Monday, May 20, 2019

Comments by ChuckSigler

Showing 68 of 68 comments.

  • Very much worth the time to read this article. It clearly shows evidence of how Zimbardo influenced the experiment and perpetuated falsehoods about what happened. Using the term of one of the “guards,” it was more like an improv skit than it was a social psychology experiment. The supposed implications the Stanford prison experiment made about human nature may be true to some extent, but Zimbardo’s classic study wasn’t.

  • There has been research into what are known as “common factors” and the dodo bird effect that shows there are factors common in various therapies suggesting the therapeutic alliance is the most significant factor predicting positive change in therapy. See an article I wrote “Another Brick in the Wall” (http://faith-seeking-understanding.org/2017/05/19/another-brick-in-the-wall/) or “A Meta-analysis of Outcome Studies Comparing Bona Fide Psychotherapies: Empirically, ‘All Must Have Prizes’” (https://pdfs.semanticscholar.org/dd7b/49df39a831af1c0d8423ff888813a5246688.pdf). Also look at the research in “The Heart and Soul of Change.”

  • Kirstie Alley’s comments are getting ridiculed simply because she’s a Scientologist. As readers of this site would know, there is some evidence of a connection between a rare genetic disorder and violence with some psychiatric medications. Yolande Lucire is a forensic psychiatrist who has researched and written on the topic. Here is the title of one of her journal articles on the subject: “Antidepressant-induced akathisia-related homicides associated with diminishing mutations in metabolizing genes of the CYP450 family.” There is also a YouTube video of a lecture she gave: “Adverse Reactions to Psychiatric Drugs: Yolande Lucire MBBS.” Google either of these to read or watch them.

  • From an article I wrote: “Listening to Marijuana Research”:

    Staci Gruber, who is the director of the MIND project, has been doing research into the effects of MJ since the early 1990s and has documented some interesting neurological effects from MJ. She led a 2013 study that found there were differences in the brain’s white matter and impulsivity between teenagers and young adults smoked an average of 25.5 joints of MJ per week and a control group who did not smoke MJ. Their research suggested that in some individuals who begin smoking MJ at an early age, differences in brain function and structure emerge during development. The study sample was small and it was not clear if the brain changes resulted from MJ use or predated MJ use. The changes could have occurred as the result of either chronic MJ use or reflect a delay in brain development in MJ smokers.

    “These data represent the first report of significant alterations in frontal white matter fiber tract integrity that are associated with self-report measures of impulsivity in chronic, heavy MJ smokers, and appear to be related to age of onset of MJ use. . . . Future investigations should include additional measures of behavioral impulsivity and their relationship to age of onset of MJ use to more fully explore the potential neurodevelopmental aspects of white matter changes in MJ smokers. Findings from this study suggest that changes in white matter microstructure may be predictive or associated with increased impulsivity, and may ultimately contribute to the initiation of MJ use or the inability to discontinue use.”

    A follow up study done by Gruber and others was published that same year, 2013. The study confirmed that heavy MJ smokers had lower levels of white matter in the corpus callosum region of the brain; and that earlier age of MJ use was associated with these lower levels of white matter. MJ smokers also had higher levels of impulsivity.

    “Taken together, these findings reinforce the idea that early onset of MJ use negatively impacts white matter development and is associated with behavioral impulsivity, a combination that may have enduring negative effects, particularly on the developing brain. Data from this study highlight the importance of early identification of MJ use among emerging adults and the need for efforts aimed at delaying or preventing the onset of MJ use.”

    Then a third study by Gruber and her research team at MIND published in the March 2016 issue of the Journal of Studies on Alcohol and Drugs found that MJ smokers had poorer executive brain function than the control group. The difference seemed to be primarily the result of early onset of MJ use, before the age of 16. The differences remained even after the frequency and amounts of MJ used were controlled. Additionally, the early MJ use and the greater amounts of MJ used predicted poorer performance and errors on the Wisconsin Card Sorting Test (WCST), which is used to assess abstract thinking. “The WCST is also considered a measure of executive function because of its reported sensitivity to frontal lobe dysfunction.”

    “These findings underscore the impact of early onset of marijuana use on executive function impairment independent of increased frequency and magnitude of use. In addition, poorer performance on the WCST may serve as a neuropsychological marker for heavy marijuana users. These results highlight the need for additional research to identify predictors associated with early marijuana use, as exposure to marijuana during a period of developmental vulnerability may result in negative cognitive consequences.”

    Here is a link to the full article: http://faith-seeking-understanding.org/2017/02/20/listening-to-marijuana-research/

    Here is a link to MIND (Marijuana investigations for Neuroscientific Discovery): http://drstacigruber.com/mind/

  • Studies looking at whether marijuana is a “gateway” to other drug use have typically looked at the general population level and they have found that marijuana is not a gateway drug. BUT I don’t ever recall seeing or hearing of an investigation of the marijuana “gateway” theory that looked at a sub-population of individuals at high risk, say individuals with a family history of at least one parent with a drug/alcohol misuse problem; or some other sub-population factor or history of personal or family dysfunction. So Dr. Stuyt’s comment that she has “definitely” seen marijuana as a gateway drug to using opiates and to relapse back into using opiates after they quit is valid. I have regularly seen the same thing in my clinical experience.

