Tag: Carrie Fisher death

10/31/17

Mistaken Beliefs About Addiction Relapse

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The coroner’s report on Carrie Fisher’s death listed sleep apnea as the primary cause of death with drug intake as a contributing factor. In addition to the medications prescribed for her bipolar disorder (Abilify, Lamictal and Prozac), toxicology results found cocaine, methadone, heroin, oxycodone, and MDMA (ecstasy) in her system at the time of her death. Fisher’s family objected to a full autopsy, so the coronor’s conclusions were based on the toxicology results and an external examination of her body. “Based on the available toxicological information, we cannot establish the significance of the multiple substances that were detected in Ms. Fisher’s blood and tissue, with regard to the cause of death.”

The above information was from an article in Variety, but several media outlets were citing the coroner’s report and the same information. People said the coroner’s report indicated Ms. Fisher used cocaine sometime in the 72 hours prior to her death. During her 10-hour flight, she had multiple apneic episodes, which her personal assistant said was normal for her. Towards the end of the flight, she could not be roused. The report also noted she suffered from atherosclerotic heart disease, but then said: “The manner of death has been ruled undetermined.”

Although the official coroner’s report listed the manner of death as undetermined, it seems reasonable to assume from the toxicological information that Ms. Fisher had relapsed into active substance use. Billie Lourd, her daughter, said in a statement to People: “My mom battled drug addiction and mental illness her entire life. She ultimately died of it.” The cocktail of substances in Carrie Fisher’s system at the time of death, along with her history of heart disease, coupled with the increased risk of sudden cardiac death due to the medications used to treat her bipolar disorder lends credibility to Ms. Lourd’s statement.

The use of psychiatric medication to treat her bipolar disorder may have been a contributing factor to Ms. Fisher’s heart failure. See the article, “Blind Spots with Antipsychotics” Part 1 and Part 2 for more on the health problems with antipsychotics. But the range of substances she used just before her death may also have been enough to precipitate a sudden cardiac death, particularly since she already suffered from heart disease. Struggling with a concurrent bipolar disorder and a substance use disorder is a double whammy to anyone in recovery. Instability with either issue is a serious risk factor for relapse. I knew of someone with a bipolar diagnosis and cocaine dependence. They bounced back-and-forth between active cocaine use and inpatient psychiatric treatment for depression ten times within a single year.

Ms. Lourd said her mother would want her death to encourage people to be open about their struggles, and to seek help for them. Historically, Carrie Fisher talked openly about her proneness to relapse. She told People in 1987: “I couldn’t stop, or stay stopped. It was never my fantasy to have a drug problem.” She would stop for a couple of months and then celebrate her abstinence by using again. “I got into trouble each time. I hated myself. I just beat myself up. It was very painful.” With that in mind, let’s assume the immediate cause for her untimely death was due to an apparent relapse into active drug use, and then discuss some mistaken beliefs about addiction relapse.

Terrance Gorski is a leading expert on addiction relapse prevention. He’s written several books on the subject, many of which are available through Herald House Independence Press at relapse.org. He also has a blog, Terry Gorski’s Blog, where he has made a significant amount of his material available for free. Here we’ll concentrate on his article, “Relapse Does not Mean Failure?”

Gorski said there were three mistaken beliefs that often interfered with helping relapse prone individuals. They are: (1) Relapse is self-inflicted; (2) Relapse is an indication the person is a failure who doesn’t want to recover; and (3) Once relapse occurs the patient will never recover.

In most cases, relapse is not self-inflicted. There isn’t a fully conscious, willful decision to throw over abstinence and return to active drinking or drug use. Relapse-prone individuals “experience a gradual progression of symptoms in sobriety that create so much pain that they become unable to function in sobriety. They turn to addictive use to self-medicate the pain.” They can learn to stay sober by recognizing these symptoms as early relapse warning signs. Next is identifying the self-defeating thoughts, feelings and actions used to cope with the symptoms and then learn more effective coping mechanisms, more healthy ways of responding to them.

Unfortunately, most relapse-prone patients never receive relapse prevention therapy, either because treatment centers don’t provide it or their insurance or managed care provider won’t pay for it.

