeks.4 Another meta-analysis found placebo improvement levels of between 6.7 and 8.9 points in placebo groups across trials involving a variety of antidepressants.5
The proportion of people classified as showing a ‘response’ (using the arbitrary but commonly used definition of a 50% decrease in HRSD score as per the original protocol) was 32.5% in the STAR-D study, and the proportion classified as showing remission (HRSD score ≤7) was 25.6%. The meta-analysis of placebo-controlled trials of fluoxetine and venlafaxine reported response rates of 39.9% among people allocated to placebo, and remission rates of 29.3%. In another antidepressant meta-analysis, the response rate on placebo was just above the STAR-D level at 34.7%,6 and in another it was just below at 30.0%.7
The authors of the current paper point out, however, that improvement is lower in placebo-controlled trials, even in the people treated with antidepressants, than it is in trials that compare one antidepressant against another without placebo controls. This is presumably because people in placebo controlled trials are told that there is a chance that they will receive a dummy tablet, while in comparative trials, they know they will receive some sort of active drug. Therefore they compare the results of the STAR-D study to the results of a large meta-analysis of comparative trials (cited in (6)). These find average HRSD improvement levels of 14.8 points; response rates of 65.2% and remission rates of 48.4%. Therefore the STAR-D results are approximately half the magnitude of those obtained in standard comparative drug trials.
The authors propose that the reasons for this poor performance of antidepressants in the STAR-D study is due to the selection of more complex patients. Industry studies in particular exclude people with ‘co-morbid’ conditions and symptoms or history of self-harm, and often recruit people via advertisements. It may also be due to the intensive attention and assessment procedures people undergo in industry-funded studies, and the added placebo effect of being in a trial of a ‘new’ treatment, which most trials involve.
Whatever the reason, STAR-D suggests that in real life situations (which the STAR-D mimicked better than other trials) people taking antidepressants do not do very well. In fact, given that for the vast majority of people depression is a naturally remitting condition, it is difficult to believe that people treated with antidepressants do any better than people who are offered no treatment at all.
It seems this may be the reason why the results of the main outcome of the STAR-D study have remained buried for so long. Instead, a measure was selected that showed results in a slightly better light. Incidentally, even then results were pretty poor, especially over the long-term, as Piggott et al have showed in a previous analysis.8
Whether this was deliberate on the part of the original STAR-D authors or not, it was certainly not made explicit. There should surely be uproar about the withholding of information about one of the world’s most widely prescribed class of drugs. We must be grateful to Kirsch and his co-authors for finally putting this data in the public domain.
Show 8 footnotes
Thank You Dr Moncrieff and MIA.
Showing posts with label Drs For Reform. Show all posts
Showing posts with label Drs For Reform. Show all posts
Friday, October 12, 2018
Wednesday, October 10, 2018
How Well Do Neuroleptics Work?
madinamerica
Sandra Steingard, MD October 9, 2018
I recently received an email from Psychiatric Times highlighting current articles. Psychiatric Times is a newspaper that is distributed for free to psychiatrists in the US. To put this in context, the paper appears to be heavily subsidized by pharmaceutical company advertising, and its former editor, Ronald Pies, is a psychiatrist who has been critical of views expressed on Mad In America.
It caught my eye when the first article mentioned had the title, “Antipsychotic Discontinuation: When is it OK?” I clicked on the link to find a slide show authored by Brian Miller, M.D., P.D., M.P.H. which was titled, “Antipsychotics – To Respond or Not to Respond?”
This was intriguing but confusing. Dr. Miller’s slides reviewed a paper just published in Schizophrenia Bulletin titled, “How Many Patients With Schizophrenia Do Not Respond to Antipsychotic Drugs in the Short Term? An Analysis Based on Individual Patient Data From Randomized Controlled Trials.” As pointed out in the slide show, the paper reported on a meta-analysis of 16 randomized controlled studies of antipsychotic drugs over the first 4-6 weeks of treatment. The authors found that a significant number of people do not respond or have relatively poor responses and the majority do not experience a remission of psychotic symptoms. While important, this article addressed short-term rather than long-term care. It is, nevertheless, informative. [Editor’s note: click here to see the MIA research news report on this paper.]
The senior author of the paper, Stefan Leucht, is a well-known and highly regarded expert in meta-analysis. As noted in the disclosures, he is also well-connected to many pharmaceutical companies. Meta-analysis is a statistical technique that allows for investigation of multiple studies. This provides a broader view of the available data in the field.
Since this was a study of response to drugs, it is important to understand how researchers define that term. When drug studies are conducted, subjects are assessed via rating scales which address the presence and severity of symptoms. A person is asked about a variety of experiences, such as hearing voices or feeling sad, and their responses are scored according to a predetermined rubric. Scores will thus fall on a continuum. The Positive and Negative Symptoms Scale (PANSS) is commonly used in antipsychotic drug trials. It includes 30 items and each can be scored on a scale of one (absent) to seven (extreme). Scores can therefore fall anywhere from 30 to 210.
There are many ways that researchers can analyze the myriad bits of data that are collected in these studies. Researchers are required to determine in advance how they will analyze their data, including what change would allow them to classify a person as a “responder.” Researchers can also define what would be considered a “remission.” To be counted as a responder, a person needs to have a certain percentage drop in the rating scale score from beginning to end of study. To be considered in remission, a person’s final score needs to fall below a set point on the scale. Unless one reads a study carefully, these distinctions can be missed and the notion of “response,” often cited in promotional material, can be misleading. Many studies consider a 20% reduction in score as a response. For some people, this can be a clinically insignificant change in symptoms. When large numbers of people are included in a study, it is easier to detect small differences among groups and these differences can reach statistical significance. A drug may be promoted as effective when what has been found is that the group of people who took it had a clinically minor reduction in symptoms as compared to the group on placebo.
The authors of this study, recognizing some of these challenges, set out to look more carefully at the range of response in the studies under review. They did this by not only reporting on the common 20% reduction often used as a marker for “response” but also 25%, 50%, and 75% reduction in the ratings.
The authors also analyzed the percentage of subjects who reached remission. In this case, remission was defined as not scoring above the “mildly present” rating on 8 key items of the PANSS.
The results:
Those who had no change or worsened – 19.8%
Less than 25% improvement – 43%
Less than 50% improvement – 66.5%
Less than 75% – 87%.
For those who were listed as “non-remission” – 66.9%.
To put this another way, only 33.1% of those in the studies were in remission. Only 33.5% had more than a 50% reduction in the rating scale.
The authors offer some insights into what I consider the paradoxes of common psychiatric practice as well as the problems with the way many research studies are conducted.
They begin their paper, “A considerable number of patients with schizophrenia do not respond to antipsychotic drugs.” They go on to cite what they describe as “vague statements” that “can be found in other reports and textbooks such as ‘most controlled trials continue to find a subgroup of 10-20% of patients who derive little benefit from typical neuroleptic drug therapy.’” They offer similar quotes from a variety of texts and conclude that “all of these statements are not based on firm evidence.”
In their discussion, the authors provide insight into the current state of pharmaceutical studies as well as offering their thoughts on why the response rates are so low:
“Pharmaceutical companies are trying to conduct large trials to assure statistical significance which leads to more recruitment pressure; the ‘patient clock’ is running down, thus patients are recruited quickly by professional centers; most of them are improved and stabilized on antipsychotics and enter an RCT after a short wash-out phase of a few days. As most of the antipsychotic effect occurs early on, further response may not be observed which could, at least partly, explain the relatively low number of responders. The increased ‘relapse’ rates on placebo also point to the direction that previous antipsychotics were beneficial.”
I found this rationale to be somewhat tortured. A major issue not addressed is that if people who are stabilized on neuroleptics are withdrawn abruptly and then restarted on drug or placebo, this would favor the drug since those given placebo would be experiencing withdrawal effects. But the authors bring up important issues about who gets recruited into studies these days and the extent to which they mirror the experiences of most people who are offered these drugs in clinical practice. Carl Elliott has written about this problem and it is critical to understand the context in which many drugs studies are conducted.
I still work as a psychiatrist and I know people who appear to benefit from these drugs. However, I want to use them in a way that is most helpful and minimizes harm. I also want to share the available data since this is what constitutes informed consent. What seems equally important is to provide this information to the public, including policy makers, since common misconceptions have had great influence on the structure of our system of care. Deinstitutionalization was driven by many forces but it is sustained by the notion that most people have robust responses to these drugs. We have a system of care and a societal expectation that these drugs are highly effective. When people are struggling in the community, the common response is that we need to adjust “their meds,” even though this is only likely to be helpful in a minority of cases.
Many of my colleague tend to focus on the need to find better drugs or design better studies as a way to address this problem. We tend to overlook so-called “alternative approaches,” such as the Hearing Voices Network. Oddly, given the context of this blog, these approaches are often discounted because they lack an evidence base. Sadly, adequate money to develop an evidence base is not offered because, well, they lack an evidence base. I suspect there is another bias at play.
In another recent email, this time from Medscape, there was a link to a video, “How to ‘Brand’ Psychiatry Today.” In the video, Dr. Stephen Strakowski, chair of the Department of Psychiatry at Dell Medical School at the University of Texas in Austin, proposes this definition of the specialty: “Psychiatry is a medical specialty that studies and treats disturbances in brain function that predominantly affect behavior — behavioral brain disorders.”
I appreciated Dr. Strakowski’s attempt to define our profession and I think he captures the way most psychiatrists conceptualize the field. This is informative. He both touts but then acknowledges the risks of the medical model: “We need to be careful to not confuse the medical model with using only medication for treatment. Rather, the medical model uses the medical approach to define the treatment evidence base and decide on the treatment.” Dr. Strakowski also suggests some limits to what psychiatrists should be doing and urges psychiatrists to let others work at the top of their expertise, “to allow those who are the best therapists to be the therapy providers, for example.” My major disagreement with him is that he does not challenge some of the negative consequences of applying the medical frame so broadly; even when he suggests that we consider social factors and invite others to offer psychotherapy, it is all done in the context of a medical conceptualization of the problems at hand. But that is a subject for another time.
For now, I would call upon physicians who claim to value the medical frame “to define treatment evidence and decide on treatment” to do just that. The evidence base suggests that it is time for us to reappraise the effectiveness of these drugs and shift our practice patterns accordingly.
Previous articleTwo-Thirds of Schizophrenia Patients Do Not Remit on Antipsychotics
Thank You Dr Steingard and MIA.
Sandra Steingard, MD October 9, 2018
I recently received an email from Psychiatric Times highlighting current articles. Psychiatric Times is a newspaper that is distributed for free to psychiatrists in the US. To put this in context, the paper appears to be heavily subsidized by pharmaceutical company advertising, and its former editor, Ronald Pies, is a psychiatrist who has been critical of views expressed on Mad In America.
It caught my eye when the first article mentioned had the title, “Antipsychotic Discontinuation: When is it OK?” I clicked on the link to find a slide show authored by Brian Miller, M.D., P.D., M.P.H. which was titled, “Antipsychotics – To Respond or Not to Respond?”
This was intriguing but confusing. Dr. Miller’s slides reviewed a paper just published in Schizophrenia Bulletin titled, “How Many Patients With Schizophrenia Do Not Respond to Antipsychotic Drugs in the Short Term? An Analysis Based on Individual Patient Data From Randomized Controlled Trials.” As pointed out in the slide show, the paper reported on a meta-analysis of 16 randomized controlled studies of antipsychotic drugs over the first 4-6 weeks of treatment. The authors found that a significant number of people do not respond or have relatively poor responses and the majority do not experience a remission of psychotic symptoms. While important, this article addressed short-term rather than long-term care. It is, nevertheless, informative. [Editor’s note: click here to see the MIA research news report on this paper.]
The senior author of the paper, Stefan Leucht, is a well-known and highly regarded expert in meta-analysis. As noted in the disclosures, he is also well-connected to many pharmaceutical companies. Meta-analysis is a statistical technique that allows for investigation of multiple studies. This provides a broader view of the available data in the field.
Since this was a study of response to drugs, it is important to understand how researchers define that term. When drug studies are conducted, subjects are assessed via rating scales which address the presence and severity of symptoms. A person is asked about a variety of experiences, such as hearing voices or feeling sad, and their responses are scored according to a predetermined rubric. Scores will thus fall on a continuum. The Positive and Negative Symptoms Scale (PANSS) is commonly used in antipsychotic drug trials. It includes 30 items and each can be scored on a scale of one (absent) to seven (extreme). Scores can therefore fall anywhere from 30 to 210.
There are many ways that researchers can analyze the myriad bits of data that are collected in these studies. Researchers are required to determine in advance how they will analyze their data, including what change would allow them to classify a person as a “responder.” Researchers can also define what would be considered a “remission.” To be counted as a responder, a person needs to have a certain percentage drop in the rating scale score from beginning to end of study. To be considered in remission, a person’s final score needs to fall below a set point on the scale. Unless one reads a study carefully, these distinctions can be missed and the notion of “response,” often cited in promotional material, can be misleading. Many studies consider a 20% reduction in score as a response. For some people, this can be a clinically insignificant change in symptoms. When large numbers of people are included in a study, it is easier to detect small differences among groups and these differences can reach statistical significance. A drug may be promoted as effective when what has been found is that the group of people who took it had a clinically minor reduction in symptoms as compared to the group on placebo.