    Marijuana is not a “gateway” drug to using harder drugs at the general population level. But with sub-populations of high risk individuals or individuals who have a history of opioid misuse, alcohol misuse, etc. social/recreational use of marijuana can lead to experimenting with opiates or cocaine, etc., or lead the person back to the active opioid use they were trying to avoid while “recreationally” using marijuana.

  • There was an experiment at the Institute of Psychiatry at King College, London, that looked at the relationship of the effects of the two main ingredients in cannabis, THC and CBD. You can see a video of a reporter participating in the experiment here. Her mixture of THC and CBD left her with the giggles: “No matter how hard I tried to take the experiment seriously, it all seems hilarious.” But with pure THC, it was a different story. “It’s horrible. It’s like being at a funeral . . . Worse . . . It’s just so depressing. You want to top [kill] yourself.” Here’s a link to a video of the above: https://www.youtube.com/watch?v=6U8XARojnbM

    The concerns with the rapidly growing strength of marijuana in its THC content is because of its relationship with psychosis. Nora Volkow, the current NIDA director, published a study noting where the adverse health effects related to the recreational use of marijuana was the highest in adolescents, “Adverse Health Effects of Marijuana Use.” Cannabis use as a component in the emergence of psychosis is reliably documented, and was noted anecdotally as far back as 1845 in “Hashish and Mental illness.” Read about these claims and more, if you are interested, in my articles, “Shatter and Psychosis” and “Marijuana & Adverse Health Effects” on http://faith-seeking-understanding.org/

  • I was encouraged to see your article, Dr. Stuyt. As a therapist working primarily in addiction settings for about thirty years, I’ve had similar concerns about the issues you noted here, namely the growing strength of marijuana, the backdoor strategy with medical marijuana approval as a gateway to recreational marijuana, and the largely under-regulated or unregulated nature of the market. I recently wrote an article on how legalization has helped the black market for marijuana to flourish, “Pot Market Getting A ‘Black’ Eye,” instead of the rhetoric that it would lead to weakening or the end of illegal marijuana sales. Here’s a link to the article, if anyone is interested: http://faith-seeking-understanding.org/2017/09/08/pot-market-getting-a-black-eye/

  • The research results of psychodynamic therapy equaling CBT is because of the dodo bird effect. Read: “The Legacy of Saul Rosenzweig: The Profundity of the Dodo Bird” by Barry Duncan. It’s available here: http://www.personal.kent.edu/~dfresco/CRM_Readings/Duncan_dodo_2002.pdf.

    Duncan’s article explores the history of what he calls “common factors” in psychotherapy, a reconceptualizing of what Lambert identified in 1992 as “therapeutic factors.” The idea that common factors to different psychotherapies could account for therapeutic change dates back to Saul Rosenzweig’s 1936 paper. Quoted from the Duncan article:

    “Lambert (1992) identified four therapeutic factors (extratherapeutic, common factors, expectancy or placebo, and techniques) as the principal elements accounting for improvement in psychotherapy. Inspired by Lambert’s proposal, Miller et al. (1997) expanded the use of the term common factors from its traditional meaning of nonspecific or relational factors to include four specific factors: client, relationship, placebo, and technique.”

    “The Heart and Soul of Change,” by Mark Hubble, Barry Duncan and Scott Miller (now in its 2nd edition) showed how these common factors demonstrate that improvement during psychotherapy can be attributed as follows: client (40%), relationship (30%), placebo (15%), and technique (15%). The relationship factor is seen as fifty-fifty client and therapist. So improvement in psychotherapy from this perspective is 70% due to the client and 30% due to a therapist and technique.

    Also try “The Dodo Bird Effect” or “Another Brick in the Wall” on my website: http://faith-seeking-understanding.org/

  • I did some quick research on the PHQ-9 Patient Health Questionnaire with interesting results. Robert Spitzer and Janet Williams were two of its original authors (http://onlinelibrary.wiley.com/doi/10.1046/j.1525-1497.2001.016009606.x/full). Spitzer and Williams (husband and wife) are historically tied to the development of the DSM-III. Additionally, there is a TWO item scale (PHQ-2; http://journals.lww.com/lww-medicalcare/Abstract/2003/11000/The_Patient_Health_Questionnaire_2__Validity_of_a.8.aspx) and there is a brief scale used to assess anxiety, the GAD-7 (http://www.sciencedirect.com/science/article/pii/S0163834310000563)!

  • Read: “The Legacy of Saul Rosenzweig: The Profundity of the Dodo Bird” by Barry Duncan. It’s available on Researchgate. Duncan’s article explores the history of what he calls “common factors” in psychotherapy, a reconceptualizing of what Lambert identified in 1992 as “therapeutic factors.” The idea that factors common to different psychotherapies could account for therapeutic change dates back to Saul Rosenzweig’s 1936 paper. Quoted from the Duncan article:

    “Lambert (1992) identified four therapeutic factors (extratherapeutic, common factors, expectancy or placebo, and techniques) as the principal elements accounting for improvement in psychotherapy. Inspired by Lambert’s proposal, Miller et al. (1997) expanded the use of the term common factors from its traditional meaning of nonspecific or relational factors to include four specific factors: client, relationship, placebo, and technique.”

