Perhaps you have read Robert Whitaker’s 2010 “Anatomy of an Epidemic.” I have given considerable attention to the book on my personal blog, “Knowledge is Necessity,” but I have only made passing reference to it here, which I will explain later. Let’s begin ...

Robert Whitaker is a journalist and outspoken critic of psychiatry. His 2002 book, “Mad in America,” is a scathing indictment of medical (mis)treatments for the mentally ill over the past couple of hundred years, and “Anatomy” picks up where “Mad” left off. In “Anatomy,” Whitaker makes the extraordinary assertion that mental illness is on the rise because of meds, not in spite of meds.

Part of his argument concerns a point I have been raising for years, one advanced by the leading bipolar authorities and backed by patient testimony - that antidepressants may considerably worsen the course of bipolar disorder by inducing mania and speeding up cycling. In addition, certain individuals with unipolar depression (especially those with highly recurrent episodes) may find themselves at risk.

Whitaker presses this line of attack by noting that certain individuals have experienced their first manic episode on an antidepressant, essentially turning someone with unipolar depression into someone with bipolar disorder. Likewise, antidepressants have complicated the course of bipolar to the extent that the illness is far less manageable than it used to be.

One of the problems with antidepressants, according to Whitaker, is that patients build up a tolerance to the drug. The drug may boot you out of your current state, but long-term administration may actually create the ironic effect of raising the risk of a reoccurring depressive episode. Giovani Fava of the University of Bologna uses the term “oppositional tolerance,” where the brain essentially fights back against the antidepressant.

Something similar may be going on with antipsychotics. Whitaker cites Guy Chouinard and Barry Jones of McGill University in support of the proposition that long-term antipsychotic use may induce “supersensitivity psychosis,” again based on the principle of of the brain fighting back against the drug and overshooting back to the condition it was meant to prevent.

Whitaker carries the argument further by pointing to a study by Harrow and Jobe of the University of Illinois that tracked 64 patients with schizophrenia over 15 years. The true finding of the study was that patients identified at intake with a “good prognosis” (such experiencing their first outbreak at a later age) were far more likely to have better long-term outcomes. Many of these patients had also been successfully weaned off their antipsychotics.

Whitaker interpreted the study to mean that the patients in the study who remained on antipsychotics fared worse over 15 years than the ones who went off. This may have been a legitimate “secondary analysis,” but this is not what the study measured for. Otherwise, the study would have been conducted on two “randomized” (ie very similar) patient groups, and such a study may well have produced a very different finding.