The authors of this study, recognizing some of these challenges, set out to look more carefully at the range of response in the studies under review. They did this by not only reporting on the common 20% reduction often used as a marker for “response” but also 25%, 50%, and 75% reduction in the ratings.
The authors also analyzed the percentage of subjects who reached remission. In this case, remission was defined as not scoring above the “mildly present” rating on 8 key items of the PANSS.
The results:
Those who had no change or worsened – 19.8%
Less than 25% improvement – 43%
Less than 50% improvement – 66.5%
Less than 75% – 87%.
For those who were listed as “non-remission” – 66.9%.
To put this another way, only 33.1% of those in the studies were in remission. Only 33.5% had more than a 50% reduction in the rating scale.
The authors offer some insights into what I consider the paradoxes of common psychiatric practice as well as the problems with the way many research studies are conducted.
They begin their paper, “A considerable number of patients with schizophrenia do not respond to antipsychotic drugs.” They go on to cite what they describe as “vague statements” that “can be found in other reports and textbooks such as ‘most controlled trials continue to find a subgroup of 10-20% of patients who derive little benefit from typical neuroleptic drug therapy.’” They offer similar quotes from a variety of texts and conclude that “all of these statements are not based on firm evidence.”
In their discussion, the authors provide insight into the current state of pharmaceutical studies as well as offering their thoughts on why the response rates are so low:
“Pharmaceutical companies are trying to conduct large trials to assure statistical significance which leads to more recruitment pressure; the ‘patient clock’ is running down, thus patients are recruited quickly by professional centers; most of them are improved and stabilized on antipsychotics and enter an RCT after a short wash-out phase of a few days. As most of the antipsychotic effect occurs early on, further response may not be observed which could, at least partly, explain the relatively low number of responders. The increased ‘relapse’ rates on placebo also point to the direction that previous antipsychotics were beneficial.”
I found this rationale to be somewhat tortured. A major issue not addressed is that if people who are stabilized on neuroleptics are withdrawn abruptly and then restarted on drug or placebo, this would favor the drug since those given placebo would be experiencing withdrawal effects. But the authors bring up important issues about who gets recruited into studies these days and the extent to which they mirror the experiences of most people who are offered these drugs in clinical practice. Carl Elliott has written about this problem and it is critical to understand the context in which many drugs studies are conducted.
I still work as a psychiatrist and I know people who appear to benefit from these drugs. However, I want to use them in a way that is most helpful and minimizes harm. I also want to share the available data since this is what constitutes informed consent. What seems equally important is to provide this information to the public, including policy makers, since common misconceptions have had great influence on the structure of our system of care. Deinstitutionalization was driven by many forces but it is sustained by the notion that most people have robust responses to these drugs. We have a system of care and a societal expectation that these drugs are highly effective. When people are struggling in the community, the common response is that we need to adjust “their meds,” even though this is only likely to be helpful in a minority of cases.
Many of my colleague tend to focus on the need to find better drugs or design better studies as a way to address this problem. We tend to overlook so-called “alternative approaches,” such as the Hearing Voices Network. Oddly, given the context of this blog, these approaches are often discounted because they lack an evidence base. Sadly, adequate money to develop an evidence base is not offered because, well, they lack an evidence base. I suspect there is another bias at play.
In another recent email, this time from Medscape, there was a link to a video, “How to ‘Brand’ Psychiatry Today.” In the video, Dr. Stephen Strakowski, chair of the Department of Psychiatry at Dell Medical School at the University of Texas in Austin, proposes this definition of the specialty: “Psychiatry is a medical specialty that studies and treats disturbances in brain function that predominantly affect behavior — behavioral brain disorders.”
I appreciated Dr. Strakowski’s attempt to define our profession and I think he captures the way most psychiatrists conceptualize the field. This is informative. He both touts but then acknowledges the risks of the medical model: “We need to be careful to not confuse the medical model with using only medication for treatment. Rather, the medical model uses the medical approach to define the treatment evidence base and decide on the treatment.” Dr. Strakowski also suggests some limits to what psychiatrists should be doing and urges psychiatrists to let others work at the top of their expertise, “to allow those who are the best therapists to be the therapy providers, for example.” My major disagreement with him is that he does not challenge some of the negative consequences of applying the medical frame so broadly; even when he suggests that we consider social factors and invite others to offer psychotherapy, it is all done in the context of a medical conceptualization of the problems at hand. But that is a subject for another time.
For now, I would call upon physicians who claim to value the medical frame “to define treatment evidence and decide on treatment” to do just that. The evidence base suggests that it is time for us to reappraise the effectiveness of these drugs and shift our practice patterns accordingly.
Previous articleTwo-Thirds of Schizophrenia Patients Do Not Remit on Antipsychotics
Thank You Dr Steingard and MIA.
Thursday, September 27, 2018
75% Of Med Students Are On Antidepressants or Stimulants (Or Both)
It's going, going, . . . . It's Over the Back Wall and It's OUTTA Here.
Any pretense of legality Psychiatric/Psychologically imposed disability ever pretended to just got nuked, along with every protection our legal system extended to the disablers themselves and everyone harboring/assisting them.
See our intro to the following post if you need clarity.
Pamela Wible MD
Posted on September 4, 2017 by Pamela Wible MD
“Have you ever been depressed as a physician?” I asked 220 doctors. Ninety percent stated yes. Yet few seek professional help. Here’s what depressed doctors do (when nobody’s looking). Some drink alcohol, exercise obsessively, even steal psychiatric meds. Still more shocking—I discovered that 75% of med students (and new doctors) are now on psychiatric medications.
“I was told by the psychologist at my med school’s campus assistance program, that 75% of the class of 175 people were on antidepressants,” shares psychiatrist Dr. Jaya V. Nair. “He wasn’t joking. How broken is the system, that doctors have to be pushed into illness in order to be trained to do their job?”
“During my internship, I found out that at least 75% of my fellow residents were on SSRIs or other antidepressants, just ‘to get through it’ because it was so horrible.” states Dr. Joel Cooper, “Depression, or a constantly depressed state, is more or less the norm in medical school and throughout one’s residency.”
“When I left my residency, I was alarmed to find out that about 75% of my fellow residents had started antidepressants since their intern year,” says Dr. Jill Fadal.
Seems the epidemic of depressed doctors begins in medical school. I wondered how best to verify this oft-repeated 75% statistic. Just then a student called to tell me what her professor said during orientation: “Look around the room. By the end of your first year, two-thirds of your class will be on antidepressants.”
I’m appalled. Yet she’s grateful. Why? Her school is so progressive. They normalize the need for antidepressants.
I must be out of touch. Do most med students require psych drugs for day-to-day survival? I turned my question over to Facebook: “75% of med students and residents are taking either stimulants or antidepressants or both. True or false?”
“It’s absolutely, horrifyingly, true. It is a symptom of a great sickness in MedEd.”
“Sadly I am guessing true as I prescribed some for my residents every year that I worked in a residency.”
“True, but I’m sure a lot is unprescribed.”
“I would assume definitely true, Ritalin, Adderall, energy drinks, ephedrine. Yep.”
“While working as a nurse at a major Army hospital, I was astounded by the number of medical students on Adderall or Ritalin.”
I’ve been on an antidepressant since being premed—18 years now. Little did I know it would be impossible to wean myself off and that my entire class was using Adderall.”
“True but most take them in secret as there are negative consequences and stigma that come with getting your mental health addressed.”
“Very true. From my practical point of view, I’d put medical students & residents at 100%.”
“I take both Zoloft and Adderall daily.”
“Very much so true—the percentages may actually be higher. I see it in my classes and I’m only a premed student.”
“If coffee counts as a stimulant it’s definitely 100%.”
“The only way I’d say false is to say it’s higher. I’d say a quarter of my class had to take a leave for a mental health break.”
Having received Facebook confirmation that most med students are on psych drugs, I then queried 1800 medical students via email with the same question and encouraged respondents to share personal experiences. To prevent professional retaliation, all quotes are published anonymously (with permission).
“I am one of the many who are currently on BOTH antidepressants (2 types) & a stimulant (amphetamine). I lost my very dear friend (also a classmate) to suicide in my third year of med school. I have been on psych treatment since then.”
“Hi Dr. Wible. The number sounds high, but whether it is right or wrong is anybody’s guess. I can tell you about myself and my girlfriend—we both just started our third year at a DO medical school. I use 100 mg Sertraline to treat panic/anxiety attacks that were very bad when we had practical exams. I am also very depressed, but the Sertraline does nothing for this. I was diagnosed with ADD in 2013, right before taking the MCAT. I have been on and off of amphetamines and Concerta since then. Then there’s the alcohol and marijuana for the end of the day when I just get too tired of thinking. I have been offered various benzos by my family doctor to help treat the anxiety attacks. I haven’t filled that prescription, but do use them (from a friend) occasionally to help sleep, escape life etc. This is coming from someone who never touched alcohol or other drugs/mind-altering substances until I was 25-ish right at the time of taking the MCAT. My now significant other also uses Sertraline, Adderall, and Benzos to treat anxiety/panic attacks and ADD. Coincidence? I doubt it. So my sample size is two, but 100% are taking antidepressants and stimulants.”
“True. I’m on them, and every student I know is on them too. I’m on both; never took them before med school. Same with all of my friends. Eek!”
“I do recall around board study season hearing from half of my classmates about sharing Adderall and getting Rx from doctors they knew. I was even offered it, but never tried. However, my coffee intake has definitely gone up since school to the point having trouble controlling my bladder. I also know of about half of my friends taking antidepressants throughout school. So I would guess at least 50-75% of my class took stimulants and/or antidepressants.”
“I tried two types of antidepressants in medical school, lost more than 200 thousand dollars, and almost ended up homeless from medical school. All [my depression and debt] started in medical school. Yet my passion remains.”
“Hi Pamela, I agree! Students are afraid to speak about it and I know some who have even asked friends/family to get meds under their name so it isn’t on their record. I finally started talking about it with my classmates and found that many of my close friends were taking them and we had individually struggled alone not knowing there were others going through the same thing. Also, if everyone’s doing it and it gives you an edge, then everyone else has to do it.”
“Sounds about right. I never needed antidepressants before medical school. And it definitely made me rely on higher doses of methylphenidate than I’ve needed in the past.”
“I never thought I would take study drugs. But I was near the bottom of the class in my exam results, and then found out that several who were best in our year were taking study drugs. I cut my losses and copied them. Low and behold, my results improved drastically. I don’t like it, but for me it is better than falling behind and doing poorly. All my friends at other med schools use Modafinil and Adderall too. They also use recreational drugs like ecstasy, cocaine and acid when they’re partying. Drug use is very common amongst the med students I know.”
“In my med school class, I’ve heard of people on antidepressants, on sleeping pills, using pot to calm down, and then also on some kind of uppers for test days and days after partying which the partying was to de-stress..but I have no idea if it’s 75%…I don’t know enough of my class well enough to have that info, nor do I think anyone does…there are usually cliques of up to 25 people, but for people to say they know for sure details of 75% of their class would be hard for me to believe but maybe…there is a lot of it, I agree with that.”
“True. As a med student I was on antidepressants. No different now I am intern. Having just finished 12 days straight and >120 hrs. I can understand why people are also using stimulants.”
“True. I only have four friends in medical school that I know well enough to know which meds they take. All are on both. I went to the university psychiatrist in my Texas premed program for depression he asked when I felt better I told him when I took my friends stimulants to study, I expected him to give me a verbal wrist slap instead he gave me a script. I was on a steady dose for years but the first year of med school I kept upping the dose to try and keep up, ended up deciding I needed to stop after one episode of not sleeping for four days and having auditory hallucinations. Failed second year when I quit them cold turkey, didn’t feel like I was keeping up without them so switched to Modafinil which is much mellower than amphetamine but definitely not good for me. Everyone started antidepressants in school even folks without a history of depression. Being completely honest 75% seems a bit high, but I wouldn’t be that surprised if it were true, in my n=5 study it’s 100%.”
“True. But that number may be higher or lower depending on the school and year in med school. I was on an antidepressant in the last month of last semester because all my other coping skills weren’t enough. I’m on summer break and I haven’t needed any medications to be functional and happy. My depression was entirely induced by the stress and frustrations encountered during medical school.”
“I was on an inpatient internal medicine rotation working 12-14 hour days 6 days a week (as a 3rd year med student) and would ‘keep it together’ at the hospital and fall apart on the way home, cry and sleep to cope. It was the first time in my life I felt suicidal, no plans—just wanted to fade away. My husband was afraid to leave me alone. I put myself back on the Lexapro, equalized somewhat and kept pushing on. That all happened around Christmas of last year. In June I finally was able to find a psychiatrist. He put me on a trial of Adderall. I was hesitant due to the abuse potential but decided to give it a try. With the two meds I have less anxiety, way better at prioritizing, and my focus is improved. I’m studying for step 2 currently so time will tell.”
