NPR’s akathisia blind spot
As a writer you never set out to return, again and again, to a topic as painful as suicide, or as divisive as the risk of side effects with popular mental health medications, but for whatever reason this very fate emerged in the course of my reporting several years ago and here we are. Unlike so many other pressing health questions in our time, however, the problems with SSRI’s and suicide seems no closer to being articulated in the culture at large, let alone resolved, beyond a few ardent voices and the small print on some drug labels that, thanks to the silent skepticism of so many, no one really knows what to think of. And then the questions raised by the topic shows up in the most glaring fashion in the middle of an evening news report on a respected news source, a sensitive, thoughtful outlet that is nonetheless unwilling to connect the dots, or even broach the subject, in spite of all that we now know.
The media is loathe to single out antidepressants, drugs created to funnel billions into the pockets of the pharmaceutical industry. The editors of magazines treat the topic like the plague. Friends and family and neighbors in conversations would rather talk to you about water-boarding. Perhaps people become sensitive to the idea they may be taking a drug for a private condition and that you are raising the fact of data showing the drug is oversold and risky. To which I can only add that I have taken them too, in another life, and I somehow came to peace with their nature, and I can’t imagine why anyone else could not do so much more easily. I am a stubborn, emotionally turgid, self-obsessed and defensive man, and yet my thinking was somehow flexible on this one. So this is my reluctant post on a grim reality. I understand if you wanted to go read about something else.
According to a meta-analysis by the FDA, antidepressants raise the risk of suicide in users under 25 and lower the risk of suicide in users over 65. That’s the promising version. According to the smarter analyses of the clinical trials, they do not lower your risk of suicide, despite everyone assuming they do, and are linked with more suicides in people on the pills than on sugar pills. It once was controversial but now is largely accepted that they do not even perform better than sugar pills except for the very extremely depressed. They do not lift depression by virtue of their chemical mechanism. They do not reduce suicides. Yet they are called antidepressants. It’s a wild notion that somehow cannot puncture the bubble of our times.
The FDA determination came about in 2006 at a moderately publicized yet historic and remarkable pharmaceutical advisory committee hearing I attended in Bethesda, MD. I will never forget the way in which, at that hearing, dozens of families who had travelled from across the country to be there, patiently waited for three alloted minutes at the microphone to tell regulators about their inexplicable loss: previously functioning, non-suicidal children or adults who had been given an antidepressant for an ambiguous condition such as insomnia, test anxiety or agitation, and shortly thereafter took their own life, often in gruesome manner, often as if they were no longer themselves, not caring about who found them, not leaving a note.
And yet it was memorable not so much for its wrenching line of widows, stoic parents of deceased children, brothers and sisters of the deceased, but because of the remarkable sense of disinterest in these stories one observed on the part of both the regulators on the panel and the mental health patient advocacy community also present to testify. These parties appeared determined only to prevent any warning from being issued that might harm the sales or respectability and increase the supposed stigma of taking antidepressants, by then some of the most widely sold drugs in the world. Microphones were turned off after the three minutes alloted, often in mid-sentence, often on leading researchers their to present important data.
What’s more remarkable, I would later learn, is how personal the impersonal stance actually was. One of the regulators, Thomas Laughren, MD of the FDA, actually lived down the street from Mathy Downing, one of the grieving mothers in front of him. Candace Downing, a little girl of 12 just down his street, and who had been given Zoloft for test anxiety, had gone from seated in her father’s lap and watching Animal Planet to taking her life in her bedroom closet. It speaks for itself — 12 year olds are not tormented little depressed adults on a death wish, they simply are not, and yet nearly to a person, the families I spoke with struggled with the wall of skepticism with which our society greets the topic of SSRI-induced suicide, a skepticism that is not even as widely shared the in medical community charged with dispensing the pills or the earliest researchers involved in their approval.
