Cracked (29 page)

“Supposing you are right,” I said to Breggin, “then how do you get people to stop going? How is that going to happen?”

“I think we need braver journalists and authors, dissident psychiatrists and psychologists,” answered Breggin. “This has to be an educational movement, a political movement. We need grassroots disillusionment among professionals, among consumers, and the sciences. From this we can only hope there will be manifested new kinds of organizations, research, and journals.”

Could this be the route to reform, then—a reliance on
us
? From everything I have learned from all my encounters, I have to say as inadequate as this solution feels, it may well offer the most hope in the coming years. As Timimi put it, “The things that get powerful institutions to change don't usually come from inside those institutions. They usually come from outside. So anything that can put pressure on psychiatry as an institution to critique its concepts and reform its ways must surely be a good thing.”

4

It is 2:00 a.m. on November 29, 2012. I am sitting alone at my kitchen table, the lights are dimmed, the shutters closed, and I am writing these words with only a large pot of coffee to prop me up. My wife and baby daughter are tucked up safely in bed. I wish I were there too. But I know this will be a long night. My publishers expect this book by the morning. There have been too many nights like this in recent months, too much fretting, too much vacillation, too few hours to spare. Don't get me wrong, I have enjoyed the journey I have been on immensely; but even so, I am now looking forward to a little rest, and most of all to spending more time with my family.

But even during those times when I have been away from them, during my various lockdowns in airport lounges, my disrupted nights in strange hotels, my long and uncomfortable journeys by car, plane, and bus, I haven't in truth ever been entirely alone. Because you, the reader, have always been there. You have been at the front of my mind as I have struggled to honestly and clearly communicate the revelations set down in these pages. I know that everything I have said won't resonate with you, that you will formulate your own opinions. But I also hope that some of the facts here disclosed will leave their mark on your views and future actions.

I believe that psychiatry is not the enemy, that the people I have disagreed with are not the enemy. No, I believe the only enemy is anything that actively tries to conceal the inconvenient facts. And the good news is that today in psychiatry the cell of concealment is cracking. The truths are finally seeping out. As to what role you choose to play in furthering this seepage is naturally a matter for you alone. But insofar as I have succeeded in making what is not generally known more freely available, then I have to admit it is with a lighter heart that I finally bring this book to a close and bid you good night.

A
ntipsychotics (neuroleptics)—Breaking the Brain? In what follows I draw upon these books, but especially the excellent work of Robert Whitaker.

As I have not really discussed the effects of antipsychotic medications in the main body of this book, and because this is such an important topic, let me at the very least say a few brief words before I close. What follows can in no way do justice to the vast body of research pursuing the pros and cons of antipsychotic medication—their benefits, their side effects, and their harmful neurological effects. As I can only provide the most cursory survey here, I have placed a short list of useful books at the end of this appendix for those interested in pursuing this topic further.

While it is true that antipsychotics can help certain people some of the time, inflated claims about their ability to “cure” mental disorders are as unsubstantiated as are claims made for the “curing” powers of antidepressants. Like the claims for antidepressants, those made in favor of antipsychotics must also be weighed against the facts. And any serious reading of the research literature on antipsychotics reveals that the facts are problematic.

Antipsychotics (or neuroleptics, as they are more technically known) are administered for what are considered to be the more severe forms of mental disorder, including schizophrenia, bipolar disorder, delusional disorder, and psychotic depression. These drugs are broadly classed under first-, second-, and third-generation headings—third-generation being the newest wave of antipsychotic medications. All antipsychotics are said to work in a similar way, most purporting to block dopamine (the chemical thought responsible for psychotic experiences) receptors in different brain pathways. It is important to note, however, that just as for the antidepressants, there is no research confirming that antipsychotics fix any known brain abnormality or that they “rebalance” brain chemistry to some optimal level.
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Rather, like any mood-altering substance, they simply alter the brain's functioning, and in ways that are still mostly opaque to researchers.

Despite the uncertainty as to how antipsychotics work neurologically, studies of their effects over the short term do reveal them to have moderately better results than placebos at reducing certain psychotic symptoms, helping people stabilize after a psychotic episode. That conclusion is now rarely disputed. What is disputed, however, is the precise value of this “stabilized” state, especially for people who may have recovered spontaneously or may have responded well to other therapeutic support. For instance, using antipsychotics over the short term does not just lead to a reduction in the intensity of psychotic symptoms. Their effects are less specific than that: they also diminish other physical and emotional functions integral to all our mental activity. Psychiatrist Peter Breggin has referred to this state of diminished activity as “deactivation.”

To give a sense of what the very common experience of deactivation looks like for people taking antipsychotics, let me quote a patient's description of deactivation documented in the
British Medical Journal
. While this patient felt his psychotic symptoms had somewhat abated after antipsychotic use, he also bemoaned other disturbing changes: “My personality has been so stifled that sometimes I think the richness of my pre-injections days—even with brief outbursts of madness—is preferable to the numbed cabbage I have now become … In losing my periods of madness I have had to pay with my soul.”
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It is of course up to the individual patient to decide whether paying with one's soul is an acceptable price for the mitigation of their symptoms, assuming first that the patient is in an able enough emotional state to make this decision for himself, and second that the patient has been provided by his doctor the information necessary for making an informed decision (which generally does not happen).

So let's provide some of this information here, by way of assessing the long-term effects of antipsychotic treatment. First, despite many claims that neuroleptics improve the outcome of schizophrenia, the actual evidence for this is scant.
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On the contrary, research conducted over consecutive decades since the 1950s indicates that long-term usage may actually make outcomes worse for the majority of patients. A particularly pertinent suite of studies in the 1970s revealed this paradoxical conclusion.

