Pillaged

Psychiatric Medications and Suicide Risk

Ronald W. Maris

• Publisher: University of South Carolina Press
• Year: 2015
• Print ISBN: 9781611174618, 9781611174601
• eBook ISBN: 9781611174625
• Topic: Psychology
• Subtopic: Pharmacology
• Index: Psychology

An examination of the efficacy and safety of psychiatric medications in light of how little is understood about how they work

It is estimated that forty-five to fifty percent of all Americans will suffer a mental disorder at some time during their lives. Increasingly, the treatment for these disorders is management with one or more psychiatric drugs, often prescribed by general practitioners. In Pillaged Ronald William Maris evaluates the psychiatric medications commonly used to treat several major types of psychiatric disorders—-including depression and mood disorders, bipolar disorders, anxiety disorders, and psychotic disorders—asking "do they work as advertised?" and, more importantly, "are they safe?"

Answers to these questions are more ambiguous than we might think, Maris explains, because drug manufacturers tend to minimize the adverse effects of their products. Furthermore, the underlying neurobiological theories of how psychiatric drugs work are complex, poorly understood, and often conflicting. Still Americans spend tens of billions of dollars a year on antidepressants and antipsychotics alone.

While Maris questions the rampant prescribing of psychiatric medications especially in young people, Pillaged does not suggest that anyone cavalierly discontinue potentially beneficial psychiatric medications without the advice of a qualified mental health professional. The book acknowledges that psychiatric medications are often necessary in treating some psychiatric conditions, but it reminds readers of medication's potential for degrading one's quality of life, contributing to self-destructive behaviors, and even leading to death in a vulnerable minority of patients. Maris advocates an open and honest discussion of data on psychiatric drugs, their effects, and their dangers, and he reminds readers of available alternative, nondrug treatments for psychiatric disorders. By reviewing the history and effects of medications for mental disorders, Maris hopes to educate health care consumers and prescribers to make careful, informed decisions about the treatment of psychiatric disorders.

Part I

Overview of the Problems

1

The Suicide Risks of Psychiatric Medications

The argument in a nutshell is that psychiatric medications are powerful and psychotropic (mind or mood altering). Ingesting them can do harm in a small, vulnerable minority of patients (much like allergies to peanuts or shellfish); they can contribute to suicide or worsen mental disorder (see Angell, 2011; compare Schwarz, 2013). Also, psychiatric medications may simply be ineffective or not work as neurobiological theories claim they do. All the manufacturers of psychiatric medications flatly deny that their products cause suicide. However, David Healy (in Whitaker, 2010: 283; compare Healy, 2012) says there are more “dead bodies” in psychiatric medication treatment groups than there are in placebo control groups.

If psychiatric drugs do harm, then the public should be warned about their adverse effects, have full access to the clinical trial data (see Leaf, 2013) and be able to make informed consent about their use. It is not just the mental illness (such as a depressive disorder) that causes suicide; sometimes it is the treatment of that illness with psychiatric medications (see Maris, 2007).

You should not take psychiatric medications cavalierly or whimsically. For example, you should probably take antidepressants only for severe to moderate depressive disorder (not for mild depression), other things being equal (compare Whitaker, 2010: 353; about two-thirds of the patients clinicians give antidepressants to do not meet the criteria for major depression), even though most psychiatrists routinely pharmacologically manage their patients’ mental disorders through fifteen-minute “medication checks.” Psychiatric diagnoses have grown astronomically, such as the hotly contested bipolar disorder diagnosis in children (see Carlat, 2010, chap. 7, “The Frenzy of Diagnosis”; Angell, 2011; and Whitaker, 2010: 208; compare the new “Dysruptive Mood Dysregulation Disorder,” code 296.99 in the DSM-5).

Unless you clearly benefit from them and only if your risks do not outweigh your benefits, perhaps in some cases you should not take psychiatric medications at all. It may be hard to determine your drug risks, since drug manufacturers obviously do not advertise them, even though they purport (see Turner, 2008, on how negative clinical trials are often not published at all) to list them in their package inserts from the pharmacy. When you look at all the possible side effects of psychiatric drugs without the guidance of a trusted physician, the possibilities can make your head swim.