    “The Heart and Soul of Change,” by Mark Hubble, Barry Duncan and Scott Miller (now in its 2nd edition) showed how these common factors demonstrate that improvement during psychotherapy can be attributed as follows: client (40%), relationship (30%), placebo (15%), and technique (15%). The relationship factor is seen as fifty-fifty client and therapist. So improvement in psychotherapy from this perspective is 70% due to the client and 30% due to a therapist and technique. So feedback from clients is an important part of making therapy work.

  • In 1998 Robert Whitaker co-wrote a series of articles on psychiatric research for the Boston Globe (the series was a finalist for the Pulitzer Prize for Public Service). The first installment of the series, “Testing Takes Human Toll” was published on November 15, 1998. In this article (http://web.archive.org/web/19991008230951/http://boston.com/globe/nation/packages/doing_harm/day1.htm), Whitaker and others described how beginning in 1972, psychiatric researchers used a variety of agents such as methylphenidate (Ritalin, Concerta), ketamine, and tetrahydrocannabinol (THC) “to deliberately provoke psychotic symptoms in more than 1,200 schizophrenic patients.” In some cases, the level of psychosis experienced by these patients was called “severe.” Jeffrey Lieberman was one of those researchers. So Lieberman’s dislike of Whutaker goes back 20 years.

  • 25-30 years ago, Lieberman participated in “research” that sought “to deliberately provoke psychotic symptoms” in schizophrenic patients. He conducted methylphenidate challenge tests for more than a decade.
    Here is a sampling of three articles where Lieberman was a co-author of studies where methylphenidate was given to schizophrenic patients in order to activate psychotic symptoms.

    In a 1987 study (https://www.ncbi.nlm.nih.gov/pubmed/2886110), 34 stable outpatients receiving neuroleptic treatment were given an infusion of methylphenidate and then withdrawn from their neuroleptic medication. Three weeks after they were withdrawn from their psych meds, they were given another infusion of methylphenidate. Then the unmedicated patients were followed up for 52 weeks—or until they relapsed; in other words their symptoms returned.

    A 1994 study (https://www.nature.com/npp/journal/v11/n2/pdf/npp199440a.pdf) had a similar methodology, 41 stable patients receiving neuroleptic treatment were given an infusion of methylphenidate. They were also withdrawn from their neuroleptic meds and followed for 52 weeks, or until relapse.

    In a 1990 study (https://www.ncbi.nlm.nih.gov/pubmed/2236460), 38 patients who met the criteria for schizophrenia or schizoaffective disorder were given an infusion of methylphenidate, followed by a regimen of standard acute neuroleptic treatment. This time the patients were individuals who were experiencing their first acute episode of psychosis. The methylphenidate produced an increase in psychopathology reflected by a worsening of their symptoms.

    Another 1987 article (https://www.ncbi.nlm.nih.gov/pubmed/2884687) with Lieberman as a co-author was a meta-analysis of 36 studies that used psychostimulants (PS) in schizophrenia. The authors noted that non-amphetamine drugs like methylphenidate appeared to have a greater “psychotogenic potency.” In other words, they elicited a greater psychotic reaction than amphetamine drugs. “Approximately 40% evidence a psychotogenic response to PS administration in doses that are subpsychotogenic in normal’s.” Don’t miss the fact that Lieberman knowingly used a psychostimulant in his own studies that he knew would elicit a greater, more intense psychotic reaction than amphetamine drugs.

  • FYi regarding your comment about Ana Sandoiu’s quotation of Lieberman. Her quotation is accurate and seems to have been Lieberman’s intent. Here is a link to a press release by Columbia University Medical Center, that has the quote: https://eurekalert.org/pub_releases/2017-05/cumc-boa050217.php

    Lieberman said in the press release:

    “The evidence from randomized clinical trials and neuroimaging studies overwhelmingly suggests that the majority of patients with schizophrenia benefit from antipsychotic treatment, both in the initial presentation of the disease and for longer-term maintenance to prevent relapse. . . . Anyone who doubts this conclusion should talk with people whose symptoms have been relieved by treatment and literally given back their lives.”

  • The National Institute on Drug Abuse (NIDA) gives a definition of addiction that is often applied reductionistically as a pure medical model of addiction. But we are not our brains (as Jeffery Schwartz said in his book, “You Are not Your Brain”) or flesh robots. The definition on the NIDA web page is the following: “Addiction is defined as a chronic, relapsing brain disease that is characterized by compulsive drug seeking and use, despite harmful consequences. It is considered a brain disease because drugs change the brain; they change its structure and how it works.” I think a failure to see humans as more than just molecules and nerve cells is the problem. We are brains and minds. Addiction is as much a “disease” of the immaterial soul/mind as it is the brain.

    There is an effect in the pleasure center of the brain, namely the mesolimbic dopamine pathway area. But there is also an effect on the prefrontal cortex, where decision making and judgments are made. Here is where we exercise self control and evaluate whether or not we should do something, including whether or not to drink or use drugs.