“I take Effexor 150mg QD. In addition to 10mg of amphetamine salts TID. I used to drink 2 quad shot white chocolate mochas from Starbucks a day, but with the stimulant I threw myself into SVT too frequently.”
“I cannot talk about anything beyond what I know of my immediate friend circle but I have in mind about 10 examples of people who started NEW prescriptions for 1) Stimulants for studying and staying awake 2) Antidepressants and/or mood stabilizers and one person who was started on 3) Beta blockers for new onset panic. These are people with new diagnoses since starting school. I know a few others who came in on these medications after having hard times as premeds (or earlier, I don’t know) That’s just those who actually got the prescription…. As I’m sure you know there is unfortunately also a great deal of illegal procurement of prescription medications as well as abuse of illegal drugs. An increase in alcohol abuse is also a major concern. People are self-medicating left and right.”
“Oh, I would not be surprised! I know 10 people from 5 different schools and at least 7 are on either.”
“I am lucky to have a great support structure and have coped quite well so far without needing any medication. I am actually diagnosed with ADHD and have a prescription for two medications which I don’t really use. The pressure to use them every day rather than relying on my own hard-won compensatory skills is certainly there. Interestingly, I am not shy about my diagnosis and talk about it openly to destigmatize it but I have actually cut back on that because if I’m not careful I inevitably get a lot of classmates asking if they can have some of my medication. For a future doctor to brazenly ask for illegal sharing of medicine is worrisome to me but again I do understand the pressure (to stay up just one more hour studying) that drives the behavior.”
“Popping prescription bottle caps and chafing of pills while studying in the library is a fixture of how daunting the pressures of medical school really are. Med school libraries are dungeons where souls came to die. You’re surrounded by absolute dread—the look of despair painted across the faces of your fellow classmates who feel at any second their life could be ruined with one failing grade. Most of my friends were on SSRI’s, Benzodiazepines, and various types of stimulants. I once asked a friend if he had anything to help me go to sleep and he recommended Lorazepam, which he gave me. The ‘top student’ in our class was rumored to be a serial user of cocaine. To avoid having a drug test reveal his dirty little secret prior to third year, he took a hiatus by engineering a family emergency to give himself adequate time to pass the contents of amphetamine (he passed). Elicit substances in medical school may seem like taboo to lay persons, however in our eyes, it’s a natural and regular experience. In fact, it is astounding how many medical students (myself included) smoke marijuana in order to experience a night of restful sleep. With each puff, it’s as if I escape a bit from my hectic reality. A reality dominated by judging, vengeful, and heartless administrators/faculty who can care less if we live or die, as long as we perform on USMLE Step 1. Yup, its that bad.”
In 1990, even I was severely depressed as a first-year med student. So my mom (a psychiatrist) mailed me a bottle of Trazodone. I thought I was the only one crying myself to sleep. Turns out occupationally-induced depression is rampant in medical training. Now schools dole out antidepressants like candy. Stimulants are used by med students like steroids in athletes. So where do we go from here? Should “progressive” med schools distribute samples of Zoloft and Adderall during orientation?
Problem is physicians must answer mental health questions (right next to questions on felonies and DUIs) to secure a medical license, hospital privileges, and participate with insurance plans. Check the YES box and be forced to disclose your “confidential” medical history and defend yourself—again and again for your entire career. Treated like a criminal for taking meds to cope with the torment of medical training (and practice).
Maybe that’s why so many future (and current) physicians sneak drugs and go off-the-grid for mental health care.
“I’ve been in practice 20 years and have been on antidepressants and anxiolytics for all of that time,” says Jason. “I drive 300 miles to seek care and always pay in cash. I am forced to lie on my state relicensing every year. There is no way in hell I would ever disclose this to the medical board—they are not our friends.”
What if we stop the mental health witch hunt on our doctors? Why not replace threats and punishment with safe confidential care? What if we address the root of the problem—the great sickness in medical education—rather than shifting blame to 75% of medical students for not having enough serotonin or dopamine or norepinephrine in their brains?
As scientists, we can’t continue to approach medical education reform as a neurotransmitter deficiency in medical students. Can we?
___
Pamela Wible, M.D., is a family physician in Oregon. She is happy in her solo practice and takes no psychiatric medication. Turns out her depression was environmental—entirely related to the culture of medical education. Dr. Wible is author of Physician Suicide Letters—Answered. View her TEDMED talk Why doctors kill themselves.
Thank You Very Much Dr Wible.
HT to MadInAmerica
Any pretense of legality Psychiatric/Psychologically imposed disability ever pretended to just got nuked, along with every protection our legal system extended to the disablers themselves and everyone harboring/assisting them.
See our intro to the following post if you need clarity.
State Medical Board Has A Simple Solution To Help Amid Physician Mental Health Crisis
Then read Title 18 Sec 241 & 242 of the Federal Criminal Code regarding Civil Rights
75% of med students are on antidepressants or stimulants (or both)
Pamela Wible MD
Posted on September 4, 2017 by Pamela Wible MD
“Have you ever been depressed as a physician?” I asked 220 doctors. Ninety percent stated yes. Yet few seek professional help. Here’s what depressed doctors do (when nobody’s looking). Some drink alcohol, exercise obsessively, even steal psychiatric meds. Still more shocking—I discovered that 75% of med students (and new doctors) are now on psychiatric medications.
“I was told by the psychologist at my med school’s campus assistance program, that 75% of the class of 175 people were on antidepressants,” shares psychiatrist Dr. Jaya V. Nair. “He wasn’t joking. How broken is the system, that doctors have to be pushed into illness in order to be trained to do their job?”
“During my internship, I found out that at least 75% of my fellow residents were on SSRIs or other antidepressants, just ‘to get through it’ because it was so horrible.” states Dr. Joel Cooper, “Depression, or a constantly depressed state, is more or less the norm in medical school and throughout one’s residency.”
“When I left my residency, I was alarmed to find out that about 75% of my fellow residents had started antidepressants since their intern year,” says Dr. Jill Fadal.
Seems the epidemic of depressed doctors begins in medical school. I wondered how best to verify this oft-repeated 75% statistic. Just then a student called to tell me what her professor said during orientation: “Look around the room. By the end of your first year, two-thirds of your class will be on antidepressants.”
I’m appalled. Yet she’s grateful. Why? Her school is so progressive. They normalize the need for antidepressants.
I must be out of touch. Do most med students require psych drugs for day-to-day survival? I turned my question over to Facebook: “75% of med students and residents are taking either stimulants or antidepressants or both. True or false?”
“It’s absolutely, horrifyingly, true. It is a symptom of a great sickness in MedEd.”
“Sadly I am guessing true as I prescribed some for my residents every year that I worked in a residency.”
“True, but I’m sure a lot is unprescribed.”
“I would assume definitely true, Ritalin, Adderall, energy drinks, ephedrine. Yep.”
“While working as a nurse at a major Army hospital, I was astounded by the number of medical students on Adderall or Ritalin.”
I’ve been on an antidepressant since being premed—18 years now. Little did I know it would be impossible to wean myself off and that my entire class was using Adderall.”
“True but most take them in secret as there are negative consequences and stigma that come with getting your mental health addressed.”
“Very true. From my practical point of view, I’d put medical students & residents at 100%.”
“I take both Zoloft and Adderall daily.”
“Very much so true—the percentages may actually be higher. I see it in my classes and I’m only a premed student.”
“If coffee counts as a stimulant it’s definitely 100%.”
“The only way I’d say false is to say it’s higher. I’d say a quarter of my class had to take a leave for a mental health break.”
Having received Facebook confirmation that most med students are on psych drugs, I then queried 1800 medical students via email with the same question and encouraged respondents to share personal experiences. To prevent professional retaliation, all quotes are published anonymously (with permission).
“I am one of the many who are currently on BOTH antidepressants (2 types) & a stimulant (amphetamine). I lost my very dear friend (also a classmate) to suicide in my third year of med school. I have been on psych treatment since then.”
“Hi Dr. Wible. The number sounds high, but whether it is right or wrong is anybody’s guess. I can tell you about myself and my girlfriend—we both just started our third year at a DO medical school. I use 100 mg Sertraline to treat panic/anxiety attacks that were very bad when we had practical exams. I am also very depressed, but the Sertraline does nothing for this. I was diagnosed with ADD in 2013, right before taking the MCAT. I have been on and off of amphetamines and Concerta since then. Then there’s the alcohol and marijuana for the end of the day when I just get too tired of thinking. I have been offered various benzos by my family doctor to help treat the anxiety attacks. I haven’t filled that prescription, but do use them (from a friend) occasionally to help sleep, escape life etc. This is coming from someone who never touched alcohol or other drugs/mind-altering substances until I was 25-ish right at the time of taking the MCAT. My now significant other also uses Sertraline, Adderall, and Benzos to treat anxiety/panic attacks and ADD. Coincidence? I doubt it. So my sample size is two, but 100% are taking antidepressants and stimulants.”
“True. I’m on them, and every student I know is on them too. I’m on both; never took them before med school. Same with all of my friends. Eek!”
“I do recall around board study season hearing from half of my classmates about sharing Adderall and getting Rx from doctors they knew. I was even offered it, but never tried. However, my coffee intake has definitely gone up since school to the point having trouble controlling my bladder. I also know of about half of my friends taking antidepressants throughout school. So I would guess at least 50-75% of my class took stimulants and/or antidepressants.”
“I tried two types of antidepressants in medical school, lost more than 200 thousand dollars, and almost ended up homeless from medical school. All [my depression and debt] started in medical school. Yet my passion remains.”
“Hi Pamela, I agree! Students are afraid to speak about it and I know some who have even asked friends/family to get meds under their name so it isn’t on their record. I finally started talking about it with my classmates and found that many of my close friends were taking them and we had individually struggled alone not knowing there were others going through the same thing. Also, if everyone’s doing it and it gives you an edge, then everyone else has to do it.”
“Sounds about right. I never needed antidepressants before medical school. And it definitely made me rely on higher doses of methylphenidate than I’ve needed in the past.”
“I never thought I would take study drugs. But I was near the bottom of the class in my exam results, and then found out that several who were best in our year were taking study drugs. I cut my losses and copied them. Low and behold, my results improved drastically. I don’t like it, but for me it is better than falling behind and doing poorly. All my friends at other med schools use Modafinil and Adderall too. They also use recreational drugs like ecstasy, cocaine and acid when they’re partying. Drug use is very common amongst the med students I know.”
“In my med school class, I’ve heard of people on antidepressants, on sleeping pills, using pot to calm down, and then also on some kind of uppers for test days and days after partying which the partying was to de-stress..but I have no idea if it’s 75%…I don’t know enough of my class well enough to have that info, nor do I think anyone does…there are usually cliques of up to 25 people, but for people to say they know for sure details of 75% of their class would be hard for me to believe but maybe…there is a lot of it, I agree with that.”
“True. As a med student I was on antidepressants. No different now I am intern. Having just finished 12 days straight and >120 hrs. I can understand why people are also using stimulants.”
“True. I only have four friends in medical school that I know well enough to know which meds they take. All are on both. I went to the university psychiatrist in my Texas premed program for depression he asked when I felt better I told him when I took my friends stimulants to study, I expected him to give me a verbal wrist slap instead he gave me a script. I was on a steady dose for years but the first year of med school I kept upping the dose to try and keep up, ended up deciding I needed to stop after one episode of not sleeping for four days and having auditory hallucinations. Failed second year when I quit them cold turkey, didn’t feel like I was keeping up without them so switched to Modafinil which is much mellower than amphetamine but definitely not good for me. Everyone started antidepressants in school even folks without a history of depression. Being completely honest 75% seems a bit high, but I wouldn’t be that surprised if it were true, in my n=5 study it’s 100%.”
“True. But that number may be higher or lower depending on the school and year in med school. I was on an antidepressant in the last month of last semester because all my other coping skills weren’t enough. I’m on summer break and I haven’t needed any medications to be functional and happy. My depression was entirely induced by the stress and frustrations encountered during medical school.”
“I was on an inpatient internal medicine rotation working 12-14 hour days 6 days a week (as a 3rd year med student) and would ‘keep it together’ at the hospital and fall apart on the way home, cry and sleep to cope. It was the first time in my life I felt suicidal, no plans—just wanted to fade away. My husband was afraid to leave me alone. I put myself back on the Lexapro, equalized somewhat and kept pushing on. That all happened around Christmas of last year. In June I finally was able to find a psychiatrist. He put me on a trial of Adderall. I was hesitant due to the abuse potential but decided to give it a try. With the two meds I have less anxiety, way better at prioritizing, and my focus is improved. I’m studying for step 2 currently so time will tell.”
“I take Effexor 150mg QD. In addition to 10mg of amphetamine salts TID. I used to drink 2 quad shot white chocolate mochas from Starbucks a day, but with the stimulant I threw myself into SVT too frequently.”
