The debate over how antidepressants work puts millions of people at risk
The debate over how antidepressants work puts millions of people at risk

The debate over how antidepressants work puts millions of people at risk

Nearly 10% of all Americans will experience symptoms of depression each year. One common form of treatment includes a combination of therapy and antidepressants. According to the CDC, about 13 percent of Americans over the age of 18 took antidepressants between 2015 and 2018. The most commonly prescribed form of them are 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 obsessive-compulsive disorder. Before I talked to a psychiatrist about using this drug, I was dealing with feelings of impending disappointment and dread that would appear on a whim, as well as dozens of intrusive thoughts and emotions every minute. It’s basically like having your own shaker yelling at you all day. Taking medication has been extremely helpful for me, as it has been for many others.

And that makes it all the weirder to admit that, as with many other complex illnesses, researchers still aren’t sure what causes depression and whether serotonin is one of the main culprits. In the 1960s, scientists accidentally discovered that certain drugs used as sedatives helped relieve depression. Because these drugs acted on the serotonin system, it led to “a very simplistic idea that low serotonin levels lead to depression,” Gerard Sanacora, a psychiatrist at Yale University and director of the Yale Depression Research Program, told The Daily Beast.

Most scientists now agree that there are many genetic, social, and biological factors that contribute to depression; and yet the idea of ​​a chemical or serotonin imbalance is stuck in the popular zeitgeist. It persisted largely because of its prominent placement in advertisements for drugs like Prozac in the late 1980s—even as psychiatric research was already changing its outlook.

That brings us to the current debate about SSRIs. Most neuroscientists, psychiatrists, and clinicians who study and treat depression agree: antidepressant drugs like SSRIs work just as well as cognitive therapy. With the right treatment, remission rates for depression can range from 5 to 50 percent. There is no doubt that people like me find real relief from these drugs.

But if depression isn’t as related to serotonin levels as we once thought, then the problem is that we don’t really know how SSRIs work and why they can help some depressed people. There are several promising theories that suggest that they play a role in mediating gut bacteria to help the brain grow new cells and require itself to create larger and more complex physiological changes beyond simply increasing serotonin levels. But none of these theories have yet been proven.

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The ensuing discussion turned into a full-blown debate, pitting mainstream psychiatry against a minority of researchers who don’t believe antidepressants really work.

Every few years, a new series of studies emerges from the shadows, purporting to “debunk” the notion of the serotonin hypothesis. These studies suggest that depression is either a result of social factors or caused by traumatic experiences, and that antidepressants either don’t work, numb emotions, or actively cause harm. Instead of medication, they believe that depression is best treated with therapy alone.

The ensuing discussion turned into a full-blown debate, pitting mainstream psychiatry against a minority of researchers who don’t believe antidepressants really work.

The conflicts between academics and competing researchers are as intense and vicious as any other battle that takes place on the Internet – featuring Twitter fights, opinion pieces for think tanks and the news outlets themselves. The shady history of the pharmaceutical industry further fuels skepticism about the effectiveness of antidepressants. When clinical trials of antidepressants did not confirm the hoped-for results, pharmaceutical companies essentially buried the evidence and biased the record in favor of antidepressants, which only increased the distrust of these drugs and their manufacturers.

Adding fuel to the fire, a study recently published in the journal Molecular psychiatry re-evaluated 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 do not work or only work by dampening emotions. That conclusion drew criticism from many psychiatrists and clinicians—the study didn’t even look at whether antidepressants worked—but with the support of the study’s authors, the right-wing media pushed the message anyway.

“If there are benefits, I would say it’s because of this emotion-numbing effect, and otherwise the evidence shows these very small differences between drugs and placebo,” said Joanna Moncrieff, a psychiatrist at University College London, who led the study. . study, The Daily Beast said. “Antidepressants are drugs that change the normal state of your brain, which is generally not a good idea to do [that] long-term.”