    The individual who needs a couple of drinks before they get on the dance floor has alcohol working in both areas of their brain: the high or euphoria in the pleasure center and the relaxation of the judgement in their prefrontal cortex saying they should not go on the dance floor because they will look ridiculous. This is not addiction, but it is how alcohol can work on any human brain. At some point in drug or alcohol “misuse,” damage or dysregulation can occur in the pleasure center of the brain. Here is where compulsive drug seeking or drinking comes in. I think this is fair summary of how Carleton Erickson described drug dependence in his book, “The Science of Addiction.”

    The prefrontal cortex of our brains distinguishes human cognitive functioning from other animals, including rats, so I don’t think the rat park experiments tell us a whole lot about the human addiction experience. It may illustrate effects on the pleasure pathway, but rats just don’t have the prefrontal lobes humans do. I always thought the reports of soldiers coming back from Vietnam who used heroin in Nam was a better illustration of the limits of a purely medical addiction model. Some soldiers stopped when they returned to the States and others didn’t. Dysregulation differences in the brain could have played a role on the difference along with social, psychological and environmental factors. But I don’t think brain dysregulation would have accounted for all the differences. If addiction is mind and brain disease, it’s never simply an an account of what happened physiologically when using.

    The concept of powerlessness in addiction originates with the First Step in AA: “We admitted we were powerless over alcohol—that our live had become unmanageable.” Yet I don’t think even the early AAs thought they were powerless to heal themselves—why form a fellowship to help ”the still suffering alcoholic” if they were powerless to heal themselves? If you keep the concept of powerlessness focused on neurological dysregulation or the neurological explanation of habit formation, I think it can be helpful. But never to say you are powerless to heal yourself.

    I’ve talked with an individual whose experience as he drove to a liquor store was to cry, because part of him didn’t want to drink; and yet he did drink, knowing it would lead again to pancreatitis. That was an experience of powerlessness. He’s sober today, so even that level of powerlessness didn’t doom him. The initial group of individuals who formed AA were all alcohol dependent; they had the emotional center dysregulation and compulsion to drink. But they broke the neurological habit patterns formed over the years as they drank through the change process they practiced in their fellowship. I think we could say they “rewired” their prefrontal neural pathways to support abstinence. And as long as they stayed away from reactivating the pleasure center dysregulation by drinking again, they would be sober and in that sense, healed. We are not flesh robots, but we can develop some faulty neurological circuits if we’re not careful.

  • The article sets up a straw man and then proceeds to knock it down. Using psychedelics to “treat” mental health “disorders” dates beck to the 1950s and the experiments of Timothy Leary and Richard Alport (before he was Ram Dass). I think turning to drugs primarily seen as recreational is a sign of how the medical model for the treatment of these “disorders” is bankrupt. Remember that whether you are “treating” depression with Paxil or ketamine, or addiction with ayahuasca or methadone, a drug is a drug is a chemical. And there are potential adverse side effects with them all. We don’t need ecstasy and cocaine to replace Prozac and Xanax—we need a better treatment paradigm than simply turning to another chemical “cure.”

  • In his article, Pies references Thomas Kuhn’s idea of “paradigm,” saying that psychiatry is not a failed paradigm since “there is no one paradigm the defines all of psychiatry or that dictates practice on the part of all psychiatrists.” But I wonder if he truly understood the implications to his comment. If you apply Kuhn’s notion of paradigm here with Pies’ application of the term to psychiatry, then you would have to conclude that psychiatry as it’s practiced, is NOT science. Rather, it would be what Kuhn calls a “pseudoscience.”

    He also seems to be oblivious to the implied paradigm in psychiatric practice generated by DSM diagnosis—that it classifies a real “illness” or “disease.”

  • The mesolimbic dopamine system (MDS), the reward pathway of the brain, is one of those later maturing brain regions. Incidentally, it is the likely region where drugs produce dependence and abuse.

    In his book, “The Science of Addiction,” Carleton Erickson said neuroscientists believe that when the functioning of certain MDS neurotransmitter systems are disrupted from genetic “miswiring” and/or long-term exposure to a drug, “chemical dependence as a bran disease” can develop.

    The Schrantee et al. study was said to be the first evidence that using ADHD medications can alter brain development. So when studies of the long-term consequences are done, one of the questions that should be investigated is does the long-term use of stimulant medications effect changes to the MDS of the brains of adolescents and young adults; and are those changes related to a greater risk of substance abuse.

  • Read about this study reported in the January issue of “JAMA Internal Medicine” and thought it was ironic to have been published in the midst of the FDA settlement with Amarin. Eguale et al. systematically looked at the association between off-label use of prescription drugs and adverse drug events (ADEs). They found a higher rate for off-label use that was not supported by strong scientific evidence. Here’s a link to the abstract: http://archinte.jamanetwork.com/article.aspx?articleid=2467782

    Here’s a link to a Medscape article on the study: http://www.medscape.com/viewarticle/854200

    “[P]hysicians and physician organizations should recognize the enormity of the problem and be active participants in the promotion of cautious prescribing of drugs for off-label uses lacking strong scientific evidence.”