“I cannot talk about anything beyond what I know of my immediate friend circle but I have in mind about 10 examples of people who started NEW prescriptions for 1) Stimulants for studying and staying awake 2) Antidepressants and/or mood stabilizers and one person who was started on 3) Beta blockers for new onset panic. These are people with new diagnoses since starting school. I know a few others who came in on these medications after having hard times as premeds (or earlier, I don’t know) That’s just those who actually got the prescription…. As I’m sure you know there is unfortunately also a great deal of illegal procurement of prescription medications as well as abuse of illegal drugs. An increase in alcohol abuse is also a major concern. People are self-medicating left and right.”
“Oh, I would not be surprised! I know 10 people from 5 different schools and at least 7 are on either.”
“I am lucky to have a great support structure and have coped quite well so far without needing any medication. I am actually diagnosed with ADHD and have a prescription for two medications which I don’t really use. The pressure to use them every day rather than relying on my own hard-won compensatory skills is certainly there. Interestingly, I am not shy about my diagnosis and talk about it openly to destigmatize it but I have actually cut back on that because if I’m not careful I inevitably get a lot of classmates asking if they can have some of my medication. For a future doctor to brazenly ask for illegal sharing of medicine is worrisome to me but again I do understand the pressure (to stay up just one more hour studying) that drives the behavior.”
“Popping prescription bottle caps and chafing of pills while studying in the library is a fixture of how daunting the pressures of medical school really are. Med school libraries are dungeons where souls came to die. You’re surrounded by absolute dread—the look of despair painted across the faces of your fellow classmates who feel at any second their life could be ruined with one failing grade. Most of my friends were on SSRI’s, Benzodiazepines, and various types of stimulants. I once asked a friend if he had anything to help me go to sleep and he recommended Lorazepam, which he gave me. The ‘top student’ in our class was rumored to be a serial user of cocaine. To avoid having a drug test reveal his dirty little secret prior to third year, he took a hiatus by engineering a family emergency to give himself adequate time to pass the contents of amphetamine (he passed). Elicit substances in medical school may seem like taboo to lay persons, however in our eyes, it’s a natural and regular experience. In fact, it is astounding how many medical students (myself included) smoke marijuana in order to experience a night of restful sleep. With each puff, it’s as if I escape a bit from my hectic reality. A reality dominated by judging, vengeful, and heartless administrators/faculty who can care less if we live or die, as long as we perform on USMLE Step 1. Yup, its that bad.”
In 1990, even I was severely depressed as a first-year med student. So my mom (a psychiatrist) mailed me a bottle of Trazodone. I thought I was the only one crying myself to sleep. Turns out occupationally-induced depression is rampant in medical training. Now schools dole out antidepressants like candy. Stimulants are used by med students like steroids in athletes. So where do we go from here? Should “progressive” med schools distribute samples of Zoloft and Adderall during orientation?
Problem is physicians must answer mental health questions (right next to questions on felonies and DUIs) to secure a medical license, hospital privileges, and participate with insurance plans. Check the YES box and be forced to disclose your “confidential” medical history and defend yourself—again and again for your entire career. Treated like a criminal for taking meds to cope with the torment of medical training (and practice).
Maybe that’s why so many future (and current) physicians sneak drugs and go off-the-grid for mental health care.
“I’ve been in practice 20 years and have been on antidepressants and anxiolytics for all of that time,” says Jason. “I drive 300 miles to seek care and always pay in cash. I am forced to lie on my state relicensing every year. There is no way in hell I would ever disclose this to the medical board—they are not our friends.”
What if we stop the mental health witch hunt on our doctors? Why not replace threats and punishment with safe confidential care? What if we address the root of the problem—the great sickness in medical education—rather than shifting blame to 75% of medical students for not having enough serotonin or dopamine or norepinephrine in their brains?
As scientists, we can’t continue to approach medical education reform as a neurotransmitter deficiency in medical students. Can we?
___
Pamela Wible, M.D., is a family physician in Oregon. She is happy in her solo practice and takes no psychiatric medication. Turns out her depression was environmental—entirely related to the culture of medical education. Dr. Wible is author of Physician Suicide Letters—Answered. View her TEDMED talk Why doctors kill themselves.
Thank You Very Much Dr Wible.
HT to MadInAmerica
Monday, January 30, 2017
More On The Biological Evidence For "Mental Illness"
Dr Phil Hickey
On January 10, 2017, I put up a post titled The Biological Evidence for “Mental Illness”. It was published simultaneously on Mad in America. The post was a response to an earlier comment from Carolina Partners in Mental Healthcare PLLC, which included the assertion “mental illnesses have a long history of biological evidence.” In my January 10 article, I challenged this assertion and pointed out that no such evidence existed. The article generated some comments, most of which were favorable. There was one comment, however, from Michael, who asserted:
“Your rebuttal that there are no scientific studies to these cases can be dismissed with a quick google search.”
In my response to Michael, I asked him to cite me some references to support this assertion. On January 15, Michael wrote back citing three studies: the first on the neurobiology of depression; the second on the neurobiology of “schizophrenia”; and the third on the neurobiology of “bipolar disorder”.
I examined these studies, and started to draft a response to Michael, but as I was writing, I realized that the subject matter warranted a wider audience and needed to be put up as a post. This is not because the studies cited are particularly compelling. As we shall see below, they are not. But rather, because what has happened here is something that occurs routinely in these debates. Psychiatry proponents claim there is evidence to support their position that “mental illnesses” are caused by biological malfunctions – but when pressed for references, they either don’t respond at all, or they dish up the kind of references cited by Michael.
Continue Reading
Thank You Dr Hickey
On January 10, 2017, I put up a post titled The Biological Evidence for “Mental Illness”. It was published simultaneously on Mad in America. The post was a response to an earlier comment from Carolina Partners in Mental Healthcare PLLC, which included the assertion “mental illnesses have a long history of biological evidence.” In my January 10 article, I challenged this assertion and pointed out that no such evidence existed. The article generated some comments, most of which were favorable. There was one comment, however, from Michael, who asserted:
“Your rebuttal that there are no scientific studies to these cases can be dismissed with a quick google search.”
In my response to Michael, I asked him to cite me some references to support this assertion. On January 15, Michael wrote back citing three studies: the first on the neurobiology of depression; the second on the neurobiology of “schizophrenia”; and the third on the neurobiology of “bipolar disorder”.
I examined these studies, and started to draft a response to Michael, but as I was writing, I realized that the subject matter warranted a wider audience and needed to be put up as a post. This is not because the studies cited are particularly compelling. As we shall see below, they are not. But rather, because what has happened here is something that occurs routinely in these debates. Psychiatry proponents claim there is evidence to support their position that “mental illnesses” are caused by biological malfunctions – but when pressed for references, they either don’t respond at all, or they dish up the kind of references cited by Michael.
Continue Reading
Thank You Dr Hickey
Thursday, January 26, 2017
Mental Health First Aid: Another Psychiatric Expansionist Tool
Dr Phil Hickey
On December 25, 2016, the Baltimore Sun published an excellent article titled Drug companies prey on children, by Patrick D. Hahn, PhD. Dr. Hahn is an affiliate professor of biology at Loyola University, Maryland. Here are some quotes:
Please take a look at Dr. Hahn’s article, and pass it on. Mental
Health First Aid is not a good thing. Rather, it is just another
psychiatric expansionist tool.
Continue Reading.
Thank You Dr Hickey
And bookmark Dr Hickey's URL.
On December 25, 2016, the Baltimore Sun published an excellent article titled Drug companies prey on children, by Patrick D. Hahn, PhD. Dr. Hahn is an affiliate professor of biology at Loyola University, Maryland. Here are some quotes:
“I recently attended Youth Mental Health First Aid Training at a local public school. It was an eye-opening experience.”
“Youth Mental Health First Aid Training,
sponsored by the National Council for Behavioral Health, is intended to
enable teachers, parents and others in contact with young people to
identify potential ‘mental illnesses’ in order to facilitate early
detection and treatment by our mental health care system. My fellow
attendees were surprisingly open about their own experiences with that
system. One mentioned that her son became manic after being diagnosed
for ADHD. Another said that both she and her roommate became bipolar
after being diagnosed for depression. Neither our facilitators nor
anyone else present pointed out that mania and bipolar disorder are
toxic effects of medications commonly prescribed for ADHD and
depression.”
“Our training manual didn’t say anything
about this either, although it did claim that depression is caused by a
deficiency of serotonin — a fable that by now has become as discredited
as the phlogiston theory of chemistry. It also stated that mental health
interventions are ‘evidence-based’ and ‘scientifically tested’ —
neglecting to mention that much of that evidence is put forth by drug
companies who have a fiduciary duty to do everything they can to
maximize sales of their products.”
“So is all this a scheme to push more drugs to more kids? The 2013/2014 annual report
for the National Council for Behavioral Health, titled ‘A Legacy of
Excellence and Impact,’ gives us a hint. It lists the organization’s
supporters as including the Pharmaceutical Research and Manufacturers of
America (PhRMA) along with no fewer than 12 different drug companies.
Would these folks be ponying up the cash if they weren’t confident this
program would increase sales? And do the parents and teachers who attend
the council’s training program — no doubt with the best intentions in
the world — realize that they are essentially sitting through an
eight-hour infomercial bought and paid for by the drugmakers?”
“One out of 13 American children between the ages of 6 and 17 has taken a psychotropic medication within the last six months, according to the Centers for Disease Control. Meanwhile, youth suicide rates are at their peak
going back at least as far back as 1999, while the number of children
receiving disability benefits for mental illness is at an all-time high.”
Continue Reading.
Thank You Dr Hickey
And bookmark Dr Hickey's URL.
Tuesday, January 10, 2017
The Biological Evidence For "Mental Illness"
Behaviorism and Mental Health
by Phil Hickey on January 10, 2017
On January 2, 2017, I published a short post titled Carrie Fisher Dead at Age 60 on Behaviorism and Mental Health. The article was published simultaneously on Mad in America.
On January 4, a response from Carolina Partners was entered into the comments string on both sites.
Carolina Partners in Mental Healthcare, PLLC, is a large psychiatric group practice based in North Carolina. According to their website, they comprise 14 psychiatrists, 7 psychologists, 34 Advanced Practice Nurse Practitioners/Physicians Assistants, and 43 Therapists and Counselors. They have 27 North Carolina locations.
Partners’ comment consists essentially of unsubstantiated assertions, non sequiturs, and appeals to psychiatric authority. As such, it is fairly typical of the kind of “rebuttals” that psychiatry’s adherents routinely direct towards those of us on this side of the issue. For this reason, and also because it comes from, and presumably represents the views of, an extremely large psychiatric practice, it warrants a close look.
I will discuss each paragraph in turn.
“We strongly disagree with this article, which neglects a lot of important information and uses selective hearing to distort what Carrie Fisher was about and also to distort the evidence for mental illness as a real disorder.”
My Carrie Fisher article was brief (566 words), and was intended as a counterpoint to the very widespread obituaries that lionized her as a champion of “bipolar disorder”. The essential point of my article was that Ms. Fisher had been a victim of psychiatry, and like a great many such victims, died prematurely. Obviously I neglected a lot of important information. I could have gone into great length as to the recklessness of psychiatry assigning the bipolar label, with all its implications of helplessness, disempowerment, and “chemical imbalance” to a young woman who by her own account was, at the time, using any drugs she could get her hands on. But I felt that a brief and respectful statement of the facts was all that was needed.
. . . . . . . . . . . . . . . .
“Mental illnesses have a long history of biological evidence. For example, researchers have demonstrated that people with depression have an overactive area of the brain, called Brodmann area 25. Schizophrenia has been linked to specific genes, as PTSD and autism have been linked to specific brain abnormalities. Suicide has been linked to a decreased concentration of serotonin in the brain. OCD has been linked to increased activity in the basal ganglia region of the brain.”
Brodmann area 25 (BA25)
Partners did not provide a specific reference in support of this contention, but my best guess is that the reference is Mayberg, HS, et al (1999) Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness (Am J Psychiatry 1999; 156:675–682). Here’s the study’s primary conclusion:
“Reciprocal changes involving subgenual cingulate [which includes Brodmann area 25] and right prefrontal cortex occur with both transient and chronic changes in negative mood.”
What this means essentially is that negative mood, whether transient or enduring, is correlated with changes in both the subgenual cingulate (Brodmann area 25) and the right pre-frontal cortex, and that when the depression is relieved, the changes are reversed.
This, of course, is an interesting finding, but provides no evidence that depression, mild or severe, transient or enduring, is caused by a biological pathology.
The reality is that all human activity is triggered by brain activity. Every thought, every feeling, every action has its origins in the brain. I cannot lift a finger, blink an eye, scratch my head, or recall my childhood home without a characteristic brain function initiating and maintaining the action in question. Without stimuli from the brain, my heart will stop beating, my respiratory apparatus will shut down, and I will die, unless these functions are maintained by machines.
So there is absolutely no surprise in the discovery that sadness and despondency have similar neural triggers and maintainers. It would be amazing if they didn’t. But – and this is the critical point – this does not warrant the conclusion that sadness which crosses arbitrary and vaguely-defined thresholds of severity, duration, and frequency is best conceptualized as an illness caused by pathological or excessive activity in BA 25.
