Whitaker vs Quack Psychiatry - Part One

On Jan 13, 2011, journalist Robert Whitaker, author of “Anatomy of an Epidemic,” delivered a grand rounds at Mass General (which is affiliated with Harvard). Originally, Whitaker was to speak for about 40 minutes, with leading psychiatric researcher Andrew Nierenberg following with his 10-minute shared “perspective.” Then, the organizers decided to allot about 30 minutes each to the two speakers.

Background

Whitaker’s "Anatomy of an Epidemic," which came out early in 2010, makes a well-reasoned case for why psychiatric meds over the long term may significantly worsen - rather than improve - the course of mental illness. A “well-reasoned case” is hardly the same as an airtight argument, but nonetheless demands a very high level of respect.

The book placed heavy emphasis on two pieces of research:

The first, by Guy Chouinard of McGill University, pointed to the possibility of “supersensitivity psychosis” from abrupt discontinuation (or lowered doses) of antipsychotic meds, analogous to rebound symptoms observed in other classes of drugs.

In the second, Whitaker interpreted findings by Martin Harrow of the University of Illinois to indicate that over the long term, patients with schizophrenia who went off their meds had far better outcomes than patients who stayed on their meds.

Taking these studies together, along with other supporting evidence, Whitaker concluded that long-term administration of psychiatric meds is likely to result in structural changes to the brain that greatly worsens symptoms and sabotages any hope of recovery. This argument goes much further than the standard critiques involving meds and those who prescribe them.

My Blog Critiques

Over the course of October and into November, I ran about 10 or 11 pieces based on “Anatomy of an Epidemic,” and also a post-book observation from Whitaker that cited a very recent piece from Giovani Fava of the University of Bologna pointing to the possibility of “oppositional tolerance” to antidepressants.

The gist of my pieces was that Whitaker had basically made his case, which is not the same as saying I agreed with Whitaker. I carefully examined all the studies he cited, plus other research, and concluded there were other ways of interpreting the Choinard and Harrow and Fava findings, namely:

1. Supersensitivity psychosis is a valid hypothesis - and clearly there is a compelling need to prioritize this research - but even those working in the field acknowledge it is virtually impossible to distinguish a drug-effect rebound psychosis from an illness-effect psychosis. Choinard’s answer to supersensitivity psychosis was not to wean patients off of these meds (a conclusion easy to make from reading Whitaker) but to keep patients on their meds using smarter strategies (such as adding a mood stabilizer to the mix).
2. The purpose of the Harrow study was to identify types of patients with schizophrenia (say those with prior work histories) most likely to do well going off their meds, which is very different than the type of standard long-term clinical efficacy trial that Whitaker led us to believe in his book. The Harrow study identified these populations, and his findings point to a much smarter way of treating schizophrenia than current practice.
3. Fava’s “oppositional tolerance” thesis (which parallels Choinard’s supersensitivity psychosis) is very compelling, but there are many other reasons for explaining the very poor long-term results from antidepressants, such as doctors handing out these meds like candy to individuals who never should be on them in the first place.

My own interpretations in no way refute Whitaker’s, nor were they intended to. The evidence clearly justifies Whitaker in making the type of conclusions that researchers in academic journals are not allowed to make (except, of course, in creatively spinning data to make the test drug look good, but that is another story).

In my pieces, I did take Whitaker to task for failing to cite these studies in their proper context and without recognizing that there were other ways of looking at the evidence. I also cited him on a number of moving violations such as his over-reliance on antipsychiatry sources and his gratuitous cheap-shots of advocacy organizations (such as NAMI) who actually get off their asses and do things.

But I also added my unambiguous concurring voice to his $64,000 question, namely: Why do patients often seem to get worse on psychiatric meds rather than better?

Tying This Into a Bow (for Now)

As I said in the beginning of this piece, Whitaker makes a “well-reasoned” case. It is hardly airtight, but it is a far more compelling one than the extremely specious arguments that psychiatry advances for us having to stay on meds (particularly at high doses) the rest of our lives.

But even if one thinks that Whitaker is off-base, the only answer to a “well-reasoned” argument is another well-reasoned argument. Reason, even in opposition, sheds light and moves the discussion forward. We all benefit - patients, loved ones, researchers, clinicians.

What we do not want to see are petty personal attacks, red herrings, misinformation, and self-serving “refutations” that fail to address the issues. Our well-being is way too important for any psychiatry thought-leader - one who has taken an oath to do no harm - to even consider such a thing.

Next: A psychiatry thought-leader delivers petty personal attacks, red herrings, misinformation, and self-serving “refutations” that fail to address the issues.