    Referring to the Amarin court decision, Good and Gellad commented on the Eguale et al. study and said: “In light of these concerns, the study of off-label drug use and adverse drug events by Eguale and colleagues … is particularly timely.” Here’s a link to their commentary: http://archinte.jamanetwork.com/article.aspx?articleid=2467779

  • There is a buprenorphine-based antidepressant now in clinical trials that was fast tracked by the FDA. Alkermes has designated it as ALKS-5461. Alkermes stock dropped over 40% in value after the announcement. It recently failed in two late-stage clinical trials, but Alkermes isn’t giving up. Here’s a link to a Reuters article on the failures: http://www.reuters.com/article/us-alkermes-study-idUSKCN0UZ1L4. Here’s a link to an article I wrote on ALKS-546, “The coming Depression Apocalypse”: http://faith-seeking-understanding.org/2015/06/17/the-coming-depression-apocalypse/

  • This is good news! The active ingredient in Alkermes’ drug, ALKS 5461, is buprenorphine, an opioid. Buprenorphine is found in Suboxone, which is used as an opioid substitution drug. It has a serious addiction potential; and it is a Schedule III controlled substance. I’ve talked with heroin addicts who said it’s harder to taper off of, or withdraw from than heroin or methadone.

  • I think it would be fine to schedule alcohol and nicotine products as controlled substances; it is insane that they are not scheduled as controlled substances. But that isn’t going to happen. Using the fact that they aren’t scheduled to rationalize removing marijuana completely as a controlled substance seems to me as repeating the same mistake with marijuana that has been made with alcohol and nicotine.

    And marijuana is far from being near benign. Even pro medical marijuana supporters admit that. Here is a link to a short video by SC Labs and WeedMaps on overmedicating with cannabis. https://www.youtube.com/watch?v=USELNiFEP1c.

    In the video, Michael Backes, the Founder/Director of Cornerstone Research Collective, said: “Just because something has a drug safety profile that’s favorable, like cannabis does, doesn’t mean there aren’t potentially some issues.”

  • IF the goal is to promote greater research of the MEDICAL use of marijuana, then it will likely have to remain classified as a controlled substance. Cannabis is addictive and should fall somewhere in the Schedules. If it was just reclassified as a Schedule II controlled substance, the current restrictions on research would be lifted as it would no longer be a Schedule I substance. Getting a Schedule II classification is more likely to happen than a sitting president removing it as a controlled substance.

  • I’m concerned with the discussion of medical marijuana here. The overall tone seems to leave open the potential for using it now for the treatment of psychiatric problems. But there is a significant amount of research that needs to be done first. Towards that end, marijuana should be reclassified as a Schedule 2 controlled substance, and there should be a significant increase in research funding for medical marijuana. The existing FDA structure, as poor as it is, isn’t applied to regulate marijuana, which makes it even more of a crapshoot with the cannabis products that are on the market now than with psychotherapeutic drugs.

    I agree that there is a clear future for the medicinal use of marijuana, but not within the existing piecemeal regulatory structure. The June 23/30 2015 issue of JAMA, The Journal of the American Medical Association, contained several articles related to medical marijuana. Vandry et al. reported on edible cannabis products that they purchased from three randomly selected dispensaries in three cities: Los Angeles, San Francisco, and Seattle. Of the 75 different products purchased from 47 different brands, only 17% were accurately labeled with respect to their THC content. Twenty-three percent were underlabeled (contained more THC than claimed on the label); and 60% were overlabeled (contained less THC than claimed on the label). Some of the overlabled products contained negligible amounts of THC.

    The non-THC content of tested products was generally low. Forty-four products (59%) contained detectable levels of CBD. But only 13 had their CBD content labeled. Four products were overlabeled and nine were underlabeled.

    Another study, in that issue, Whiting et al. did a systematic review and meta-analysis of randomized clinical trials of cannabinoids for various medical conditions. The study concluded there was moderate-quality evidence for the use of cannabinoids (smoked THC and nabiximols) to treat chronic pain and spasticity. There was low-quality evidence to support using cannabinoids for nausea and vomiting due to chemotherapy, weight gain in HIV infection, sleep disorders and Tourette syndrome. There was very low quality evidence for improvement in anxiety as assessed by a public speaking test. There was some evidence that cannabinoids (mainly nabiximols) were associated with an improvement in sleep. There was no evidence showing that cannabinoids helped in the treatment of depression or glaucoma. Most of the indications that qualify by state law for medical marijuana is supported by poor quality scientific evidence.

    Andy LaFrate presented data to the American Chemical Society on the results from his lab on its analysis of marijuana. The average potency of THC is around 20%. An unexpected consequence of breeding for higher THC strains has been that CBD levels have been lowered. Much of the time the CBD concentration in marijuana is low, meaning that the variety of strains are actually very similar, chemically. This is changing, but there has been evidence of serious mislabeling of edible products, as noted above.
    LaFrate also tested for biological and chemical contaminants and found that it had a surprisingly high amount of microbial growth. . “You’ll see a marijuana bud that looks beautiful. And then we run it through a biological assay, and we see that it’s covered in fungi.” Contaminant testing is not mandatory yet, but should be soon in Colorado. LaFrate noted that many samples had fungi or bacteria. Some marijuana products tested have butane, used to strip and concentrate THC from the plant. Other samples had heavy metals.