Relapse is not automatically a sign that treatment has failed or the person really doesn’t want to recover. It is more likely that the root-cause of the person’s problems wasn’t addressed by the “standard package of treatment offered.” If this is the case, the risk of relapse increases dramatically. Learning to recognize relapse warning signs and how to cope with them would minimize this risk.

Gorski said that between one half and two-thirds of all individuals treated for alcohol and drug use problems will relapse. At least one half of those who relapse will establish long-term recovery within five to seven years of their first treatment experience. Believing that relapse means both the person and the treatment failed ignores the reality that for many, recovery involves a series of relapse episodes. “Each relapse, if properly dealt with in a subsequent treatment, can become the a learning experience which makes the patient less likely to relapse in the future.”

Chemically dependent people can be grouped into three types based upon their recovery and relapse histories. The first type is recovery prone and maintains total abstinence from their first serious attempt at change. Another type is relapse prone, with a series of short-term, low consequence relapse episodes before finding long-term abstinence. The third type is chronically relapse prone, who can’t seem to find long-term sobriety regardless of what they do.

Recovery prone individuals tend to be dependent on a single drug. They also have higher levels of social and economic stability. They may have steady employment, friendships and stable living situations. And they don’t have coexisting mental health issues, as Carrie Fisher did, or physical health issues, like chronic pain problems. These “garden variety addicts” have chemical addictions with few additional serious personal or social problems.

The second type of transitionally relapse-prone individuals, seem to have more severe addictions that are complicated by other problems. However, they learn from each relapse episode and take steps to modify their recovery programs to avoid future relapses. For example, they may downplay the risks of going around good friends who still drink or use drugs until they find themselves actively drinking or drugging again. Afterwards, they set and keep boundaries with those friends that better support their recovery.

The third type— chronically relapse-prone individuals—not only have the primary addiction for which they are being treated, but also a combination of the following coexisting issues. They may have multiple drug addictions, especially with opiates and methamphetamines. They can have an undiagnosed physical condition, a personality disorder or other mental health problem. There could be issues with severe post acute withdrawal (PAW), which becomes even more severe when the person is under high levels of stress.

Many relapse-prone patients fail to recover because these coexisting [issues] are not properly diagnosed and treated and they interfere with the primary treatment being given.

The third mistaken belief sees recovery as an all-or-nothing process—you either have it or you don’t. And if you relapse, you just don’t want recovery bad enough. Actually, recovery is a learned skill, acquired mostly by trial and error.  Rarely does someone with long-term recovery get there without one or more short series of relapse episodes. “They learned from these experiences and figured out how to put together a meaningful and comfortable long-term recovery.”

So when you think about Carrie Fisher’s toxicology report, don’t assume she threw away her sobriety like it was an old, worn out Alderaan gown. Her relapse was likely the result of a gradual progression of symptoms occurring in her life. In time, they created so much pain in sobriety that she wasn’t able to function. So she tried to self-medicate. She also wasn’t a failure who didn’t want to recover. The openness in her life about her struggles with addiction and mental health belie such an assessment.

Like thousands of others each year, she died with multiple psychoactive substances in her system. But that doesn’t mean she would have never made it back to abstinence. Remember, she was Princess Leia; and Leia Organa never gave in to the tyranny of the Empire. Carrie Fisher would never have given up fighting against her addiction and mental health demons.

I have read and used Terence Gorski’s material on relapse and recovery for most of my career as an addictions counselor. I’ve read several of his books and booklets; and I’ve completed many of his online training courses. He has a blog, “Terry Gorski’s Blog”, where he graciously shares much of what he has learned, researched and written over the years. This is one of a series of articles based upon the material available on his blog and website.

07/21/17

Blind Spots with Antipsychotics, Part 2

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The American Journal of Psychiatry published an article by Goff et al. that addressed concerns that antipsychotic medications can adversely effect long-term outcomes of people with schizophrenia. Their conclusion was that there was little evidence to support “a negative long-term effect of initial or maintenance antipsychotic treatment on outcomes,” when compared to withholding medication treatment. Additionally, the researchers said while a subgroup of patients may benefit from “nonpharmacological treatment approaches,” they warned of the potential for an “incremental risk of relapse” and recommended the need for further research into the question. But did these researchers have a blind spot in how they evaluated their evidence?