Depression is a normal state. It is the normal human reaction to significant loss and/or living in sub-optimal conditions/circumstances. It is also an adaptive mechanism, the purpose of which is to encourage us to take action to restore the loss and/or improve the conditions.
All consciously-felt human drives stem from unpleasant feelings. Thirst drives us to seek water; hunger, food; hypothermia, warmth; hyperthermia, coolness; danger, safety, etc. Sadness and despondency are no exceptions. They drive us to seek change, and have been serving the species well since prehistoric times.
But – as is the case with all the above examples – when a drive is not acted upon, for whatever reason, the unpleasant feelings worsen. Just as unrequited hunger and thirst increase in strength, so the depression drive when not requited deepens.
The reality is that most people deal with depression in appropriate, naturalistic, and time-honored ways. If the source of the depression is the loss of a job, they start job-hunting. If the source is an abusive relationship, they seek ways to exit or remediate the situation. If the source is a shortage of money, they seek ways to budget more sensibly, or increase their earnings; etc.
Depression, either mild or severe, transient or lasting, is not a pathological condition. It is the natural, appropriate, and adaptive response when a feeling-capable organism confronts an adverse event or circumstance. And the only sensible and effective way to ameliorate depression is to deal appropriately and constructively with the depressing situation. Misguided tampering with the person’s feeling apparatus is analogous to deliberately damaging a person’s hearing because he is upset by the noise pollution in his neighborhood, or damaging his eyesight because of complaints about litter in the street.
Our feeling apparatus is as valuable and adaptive as our other senses. But psychiatry routinely numbs, and in many cases permanently damages, this apparatus to sell drugs and to promote the fiction that they are real doctors. Their justification for this blatantly destructive activity hinges on the false notion that depression becomes a diagnosable illness when its severity crosses arbitrary and vaguely-defined thresholds. But deep despondency is no more an illness than mild despondency. The latter is the appropriate and adaptive response to minor losses and adversity. The former is the appropriate and natural response to more profound or more enduring adversity. Though, of course, what constitutes profound adversity will vary enormously from person to person. An individual, for instance, raised to the expectation of stable and permanent employment may be truly heartbroken at the loss of a job. Another individual, raised to the notion that there’s always another job “around the corner” will, other things being equal, be less affected. And so on.
In this regard, it’s noteworthy that Partners’ comment refers to overactivity in BA 25. The use of the prefix over implies pathology, but in reality there is no yardstick to determine what would be a correct amount of activity for BA 25. All that can be said, on the basis of Mayberg et al’s findings, and subsequent BA 25 research, is that when a person is sad, there is more activity than when he is happy. So the use of the term “overactivity” is deceptive – sneaking in the notion of pathology without any genuine or valid reasons to consider it so. The “reasoning” here is:
– depression is an illness
– depression is correlated with high activity in BA 25
– therefore high activity in BA 25 is pathological
In other words, the contention of pathology rests on the assumption that depression is an illness. To turn around and use this falsely inferred pathology to prove that depression is an illness is obviously fallacious. It is also typical of the kind of circular reasoning that permeates psychiatric contentions. In reality, there is nothing in Mayberg et al or in subsequent research that warrants the conclusion that the increased activity in BA 25 is pathological or excessive.
. . . . . . . . . . . . . . . .
Schizophrenia linked to specific genes
This assertion, that schizophrenia is linked to specific genes, is frequently adduced in these debates, as evidence that “schizophrenia” is a real illness with a biological pathology. Here again, Partners do not provide any references in support of this assertion, but there have been a number of studies in the past fifteen years or so that have found links of this kind. However, in all cases, the correlations have been small. In other words, there are always a great many individuals who have been assigned the “schizophrenia” label, but who do not have the gene variant in question; and there are a great many who have the gene variant, but who do not acquire the label “schizophrenia”. To date, no genetic test has been found helpful in confirming or refuting a “diagnosis of schizophrenia”.
An additional problem arises here, in that the assertion that “schizophrenia has been linked to specific genes” is often interpreted as meaning that “schizophrenia” is a genetic disease, which it emphatically is not. To illustrate this, let’s look briefly at a real genetic illness: polycystic kidney disease (PKD). This is a well established genetic illness caused by cysts in the kidneys. The cysts progressively block the flow of blood through the kidneys, causing tissue death.
Most cases of PKD are caused by the defective gene (PKD-1). In polycystic kidney disease, the pathology occurs because the PKD-1 gene causes the nephrons to be made from cyst wall epithelium rather than nephron epithelium. And cyst wall epithelium produces fluid which accumulates in, and ultimately destroys, the nephrons and the kidney.
So the gene determines the structure of the nephron wall. This is the primary genetic effect. This structure causes the wall to produce fluid. As the nephrons become increasingly blocked, the kidneys produce less urine. So, reduced urination is a secondary effect of the gene PKD-1. Symptoms of PKD don’t usually emerge until adulthood, but about 25% of children with PKD1 experience pain and other symptoms. So a child growing up with polycystic kidney disease may feel sick much of the time. Such a child, other things being equal, is likely to be fussier and more distressed than other children, and it is entirely possible that one could find a weak correlational link between gene PKD-1 and childhood fussiness, though, of course, any search for such a correlation will be confounded by the obvious fact that children can be habitually fussy for other reasons. The fussiness would be a tertiary effect of the gene PKD1.
And from there the causal chain could continue in various ever-weakening directions. For instance, the child might become somewhat sad and despondent. Or it could be that the child received extra attention and comforting from his parents and was fairly content, and so on. Ultimately the outcome is impossible to predict with any kind of precision, and the best we can expect from genes vs. subsequent behavior studies are weak, tenuous correlations.
Cleft palate is another example of a pathology that is caused by a gene defect; actually a gene deletion. This condition results in a characteristically strained and nasal speech quality which can be quite stigmatizing. The nasal speech is a secondary effect of the gene deletion.
Children with this kind of speech are sometimes mocked and bullied by their peers. The child might react to this kind of stigmatizing by speaking as little as possible, by withdrawing socially, or in various other ways. These reactions would be considered tertiary effects of the defect. And so on. As with the PKD, each step in the chain takes us further from the genetic defect, and the statistical associations grow proportionally weaker, and it would be stretching the matter to say that the lack of speech was caused by the gene deletion. Nor would one conclude that the child’s social withdrawal was a symptom of a genetic disease. And this is true even though the link between the deletion and the cleft palate is clear-cut and direct.
In the same way, it is simply not tenable to claim that “schizophrenic” behaviors (e.g. disorganized speech) are symptoms of a genetic disease. This is particularly the case in that correlations between the “diagnosis” and genetic anomalies are typically very small. The effects of any minor genetic anomalies that might exist have had ample opportunity to be shaped by social and environmental factors, and these are more credible causal constructs.
“Schizophrenia” is not a unified condition. Rather, it is a loose collection of vaguely defined behaviors. For this reason, any genetic research done on this condition will inevitably result in conflicting and confusing results. It’s like looking for genetic similarities in all the people who play bridge, or read romance novels, visit libraries, play football, or whatever. If the sample sizes are large enough, and in genetic research sample sizes are often enormous, one could probably find small effects in all or most of these areas, but no one would conclude from this that these are genetically determined activities, much less illnesses.
A person’s ability to learn depends on two general factors: a) the structure of his brain, as determined by his DNA, and b) his experiences since birth.
One can’t learn to play the piano, for instance, unless one has appropriate neural apparatus, and fingers, both of which require appropriate DNA. But even a person with good genetic endowment in these regards, will never learn to play unless he is exposed to certain environmental factors. He must, at the very least, encounter a piano. In the same way, a person whose genetic endowment might be relatively marginal might become an excellent pianist, if he were to receive persistent environmental encouragement and support.
Similar reasoning can be applied to the behavior of not-being-“schizophrenic.” This behavior involves navigating the pitfalls of late adolescence/early adulthood, and establishing functional habits in interpersonal, occupational, and other important life areas. Obviously it requires appropriate neural apparatus, hence the weak correlations with genetic material, but equally clearly it calls for a nurturing childhood environment, with opportunities for emotional growth and acquisition of social, occupational, and other skills.
Given all of this, it’s not surprising that researchers are finding correlations between DNA variations and a “diagnosis” of schizophrenia, but given the number of links in the causal chain and the multiplicity of possible pathways at each link, it is also not surprising that the correlations are always found to be weak, and of little or no practical consequence.
Nor is it surprising that the correlations between being labeled “schizophrenic” and various psychosocial factors are by contrast generally strong. Having a schizophrenia label is correlated with childhood social adversity, childhood abuse and maltreatment, poverty, and a family history of migration.
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Generally similar considerations apply to Partners contentions with regards to “PTSD”, “autism”, suicide, and “OCD”, but space precludes a detailed discussion here.
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“Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, says, ‘All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases…The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?'”
Dr. Kandel (now 87 years old) is an eminent neuroscience researcher at Columbia University. There’s an extensive biography in Wikipedia. His early research focused on the neurophysiology of memory. He has received numerous awards, including the Nobel Prize in Physiology/Medicine (2000), and is widely published. His record of research achievements is enormous, and his knowledge and expertise are vast, but in the statement quoted by Partners, and, incidentally, by other psychiatry adherents, he is simply wrong.
Let’s take a closer look. Logically, the Kandel quote can be stated symbolically as: A is identical to B; therefore malfunctions or aberrations in A are malfunctions or aberrations in B.
On the face of it, this seems sound, and indeed, it is a valid inference in some situations. For instance, the furnace in a person’s home is the primary heating appliance; therefore, malfunctions in the furnace are malfunctions in the primary heating appliance. Indeed, in a simple example of this sort, the statement is tautological. We are simply substituting the synonyms furnace and primary heating appliance, and the inference contains no new information or insights. But the inference is fallacious in more complex matters.
Let’s concede, for the sake of discussion, that the premise of the Kandel quote is true, i.e., that all mental processes are brain processes. The term mental processes embraces a wide range of activities, including sensations, perceptions, thoughts, choices, positive feelings, negative feelings, hopes, beliefs, speaking, singing, general behavior, etc.
The term “disorders of mental functioning” is harder to define, but, again for the purposes of discussion, let’s accept the APA’s catalog as definitive in this regard. Let’s accept that anything listed in the DSM is a “disorder of mental functioning”.
It’s immediately obvious that some of the DSM entries are indeed the result of brain malfunctioning. In the text these are referred to as disorders due to a general medical condition or to the effects of a substance. But in the great majority of DSM labels, no such biological cause is identified, and so the conclusion in the Kandel quote would appear to call for some kind of evidence or proof. However, in the Kandel quote, the conclusion is not presented as something that has been, or even needs to be, proven. Rather, it is presented as a logical conclusion inherent in, and stemming directly from, the premise. And it is from this perspective that the Kandel quote needs to be evaluated.
To pursue this, let’s consider the example of “oppositional defiant disorder”. This is a disorder of mental functioning as defined above, because it is listed in the DSM. And according to Dr. Kandel’s “logic”, it is also therefore a “biological disease”. The “symptoms” of oppositional defiant disorder as listed in DSM-5 are:
Often loses temper.
Is often touchy or easily annoyed.
Is often angry and resentful.
Often argues with authority figures or, for children and adolescents, with adults.
Often actively defies or refuses to comply with requests from authority figures or with rules.
Often deliberately annoys others.
Often blames others for his or her mistakes or misbehavior.
Has been spiteful or vindictive at least twice within the past 6 months. (p 462)
Obviously for any of these behaviors to occur, there has to be corresponding neural activity. But there is no necessity that the neural activity is diseased or malfunctioning in any way. A child learning from his environment, developing his behavioral repertoire in accordance with the ordinary principles or learning, could acquire any or all of these behavioral habits without any malfunctioning in his neural apparatus. We acquire counterproductive habits as readily, and by essentially the same processes, as we acquire productive ones. In general, if a child discovers that he can acquire power and control in his environment by throwing temper tantrums, he will, other things being equal, acquire the habit of throwing temper tantrums. Similarly, if arguing with parents and other authority figures yields positive results, there is a good chance that this also will become habitual. And this is not because there is anything wrong with the child’s brain. Rather, it’s because his brain is functioning correctly. He is internalizing as habits those decisions and actions that pay off. It is often observed in child-raising practice that if you’re not training your children, they’re training you.
Similar observations can be made about the other seven “symptoms” of oppositional defiant disorder, and indeed all the DSM labels. A person with a perfectly normal-functioning brain can acquire the habits in question if the circumstances are conducive to this learning.
So to return to the question in the Kandel quote: “Where else could [mental illness] be if not in the brain?”, the answer is clear: In the self-serving and unwarranted perception of psychiatrists. Mental illness is the distorting lens through which psychiatrists view all problems of thinking, feeling, and behaving. It is the device they use to legitimize their drug-pushing and to maintain the fiction that they are practicing medicine.
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“You’re right that mental illness is also affected by social and environmental conditions–by a person’s disposition, or upbringing, or current environment. It’s also true that mental illness is affected by drug use (both prescribed and not prescribed). So are other medical conditions, such as heart disease and cancer.”
