The Troubled History of Psychiatry

Jerome Groopman
The New Yorker
Originally posted May 20, 2019

Here is an excerpt:

Yet, despite the phenomenal success of Prozac, and of other SSRIs, no one has been able to produce definitive experimental proof establishing neurochemical imbalances as the pathogenesis of mental illness. Indeed, quite a lot of evidence calls the assumption into question. Clinical trials have stirred up intense controversy about whether antidepressants greatly outperform the placebo effect. And, while SSRIs do boost serotonin, it doesn’t appear that people with depression have unusually low serotonin levels. What’s more, advances in psychopharmacology have been incremental at best; Harrington quotes the eminent psychiatrist Steven Hyman’s assessment that “no new drug targets or therapeutic mechanisms of real significance have been developed for more than four decades.” This doesn’t mean that the available psychiatric medication isn’t beneficial. But some drugs seem to work well for some people and not others, and a patient who gets no benefit from one may do well on another. For a psychiatrist, writing a prescription remains as much an art as a science.

Harrington’s book closes on a sombre note. In America, the final decade of the twentieth century was declared the Decade of the Brain. But, in 2010, the director of the National Institute of Mental Health reflected that the initiative hadn’t produced any marked increase in rates of recovery from mental illness. Harrington calls for an end to triumphalist claims and urges a willingness to acknowledge what we don’t know.

Although psychiatry has yet to find the pathogenesis of most mental illness, it’s important to remember that medical treatment is often beneficial even when pathogenesis remains unknown. After all, what I was taught about peptic ulcers and stress wasn’t entirely useless; though we now know that stress doesn’t cause ulcers, it can exacerbate their symptoms. Even in instances where the discovery of pathogenesis has produced medical successes, it has often worked in tandem with other factors. Without the discovery of H.I.V. we would not have antiretroviral drugs, and yet the halt in the spread of the disease owes much to simple innovations, such as safe-sex education and the distribution of free needles and condoms.

The info is here.

A Waste of 1,000 Research Papers

Ed Yong
The Atlantic
Originally posted May 17, 2019

In 1996, a group of European researchers found that a certain gene, called SLC6A4, might influence a person’s risk of depression.

It was a blockbuster discovery at the time. The team found that a less active version of the gene was more common among 454 people who had mood disorders than in 570 who did not. In theory, anyone who had this particular gene variant could be at higher risk for depression, and that finding, they said, might help in diagnosing such disorders, assessing suicidal behavior, or even predicting a person’s response to antidepressants.

Back then, tools for sequencing DNA weren’t as cheap or powerful as they are today. When researchers wanted to work out which genes might affect a disease or trait, they made educated guesses, and picked likely “candidate genes.” For depression, SLC6A4 seemed like a great candidate: It’s responsible for getting a chemical called serotonin into brain cells, and serotonin had already been linked to mood and depression. Over two decades, this one gene inspired at least 450 research papers.

But a new study—the biggest and most comprehensive of its kind yet—shows that this seemingly sturdy mountain of research is actually a house of cards, built on nonexistent foundations.

Richard Border of the University of Colorado at Boulder and his colleagues picked the 18 candidate genes that have been most commonly linked to depression—SLC6A4 chief among them. Using data from large groups of volunteers, ranging from 62,000 to 443,000 people, the team checked whether any versions of these genes were more common among people with depression. “We didn’t find a smidge of evidence,” says Matthew Keller, who led the project.

The info is here.

Notes From Psychiatry’s Battle Lines

By George Makari
The New York Times - Opinionator
February 23, 2016

Here is an excerpt:

Consider this: Like most clinicians, I am eager for scientific progress, something new that will yield more clarity and provide my patients with faster or deeper relief. However, as I take stock of a new “neuroenhancer,” or the latest genetic correlation that may point to the cause of an illness, or a suddenly popular diagnosis, the historian in me senses ghosts beginning to stir.

Historians have shown that psychiatry has long suffered from the adoption of scientific-sounding theories and cures that turned out to be dogma. Perhaps the clearest example of such “scientism” was psychiatry’s embrace, in the early 19th century, of Franz Joseph Gall’s phrenology, in which all mental attributes and deficiencies were assigned to specific brain locales, evidence be damned. During much of the 20th century, psychoanalysis proposed far more conclusive answers than it could support, and today, the same could be said for some incautious neurobiological researchers.

The article is here.

How to Know Whether to Believe a Health Study

By Austin Frakt
The New York Times - The Upshot
Originally posted on August 17, 2015

Here is an excerpt:

Unfortunately, there’s no substitute for careful examination of studies by experts. Yet, if you’re not an expert, you can do a few simple things to become a more savvy consumer of research. First, if the study examined the effects of a therapy only on animals or in a test tube, we have very limited insight into how it will actually work in humans. You should take any claims about effects on people with more than a grain of salt. Next, for studies involving humans, ask yourself: What method did the researchers use? How similar am I to the people it examined?

Sure, there are many other important questions to ask about a study — for instance, did it examine harms as well as benefits? But just assessing the basis for what researchers call “causal claims” — X leads to or causes Y — and how similar you are to study subjects will go a long way toward unlocking its credibility and relevance to you.

The entire article is here.

Dealing with all the behavioral conditions of unknown etiology

By Steven Reidbord
KevinMD.org
Originally published May 1, 2014

Here are some excerpts:

A few years ago I wrote that uncertainty is inevitable in psychiatry.  We literally don’t know the pathogenesis of any psychiatric disorder.  Historically, when the etiology of abnormal behavior became known, the disease was no longer considered psychiatric.  Thus, neurosyphilis and myxedema went to internal medicine; seizures, multiple sclerosis, Parkinson’s, and many other formerly psychiatric conditions went to neurology; brain tumors and hemorrhages went to neurosurgery; and so forth.

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Patients are told they suffer a “chemical imbalance” in the brain, when none has ever been shown.  Rapid advances in brain imaging and genetics have yielded an avalanche of findings that may well bring us closer to understanding the causes of mental disorders.  But they haven’t done so yet — a sad fact obscured by popular and professional rhetoric.  In particular, functional brain imaging (e.g., fMRI) fascinates brain scientists and the public alike.  We can now see, in dramatic three-dimensional colorful computer graphics, how different regions of the living brain “light up,” that is, vary in metabolic activity.  Population studies reveal systematic differences in patients with specific psychiatric disorders as compared to normals.  Don’t such images prove that psychiatric disorders are neurobiological brain diseases?

Note quite.

The entire article is here.

Thanks to Ed Zuckerman for this information.