I haven’t written about my opposition to the widespread use of psychiatric medications in quite some time, mostly because I feel I’ve already said most of what I have to say on this issue. (See the collection of posts under the heading “The Medicalization of Mental Health,” to be found at the lower right of this page.) But a new study was recently released which demonstrates a link between the use of benzodiazepines and the risk of developing Alzheimer’s disease. While this study says nothing about the long-term effects of SSRIs, the history of benzodiazepine usage offers a cautionary tale as to how little we truly understand about a drug’s side effects during the years immediately after psychiatrists and physicians begin prescribing it.
In the study, a team of researchers from France and Canada linked benzodiazepine use to an increased risk of being diagnosed with Alzheimer’s disease. Relying on a database maintained by the Quebec health insurance program, they identified nearly 2,000 men and women over age 66 who had been diagnosed with Alzheimer’s disease and then looked at their drug prescriptions during the five to six years preceding the Alzheimer’s diagnosis. These people were compared to a larger group of subjects who were matched for age and sex.
People who had taken a benzodiazepine for three months or less had about the same dementia risk as those who had never taken one. But taking the drug for three to six months raised the risk of developing Alzheimer’s by 32%, and taking it for more than six months boosted the risk by an astonishing 84%. Those who had taken longer-acting drugs like Valium and Dalmane were at greater risk than those who had taken a shorter acting one.
One major caveat: men and women in the early stages of Alzheimer’s might turn to benzodiazepines in order to cope with anxiety and sleep disruption – two common symptoms of early Alzheimer’s disease. In that case, their use of a benzodiazepine may not be a factor in causing dementia but rather an indication that it is already in progress. In other words, based on the results of this study, we can’t identify an actual causal relationship with certainty.
Still, it’s enough to make one worry. For me personally, this study helped me to understand what likely happened to my own mother, who began demonstrating early symptoms of Alzheimer’s in her late-50s and died in her early 70s, by which time she hadn’t known who I was for many years. Our family physician and a dentist friend kept Mom well-stocked first with Miltown and later with Valium. She took them on a daily basis throughout my childhood. The study made me wonder whether her benzodiazepine usage actually brought on her dementia.
Librium, the first benzodiazepine, was made available to the public in 1960; Valium has been available since 1963. Not until 2014 — fifty years later — did results from a controlled study indicate a probable connection between benzodiazepines and the risk of developing dementia. Prozac hit the U.S. market in 1987, followed by Zoloft in 1991 and Paxil in 1992. Twenty years from now, who knows what future studies may demonstrate about their long-term side effects. Recent meta-analyses have debunked the “miracle pill” hype that surrounded Prozac in the early 90s, proving anti-depressants to be no more effective than a placebo for most forms of depression, but not enough is known about what damage they may be doing to those who have already taken them for years.
Even now, doubts about their safety are beginning to surface. In a 2012 article published in Frontiers in Psychology, the authors discuss growing evidence that anti-depressants cause neurological damage: they may kill neurons in a way that causes structural damage to the brain, the kind that produces symptoms of Parkinson’s disease and tardive dyskinesia, a condition characterized by involuntary and repetitive body movements. Other evidence links anti-depressants to cognitive decline and an increased risk of developing breast cancer.
On an entirely different subject: another study recently published in Nature has demonstrated a link between the use of artificial sweeteners like saccharine or Splenda and the development of glucose intolerance – a condition that leads to obesity. For decades, these products have been marketed to the public as entirely safe and guilt-free sugar substitutes, trusty weapons in the battle against weight gain; ironically, it now turns out they are likely implicated in the obesity “epidemic” sweeping our country.
I bring up this further study to point out the unknown risks we run by loading our bodies with chemical substances produced in the laboratory, be they psychiatric medications or artificial sweeteners. In truth, there are no “miracle pills” for depression and there’s no “free lunch” when it comes to sugar substitutes. Exercise has been shown to be an effective treatment for depression, along with psychotherapy and exposure to sunlight. Reducing the intake of carbohydrates and eating more protein (combined with moderate exercise) leads to weight loss. I speak from personal experience, but much has been written on this subject, in particular by Gary Taubes, a man I deeply admire.
Both of these approaches to change involve more personal activity on our parts, rather than the passive approach promoted in particular by the pharmaceutical industry. “Here, take this pill and it will correct the imbalance in your serotonin levels.” I understand the simplistic appeal of this approach but it’s important to understand the grave risks we run when we buy into the lie, despite the growing evidence as to the ineffectiveness and potential dangers involved in taking anti-depressants.