Nearly 10 percent of all Americans will experience symptoms of depression every year. One of the common forms of treatment includes a combination of therapy and antidepressants. According to the CDC, about 13 percent of Americans over the age of 18 were taking antidepressants between 2015 and 2018. The most commonly prescribed form of these is called selective serotonin reuptake inhibitors (SSRIs), developed to alter the flow of serotonin in the brain.
I’m one of the millions who take an SSRI, one called sertraline, to manage symptoms of anxiety, depression, and OCD. Before talking to a psychiatrist about taking this drug, I dealt with feelings of impending doom and terror that appeared on a whim, as well as dozens of intrusive thoughts and emotions every minute. Basically, it’s like having your own jammer yelling at you all day. Taking the drug has been of great help to me, as it has been for many others.
And that makes it even stranger to recognize that, as with many other complex diseases, researchers are still not sure what exactly causes depression and whether serotonin is a major culprit. In the 1960s, scientists accidentally discovered that certain drugs used as sedatives helped relieve depression. Since these drugs acted on the serotonin system, it led to a “very simplistic idea that low serotonin levels lead to depression,” Gerard Sanacora, Yale University psychiatrist and program director, told the Daily Beast. Yale Depression Research.
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Most scientists now adhere to the idea that there are many genetic, social and biological factors that contribute to depression; yet the idea of a chemical or serotonin imbalance is stuck in the popular spirit of the time. It remained largely thanks to its prominent position in advertising for drugs like Prozac in the late 1980s, even when psychiatric research was already changing its perspective.
This brings us to the current debate on SSRIs. Most neuroscientists, psychiatrists, and clinicians who study and treat depression agree: antidepressant drugs like SSRIs work as well as cognitive therapy. With the right treatment, depression remission rates can range between 5 and 50 percent. There is no doubt that people like me are finding real relief thanks to these drugs.
But if depression isn’t as related to serotonin levels as we once thought, then it raises the question that we don’t really know how SSRIs work and why they can help some depressed people. There are several promising theories that suggest they play a role in mediating gut bacteria, in helping the brain grow new cells and demand itself, in creating larger and more complex physiological changes beyond simply increasing serotonin levels. But none of these theories have yet been proven.
The ensuing discussion has resulted in a full debate, pitting traditional psychiatry against a minority of researchers who think antidepressants don’t really work.
Every few years, a new wave of studies comes out of the shadows, presumably “debunking” the notion of the serotonin hypothesis. These studies suggest that depression is the result of social factors or caused by traumatic experiences and that antidepressants don’t work, numb emotions, or actively cause harm. Instead of drugs, they believe depression is best treated only through therapy.
The quarrels between competing academics and researchers are as intense and ferocious as any other struggle that takes place on the Internet, with Twitter feuds, editorials for think-tanks and newspapers themselves. The dark history of the pharmaceutical industry further fuels skepticism about the effectiveness of antidepressants. When clinical trials on antidepressants didn’t confirm the hoped-for results, drug companies essentially buried the evidence and skewed the record in favor of antidepressants, which only exacerbated distrust of these drugs and their manufacturers.
Adding fuel to the fire, a recent review study published in the journal Molecular Psychiatry reassessed decades of past data on serotonin levels in depression, finding no evidence of a link between the two and offering this as evidence that SSRIs either don’t work or only work by dulling emotions. This conclusion has drawn criticism from many psychiatrists and clinicians – the study didn’t even analyze whether antidepressants work – but with the support of the study’s authors, the right-wing media still spread this message.
“If there are any benefits, I would say they are due to this paralyzing effect of emotions, and if not, what the evidence shows is these very small differences between drugs and placebo,” Joanna Moncrieff, a psychiatrist at University College of London who led the study, told The Daily Beast. “Antidepressants are drugs that change the normal state of the brain, generally not a good idea to do [that] long-term”.
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Moncrieff herself is an influential figure in what is called “critical psychiatry,” The Critical Psychiatry Network, of which Moncrieff co-chair, describes the movement on its website: “Moncrieff scientifically challenges claims about the nature and causes of the disorder. mental health and the effects of psychiatric interventions. ”Researchers associated with this movement campaign against drug use for mental health conditions and have even promoted COVID-19 conspiracies.