I’m not sure where Partners are coming from here, because I never made any such statement. In my view, which I have stated clearly on numerous occasions, “mental illness” is a psychiatric invention, self-servingly created to promote the spurious notion that all problematic thoughts, feelings, and/or behaviors are illnesses. And not just illnesses in some vague allegorical sense, but real illnesses “just like diabetes”, which need to be treated by medically trained psychiatrists with mood-altering drugs and high voltage electric shocks to the brain.
Partners’ vague concessions concerning environment, child-rearing, and drug effects is a fairly standard psychiatric sop, but doesn’t mitigate their earlier contentions on the “long history of biological evidence” and their uncritical endorsement of the logically spurious Kandel quote.
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“And it’s true that mental illness is often difficult to diagnose because of
1) the current limitations of the field of research. Thomas R. Insel, MD, director of the National Institute of Mental Health, for example, talks about how the diagnosis and treatment of mental illness today is where cardiology was 100 years ago, concluding that we need to continue scientific research of mental illnesses. (There’s a longer quote on this below.)”
And (from later in the comment)
“Longer aforementioned quote:
Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient’s physical presentation and listen to the patient’s subjective complaints. Today they can measure cholesterol levels, examine the heart’s electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. ‘In most areas of medicine, we now have a whole toolkit to help us know what’s going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine,’ he says.
Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. ‘We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We’re finally able to answer some of the fundamental questions.'”
It is at least forty years since I started hearing about psychiatry’s great biological breakthroughs that were just around the proverbial corner, and the promise, if my readers will pardon the pun, is getting a little old.
What’s noteworthy, however, is that in other disciplines, where there is hope or expectation of breakthroughs, the proponents of these endeavors generally wait until the evidence is in, before implementing practices based on these hopes. In fact, to the best of my knowledge, psychiatry is the only profession whose entire work, indeed, whose entire conceptual framework, is based on “evidence” and “breakthroughs” that are not yet to hand.
Note also the truly exquisite contrast between Partners’ earlier and confident contention that “mental illnesses have a long history of biological evidence” with the assertion here that the “diagnosis” and “treatment” of “mental illness” today is where cardiology was 100 year ago.
Incidentally, Dr. Insel, former Director of the NIMH, also said:
“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.” (Transforming Diagnosis, 2013)
And let us be quite clear. “Lack of validity” in this context means that the “diagnoses” don’t actually correspond to any disease entities in the real world. Note also that Dr. Insel didn’t say poor validity, or low validity. He said lack of validity – meaning none.
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Back to the Carolina Partners comment:
“2) mental illness symptoms often overlap with symptoms caused by other illnesses, for example, someone with cancer may also become depressed after diagnosis. Or someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.
While considering all these factors, it is still completely inaccurate to state that there is no biological foundation for mental illnesses. They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones. As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
This is a little rambling, but let’s see if we can unravel it.
“… someone with cancer may also become depressed after diagnosis.”
This is true. In fact, I would say that most people who contract serious illness become somewhat sad and despondent. But this in no way establishes the notion that the sadness should be considered an additional illness.
“…someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.”
This quote contains one of psychiatry’s core fallacies: that the various “mental illnesses” are the causes of their respective symptoms (as is the case in real illness). To illustrate the fallacy, consider the hypothetical conversation:
Client’s wife: Why is my husband so tired all the time?
Psychiatrist: Because he has an illness called major depressive disorder.
Client’s wife: How do you know he has this illness?
Psychiatrist: Because he is tired all the time.
Psychiatry defines major depression (the so-called illness) by the presence of five “symptoms” from a list of nine, one of which is fatigue, and then routinely adduces the “illness” to explain the symptoms. In reality, the “symptoms” are entailed in the definition of the “illness”, and the explanation is entirely spurious. There are many valid reasons why a person might feel fatigued, but none of these is because he “has a mental illness”. Mental illnesses are merely labels with no explanatory significance. And because of the inherent vagueness in the criteria, they’re not even good labels.
“…it is still completely inaccurate to state that there is no biological foundation for mental illnesses.”
As stressed above, there is a biological foundation to everything we do – every thought, every feeling, every eye blink, every action. But – and this is the point that seems to evade psychiatry – there is no good reason to believe that the various problems catalogued in the DSM are underlain by pathological biological processes. And there are lots of very good reasons to believe that they are not.
“They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones.”
I don’t think I’ve ever used the term “make-believe” to describe psychiatric “illnesses”, though I do routinely describe psychiatric labels as invented. The two terms are not synonymous. What psychiatry calls mental illnesses are actually nothing more than loose collections of vaguely-defined problems of thinking, feeling, and/or behaving. In most cases the “diagnosis” is polythetic (five out of nine, four out of six, etc.), so the labels aren’t coherent entities of any sort, let alone illnesses.
But the problems set out in the so-called symptom lists are real problems. That’s not the issue. I refer to these labels as inventions, because of psychiatry’s assertion that the loose clusters of problems are real diseases. In reality, they are not genuine diseases; they are inventions. They are not discovered in nature, but rather are voted into existence by APA committees.
“As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
But meanwhile psychiatry has made up its mind. Within psychiatric dogma, all significant human problems of thinking, feeling, and behaving are illnesses that need to be “treated” with drugs and electric shocks.
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FINALLY
All of this is interesting, and I suppose it’s important to refute the more or less steady stream of unsubstantiated assertions, fallacious reasoning, and spin that flows from the psychiatric strongholds.
But meanwhile the carnage continues. There is abundant prima facie evidence that psychiatric drugs are causally implicated in the suicide/murders that have become almost daily occurrences here in the US. My challenge to organized psychiatry is simple: call publicly for an independent, definitive study to explore this relationship. And my challenge to rank and file psychiatrists is equally simple: pressure the APA to call for such a study. If what you are doing is unqualifiedly wholesome, safe, and effective, then what do you have to fear?
Thank You Dr Hickey.
by Phil Hickey on January 10, 2017
On January 2, 2017, I published a short post titled Carrie Fisher Dead at Age 60 on Behaviorism and Mental Health. The article was published simultaneously on Mad in America.
On January 4, a response from Carolina Partners was entered into the comments string on both sites.
Carolina Partners in Mental Healthcare, PLLC, is a large psychiatric group practice based in North Carolina. According to their website, they comprise 14 psychiatrists, 7 psychologists, 34 Advanced Practice Nurse Practitioners/Physicians Assistants, and 43 Therapists and Counselors. They have 27 North Carolina locations.
Partners’ comment consists essentially of unsubstantiated assertions, non sequiturs, and appeals to psychiatric authority. As such, it is fairly typical of the kind of “rebuttals” that psychiatry’s adherents routinely direct towards those of us on this side of the issue. For this reason, and also because it comes from, and presumably represents the views of, an extremely large psychiatric practice, it warrants a close look.
I will discuss each paragraph in turn.
“We strongly disagree with this article, which neglects a lot of important information and uses selective hearing to distort what Carrie Fisher was about and also to distort the evidence for mental illness as a real disorder.”
My Carrie Fisher article was brief (566 words), and was intended as a counterpoint to the very widespread obituaries that lionized her as a champion of “bipolar disorder”. The essential point of my article was that Ms. Fisher had been a victim of psychiatry, and like a great many such victims, died prematurely. Obviously I neglected a lot of important information. I could have gone into great length as to the recklessness of psychiatry assigning the bipolar label, with all its implications of helplessness, disempowerment, and “chemical imbalance” to a young woman who by her own account was, at the time, using any drugs she could get her hands on. But I felt that a brief and respectful statement of the facts was all that was needed.
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“Mental illnesses have a long history of biological evidence. For example, researchers have demonstrated that people with depression have an overactive area of the brain, called Brodmann area 25. Schizophrenia has been linked to specific genes, as PTSD and autism have been linked to specific brain abnormalities. Suicide has been linked to a decreased concentration of serotonin in the brain. OCD has been linked to increased activity in the basal ganglia region of the brain.”
Brodmann area 25 (BA25)
Partners did not provide a specific reference in support of this contention, but my best guess is that the reference is Mayberg, HS, et al (1999) Reciprocal Limbic-Cortical Function and Negative Mood: Converging PET Findings in Depression and Normal Sadness (Am J Psychiatry 1999; 156:675–682). Here’s the study’s primary conclusion:
“Reciprocal changes involving subgenual cingulate [which includes Brodmann area 25] and right prefrontal cortex occur with both transient and chronic changes in negative mood.”
What this means essentially is that negative mood, whether transient or enduring, is correlated with changes in both the subgenual cingulate (Brodmann area 25) and the right pre-frontal cortex, and that when the depression is relieved, the changes are reversed.
This, of course, is an interesting finding, but provides no evidence that depression, mild or severe, transient or enduring, is caused by a biological pathology.
The reality is that all human activity is triggered by brain activity. Every thought, every feeling, every action has its origins in the brain. I cannot lift a finger, blink an eye, scratch my head, or recall my childhood home without a characteristic brain function initiating and maintaining the action in question. Without stimuli from the brain, my heart will stop beating, my respiratory apparatus will shut down, and I will die, unless these functions are maintained by machines.
So there is absolutely no surprise in the discovery that sadness and despondency have similar neural triggers and maintainers. It would be amazing if they didn’t. But – and this is the critical point – this does not warrant the conclusion that sadness which crosses arbitrary and vaguely-defined thresholds of severity, duration, and frequency is best conceptualized as an illness caused by pathological or excessive activity in BA 25.
Depression is a normal state. It is the normal human reaction to significant loss and/or living in sub-optimal conditions/circumstances. It is also an adaptive mechanism, the purpose of which is to encourage us to take action to restore the loss and/or improve the conditions.
All consciously-felt human drives stem from unpleasant feelings. Thirst drives us to seek water; hunger, food; hypothermia, warmth; hyperthermia, coolness; danger, safety, etc. Sadness and despondency are no exceptions. They drive us to seek change, and have been serving the species well since prehistoric times.
But – as is the case with all the above examples – when a drive is not acted upon, for whatever reason, the unpleasant feelings worsen. Just as unrequited hunger and thirst increase in strength, so the depression drive when not requited deepens.
The reality is that most people deal with depression in appropriate, naturalistic, and time-honored ways. If the source of the depression is the loss of a job, they start job-hunting. If the source is an abusive relationship, they seek ways to exit or remediate the situation. If the source is a shortage of money, they seek ways to budget more sensibly, or increase their earnings; etc.
Depression, either mild or severe, transient or lasting, is not a pathological condition. It is the natural, appropriate, and adaptive response when a feeling-capable organism confronts an adverse event or circumstance. And the only sensible and effective way to ameliorate depression is to deal appropriately and constructively with the depressing situation. Misguided tampering with the person’s feeling apparatus is analogous to deliberately damaging a person’s hearing because he is upset by the noise pollution in his neighborhood, or damaging his eyesight because of complaints about litter in the street.
Our feeling apparatus is as valuable and adaptive as our other senses. But psychiatry routinely numbs, and in many cases permanently damages, this apparatus to sell drugs and to promote the fiction that they are real doctors. Their justification for this blatantly destructive activity hinges on the false notion that depression becomes a diagnosable illness when its severity crosses arbitrary and vaguely-defined thresholds. But deep despondency is no more an illness than mild despondency. The latter is the appropriate and adaptive response to minor losses and adversity. The former is the appropriate and natural response to more profound or more enduring adversity. Though, of course, what constitutes profound adversity will vary enormously from person to person. An individual, for instance, raised to the expectation of stable and permanent employment may be truly heartbroken at the loss of a job. Another individual, raised to the notion that there’s always another job “around the corner” will, other things being equal, be less affected. And so on.
In this regard, it’s noteworthy that Partners’ comment refers to overactivity in BA 25. The use of the prefix over implies pathology, but in reality there is no yardstick to determine what would be a correct amount of activity for BA 25. All that can be said, on the basis of Mayberg et al’s findings, and subsequent BA 25 research, is that when a person is sad, there is more activity than when he is happy. So the use of the term “overactivity” is deceptive – sneaking in the notion of pathology without any genuine or valid reasons to consider it so. The “reasoning” here is:
– depression is an illness
– depression is correlated with high activity in BA 25
– therefore high activity in BA 25 is pathological
In other words, the contention of pathology rests on the assumption that depression is an illness. To turn around and use this falsely inferred pathology to prove that depression is an illness is obviously fallacious. It is also typical of the kind of circular reasoning that permeates psychiatric contentions. In reality, there is nothing in Mayberg et al or in subsequent research that warrants the conclusion that the increased activity in BA 25 is pathological or excessive.
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Schizophrenia linked to specific genes
This assertion, that schizophrenia is linked to specific genes, is frequently adduced in these debates, as evidence that “schizophrenia” is a real illness with a biological pathology. Here again, Partners do not provide any references in support of this assertion, but there have been a number of studies in the past fifteen years or so that have found links of this kind. However, in all cases, the correlations have been small. In other words, there are always a great many individuals who have been assigned the “schizophrenia” label, but who do not have the gene variant in question; and there are a great many who have the gene variant, but who do not acquire the label “schizophrenia”. To date, no genetic test has been found helpful in confirming or refuting a “diagnosis of schizophrenia”.