In part one of this article, I reviewed some of the research evidence that supported concerns with long-term antipsychotic treatment. There was evidence supporting a link between long-term antipsychotic use and adverse cardiovascular events, brain shrinkage, and dopamine supersensitivity, as well as questions regarding the efficacy of antipsychotic maintenance treatment. There also seemed to be a disregard in Goff et al. of the evidence for the risk of metabolic syndrome with long-term antipsychotic use in their risk-benefit analysis of antipsychotic use. Yet health concerns from metabolic syndrome have been connected to the glaring difference in a shortened life expectancy, with persons suffering with serious mental illness dying 25 years earlier than the general population.

My previous encounters with Dr. Jeffrey Lieberman, who was the lead researcher for Goff et al., have led me to be cautious of his assertions without further investigation. I believe he has a serious blind spot when it comes to assessing and interpreting information counter to his position. See (“A Censored Story of Psychiatry, “Part 1, Part 2;  “Psychiatry, Diagnose Thyself!” Part 1, Part 2) for more on my concerns with Dr. Lieberman. So if there was a blind spot in Goff et al., what do other experts have to say about their conclusions?

Joanna Moncrieff wrote a response to Goff et al. on the Mad in America website, which can be accessed here. Moncrieff is a practicing psychiatrist, academic and author. She is one of the founding members and current co-chair person for the Critical Psychiatry Network, “a group of psychiatrists from around the world who are sceptical of the idea that mental disorders are simply brain diseases and of the dominance of the pharmaceutical industry.” She has written extensively on this issue, including a recent book on the troubling story of antipsychotic drugs entitled: The Bitterest Pill. You can read more about her thinking and her background on her website. She said she was shocked by how Goff et al. dismissed the concerns with long-term antipsychotic treatment and the evidence of brain impacts.

It is riddled with distortion, ignores the most pressing criticisms, and is shot through with the unexamined presumption that the multitude of problems currently labelled as schizophrenia or psychosis will one day be revealed to be due to a specific brain abnormality that is targeted by antipsychotics.

She doesn’t dispute the usefulness of antipsychotics for treating acute psychosis, what Goff et al. called initial antipsychotic treatment. Yet she noted where “decades of research into early intervention has not demonstrated that early antipsychotic treatment improves long-term outcomes.” She pointed out where Goff et al. stated the effectiveness of maintenance treatment has been well established, but then failed to acknowledge that randomised trials of maintenance treatment were typically maintenance treatment versus sudden withdrawal. “Thus they completely fail to address concerns that effects of withdrawal of long-term treatment inevitably confound such studies.”

The most worrying thing about the Goff et al. paper to Moncrieff was the minimization of the evidence that antipsychotics produce brain shrinkage. They claim that shrinkage of brain grey matter has been shown to be part of schizophrenia, claiming that brain differences were detected long before the introduction of antipsychotics. The paper they cited was a 1985 study by Bogerts and Schonfeldt-Bausch, which was a post mortem study done long after antipsychotics had been introduced.

The presence of differences between the brains of people with schizophrenia and controls does not establish that there is progression of brain volume loss, which is what has been clearly demonstrated in people and animals taking antipsychotics. There are no studies that show progressive brain changes in people diagnosed with schizophrenia or psychosis in the absence of antipsychotic treatment.

Dr. Moncrieff concluded her article by saying:

I still think antipsychotics can be useful, and that the benefits of treatment can sometimes outweigh the disadvantages, even in the long-term for some people. However, it does no one any service to pretend that they are innocuous substances that somehow magically transform (hypothetically) abnormal schizophrenic brains back to normal. Psychiatrists need to be fully aware of the detrimental effects of antipsychotics on the brain and body. They also need to acknowledge the way these drugs make life so miserable for many people, even for some who might have been even more distressed were they to be without them… Psychiatrists need to support people to evaluate the pros and cons of antipsychotic treatment for themselves and to keep doing this as they progress through different stages of their problems. To do this they need to be able to acknowledge the real nature of these drugs, and not sweep inconvenient truths under the carpet!