If depression is caused by the interplay of stressful events and biology, as some within the Critical Psychiatry Network claim, Sanacora doesn’t follow why this means antidepressants don’t work. “I just don’t follow logic,” she said.
Four other experts who spoke to The Daily Beast specifically dismissed Moncrieff’s findings, notably pointing out that his paper and that of his team grossly confuse two hypotheses under the serotonin theory. There is the chemical imbalance hypothesis which is quite well known, which suggests that a deficiency in the neurotransmitter serotonin in the body leads to depression. But according to Roger McIntyre, a professor of psychiatry and pharmacology at the University of Toronto, “the notion of chemical imbalance in the brain has never been put forward as a coherent, comprehensive and evidence-based proposition.”
Instead, the most prevalent hypothesis about serotonin that psychiatry takes seriously and that McIntrye and others argue is supported by evidence, is that a dysregulation of the body’s entire serotonin system is what contributes to clinical depression. This includes problems with the amount of receptors available to bind serotonin, problems with how cells become activated, and numerous other disruptions at the biomolecular level. They argue that Moncrieff is wrong when it comes to making the big claim that there is no evidence of serotonin’s involvement in depression.
Furthermore, not knowing the mechanism of a drug is not a sufficient reason to prevent its use if it is proven to help people. “We are very confident that SSRIs work for depression,” Tyler Randall Black, a child and adolescent psychiatrist at British Columbia’s Children’s Hospital, told the Daily Beast. “There are reams and reams of evidence that show us they work, but not because they work.” McIntrye pointed out that we don’t even fully know how Tylenol works, despite being one of the most widely used pain relievers around the world. Tylenol also impacts the brain in unexpected ways – although it numbs social or psychological pain, it’s no reason to remove it from the market.
Defaming these drugs can have unintended consequences because therapy is often not available, making SSRIs the only accessible option. “The demand for mental health care far exceeds the access available,” Sanacora said, adding that many Americans have to wait months to see a good cognitive behavioral therapist. Also, abruptly deciding to stop taking SSRIs can be dangerous – one in five patients who do so will experience flu-like symptoms, insomnia, imbalance, and other symptoms that can last for a year.
While psychiatrists who spoke to The Daily Beast pointed out that the serotonin hypothesis was a way of simply explaining a complex ailment like depression, they found that it favored the downsides over time. The story of a narrative “chemical” imbalance adversely affected patient decision making and patient self-understanding, “Awais Aftaib, a psychiatrist at Case Western Reserve University in Cleveland, Ohio, told the Daily Beast.
Phil Cowen, a psychopharmacologist at the University of Oxford in the UK, told the Daily Beast that socioeconomic status is a contributing factor to depression, leading those in the critical space of psychiatry to believe that it “empowers doctors and all. ‘industry “on patients. Ironically, he ignores the millions of “experienced people” who have been helped with antidepressants.
However, the million dollar question remains: How do SSRIs work? Aftaib explained that a new guiding hypothesis is that they encourage the creation of new neurons and new connections between neurons within the brain. The hippocampus, a seahorse-shaped brain region important for memory and learning, shrinks and loses neurons when depression hits. SSRIs appear to stimulate the production of neuronal stem cells, which integrate into the hippocampus to restore its function and structure. Other studies suggest that SSRIs help the brain rewire the connections that cause the clinical symptoms associated with depression.
He also added that SSRIs might work through different mechanisms in different individuals, so treatments may need to be more tailored on a case-by-case basis.
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And more specific, individual treatments may require psychiatrists to be more honest with their patients about what we know and don’t know about these drugs, rather than come up with an overly simplified (and downright inaccurate) explanation.
Black already tries to do this with his patients: “I say we know for sure it affects serotonin, but we don’t know how this changes your brain and we don’t know you lack serotonin to begin with.” He has found that these open discussions about what we know so far about therapy and medications pay off in the long run, and many of his patients will still choose to take the antidepressant as part of their quest to find what works best for them.
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