Reactions to starting on psychiatric medications should be monitored closely, especially in children and adolescents. Psychotherapeutic treatments (like Beck’s cognitive behavioral therapy or Linehan’s [1993] dialectical behavioral therapy) often work as well as pharmacologic interventions. Even no treatment at all may occasionally work better than drug treatment (see Whitaker, 2010: 103, 169, 335).

One of the great ironies of modern psychiatric treatment is that for some people the medicines designed to reduce emotional pain and suffering can paradoxically contribute to or even cause the very outcomes they were intended to mitigate or prevent. For example, antidepressants can iatrogenically exacerbate or worsen depression and even contribute to suicide risk (including ideation and behavior). “Iatrogenesis” means health care that causes illness (compare Whitaker, 2010: 30). There was recently a forensic case in which a young boy in Arizona was given Prozac. When he developed suicidal ideation, his Prozac dose was doubled and he killed himself a few weeks later. Suicide, however, seldom only has one cause, and causation is hard to determine.

Unnecessary, premature death (via “pharmacide”) is a pretty serious adverse effect, even if it happens rarely. To make matters worse, the drug companies that manufacture antidepressants systematically underestimate the actual risks of their products to their consumers (Turner, 2008; Glenmullin, 2008).

The vast majority of psychiatrists today simply medicate their patients (Carlat, 2010). They do not do psychotherapy themselves. Furthermore, the medications they prescribe are not always clearly effective (Whitaker, 2010; Kirsch, 2010). In spite of a vast panorama of psychiatric drugs on the market since the late 1950s, the incidence and prevalence of mental disorders has actually gone up (what Whitaker, 2010, calls an “epidemic”; compare Angell, June 23, 2011). Harvard psychologist Irving Kirsch (2010) goes on to claim that the majority (70 to 80 percent) of the purported antidepressant result of most antidepressants is in fact due to the placebo effect. For example, Kirsch argues that the extra effect (beyond the placebo effect) of any antidepressant is only 1.8 points (3 percent) on the 59-point Hamilton Depression Scale (a standard scale that quantifies and measures depressive disorder; see also Beck, 1996, ii). Kirsch’s book is entitled The Emperor’s New Drugs, suggesting that (like the Emperor’s New Clothes) the effects of antidepressant medications may be largely imaginary.

The whole theory of titrating brain neurotransmitters with psychiatric medications is not categorically convincing, nor well-understood; Whitaker (2010: 263) refers to it as “the dogma of biological psychiatry.” It is just that, a “theory,” not a cogent, scientific fact (Carlat, 2010; Kramer, 1993; but see Mann and Currier, 2012). Angell (2011) says that the neurobiological explanation of mental illness is a little like arguing that too little aspirin causes headaches. In spite of the simplistic claims of drug companies and their “detailers” (Carlat, 2010), the human brain is extremely complex, and we have just begun to understand it. For example, there are about fourteen times more neurons is a single human brain than there are people on our planet (100 billion neurons divided by 7 billion people).* So when Pfizer talks about “cell A” communicating with “cell B” in its Zoloft television commercials, it is nothing more than a crude, oversimplified theory.

The so-called “serotonin hypothesis” or “monoamine hypothesis” (the neurotransmitters serotonin and norepinephrine are both monoamines that are thought to be dysfunctional in the brains of depressed patients) for depression ignores the fact that mood is the result of many different neurotransmitters interacting in many different parts of the brain in subtle ways we do not yet comprehend. People diagnosed with clinical depression are thought to have lower cerebral-spinal fluid (“CSF”) brain serotonin, especially in their prefrontal cortex. This theory was first proposed by Bowers in 1969 (Whitaker, 2010: 71). Note, too, that you cannot make a healthy, normal person depressed simply by lowering their cerebral-spinal fluid serotonin level.

Perhaps even more disturbing is that psychiatric medications (such as Prozac, Paxil, Zoloft, Lexapro, Xanax, Neurontin, and so forth; see below for generic names) have suicide risks and other serious adverse effects that their manufacturers minimize (Angell, 2004; Bass, 2008; Peterson, 2008; Glenmullin, 2008; Turner, 2008: Whitaker, 2010: 170). Similarly, for years drug companies minimized the sexual dysfunction consequences of SSRI (“selective serotonin reuptake inhibitors”) antidepressants. They claimed in their package inserts (which patients get at their pharmacy along with their medication) that 1 to 5 percent of patients would experience sexual dysfunction, when the true prevalence sometimes approached 50 to 70 percent (Carlat, 2010: 93).