Miram Larsen-Barr also wrote a response to Goff et al. that appeared on Mad in America, which can be accessed here. She is a clinical psychologist with the University of Auckland, New Zealand. Larsen-Barr created and is the Service Director for Engage Aotearoa, an initiative that aims to make recovery information more easily accessible to the general public. She has “lived experience” of recovery from trauma, depression and suicidality. Her doctoral research explored experiences of taking, and attempting to stop, antipsychotic medication.

For her doctoral research she talked to 144 people who take or have taken antipsychotics. One-third thought antipsychotics had relieved their symptoms and given them back their lives—but another third said quite the opposite. She said the claim that the benefits of antipsychotic medications conclusively outweigh the adverse effects is just not true. It is true for some; entirely the opposite for others; and a mixed bag for the remaining individuals. You can access a copy of her thesis research here.

In my study, overall subjective experiences ranged on a continuum from “life-saver” to “hell” and every point between (Larsen-Barr, 2016). Around a third reported overall positive experiences such as “A major relief from the monsters […] for me they have saved my life” and “Helped me get through an unstable period of my life.” And around a third of the participants reported mixed experiences such as, “A short term help when needed then a burden” and “A double edged sword. They help me with my bad experiences but they also take away the wind in my sails.”Another third reported wholly negative experiences such as, “The worst experience of my life […] affected every aspect of my health and wellbeing.” The therapeutic benefits certainly did not outweigh the costs for those who described the overall experience of taking antipsychotics as “The ruin of my life” or said they were “Helpful to a point but […] robbed me of everything I value in myself as a person.”

Larsen-Barr reported that few people in her study reported being well-informed of the potential benefits and risks before antipsychotic treatment. While about one-third reported beneficial results, 79% overall did contemplate stopping their medication, with 73% making at least one attempt. She said her study suggested the desire to stop antipsychotic medications was not just because of negative experiences. These decisions were primarily based upon whether or not taking AMs helped the person to “function in daily life.”

A full third of her survey sample had discontinued medications at the time of the study, which was similar to the stable discontinuation rate found in Harrow’s long-term study. Larsen-Barr found half of 105 survey participants who attempted to stop remained AM-free for one year or more; some over five years ago. Her research showed “withdrawal often entails a lack of information, poor support, and a range of physical, emotional, cognitive, social and functional disruptions that can be difficult to cope with, and which may include exacerbation of symptoms to the point of relapse.” For more on the Harrow study and concerns with antipsychotics, see “The Case Against Antipsychotics” by Robert Whitaker and “Worse Results with Psych Meds” on this website.

In part 1 of this article there was a discussion of how Carrie Fisher’s sudden cardiac death may have been associated with her use of psychiatric medications. Yet the possibility of her medications being a contributing factor to her death seemed to be overlooked in many articles about her unexpected death. For example, writing for Scientific American, Tori Rodriguez raised the possibility that Fisher’s bipolar disorder played a role in her death. Not the medication used to treat her bipolar disorder, but the disorder itself.

“Did Carrie Fisher’s Bipolar Disorder Contribute to Her Death?” noted several possible connections to her bipolar disorder, but only made an oblique comment about how the medications may cause adverse effects like weight gain, diabetes higher triglycerides and even sudden cardiac death. Rodriguez noted how Fisher’s earlier substance abuse and struggles with her weight have been speculatively raised as contributing factors to her death. But she said one possibility that has been overlooked was the connection between bipolar disorder and cardiovascular disease and mortality. Individuals with bipolar disorder are twice as likely to develop or die from cardiovascular disease. The onset of cardiovascular disease occurs up to 17 years earlier in persons with bipolar disorder than in the general population. But as we’ve seen, that connection seems to be with the medications and not the disorder itself.

Rodriguez said Carrie Fisher “fit the bill” for several of the risk factors for sudden cardiac death at different points in her life. Then she said: ‘There is no definitive way to know whether her bipolar disorder or addiction history contributed to her death.” Yet there does seem to be a strong likelihood that not only did her use of antipsychotic medications help her be a better mother, friend and daughter, it may have contributed to her sudden cardiac death as well.