The condition by which an antidepressant can cause someone to become suicidal is known as akathisia, and it is well-recognized in the pharmacology literature, and it dates back, as David Healy has so very well written, to the first antidepressant — a sedative for high blood pressure called reserpine. The fact that a pill could do this was not considered controversial then as it is today — truly we have lost ground in the area of information acceptance — and reserpine was discontinued due to its recognized danger of causing suicides. (These patients could not be called depressed, moreover — they were merely being treated for high blood pressure. For what it’s worth, it was given to Hemingway in the years preceding his suicide, and his Mayo psychiatrist blamed his deteriorating condition on the drug pared with a stimulant commonly used to treat ADHD today).
Yet memory is short and the cultural embrace of the “chemical imbalance” marketing message — it was created in the 1990s within the marketing departments of Pfizer, Lilly and SmithKline Beecham, according to Healy’s fine book Pharmageddon– was strong. Critics of these historical if rare dangers inherent to SSRI’s were and still are dismissed as anti-psychiatry, cult-members or somehow hostile to the importance of safe and effective mental health treatments. The idea that a drug meant to treat depression could hide a side effect that correlates with depression was simply too much to process.
So here we are, most of the drugs having gone off patent, the much anticipated rise in suicides from a black box warning having failed to materialize, and yet there remains still our shared blind spot to the established, 50 year old fact that certain drugs which manipulate brain hormones can cause a small subset of users to become agitated and emotionally tormented, raising the risk of suicide.
On NPR yesterday, a report intended to promote the importance of physicians asking about the presence of guns in the home when treating patients for depression — still more common sense that we can’t seem to agree on — managed to illustrate this very conundrum. A doctor in Colorado “who was doing everything he could ” to reduce an elderly patient’s chance of suicide, was portrayed as heartsick that he did not ask him about the presence of guns in the home. The doctor had placed the patient on antidepressants for distress over memory problems. Memory problems, of course, have many potential causes, including some believe, popular lipid lowering medications, but surely age is one reason. Depression could be the cause of memory problems as well perhaps, but we don’t know what the family doctor did to determine the patient was in need of the drugs. The doctor saw the patient every two months. Somewhere in this timeline he recived word that the man had taken his own life with a gun.
As we said earlier, according to the analysis that informed the FDA warning, antidepressants lower suicide in people over 65. But this is based on drug industry data, and doesn’t track with the case reports presented at the hearing, stories of fathers who took their lives shortly after going on the drugs. And indeed, there’s no reason why a drug would do one thing at 25 and the opposite at 65. We also know by now that a host of medications can have this effect, including drugs for epilepsy, asthma, acne, nicotine addiction, schizophrenia, and antibiotics, to name a few.
So my question is why distress over memory problems will get you put on antidepressants, despite the fact that distress over memory problems is surely part of life and the drug is not indicated for the treatment of distress over memory problems, and yet when you die of an acknowledged side effect of that drug in younger users, the possibility of that side effect playing a role never comes up. Not by the reporter. Not by the doctor. Not in 177 comments. What is it about this notion that is so threatening, impermeable to reason, off-limits, untouchable. I’m not upset, I’ve come to accept this is the case in our time. I’m genuinely curious.
I wish Mark Bittman would stick to writing about cooking.
Mark Bittman is a great food writer.
I fact-checked one of his articles a long time ago and can tell you he is a nice guy, too!
But it’s been frustrating to watch legions of readers drive his half-right pieces on food and health up the most emailed list at the Times. Last week it was low carbohydrate eating. This week it is milk.
Were we meant to drink milk? Who knows. But unless it makes you feel miserable, which it did to Mark Bittman, high-fat milk has a lot going for it. Throwing it out of your diet seems like inviting the substitution of replacements with even less of a naturalistic entry into the food supply, like milk derived from beans. (In fact, as I wrote in Details last year, its possible that it is skim milk that’s making us fatter, not whole.)