Scientific evidence (including randomized clinical trials, experiments, epidemiological surveys, statistical analyses, and so-called “meta-analytical” studies in spite of their shortcomings) will provide illustrative examples. “Meta-analysis” usually consists not of original research, but rather of a compilation and statistical analysis of the very best peer-reviewed journal articles or clinical trials on a specific topic. Nevertheless, psychiatry is as much an art as a science. Much of the neurochemical science in psychiatry is rudimentary and inconclusive. Honest psychiatrists (see Carlat, 2010) will tell you that a lot of what they do is trial and error and that there is seldom one clearly agreed-upon way to manage a patient. Especially in the first two chapters of this book, the writing style will be somewhat conversational. That is, the reader will simply be talked with (much like Carlat does in his 2010 book, Unhinged), as a suicidologist cautioning a potential or actual drug consumer. This book is written for educated laypeople and consumers, as well for professional mental health workers. Consumers deserve to know what has been discovered before they decide whether or not to buy, ingest, or discontinue psychiatric medications.

For example, in 2006 the Columbia University Reclassification Committee, which in turn reported to the U.S. Federal Drug Administration (FDA), did an important study of antidepressants and suicidality. Consultants were to review narrative vignettes provided by drug companies (Eli Lilly, Glaxo-Smith-Kline, Pfizer, and others) concerning individuals in randomized clinical trials who were taking one of nine antidepressant medications (such as Prozac, Paxil, Zoloft, Luvox, Celexa, Lexapro, Remeron, Wellbutrin, and Serzone). These are obviously the brand names, not the generic names. In Great Britain, Paxil is called “Seroxat,” but in both the United States and Great Britain the generic drug is called “paroxetine HCl.” In a clinical trial a subject and a control group are given either the experimental drug or a placebo (neither the subjects nor the experimenters knows which subjects get the active drug or inert placebo) over a period of time (usually weeks), measurements are taken, and then the results of the trial are analyzed. For the FDA only two positive risk/benefit trials are required for approval of the new drug application (NDA) for marketing.

Suicide experts (each panel had three consultants) were to rate a highly redacted vignette as to its “suicidality.” That is, how did the antidepressant patient (the “proband”) in question rank on a seven-point scale of completed suicide, suicide attempt, preparatory actions, self-injurious behavior with and without intent, suicide ideation, and other behaviors (like accidents)? All the consultant panels reclassified cases which had originally been classified as “possibly suicide-related” serious adverse events by drug manufacturers.

The results of the consultant reclassifications were then statistically analyzed for twenty-four short-term (four to sixteen weeks; most clinical trials are relatively short and, for example, unmedicated depression may take longer than the trials are to lift [see Whitaker, 2010: 169], making the untreated group appear to have less improvement) placebo-controlled trials (the trials involved 4,400 patients for the children and adolescents sample) with the result being that the Major Depressive Disorder patients receiving any of the nine antidepressants had a statistically significant higher relative risk of 2.0 for suicidality (4 percent in the antidepressant group versus 2 percent in the placebo group [compare Carlat, 2010: 95]). To put it in ordinary English, younger patients taking antidepressants were twice as likely as placebo control patients to have suicide ideas, make suicide attempts, and so forth. This was a big surprise. After all, antidepressants were supposed to lower suicide risk.

There were no suicides in the trials, but the rate of suicide in the general population is only about one in ten thousand per year (see American Association of Suicidology). It is entirely reasonable to expect that, with larger samples (Gibbons, in Goldsmith, et al., 2002, 404 ff., suggests one would need about 100,000 subjects, along with other statistical design considerations), antidepressants would also be associated with completed suicides (Leaf, 2013, 6). The study was repeated for adults in 2006, and it was found that the doubling of suicidality risk for antidepressant patients extended up to age twenty-four, although there was some protective effect of antidepressants against suicidality in older age groups.