    THC in particular seems to be the psychoactive chemical in marijuana that triggers symptoms of psychosis. There was an experiment done at the Institute of Psychiatry at Kings College, London. That looked at the effects of THC and CBD, the two main ingredients in cannabis. You can see a video of a reporter participating in the experiment here. Her mixture of THC and CBD left her with the giggles: “No matter how hard I tried to take the experiment seriously, it all seems hilarious.” But with pure THC, it was a different story. “It’s horrible. It’s like being at a funeral . . . Worse . . . It’s just so depressing. You want to top [kill] yourself.”

    On THC and CBD mixture, she said she seemed flippant; on pure THC, she just didn’t care. With pure THC, she was suspicious, introverted; “weird.” Every question seemed to have a double meaning. She felt morbid. “It’s like a panic attack.” The researchers used the Positive and Negative Syndrome Scale (PNASS), a standard test to measure changes in psychotic symptoms. On the PNASS sub scale used, changes above four was clinically significant; what would be associated with schizophrenic psychosis. She scored fourteen. The effects were temporary.

    I’ve been a therapist working with individuals with substance use disorders for over thirty years and think that the current medical marijuana movement is more like the time patent medicines in the 1800s and early 1900s. There is a clear place for the medicinal use of marijuana, but not as it is now practiced. The lack of regulatory control over its use and the poor quality of scientific research into the benefits from specific chemicals in cannabis (that do have treatment potential) is leading to a future I fear could be worse than what currently exists with pharmaceutical medications.

    I’ve taken the information above from articles I’ve written in my own blog on marijuana and medical marijuana. Some of those article titles are: “Let’s not Get Ahead of Ourselves;” “Is the Cart Before the Horse?;” “Clearing Away the Medical Marijuana Smoke.” If are interested in more information, go to http://faith-seeking-understanding.org/.

  • Any response from Dr. Lieberman to your challenge yet? I read “Shrinks” and noticed he didn’t use any end notes or citations, so there is no way of fact checking his various claims, such as stating E. F. Torrey said Thomas Szasz and R. D. Laing privately held that schizophrenia is a brain disease.

  • I think there aree plenty of things to be concerned about with ketamine for depression. Its use is moving too fast, not allowing solid scientific research to keep up. Alan Schatzberg, in “A Word to the Wise About Ketamine,” said: “until we know more, clinicians should be wary about embarking on a slippery ketamine slope.” You can read more here as well: “Falling Down the K-Hole” http://faith-seeking-understanding.org/2014/10/08/falling-down-the-k-hole/

  • Jill,
    I thought your article was a well written critique of the twisted logic of “treating” opioid misuse with medication assisted therapy. I’ve worked in the addiction field for over 30 years and have had similar concerns. The development of buprenorphine as an antidepressant scares me. It’s formulation in ALKS-5461 is essentially another chemical version of Suboxone. I think of it as the coming of a depression apocalypse. now people treating their depression will develop a dependency to a Schedule III opioid.

  • Wait for it … “Under the umbrella of positive psychiatry, clinicians and educators would have rather different roles from today. Clinicians will evaluate not just the symptoms and diagnoses but also the levels of well-being and PPCs among their patients and employ psychotherapeutic/behavioral (AND IN THE FUTURE, BIOLOGICAL) interventions to enhance those traits, focusing on positive outcomes such as improved well-being and recovery.”

  • Sandra,
    I’ve read the critique you wrote of the McElroy study and that by Roy Poses on Health Care Renewal. I looked at the abstract of the McElroy study and the clinical trial information available on clinicaltrials.gov (https://clinicaltrials.gov/show/NCT01291173). But I don’t see anything that says whether the placebo in the study was an inert or active placebo. I’d guess it was an inert placebo.

    If it was, then it would have been easy for the study’s participants to distinguish whether or not they were in one of the drug groups or the placebo group because of the drug effect, especially with the higher dose groups. If that is the case, then the closeness of the results is even more concerning—the double-blind methodology would be broken and still there was only .8 binge day difference between the placebo group and the 70 mg group of Vyanase.

  • Murphy received his Ph.D.in psychology from the University of Pittsburgh, where he was an assistant professor. He was also in private practice in the Pittsburgh area. The Pitt-connected Western Psychiatric Institute and Clinic (WPIC) is a very entrenched medical model facility.

    David Kupfer, the DSM-5 Chair, was the chair of Pitt’s psychiatry department from 1983 to 2009. According to his page at upmc.com, under Kuyper’s direction: “WPIC became one of the nation’s preeminent university-based psychiatric centers, illustrated by the quality and number of publications and the amount of peer-reviewed federal funding for mental health research.”

  • Thanks for this information on Congressman Tim Murphy. I followed up on some of your citations and links and heard him say in his “Fixing America’s Mental Healthcare System” event last month, that he hoped to reintroduce H.R. 3717 as early as March of 2015.