William Carpenter and Thomas McGlashan at the National Institute for Mental Health explored whether patients fared better off drugs. Their study, published in the
American Journal of Psychiatry
, showed that 35 percent of the non-medicated group relapsed within a year after discharge, compared with 45 percent of the medicated group. This finding was confirmed in a later study by Jonathan Cole, published in 1977 in the
American Journal of Psychiatry,
which reviewed all of the long-term studies on schizophrenic outcomes. It concluded that at least 50 percent of all schizophrenia patients could fare well without drugs, and therefore requested a serious reappraisal of current prescription practices.

This was quickly followed by a study in
International Pharmacopsychiatry
published in 1978 by Maurice Rappaport from the University of California. He followed eighty young males diagnosed with schizophrenia over a period of three years. All had been initially hospitalized, but not all had been administered antipsychotics. He showed that those not treated with antipsychotics, again, had by far the best outcomes: of those treated with antipsychotics a full 73 percent were rehospitalized, compared with only 47 percent who were not given meds. Rappaport thus concluded that “many unmedicated-while-in-hospital patients showed greater long-term improvement, less pathology at follow-up, fewer rehospitalizations, and better overall functioning in the community than patients who were given chlorpromazine while in the hospital.”
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Studies like these gained further legitimacy in the 1980s, when two researchers from the University of Illinois, Martin Harrow and Thomas Jobe, began a long-term study of sixty-four newly diagnosed schizophrenia patients. Every few years the researchers assessed their progress. They asked whether the patients' symptoms had decreased, whether they were recovering, how they were getting on with their lives, and whether they were still taking antipsychotics. After observing the patients for two years, they noticed that the experience of those still taking antipsychotics began to diverge from those who weren't. By four and a half years into the study, nearly 40 percent of those who had stopped taking medication were “in recovery” and more than 60 percent were working. Whereas of those still taking medication, only 6 percent were “in recovery” and few were working.

As the years unfolded these dramatic differences remained: at the fifteen-year follow-up assessment, 40 percent of those off drugs were in recovery, versus 5 percent of the medicated group. These results were published in 2007 in
The Journal of Nervous and Mental Disease
and led the authors to conclude that patients who had remained on medication did far worse than patients who had stopped their medication—this latter group were more successful in their lives and at work.
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Research like this has raised many serious concerns that have often been sidelined by many working within psychiatry. One of particular importance pertains to the precise long-term damage that antipsychotics can cause the brain. This is to say, can the neurological changes antipsychotics induce explain the worse outcomes of medicated patients?

Writer Robert Whitaker has closely investigated this question in his book
The Anatomy of an Epidemic
. He builds upon the research by two physicians, Guy Chouinard and Barry Jones from McGill University, which provides a neurological explanation for why patients taking antipsychotic medication long-term regularly fare worse than non-medicated groups. They start from the accepted position that antipsychotics work by blocking dopamine receptors in the brain, for which, they theorize, the brain then compensates by increasing the number of dopamine receptors (by up to 30 percent). This then leaves the brain hypersensitive to dopamine once the medication is stopped—a hypersensitivity believed responsible for further psychotic experiences and thus further “relapses.” Whitaker summarizes the problem thus:

Neuroleptics [antipsychotics] put a brake on dopamine transmission, and in response the brain puts down the dopamine accelerator (the extra D2 receptors). If the drug is abruptly withdrawn, the brake on dopamine is suddenly released while the accelerator is still pressed to the floor. The system is now wildly out of balance, and just as a car might careen out of control, so too the dopaminergic pathways in the brain. The dopaminergic neurons in the basal ganglia may fire so rapidly that the patient withdrawing from the drugs suffers weird tics, agitation, and other motor abnormalities; the same out-of-control firing is happening with the dopaminergic pathway to the limbic region, and that may lead to “psychotic relapse or deterioration.”
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What Whitaker argues is that Chouinard and Jones's work had in theory ascertained why the outcomes of people taking antipsychotics were so comparatively low: medication escalates the likelihood of relapse by increasing dopamine activity once the person has ceased taking medication. As such relapses are then treated with yet more medication, which in turn raises the likelihood of yet another relapse, a vicious spiral of worsening mental health ensues.

It is not just the dopamine system that Whitaker has argued was being damaged by long-term antipsychotic use. Recent studies on macaque monkeys, for instance, have shown that after two years on either haloperidol or olanzapine, there was an observable shrinkage in their brain tissue.
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And similar structural changes in the brain have also been discerned in humans. One study showed that antipsychotics could increase the basal ganglia and, as with monkeys, reduce gray matter in certain brain regions.
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Furthermore, there is no definitive research indicating that these brain changes are indeed in any way positive. Just like the brain changes sustained by long-term drug or alcohol abuse, these changes may well be both deleterious and irreversible. For example, some patients who take antipsychotics long-term develop what is called “tardive dyskinesia” (TD), a gross motor dysfunction characterized by sudden, uncontrollable movements of voluntary muscle groups (e.g., constant movements of the mouth, tongue, jaw, and cheeks; constant tongue protrusion or squirming and twisting). The problem with this condition is that it remains after the drugs are withdrawn, which has been taken as evidence for their causing permanent brain damage. Whitaker argues that antipsychotic usage may not therefore be curing the brain but rather damaging the brain. This leads him to offer the following reflections:

This does not mean that antipsychotics don't have a place in psychiatry's toolbox. But it does mean that psychiatry's use of these drugs needs to be rethought, and fortunately a model of care pioneered by a Finnish group in western Lapland provides us with an example of the benefit that can come from doing so. Twenty years ago, they began using antipsychotics in a selective, cautious manner, and today the long-term outcomes of their first-episode psychotic patients are astonishingly good. At the end of five years, 85% of their patients are either working or back in school, and only 20% are taking antipsychotics.
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