07/11/17

Blind Spots with Antipsychotics, Part 1

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Carrie Fisher was flying back to her home in Los Angeles on December 23, 2016 when she went into cardiac arrest. She was removed from the plane and later died in the hospital. Her daughter, Billie Lourd, said: ““She was loved by the world and she will be missed profoundly.” She was a well-known actress, writer and humorist. She wrote six books, some of which described her life, loves and adventures, which included drug addiction and bipolar disorder. A series of articles lamented that she was taken too soon, but there wasn’t anything said about a possible connection between her sudden cardiac death (SCD) and the medication she took for her bipolar disorder.

Fisher was a vocal mental health advocate and talked freely about her bipolar disorder and over the years. An article contained the following statements made by Fisher about her mental health and use of medication. In an interview with Diane Sawyer in December of 2000, she said: “I am mentally ill. I can say that. I am not ashamed of that. I survived that, I’m still surviving it, but bring it on. Better me than you.” At a February 2001 rally in Indianapolis for increased state funding for mental health and addiction treatment, she said: “Without medication I would not be able to function in this world. Medication has made me a good mother, a good friend, a good daughter.”

Writing for Mad in America, Corinna West raised the question of whether Fisher’s too soon passing was related to her use of psych meds. West referred to an article in the European Heart Journal by Honkola et al. that concluded: “The use of psychotropic drugs, especially combined use of antipsychotic and antidepressant drugs, is strongly associated with an increased risk of SCD at the time of an acute coronary event.” Variety reported Carrie Fisher was taking Prozac (an antidepressant), Abilify (an antipsychotic) and Lamictal (a mood stabilizer).

This study confirms that combining antidepressants and old school [first generation] antipsychotics causes an 18-fold increase in death during a cardiac event. Combining antidepressants with any antipsychotic causes an over 5-fold increase in relative risk of death during a cardiac incident.

To put this into some context, West noted: “Vioxx was pulled from the market for a 2-fold increase in relative risk factor of strokes and heart attacks.” It may have led to the death of 50,000 to 70,000 people while it was on the market. She then did some speculative calculations and suggested psych meds may contribute to 74,191 additional heart attacks annually and 33,386 deaths from SCD per year.

She also noted how people with serious mental illness have a 25-year lower life expectancy than others and a significantly greater risk of myocardial infarction. The NASMHPD “Morbidity and Mortality Report” said that it has been known for several years that people with serious mental illness die younger than the general population. “In fact, persons with serous mental illness (SMI) are now dying 25 years earlier than the general population.” The report also said people with SMI also suffer from a greater percentage of modifiable risk factors associated with cardiovascular disease, such as obesity, smoking, diabetes, hypertension and dyslipidema (high cholesterol). Corrine West noted the data from the “Morbidity and Mortality Report” showed that psychiatric drugs increased 4 of the top 5 normal risk factors for cardiac disease. Smoking was included as a risk factor because many individuals using psych meds find the nicotine helps relieve some of the numbness caused by the meds. See the following chart from the report.

There is increasing evidence of multiple adverse effects from the long-term use of antipsychotics in addition to the risk of SCD. Murray et al. concluded there was a lack of evidence for the long-term effectiveness of prophylactic (maintenance) antipsychotic use; and a growing concern with the cumulative effects of antipsychotics on physical health and brain structure. “There is enough evidence concerning the adverse effects of antipsychotics on physical health to compel psychiatrists to act.”

Murray et al. said long-tem maintenance treatment with antipsychotics was “based on hope rather than evidence.” They pointed to two serious methodological problems. First, studies claiming that antipsychotic maintenance treatment substantially reduced the risk of relapse were often limited to two years of follow-up. Second, the studies compared schizophrenic patients continuing on antipsychotics with those who stopped taking antipsychotics, not individuals who never used the drugs. So the withdrawal effect from antipsychotics in the discontinuation group influenced the higher relapse rates, making it a confounding variable to the supposed positive results with antipsychotic maintenance treatment.

The Murray et al. researchers did think there was no clear link between antipsychotic-associated changes in brain structure and cognitive decline or functional impairment. However, studies like that of Ho et al. suggested antipsychotics can “have a subtle but measurable influence on brain tissue loss over time.” Ho et al. said there was also a problem with dopamine receptor supersensitivity in some antipsychotic users. This supersensitivity could be a factor in the decreased efficacy of antipsychotics with continued prescription; and it may contribute to relapse when an individuals stops using antipsychotics. “There is an urgent need for neurochemical imaging studies addressing the question of dopamine supersensitivity in patients.”  In their conclusion, the researchers gave the following recommendations.