Moncrieff herself is an influential figure in what is called “critical psychiatry,” The Critical Psychiatry Network, which Moncrieff co-chairs, describes the movement on its website: “It represents a scientific challenge to claims about the nature and causes of mental disorders and the effects of psychiatric interventions.” Researchers associated with this movement advocate against drug use for mental health conditions and have even promoted COVID-19 conspiracies.

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If depression is caused by the interaction between stressful events and biology, as some in the Critical Psychiatry Network argue, Sanacora doesn’t understand why that means antidepressants don’t work. “I just don’t follow the logic,” he said.

Four other experts who spoke to The Daily Beast specifically rejected Moncrieff’s conclusions, noting in particular that her and her team’s work grossly conflates two assumptions within the serotonin theory. There is the chemical imbalance hypothesis which is quite well known, which suggests that a deficiency of 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 a chemical imbalance in your brain has never been presented as a coherent, comprehensive, evidence-based proposition.”

Instead, the more prevalent serotonin hypothesis that psychiatry takes seriously, and that McIntrye and others say 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 fire, and numerous other disruptions at the biomolecular level. They argue that Moncrieff gets it wrong when it comes to making the big claim that there is no evidence for serotonin’s involvement in depression.

The notion of a chemical imbalance in your brain has never been presented as a coherent, comprehensive, evidence-based proposition.

Roger McIntyre, University of Toronto

Moreover, not knowing the mechanism of a drug is not a good enough reason to prevent its use if it can be shown to help people. “We’re very confident that SSRIs work for depression,” Tyler Randall Black, a child and adolescent psychiatrist at the Children’s Hospital of British Columbia, told The Daily Beast. “There’s lots and lots of evidence that shows it works, but not why it works.” McIntrye pointed out that we don’t even fully know how Tylenol works — despite it being one of the most widely used pain relievers worldwide. Tylenol also impacts the brain in unexpected ways — while it numbs social or psychological pain, that’s no reason to take it off the market.

The vilification of these drugs can have unintended consequences, as therapy is often unavailable, making SSRIs the only affordable option. “Demand for mental health care far outstrips available access,” Sanacora said, adding that many Americans have to wait months to see a good cognitive behavioral therapist. In addition, the sudden decision 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.

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While psychiatrists who spoke to The Daily Beast pointed out that the serotonin hypothesis is a simple way to explain a complex disorder like depression, they pointed out that it has created drawbacks over time. The story of a ‘chemical imbalance’ narrative negatively influenced the patient’s decision-making and self-understanding,” Awais Aftaib, a psychiatrist at Case Western Reserve University in Cleveland, Ohio, told the Daily Beast.

Demand for mental health care far exceeds available access.

Gerard Sanacora, Yale University

Phil Cowen, a psychopharmacologist at Oxford University in the UK, told The Daily Beast that socioeconomic status is a contributing factor to depression, leading those in the critical psychiatry space to believe it “gives doctors and industry power” over patients. Ironically, it ignores the millions of “experienced people” who have been helped by antidepressants.

However, the million dollar question remains: How do SSRIs work? Aftaib explained that a new leading hypothesis is that they encourage the creation of new neurons and new connections between neurons within the brain. The hippocampus, a seahorse-shaped region of the brain important for memory and learning, shrinks and loses neurons when depression strikes. SSRIs appear to stimulate the production of neural 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 by different mechanisms in different individuals, so treatments may need to be more tailored on a case-by-case basis.

Even more specifically, individual treatments might require psychiatrists to be more honest with their patients about what we know and don’t know about these drugs, rather than offering an oversimplified (and downright inaccurate) explanation.

Black is already trying to do this with his patients: “They say we know for sure it affects serotonin, but we don’t know how that changes your brain, and we don’t know that you’re missing serotonin to begin with.” He has found that these open discussions about what we know so far about therapy and medication pay off in the long run, and many of his patients will still choose to take an antidepressant as part of their search to find what works best for them. .

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