    In his speech to the American Psychiatric Association last May, he was introduced as “a friend of psychiatry;” he commented on feeling at home among like-minded people. The APA president, Paul Summergrad, said the APA was pleased to work with Congressman Murphy “to craft the best bill to benefit the American people.” He has continued to lobby for support of H.R. 3717 and as of December 2014 had 115 cosponsors of the bill, with 34 organizations supporting the bill—with several medical and psychiatric organizations.

    OpenSecrets.org reported that within Murphy’s top 20 contributions from industry were health professionals, pharmaceuticals/health products, hospitals/nursing homes, and health services/HMOs. Murphy received over $283,000 from the political action committees related to these industries for the 2014 election cycle. There were individual contributions in addition to these. His campaign committee reported that during the 2013-2014 fundraising cycle they raised $1,854,010. In his political career from 2001-2014, he has received $701,235 in contributions from health professional political action committees, and $430,030 in contributions from pharmaceuticals/health products political action committees.

  • A friend told me about the segment and I just watched it last night on YouTube. The responses by PHRMA and the AMA were nonresponses, in my opinion. They merely said they supported transparency, the one positive thing mentioned about Pharma in the bit.. None other other issues were addressed.

  • In 2007, a study published in the journal Psychiatric Services found that psychiatrists were less religious than other physicians. Psychiatrists were less likely to believe in God than other physicians (65% versus 77%). And they were less likely to say they looked to God for strength, support and guidance (36% versus 49%). See the original study here: http://ps.psychiatryonline.org/doi/full/10.1176/ps.2007.58.9.1193

  • There is a wrong-headed view of addiction as merely a brain disease. It comes from the same worldview mistake that sees “mental health disorders” as caused by biochemical imbalances. But it is equally wrong-headed to just see addiction through the lens of a “social” model.

    There is a clear cognitive difference between humans and rats. So while studying how the social life of rats influences drug use can be useful, the cognitive differences between humans and rats adds another factor to consider when interpreting the results of these addiction experts—the cognitive or psychological. Addiction is a bio-psycho-social problem.

  • There is an out-of-fashion sense of addiction as a “bio-psycho-social” disease/disorder.

    We are currently fighting against an over-emphasis on the biological sense of addiction as a neurological, brain disorder. My concern with the direction of the article is that it seems to focus only on the social aspect. Governmental policy decisions should see addiction holistically—as biological, psychological AND social.

  • The author lumps substance abuse and substance dependence together as “addiction” to make her point. This has been a pet peeve of Carlton Erickson’s (author of “The Science of Addiction”). Erickson makes a distinction between drug abuse and drug dependence (the older DSM-IV categories in substance use disorders). He said on his website Addiction Science Research and Education Center (http://www.utexas.edu/research/asrec/presentations.html) :

    “Drug abuse often precedes dependence”. The myth suggests that drug abuse causes drug dependence, when in actuality they are two different drug-use conditions. In many people dependence is preceded by abuse, but some people develop dependence without going through the progression of drug use, abuse, and dependence. In addition, many people abuse drugs for many years without developing the disease of chemical dependence.

  • Was the confounding variable of taking a stimulant medication accounted for in determining that children with “ADHD” may have sleep problems? Also, “avoiding television, computers, telephones, and other electronic devices” is recommended as part of treating ADHD by John Rosemond and Bose Ravenel in “The Diseasing of America’s Children.”

  • The concept of “post acute withdrawal” has been an accepted part of addiction treatment for decades. I believe it applies to psychiatric drug withdrawal as well. There is an “acute withdrawal” phase and a “post acute withdrawal” phase, which can last 6 to 24 months. The concept of post acute withdrawal was coined by Terrance Gorski. Here is a link to Gorski’s blog, with a search of postings he’s done about post acute withdrawal: http://terrygorski.com/?s=post+acute+withdrawal.

  • The article reports on the comparison of just TWO different therapies, CBT and psychoanalysis when applied to eating disorders; then generalizes the results to say “So when it comes to psychotherapy, it seems the dodo was wrong.” Second, Rosenzweig’s idea of common factors is not used to say that in all cases, all therapies are equal. Read Barry Duncan’s article, “The Legacy of Saul Rosenzweig: The Profundity of the Dodo Bird” in The Journal of Psychotherapy Integration (2002, vol. 12, no. 1, 32-57); or get a copy of “The Heart and Soul of Change” by Hubble, Duncan and Miller and read the overwhelming evidence that in most cases the type of therapy makes no difference. The author sets up a straw man to then knock down in his article. “The claim that all forms of psychotherapy for mental illness are winners, known as the Dodo Bird Verdict, has been dealt a blow.” This was not what Rosenzweig was claiming. This is not what “The Heart and Soul of Change” was demonstrating.

  • In 2004 Pfizer agreed to pay $430 million to resolve criminal and civil liabilities in connection with its “illegal and fraudulent promotion of unapproved uses” of Neurontin. Just earlier this month, the U.S. Supreme court upheld a $142 million award to the Kaiser Foundation Health Plan for Pfizer’s marketing Neurontin for unapproved uses. The court also allowed two additional lawsuits against Pfizer to proceed. A key factor in the court’s decision was an analysis by Meredith Rosenthal of the Harvard School of Public Health which suggested that marketing Neurontin for unapproved uses “caused physicians to write 43 million off-label prescriptions.”