This is the second piece by Bittman in the last few weeks to take his gargantuan audience at the Times and blithely wade into some hotly contested nutritional question without a lot of understanding for the politics and tenacity of outdated paradigms in medicine and science. Last time it was whether it makes sense to eat a no carb diet — even though, as a JAMA study discovered, it burned more calories than a low fat or low glycemic index diet — if it raises some surrogates for inflammation (CRP and cortisol) and by extension disease. As I wrote (Surrogates are Not Diseases), surrogates are the big no-no’s in the eyes of the medical specialty guideline-writing committees, health panel findings championed by industry and their, umm, surrogates in patient advocacy groups. But they are directives which ultimately serve to getting us hooked on pills of dubious benefit.
That was just my quick take on what was wrong with the thing, but it turns out if you actually read the study, which is above my pay grade on some mornings, it was plainly inaccurate: There’s a great post by Peter Attia, MD, here, (The Eating Academy website) about the fact that apparently the Times overplayed even the link between Atkins eating and a rise in CRP. Attia called the assertion “patently false.” Apparently, the rise of markers for inflammation in people who ate a no-carb diet was negligible.
“Each group experienced a significant decline in both PAI-1 and CRP, and there was no significant difference between the groups for either marker. However, the trend was (barely) significant favoring the low carbohydrate group for PAI-1 and favoring the low GI group for CRP. Sorry low fat, you didn’t win either.”
Bittman says milk gave him reflux and I believe him. Fine, drink water, Mark. But he then lets a dairy critic make a host of outdated assertions, like the idea that saturated fat is bad for us (wrong), and neglects something really important about dairy fat — it slows the absorption of carbohydrates into the blood stream, reducing the insulin response and the storage of carbohydrates as fat. Hey, it’s why your grandmother gave you a rich creamy glass of whole milk with your cookie.
Surrogates are not diseases.
The popular and reasonable food writer Mark Bittman at the New York Times recently acknowledged some new data showing that high-fat, high protein, very low carbohydrate diets (some people call them “Atkins” diets, but that makes it sound like all you ever do is eat pork rinds, so I respectfully decline to do so here) help you lose weight faster than low fat diets or even low processed food diets — all while eating the same number of calories. In other words, a calorie is not a calorie, or, as Gary Taubes famously wrote back 2006, there are Good Calories/Bad Calories. This is progress, surely, to read in the Times that, as Ludwig says, “the low-fat diet that has been the primary approach for more than a generation is actually the worst for most outcomes, with the worst effects on insulin resistance, triglycerides and HDL, or good cholesterol.”
But when it comes to getting rid of carbohydrates in the diet, the vast majority of the commentariat always seems to want to hedge their bets, and Bittman is no different. He highlights the caveat put forth by David O. Ludwig, that the Atkins diet, in Bittman’s telling, “raised levels of CRP (c-reactive protein), which is a measure of chronic inflammation, and cortisol, a hormone that mediates stress. “’Both of these,’ says Ludwig, ‘are tightly linked to long term-heart risk and mortality.’”
And both of these are surrogates, one could add, or stand-ins for disease, risk factors associated with disease, rather than evidence of higher levels of actual disease. At this stage in the game, I would be wary of papers that warn us about surrogates. We have a long history of surrogates being used to prop up the use of pills, or ideologies about disease, in place of actual correlations between diets and disease. LDL is a surrogate for heart disease, and it is a crude, misleading one at that. It is necessary but not sufficient, in other words, like a herniated disc can be the source of back pain, or not. The presence of elevated levels of prostate specific antigen was used to justify widespread use of aggressive prostate cancer interventions that are now being walked back. We could go on and on.
Playgrounds used to be vertical
Last night we had dinner with friends who lived on a golf course. Our kids all disappeared and then we realized they were happily climbing and straddling a stationary 10 foot iron ladder used for golfers to inspect the fairway. I couldn’t help but think about how we have scrubbed all the climbing and jumping from our playgrounds, most likely at the behest of lawyers, and then wonder why so many kids are tearing their ACL when the sign up for soccer.
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There was a time when this was a real concern…
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