An additional problem arises here, in that the assertion that “schizophrenia has been linked to specific genes” is often interpreted as meaning that “schizophrenia” is a genetic disease, which it emphatically is not. To illustrate this, let’s look briefly at a real genetic illness: polycystic kidney disease (PKD). This is a well established genetic illness caused by cysts in the kidneys. The cysts progressively block the flow of blood through the kidneys, causing tissue death.
Most cases of PKD are caused by the defective gene (PKD-1). In polycystic kidney disease, the pathology occurs because the PKD-1 gene causes the nephrons to be made from cyst wall epithelium rather than nephron epithelium. And cyst wall epithelium produces fluid which accumulates in, and ultimately destroys, the nephrons and the kidney.
So the gene determines the structure of the nephron wall. This is the primary genetic effect. This structure causes the wall to produce fluid. As the nephrons become increasingly blocked, the kidneys produce less urine. So, reduced urination is a secondary effect of the gene PKD-1. Symptoms of PKD don’t usually emerge until adulthood, but about 25% of children with PKD1 experience pain and other symptoms. So a child growing up with polycystic kidney disease may feel sick much of the time. Such a child, other things being equal, is likely to be fussier and more distressed than other children, and it is entirely possible that one could find a weak correlational link between gene PKD-1 and childhood fussiness, though, of course, any search for such a correlation will be confounded by the obvious fact that children can be habitually fussy for other reasons. The fussiness would be a tertiary effect of the gene PKD1.
And from there the causal chain could continue in various ever-weakening directions. For instance, the child might become somewhat sad and despondent. Or it could be that the child received extra attention and comforting from his parents and was fairly content, and so on. Ultimately the outcome is impossible to predict with any kind of precision, and the best we can expect from genes vs. subsequent behavior studies are weak, tenuous correlations.
Cleft palate is another example of a pathology that is caused by a gene defect; actually a gene deletion. This condition results in a characteristically strained and nasal speech quality which can be quite stigmatizing. The nasal speech is a secondary effect of the gene deletion.
Children with this kind of speech are sometimes mocked and bullied by their peers. The child might react to this kind of stigmatizing by speaking as little as possible, by withdrawing socially, or in various other ways. These reactions would be considered tertiary effects of the defect. And so on. As with the PKD, each step in the chain takes us further from the genetic defect, and the statistical associations grow proportionally weaker, and it would be stretching the matter to say that the lack of speech was caused by the gene deletion. Nor would one conclude that the child’s social withdrawal was a symptom of a genetic disease. And this is true even though the link between the deletion and the cleft palate is clear-cut and direct.
In the same way, it is simply not tenable to claim that “schizophrenic” behaviors (e.g. disorganized speech) are symptoms of a genetic disease. This is particularly the case in that correlations between the “diagnosis” and genetic anomalies are typically very small. The effects of any minor genetic anomalies that might exist have had ample opportunity to be shaped by social and environmental factors, and these are more credible causal constructs.
“Schizophrenia” is not a unified condition. Rather, it is a loose collection of vaguely defined behaviors. For this reason, any genetic research done on this condition will inevitably result in conflicting and confusing results. It’s like looking for genetic similarities in all the people who play bridge, or read romance novels, visit libraries, play football, or whatever. If the sample sizes are large enough, and in genetic research sample sizes are often enormous, one could probably find small effects in all or most of these areas, but no one would conclude from this that these are genetically determined activities, much less illnesses.
A person’s ability to learn depends on two general factors: a) the structure of his brain, as determined by his DNA, and b) his experiences since birth.
One can’t learn to play the piano, for instance, unless one has appropriate neural apparatus, and fingers, both of which require appropriate DNA. But even a person with good genetic endowment in these regards, will never learn to play unless he is exposed to certain environmental factors. He must, at the very least, encounter a piano. In the same way, a person whose genetic endowment might be relatively marginal might become an excellent pianist, if he were to receive persistent environmental encouragement and support.
Similar reasoning can be applied to the behavior of not-being-“schizophrenic.” This behavior involves navigating the pitfalls of late adolescence/early adulthood, and establishing functional habits in interpersonal, occupational, and other important life areas. Obviously it requires appropriate neural apparatus, hence the weak correlations with genetic material, but equally clearly it calls for a nurturing childhood environment, with opportunities for emotional growth and acquisition of social, occupational, and other skills.
Given all of this, it’s not surprising that researchers are finding correlations between DNA variations and a “diagnosis” of schizophrenia, but given the number of links in the causal chain and the multiplicity of possible pathways at each link, it is also not surprising that the correlations are always found to be weak, and of little or no practical consequence.
Nor is it surprising that the correlations between being labeled “schizophrenic” and various psychosocial factors are by contrast generally strong. Having a schizophrenia label is correlated with childhood social adversity, childhood abuse and maltreatment, poverty, and a family history of migration.
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Generally similar considerations apply to Partners contentions with regards to “PTSD”, “autism”, suicide, and “OCD”, but space precludes a detailed discussion here.
. . . . . . . . . . . . . . . .
“Eric Kandel, MD, a Nobel Prize laureate and professor of brain science at Columbia University, says, ‘All mental processes are brain processes, and therefore all disorders of mental functioning are biological diseases…The brain is the organ of the mind. Where else could [mental illness] be if not in the brain?'”
Dr. Kandel (now 87 years old) is an eminent neuroscience researcher at Columbia University. There’s an extensive biography in Wikipedia. His early research focused on the neurophysiology of memory. He has received numerous awards, including the Nobel Prize in Physiology/Medicine (2000), and is widely published. His record of research achievements is enormous, and his knowledge and expertise are vast, but in the statement quoted by Partners, and, incidentally, by other psychiatry adherents, he is simply wrong.
Let’s take a closer look. Logically, the Kandel quote can be stated symbolically as: A is identical to B; therefore malfunctions or aberrations in A are malfunctions or aberrations in B.
On the face of it, this seems sound, and indeed, it is a valid inference in some situations. For instance, the furnace in a person’s home is the primary heating appliance; therefore, malfunctions in the furnace are malfunctions in the primary heating appliance. Indeed, in a simple example of this sort, the statement is tautological. We are simply substituting the synonyms furnace and primary heating appliance, and the inference contains no new information or insights. But the inference is fallacious in more complex matters.
Let’s concede, for the sake of discussion, that the premise of the Kandel quote is true, i.e., that all mental processes are brain processes. The term mental processes embraces a wide range of activities, including sensations, perceptions, thoughts, choices, positive feelings, negative feelings, hopes, beliefs, speaking, singing, general behavior, etc.
The term “disorders of mental functioning” is harder to define, but, again for the purposes of discussion, let’s accept the APA’s catalog as definitive in this regard. Let’s accept that anything listed in the DSM is a “disorder of mental functioning”.
It’s immediately obvious that some of the DSM entries are indeed the result of brain malfunctioning. In the text these are referred to as disorders due to a general medical condition or to the effects of a substance. But in the great majority of DSM labels, no such biological cause is identified, and so the conclusion in the Kandel quote would appear to call for some kind of evidence or proof. However, in the Kandel quote, the conclusion is not presented as something that has been, or even needs to be, proven. Rather, it is presented as a logical conclusion inherent in, and stemming directly from, the premise. And it is from this perspective that the Kandel quote needs to be evaluated.
To pursue this, let’s consider the example of “oppositional defiant disorder”. This is a disorder of mental functioning as defined above, because it is listed in the DSM. And according to Dr. Kandel’s “logic”, it is also therefore a “biological disease”. The “symptoms” of oppositional defiant disorder as listed in DSM-5 are:
Often loses temper.
Is often touchy or easily annoyed.
Is often angry and resentful.
Often argues with authority figures or, for children and adolescents, with adults.
Often actively defies or refuses to comply with requests from authority figures or with rules.
Often deliberately annoys others.
Often blames others for his or her mistakes or misbehavior.
Has been spiteful or vindictive at least twice within the past 6 months. (p 462)
Obviously for any of these behaviors to occur, there has to be corresponding neural activity. But there is no necessity that the neural activity is diseased or malfunctioning in any way. A child learning from his environment, developing his behavioral repertoire in accordance with the ordinary principles or learning, could acquire any or all of these behavioral habits without any malfunctioning in his neural apparatus. We acquire counterproductive habits as readily, and by essentially the same processes, as we acquire productive ones. In general, if a child discovers that he can acquire power and control in his environment by throwing temper tantrums, he will, other things being equal, acquire the habit of throwing temper tantrums. Similarly, if arguing with parents and other authority figures yields positive results, there is a good chance that this also will become habitual. And this is not because there is anything wrong with the child’s brain. Rather, it’s because his brain is functioning correctly. He is internalizing as habits those decisions and actions that pay off. It is often observed in child-raising practice that if you’re not training your children, they’re training you.
Similar observations can be made about the other seven “symptoms” of oppositional defiant disorder, and indeed all the DSM labels. A person with a perfectly normal-functioning brain can acquire the habits in question if the circumstances are conducive to this learning.
So to return to the question in the Kandel quote: “Where else could [mental illness] be if not in the brain?”, the answer is clear: In the self-serving and unwarranted perception of psychiatrists. Mental illness is the distorting lens through which psychiatrists view all problems of thinking, feeling, and behaving. It is the device they use to legitimize their drug-pushing and to maintain the fiction that they are practicing medicine.
. . . . . . . . . . . . . . . .
“You’re right that mental illness is also affected by social and environmental conditions–by a person’s disposition, or upbringing, or current environment. It’s also true that mental illness is affected by drug use (both prescribed and not prescribed). So are other medical conditions, such as heart disease and cancer.”
I’m not sure where Partners are coming from here, because I never made any such statement. In my view, which I have stated clearly on numerous occasions, “mental illness” is a psychiatric invention, self-servingly created to promote the spurious notion that all problematic thoughts, feelings, and/or behaviors are illnesses. And not just illnesses in some vague allegorical sense, but real illnesses “just like diabetes”, which need to be treated by medically trained psychiatrists with mood-altering drugs and high voltage electric shocks to the brain.
Partners’ vague concessions concerning environment, child-rearing, and drug effects is a fairly standard psychiatric sop, but doesn’t mitigate their earlier contentions on the “long history of biological evidence” and their uncritical endorsement of the logically spurious Kandel quote.
. . . . . . . . . . . . . . . .
“And it’s true that mental illness is often difficult to diagnose because of
1) the current limitations of the field of research. Thomas R. Insel, MD, director of the National Institute of Mental Health, for example, talks about how the diagnosis and treatment of mental illness today is where cardiology was 100 years ago, concluding that we need to continue scientific research of mental illnesses. (There’s a longer quote on this below.)”
And (from later in the comment)
“Longer aforementioned quote:
Take cardiology, Insel says. A century ago, doctors had little knowledge of the biological basis of heart disease. They could merely observe a patient’s physical presentation and listen to the patient’s subjective complaints. Today they can measure cholesterol levels, examine the heart’s electrical impulses with EKG, and take detailed CT images of blood vessels and arteries to deliver a precise diagnosis. As a result, Insel says, mortality from heart attacks has dropped dramatically in recent decades. ‘In most areas of medicine, we now have a whole toolkit to help us know what’s going on, from the behavioral level to the molecular level. That has really led to enormous changes in most areas of medicine,’ he says.
Insel believes the diagnosis and treatment of mental illness is today where cardiology was 100 years ago. And like cardiology of yesteryear, the field is poised for dramatic transformation, he says. ‘We are really at the cusp of a revolution in the way we think about the brain and behavior, partly because of technological breakthroughs. We’re finally able to answer some of the fundamental questions.'”
It is at least forty years since I started hearing about psychiatry’s great biological breakthroughs that were just around the proverbial corner, and the promise, if my readers will pardon the pun, is getting a little old.
What’s noteworthy, however, is that in other disciplines, where there is hope or expectation of breakthroughs, the proponents of these endeavors generally wait until the evidence is in, before implementing practices based on these hopes. In fact, to the best of my knowledge, psychiatry is the only profession whose entire work, indeed, whose entire conceptual framework, is based on “evidence” and “breakthroughs” that are not yet to hand.
Note also the truly exquisite contrast between Partners’ earlier and confident contention that “mental illnesses have a long history of biological evidence” with the assertion here that the “diagnosis” and “treatment” of “mental illness” today is where cardiology was 100 year ago.
Incidentally, Dr. Insel, former Director of the NIMH, also said:
“While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’ – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment.” (Transforming Diagnosis, 2013)
And let us be quite clear. “Lack of validity” in this context means that the “diagnoses” don’t actually correspond to any disease entities in the real world. Note also that Dr. Insel didn’t say poor validity, or low validity. He said lack of validity – meaning none.
. . . . . . . . . . . . . . . .
Back to the Carolina Partners comment:
“2) mental illness symptoms often overlap with symptoms caused by other illnesses, for example, someone with cancer may also become depressed after diagnosis. Or someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.