As a result of the reclassifications of antidepressant data, the FDA ordered the relevant drug manufacturers to post black-box warnings (the most serious FDA warning) about suicidality on all of the nine antidepressants in their package inserts and product labeling descriptions (for example, in the Physicians’ Desk Reference or PDR). One wonders if the antidepressant manufacturers would have warned the consumers or warned them as dramatically (in a black box early in the product description) without the FDA-mandated warning. The warning stopped short of saying antidepressants “caused” suicidality, since statistical association is not the same as causation (see Bradford-Hill criteria for causation). Some well-known suicidologists, like Thomas Joiner (2005), doubt that any psychiatric medication ever caused a suicide (compare Goldney, 2007). The FDA alerts were issued for children and adolescents on October 15, 2004, and for young adults in December 2006. Before 1962 the FDA did not even require that drugs be certified as “effective” (Whitaker, 2010: 94).

Scope of the Problem

Is there really a big problem here? Actually, there is. It has been estimated that about 15 percent of the American population have a diagnosable psychiatric disorder in any given year (Kessler, 2006). If true, that amounts to roughly to 46,000,000 (of 315,000,000) Americans. Of course, far fewer than 15 percent ever get diagnosed or even go to a doctor, and fewer still ever get treated (maybe close to 3 percent).

The American Psychiatric Association’s Diagnostic and Statistical Manual of Psychiatric Disorders was in its fourth (DSM-IV-TR) edition, before the DSM-5 edition came out in May of 2013. Most psychiatric disorders are diagnosed by a symptom checklist and accompanying conditions. Note, too, that in every subsequent edition of the DSM the number of psychiatric disorders has increased and now totals over 300 types. There are about 17 main types of mental disorders and about 312 specific DSM-IV-TR diagnoses.

Ron Kessler (2006) claims that fully 50 percent of all Americans will suffer a mental disorder sometime during their lifetimes and that 22,000,000 take some type of psychotropic drug. Angell (2011) claims that 46 percent of the American population have had at least one psychiatric disorder during their lifetimes. Major depression (and antidepressant use) is right up there near the top, with a lifetime prevalence of 17 percent (and depression is about twice as common in women as in men), with anxiety disorders not far behind. In 2005 about 27,000,000 people in the United States were taking an antidepressant (Carlat, 2010: 69). Angell (2011) says that 10 percent of the American population over age six takes an antidepressant. Crudely, a major antidepressant like Lexapro or Prozac (earlier, before Lilly’s patent expired) could generate about one to two billion dollars profit each year.

In the Global Burden of Disease (World Health Organization, 1996, 2008, and 2012), major depression was found to be the single most disabling illness (including physical illnesses like tuberculosis) in the world. In fact, five of the ten leading causes of disability (daily activities lost per year or “DALYs”) were attributable to psychiatric disorders (that is, depression, alcohol misuse, bipolar disorder, schizophrenia, and suicide).*

Even though suicide is relatively rare (about one in ten thousand in the general population per year), with 38,285 suicides in 2011 (the latest available data) and about 1.6 percent of all deaths, suicide is the tenth leading cause of death in the United States, and the third cause of death for fifteen- to twenty-four-year-olds (for more recent data see American Association of Suicidology’s statistics). As a cause of death, suicide ranks ahead of cirrhosis, renal disease, and homicide.

Suicide has especially high rates among older white males, although recently in the United States the highest suicide rates have been in the middle ages, forty-five to fifty-four. In countries like China the female suicide rate exceeds that of males. Some like to argue that suicide is the leading cause of unnecessary death, since it is self-inflicted and intentional. We all have to die, but not by suicide.

Especially in the era of managed health care, psychiatric disorders tend to be treated pharmacologically (the euphemism is “medication management”). After a fairly brief initial assessment (normally an hour or less), most depressed and/or suicidal patients get a prescription for an antidepressant (like Lexapro, Cymbalta, or Pristiq) and perhaps also a minor tranquilizer (like Klonopin or Xanax, even though Xanax has some troubling side-effects; see p. 114) for anxiety (or even a major tranquilizer; like Zyprexa or Risperdal), not usually psychotherapy (Carlat, 2010).

Lexapro is an isomer or molecular mirror-image (which has fewer side-effects) of Celexa and is serotonin-specific (see p. 42), but Cymbalta and Pristiq block reabsorption both of serotonin and of norepinephrine (“SNRIs”). The British journal The Lancet (2009) found Remeron to be the most effective antidepressant. Psychiatric patient...

Table of contents

• Cover
• Half title
• Title
• Copyright
• Dedication
• Contents
• Illustrations
• Foreword
• Preface
• Acknowledgments
• Part I Overview of the Problems
• Part II The Medications
• Bibliography
• Index