    GSK can see the writing on the wall; the practices that pharmaceutical companies used to build their empire can’t be used in the future to maintain it. I agree with your analysis of why GSK is making the announced changes. And I agree it has nothing to do with turning over a new leaf and trying to set a new ethical business model because it is the right, honorable and moral thing to do. It’s just the right business move to make at this time.

    If it was being done for moral, ethical reasons, GSK should have done this ten years or longer ago.

  • I read your Washington Post article and I love your balanced approach. I know a family where the mother is bipolar but is now stablized on Abilify and several other medications. Her teen daughter had a brief hospitalization and at her mother’s insistence was started on Abilify as well. Mom is convinced her daughter is on her way to becoming bipolar and sees this as helping to prevent the daughter from going through all the pain she went through—until she finally accepted that she was bipolar.

  • Addiction AS disease; not addiction IS disease. The first is a conceptual metaphor, where there are some some things that correspond between the two halves, yet they are different. “War as a drug” is another conceptual metaphor. Watch the “Hurt Locker” to see it.

    Current thinking on addiction is ignoring this and creating an identity (addiction Is disease) where there is only correspondence. It is reductionistic and dehumanizing.

  • This is not junk science. Here are four articles in the literature making similar points as to the potential harm of marijuana use.

    Marijuana and Brain Shrinkage
    http://archpsyc.jamanetwork.com/article.aspx?articleid=482744

    Australian researchers reported in the June 2008 edition of the Archives of General Psychiatry that long-term use of marijuana may cause two areas of the brain, the hippocampus and amygdala, to shrink in size.

    Marijuana and Psychosis
    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2807%2961162-3/abstract

    A July 2007 article published in the British medical journal Lancet indicated a relationship between marijuana use and psychosis. The authors reported that their analysis showed the risk of psychosis increased by 40% in people who have used marijuana even one time. An even greater risk was evident with the most frequent users, where the risk of psychosis was 50 to 200% greater than normal.

    http://ajp.psychiatryonline.org/article.aspx?articleID=102388

    The results of a 10-year follow up study of 229 individuals diagnosed with schizophrenia demonstrated that cannabis use after the onset of schizophrenia was associated with more severe psychotic symptoms over the 10-year follow-up time.
    Published in the American Journal of Psychiatry.

    http://docsdrive.com/pdfs/ansinet/ijp/2010/796-807.pdf
    A study in the International Journal of Pharmacology, by T.H. Richardson concluded that there was evidence to suggest that cannabis could induce or exacerbate a number of mental health problems.

  • I’ve worked as a therapist in the field of drug and alcohol problems for over thirty years and do find that “recovery” has some utility there. Yes, there is stigma to the labels of “addict” and “alcoholic;” and there is a continuing, frustrating medicalization of addictive “disease” in the terminology of “recovering addict.” Addiction seen merely through a medical lens is reductionistic. BUT the idea of merely being “in remission” within the notion of a “recovering” addict or alcoholic is very important for their ongoing ability to get on with life and avoid falling back into a pattern of compulsive drug or alcohol use.

    To give two examples, I read of a man who had forty years of abstinence from alcohol who was found passed out (from drinking) in his closet two weeks after deciding he could have “a couple of beers” after so much elapsed time. Another man I knew had over 25 years of abstinence when he decided to try using socially again; it didn’t work and he struggled for several years before re-establishing and maintaining his abstinence.

    From a sociological perspective, referring to oneself as a “recovering addict” can also have the sense of attempting to positively redefine the unacceptable, “deviant” social role of addict. Additionally, when an individual continues to view himself or herself as a recovering addict long after they have last used any drugs or alcohol (the refrain of “once an addict, always an addict”), they reinforce a self-identified “master role” as an addict that reminds them of the very real and serious consequences if they forget or redefine their sense of self as “cured” or “recovered” to the extent that they can resume social drinking or drug use.

  • A great conversation. A resource that I’ve found with good information about the changes in psychiatry over the past forty or so years have been “Of Two Minds: An Anthropologist Looks at American Psychiatry,” by T.M. Luhrmann.

  • Hi Douglas,

    I’m not dismissing your experience in asking the following questions. I do believe in the power of prayer. Had you been off of all psychotropic medication at the time of your meeting at the spiritual center? If so, how long since the last time you used any of the medication(s)? Medication withdrawal would contribute to the symptoms you reported. There is also an expectancy or placebo effect that could also be working within your recovery.

  • I’ve worked for over 25 years in addiction treatment and think that the information on “post acute withdrawal” syndrome should be helpful with neuroleptic withdrawal. Also, the is something called the “Discontinuation-Emergent Signs and Symptoms Scale,” developed by Maurizio Fava for antidepressant withdrawal. See his article “Prospective Studies of Adverse Events Related to Antidepressant Discontinuation” in J Clin Psychiatry, 2006:67; supplement 4: 14-21.