While considering all these factors, it is still completely inaccurate to state that there is no biological foundation for mental illnesses. They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones. As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
This is a little rambling, but let’s see if we can unravel it.
“… someone with cancer may also become depressed after diagnosis.”
This is true. In fact, I would say that most people who contract serious illness become somewhat sad and despondent. But this in no way establishes the notion that the sadness should be considered an additional illness.
“…someone’s fatigue may be caused by a vitamin deficiency, rather than by depression.”
This quote contains one of psychiatry’s core fallacies: that the various “mental illnesses” are the causes of their respective symptoms (as is the case in real illness). To illustrate the fallacy, consider the hypothetical conversation:
Client’s wife: Why is my husband so tired all the time?
Psychiatrist: Because he has an illness called major depressive disorder.
Client’s wife: How do you know he has this illness?
Psychiatrist: Because he is tired all the time.
Psychiatry defines major depression (the so-called illness) by the presence of five “symptoms” from a list of nine, one of which is fatigue, and then routinely adduces the “illness” to explain the symptoms. In reality, the “symptoms” are entailed in the definition of the “illness”, and the explanation is entirely spurious. There are many valid reasons why a person might feel fatigued, but none of these is because he “has a mental illness”. Mental illnesses are merely labels with no explanatory significance. And because of the inherent vagueness in the criteria, they’re not even good labels.
“…it is still completely inaccurate to state that there is no biological foundation for mental illnesses.”
As stressed above, there is a biological foundation to everything we do – every thought, every feeling, every eye blink, every action. But – and this is the point that seems to evade psychiatry – there is no good reason to believe that the various problems catalogued in the DSM are underlain by pathological biological processes. And there are lots of very good reasons to believe that they are not.
“They are not ‘make-believe’ diseases, but rather are caused by a variety of factors, including biological ones.”
I don’t think I’ve ever used the term “make-believe” to describe psychiatric “illnesses”, though I do routinely describe psychiatric labels as invented. The two terms are not synonymous. What psychiatry calls mental illnesses are actually nothing more than loose collections of vaguely-defined problems of thinking, feeling, and/or behaving. In most cases the “diagnosis” is polythetic (five out of nine, four out of six, etc.), so the labels aren’t coherent entities of any sort, let alone illnesses.
But the problems set out in the so-called symptom lists are real problems. That’s not the issue. I refer to these labels as inventions, because of psychiatry’s assertion that the loose clusters of problems are real diseases. In reality, they are not genuine diseases; they are inventions. They are not discovered in nature, but rather are voted into existence by APA committees.
“As we understand more about mental illness through research we will (as we have with cardiology, for example) gain more precise vehicles for measuring and understanding the biological implications of these disorders.”
But meanwhile psychiatry has made up its mind. Within psychiatric dogma, all significant human problems of thinking, feeling, and behaving are illnesses that need to be “treated” with drugs and electric shocks.
. . . . . . . . . . . . . . . . .
FINALLY
All of this is interesting, and I suppose it’s important to refute the more or less steady stream of unsubstantiated assertions, fallacious reasoning, and spin that flows from the psychiatric strongholds.
But meanwhile the carnage continues. There is abundant prima facie evidence that psychiatric drugs are causally implicated in the suicide/murders that have become almost daily occurrences here in the US. My challenge to organized psychiatry is simple: call publicly for an independent, definitive study to explore this relationship. And my challenge to rank and file psychiatrists is equally simple: pressure the APA to call for such a study. If what you are doing is unqualifiedly wholesome, safe, and effective, then what do you have to fear?
Thank You Dr Hickey.
Monday, January 9, 2017
Wednesday, November 30, 2016
WARNING: A Psychiatric tsuNAMI is Upon Us.
By Lauren Tenney, PhD, MPhil, MPA, Psychiatric Survivor November 29, 2016
Well, our government is at it again.
It is not clear if this is the last stop, or where in the process we even are, but as best I can tell: happening any moment, Congressman Tim Murphy (R, Pennsylvania) will be making another speech at another hearing about the Helping Families in Mental Health Crisis Act (H.R. 2646) which is now part of a new bill, H.R. 34.
H.R. 2646 was the controversial legislative package that did everything from increasing and sanctioning state-sponsored forced and court-ordered psychiatry to the re-organization of SAMHSA. There was not a group that went unscathed: babies, pregnant and lactating women, children, teens, adults, and veterans. The mixing of drug experimentation, programming, payments, delivery, tracking systems, prison systems, psychiatric systems, medical systems, educational systems—everything accounted for in 996 pages.
This new bill, introduced on the day after Thanksgiving, November 25, 2016 is part of a pattern of the government trying to slip controversial psychiatric policy through when no one is thought to be watching. We recently saw this with the FDA's shock treatment regulation for comment being released days before the new year and due the day after a celebrated holiday.
This bill, H.R. 34, the Tsunami Warning, Education, and Research Act of 2015 [21st Century Cures Act] is the subject of a hearing at the Capitol, in H-313, tonight on Tuesday, November 29, 2016 at 5:00 PM. Among the most problematic issues this bill presents are multiple provisions for forced psychiatry not limited to IOC/AOT, ACT Teams, and Prison Psychiatry.
H.R. 34 also includes: SAMHSA reorganization, condoning of HIPPAA violations, electronic health records, a study of peer support specialists for future controls of the field, multiple attacks on young people and veterans, and a host of other potential human rights violations. Psychiatry is a fraud and this bill perpetuates it.
Tell your legislators to VOTE NO on H.R. 34!
Demand that your legislators stop sneaking controversial, damaging bills into other bills at the last minute. What is being called a “simple parliamentary procedure” seems rather shady to me. The legislature has not been able to pass some version of Murphy’s bill for years, and now they are going to try to sneak it in merged with the 21st Century Cures Act under the title Education, Research and Tsunami Warning Act of 2015. These actions further problematize our legislative processes.
It is urgent that people realize that no child will grow up without psychiatric evaluation. All people will become, in a generation or two, acclimated to being psychiatrized; psychiatry and its arms of drugs and institutions will become even more standard in our society.
At the very moment that people are becoming more vocal about the need for equality, eliminating racism and racist practices and systems, calling out sexism, homophobia, transphobia, xenophobia, and other forms of structural oppression, and addressing the outright fraud and other structural problems of psychiatry and its subdivisions, the government will solidify psychiatric practice in our society. This includes a great expansion of psychiatric reach into the prison industry and court systems.
Do not be fooled, this is a one way path that will allow the new administration the type of reach they want to keep us contained as they break down the existing structure, creating greater disparities, and further subjecting us, as a people who are already often oppressed, into further social control and subjugation to psychiatry.
Follow up with your legislators, and all legislators you can. Inform them about the dangers of psychiatry. Inform them about the dangers of this bill. Tell them that a bill that has been combined with multiple other bills totaling 996 pages (and involving who knows how many billions of dollars in taxpayer resources)—a bill that was introduced 3 business days prior to its hearing and 4 days prior to its assumed vote, under the name of a bill that has already passed, but has been deleted and replaced by this mess that has not been able to pass on its own for years—is not acceptable.
I am sure analyses of what the bill entails need to be made and many are working on making them. For now, take action. Call your elected officials today, tonight, tomorrow, and continue to do so to make your voice heard. The pro-psychiatry, pro-forced psychiatric treatment advocates are launching campaigns against us. We need to speak out, once again, for ourselves. No one else will. Make your calls now.
Find your Representatives in Congress
Find your Senators
H.R. 34 Bill Text
H.R. 34 Hearing Information
Those who want to take a closer look at this bill, please read on:
Even a cursory glance at the Table of Contents and the twenty-five titles it encompasses makes one have to take a deep breath to get the scope of how this bill can fundamentally transform our society—and not for the better.
Division A – 21st Century Cures starts off with Title I, NIH Innovation Projects and State Responses to Opioid Abuse. Title II includes Innovation Projects and includes privacy protections for human research subjects—a section called “High Risk, High Reward Research” is included here, as is the development of a “Taskforce specific to pregnant and lactating women.” These need to be read carefully.
Title III is Development and includes provisions such as patient-focused drug development, advancing new drug therapies, and a host of other sections designed for research on physical health.
Title V addresses Savings and this looks at issues of Medicare and Medicaid, and affects the Affordable Care Act.
Section VI looks at Leadership and Accountability and this is where the re-organization of SAMHSA is laid out and the provisions for the establishment of the “Interdepartmental Serious Mental Illness Coordinating Committee” can be found.
Title VII is designed for “Ensuring mental and substance use disorders prevention, treatment, and recovery programs keep pace with science and technology” and has both regional and national goals.
Title VIII is for “Supporting state prevention activities and responses to mental health and substance use disorder needs” that work on block grants.
Title IX is for “Promoting access to mental health and substance use disorder care” and these include grants for “treatment and recovery for homeless individuals”; “jail diversion programs”; “promoting integration of primary and behavioral health care”; “National Suicide Prevention Line” and other types of programs that track and turn in people to the system, acting as a pipeline to psychiatry. Section 9014 is “Assisted outpatient treatment” and Section 9015 is the Assertive Community Treatment grant program. It is important for people to specifically speak out against Sections 9014 and 9015 as inherently problematic for protecting human rights.
Subtitle B of Title IX is focused on “Strengthening the Health Care Workforce” and this includes education and training programs. Subtitle C targets college campuses.
Title X is for “Strengthening mental and substance use disorder care for children and adolescents” and increases pediatric access, programming, treatment, and interventions for young people, “screening and treatment for maternal depression” and Section 10006 is particularly worrisome, “Infant and early childhood mental health promotion, intervention, and treatment.”
Title XI is the loss of privacy rights under HIPAA (you may recall issues around Matsui’s bill that was basically incorporated into the structure).
Title XII further strengthens “Mental Health Parity” which works on the premise that psychiatry is as legitimate a science as physical health medicine, and perpetuates the fraud of the pharmaceutical and psychiatric industries, ensuring also that training, education, information and awareness of eating disorders are covered under these processes.
Title XIII is for “Mental Health and Safe Communities” Subtitle A includes the expansion and over reach of Law Enforcement and Psychiatry working hand in hand through Involuntary Outpatient Commitment (torture) “Assisted Outpatient Commitment” (as a second section in this same bill, here Section 14002. Title XIII also includes “Federal drug and mental health courts”; “mental health in the judicial system”; “Forensic Assertive Community Treatment Initiatives”; “mental health training for Federal uniformed services”; “school mental health intervention teams”; “Active-shooter training for law enforcement”; “Improving Department of Justice data collection on mental illness involved in crime”; and “Reports on the number of mentally ill offenders in prison”, further attempting to discriminate against people with psychiatric histories. In this section, the limited patients’ rights for the Department of Veterans Affairs are noted, and this of course is and continues to be a concern; for example, we know veterans and their fetuses are being subjected to shock treatment.
Subtitle B focuses on “Comprehensive Justice and Mental Health” in prisons and jails, local and federal law enforcement training, and GAO reporting and needs to be looked at very carefully in the future.
Title XV addresses Medicare Part A and reimbursements. Title XVI, Medicare Part B and treatment/payments/ and Continuing Access to Hospitals Act of 2016; all of which need thorough review.
Title XVII includes other Medicare provisions and XVIII still other provisions around employer health reimbursement.
Division D is “Child and Family Services and Support” and includes Title XIX, “Investing in Prevention and Family Services”, restructuring prevention services, programs, and payments as they relate to foster care, and perhaps one of the few sensible things, Section 19032, “Development of a statewide plan to prevent child abuse and neglect fatalities.”
Title XXI looks also and securing support for foster families and children and Title XXII addresses “reauthorizing adoption and legal guardianship incentive programs.”
Title XXIII is for “Technical Corrections” for data and programming and “Technical corrections to State requirement to address the developmental needs of young children.”
Title XXIV is for “Ensuring states reinvest savings resulting from increase in adoption assistance” and like “Title XXV, Social Impact Partnerships to Pay for Results” and the extension of the TANF program and other types of social supports, this needs to be read and understood.
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Lauren Tenney, PhD, MPhil, MPA, Psychiatric Survivor
http://www.LaurenTenney.us
Lauren Tenney, PhD, is a psychiatric survivor and activist first involuntarily committed at age 15. Her work aims to expose the institutional corruption which is a source of profit for organized psychiatry, and to abolish state sponsored human rights violations, such as murder, torture and slavery. www.laurentenney.us
Thank You Dr Tenny and MIA.
"to abolish state sponsored human rights violations, such as murder, torture and slavery"
Thank You again Dr Tenny.
wiki: Indentured Servitude.
wiki: 13th Amendment To The United States Constitution.
Section 1. Neither slavery nor involuntary servitude, except as a punishment for crime whereof the party shall have been duly convicted, shall exist within the United States, or any place subject to their jurisdiction.
Section 2. Congress shall have power to enforce this article by appropriate legislation.[1]
We know Christmas is coming and you're busy.
So is Tyranny.
Pick up the phone and tell your legislators, respectfully but without equivocating, to vote NO.
Write them a real letter: Stamp and Envelope. They get so much email that most it gets flushed unread.
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