by Dr. Joseph Mercola, Mercola:
STORY AT-A-GLANCE
- The serotonin hypothesis posits that low serotonin levels in your brain are responsible for symptoms of depression. However, there’s little to no evidence for this. A number of studies have debunked the serotonin hypothesis, which is the basis upon which drug makers market SSRI antidepressants like Prozac, Lexapro and Zoloft
- According to recent research, “The main areas of serotonin research provide no consistent evidence of there being an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations”
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- The primary effect of SSRIs is to superimpose an abnormal drug state over your symptoms, much like recreational drugs and alcohol would. The small benefits seen in some drug trials are due to emotional numbing
- This numbing effect comes at a steep price, as it also prevents you from experiencing emotional highs and does little to counteract the loss of energy, interest and motivation that are so characteristic of depression
- Researchers at the U.S. Food and Drug Administration recently published the most comprehensive analysis of antidepressant clinical trial data submitted to the FDA, including unpublished trials. The evidence showed antidepressants outperformed placebo in only 15% of patients, and almost exclusively in those with the most severe depression
As of 2018, 13.2% — approximately 1 in 8 — of American adults over the age of 18 were on antidepressant medication, with more than twice as many women taking them (17.7%) than men (8.4%).1 Curiously, though, only 7.2% had actually been diagnosed with a major depressive episode — a statistical discrepancy that hints at massive antidepressant overprescribing. As noted by Newsweek:2
“Although there is widespread agreement that SSRIs [selective serotonin reuptake inhibitors] help some people with severe depression, these patients are a small minority of people who take the drugs.”
While those statistics are already staggering, depression rates have further risen since then, thanks to COVID lockdowns and the unprecedented fearmongering that has been a hallmark of this pandemic. As reported in “What Does the Best Evidence Say About Antidepressants?” 22.4% of American adults reported symptoms of depression in June 2022, compared to 7.1% in 2017.
No Evidence to Back Serotonin Hypothesis
The fact that antidepressants are still being used to this extent is a testament to how effectively the drug industry manipulates doctors and patients alike with less than truthful propaganda, as independent studies have repeatedly shown these drugs work no better than placebo.
As Irving Kirsch — associate director of the Program in Placebo Studies and the Therapeutic Encounter at Beth Israel Deaconess Medical Center and Harvard Medical School and a long-time critic of antidepressants — told Newsweek:3
“People do get better on the drug — but in the vast majority of cases it’s not because of what’s in the drug. There are other treatments that are at least equally effective, and that don’t carry the risks.”
Indeed, a number of studies have solidly debunked the serotonin hypothesis, which is the basis upon which drug makers market SSRI antidepressants like Prozac, Lexapro and Zoloft.
In short, the idea is that low serotonin levels in your brain is responsible for symptoms of depression. The problem is, there’s little to no evidence for this. In fact, low serotonin is associated with long-term antidepressant use, which is basically the converse effect you’d expect if the serotonin theory was true. As reported in a systematic review published in Molecular Psychiatry July 20, 2022:4
“The serotonin hypothesis of depression is still influential. We aimed to synthesize and evaluate evidence on whether depression is associated with lowered serotonin concentration or activity in a systematic umbrella review of the principal relevant areas of research …
17 studies were included: 12 systematic reviews and meta-analyses, 1 collaborative meta-analysis, 1 meta-analysis of large cohort studies, 1 systematic review and narrative synthesis, 1 genetic association study and 1 umbrella review …
Two meta-analyses of overlapping studies examining the serotonin metabolite, 5-HIAA, showed no association with depression … One meta-analysis of cohort studies of plasma serotonin showed no relationship with depression, and evidence that lowered serotonin concentration was associated with antidepressant use …
One meta-analysis of tryptophan depletion studies found no effect in most healthy volunteers, but weak evidence of an effect in those with a family history of depression. Another systematic review and a sample of ten subsequent studies found no effect in volunteers.