[The wise psychiatrist] will treat acute psychosis with the minimum necessary dose of antipsychotics, employing weight sparing antipsychotics wherever possible; dopamine partial agonists have this property and may also be less likely to induce dopamine supersensitivity. Following recovery, the psychiatrist should work with each patient to decrease the dose to the lowest level compatible with freedom from troublesome psychotic symptoms; in a minority of patients, this level will be zero.

You can read a summary review of the study by Justin Karter on Mad in America here.

Not all of the above-cited researchers agreed with the conclusions of each other. But collectively they pointed to evidence of a link between antipsychotics and adverse cardio vascular events, brain shrinkage, and dopamine supersensitivity.  Murray et al. also suggested that studies of long-tem antipsychotic maintenance treatment unfairly stacked their results in favor of antipsychotic maintenance by using patients who were withdrawn/discontinued from using antipsychotics as their control group. So when the recent press release from Columbia Medical Center regarding Goff et al. concluded the benefits of antipsychotics outweigh the risks was disconcerting and confusing at first. The Goff et al. abstract asserted: “Little evidence was found to support a negative long-term effect of initial or maintenance antipsychotic treatment on outcomes, compared with withholding treatment.”

The press release acknowledged the above concerns that antipsychotic medications have been said to have toxic effects and negatively impact long-term outcomes. However it went on to say that if this view was not justified by data, it had the potential to “mislead some patients (and their families) to refuse or discontinue antipsychotic treatment.” Therefore a team of researchers led by Jeffrey Lieberman, the Lawrence C. Kolb Professor and Chairman of Psychiatry at Columbia University College of Physicians and Surgeon, undertook “a comprehensive examination of clinical and basic research studies that examined the effects of antipsychotic drug treatment on the clinical outcomes of patients and changes in brain structure.” Lieberman was liberally quoted in the Columbia press release with regard to their findings supporting how the benefits of antipsychotics outweigh the risks. He said:

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.

Lieberman went on to suggest that only a very small number of individuals recover from an initial psychotic episode without the use of antipsychotic maintenance treatment. “Consequentially, withholding treatment could be detrimental for most patients with schizophrenia.” He acknowledged where rodent studies suggested antipsychotics can sensitize dopamine receptors, but “there is no evidence that antipsychotic treatment increases the risk of relapse.” Further, although antipsychotic medications can increase the risk of metabolic syndrome, which is linked to heart disease, diabetes and stroke, their study did not include a risk benefit analysis of this concern.

Wait a minute. Why didn’t their study include a risk benefit analysis for metabolic syndrome? It seems to be one of the most reliably documented adverse effects, as noted above. Could it be that the intended message of the research—namely how strong evidence supports the benefits of antipsychotic medications—would not have been as clearly communicated if the risk benefit analysis concluded there was a substantial risk of metabolic syndrome? By the way, according to the Mayo Clinic,

Metabolic syndrome is a cluster of conditions — increased blood pressure, high blood sugar, excess body fat around the waist, and abnormal cholesterol or triglyceride levels — that occur together, increasing your risk of heart disease, stroke and diabetes. Having just one of these conditions doesn’t mean you have metabolic syndrome. However, any of these conditions increase your risk of serious disease. Having more than one of these might increase your risk even more. If you have metabolic syndrome or any of its components, aggressive lifestyle changes can delay or even prevent the development of serious health problems.

Dr. Lieberman has been a vocal advocate of modern psychiatry and equally critical of those who question many of its claims, as with those documented here. My previous encounters with his presentation of evidence and data, like his discussion of the conclusions of Goff et al. above, have led me to be skeptical of his conclusions without further investigation. I believe his fervent desire to defend modern psychiatry and current psychiatric methods has distorted how he interprets and presents conflicting evidence. He seems to have a blind spot when assessing and interpreting evidence counter to his position. The above question about the failure to include a risk benefit analysis of metabolic syndrome is one illustration of what I mean.

So what do others have to say with regard to the Goff et al. study? We’ll look at some of those critiques in Part 2 of this article.