No systematic review of tryptophan depletion studies has been performed since 2007. The two largest and highest quality studies of the SERT gene, one genetic association study and one collaborative meta-analysis, revealed no evidence of an association with depression, or of an interaction between genotype, stress and depression.
The main areas of serotonin research provide no consistent evidence of there being an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations. Some evidence was consistent with the possibility that long-term antidepressant use reduces serotonin concentration.”
Researcher’s Personal Experience With Antidepressants
An interesting backstory to this serotonin paper is that one of its coauthors, Mark Horowitz, Ph.D., a research scientist at the University College London, was on the antidepressant Lexapro for 15 years. His incentive to dive deeper into the truth behind antidepressants emerged when he tried to wean off the drug and found he couldn’t.
Panic attacks, insomnia and debilitating depression actually forced him to move back with his parents. All of these symptoms were far worse than what he suffered before taking the drug, and many others find themselves in the same situation — they can’t quit the drug because of the side effects. In essence, the addictive nature of these drugs ensures you’ll be a lifelong cash cow for the drug maker.
“Ever since beginning his calamitous effort to get off SSRIs, Horowitz has devoted himself to disproving the claims used to justify their widespread use, and lobbying lawmakers to take a second look,” Newsweek writes.5 “He now describes himself as no more neurotic than anyone in a Woody Allen movie and believes he should never have been prescribed SSRIs in the first place.”
We’ve Been Lied to About Antidepressants
But if the serotonin hypothesis is false, what is it that makes antidepressants appear to be working? In short, it’s the placebo effect. As reported by Newsweek:6
“The pharmaceutical industry used [the serotonin hypothesis] … to market the drugs to consumers for many years … As a result, according to the study’s authors, between 85 and 90% of the public believe that low serotonin levels cause depression.
After reviewing data from previous studies involving hundreds of thousands of individuals, Horowitz and his colleagues concluded that there is little to no evidence that this is true. ‘The drug companies convinced us that if you’re sad, you should go to your doctor and seek treatment,’ Horowitz told Newsweek.
‘They’ve made us all believe that normal aspects of the human condition are a medical illness called major depressive disorder — that normal reactions to difficult situations are a chemical brain problem that needs a medical solution. They convinced people these are very ‘mild’ drugs that are very easy to stop. None of this is true’ …
Horowitz and the paper’s other co-authors … call for a fundamental reassessment of how mental illness is treated. ‘We have a mistaken view of what psychiatric drugs are doing,’ says Dr. Joanna Moncrieff, professor of Critical and Social Psychiatry at University College London.
She is also Horowitz’s boss and the lead author of the serotonin paper. ‘This idea that they work by targeting the underlying biological mechanisms that produce the symptoms of mental disorders is actually not supported by evidence for any type of mental disorder, whether that’s depression or schizophrenia or whatever,’ she told Newsweek.
Instead, she argues, the drugs change ‘normal brain states’ and ‘normal mental states and processes’ in ways not that much different than recreational drugs like alcohol.”
Negative Emotions Are Part of the Human Condition
As explained by Moncrieff, the primary effect of SSRI’s is to “superimpose an abnormal drug state” over your symptoms, much like recreational drugs and alcohol would. She also stresses that the small benefits seen in some drug trials are due to emotional numbing.
This numbing effect comes at a steep price, however, as it also prevents you from experiencing emotional highs, and does little to counteract the loss of energy, interest and motivation that are so characteristic of depression. Moncrieff continues:7
“It’s not helpful to think of depression as a brain disease. I think that we should be thinking of it as an emotional reaction to life circumstances and life events. And indeed, there is very strong evidence that people who suffer from adverse life events are much more likely to get depressed.”
Adverse life events tend to be stressful, and stress is strongly linked to depression. People with depression typically report experiencing a stressful episode, such as the death of a loved one, a job loss or onset of a chronic disease, shortly before the onset of their depression.
