Depression isn’t defined as having low serotonin contrary to Gary Brecka claims in TikTok videos

In May 2025, The Guardian published an investigation finding that more than half of the top 100 TikTok videos about mental health, identified using the hashtag #mentalhealthtips, contained misinformation.

Using this hashtag, Science Feedback discovered videos showing wellness influencer Gary Brecka making certain claims about depression and serotonin (see examples here, here, here, and here). Specifically, he claimed that depression is defined as “an inadequate supply of the neurotransmitter serotonin” and that SSRI drugs, or selective serotonin reuptake inhibitors, are ineffective in treating depression.

He also claimed that “90% of [serotonin] is made in the gut before it travels up the vagus nerve to the brain” and implied that by increasing serotonin in the gut using supplements, one can reverse depression.

Brecka previously spread health misinformation about various topics ranging from folic acid in food to water fluoridation.

Serotonin is a neurotransmitter, a kind of chemical that transmits signals between neurons (nerve cells). It affects our mood, sleep-wake cycles, as well as the way we perceive pain. It’s also involved in digestion, since it controls the muscles that move food along the digestive tract.

Brecka’s claims have circulated for the past few years, as the TikTok videos posted from 2023 to 2025 show. Collectively, these videos—and Brecka’s claims—have been viewed millions of times on TikTok. But these claims are a mix of inaccurate and misleading information about depression, serotonin, and SSRIs. We explain below.

Depression not defined as having low serotonin, contrary to popular misconception

The American Psychiatry Association defines depression, also called clinical depression or major depressive disorder, as “a common and serious mental disorder that negatively affects how you feel, think, act, and perceive the world”.

The Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, describes a set of diagnostic criteria for depression. As we can see, testing for serotonin isn’t part of that criteria. Indeed, diagnosing depression currently relies on identifying specific symptoms rather than any biochemical test.

Depression is popularly described—and understood—as a “chemical imbalance” in the brain, more commonly, having insufficient serotonin. The serotonin theory of depression emerged in the mid-19th century and partly has its roots in research related to iproniazid, a drug originally used to treat tuberculosis. Some studies reported that iproniazid improved mood in people with depression, while other studies in animals found that it increased the amount of serotonin in the brain. This led scientists to hypothesize that raising serotonin levels could help treat depression.

However, our understanding of depression has advanced significantly since then. Research suggests that multiple factors, including neurotransmitters apart from serotonin as well as personality traits^[1] also play a role.

Philip Cowen, a professor of psychopharmacology at the University of Oxford, told Science Feedback in an email that “the idea that a complex heterogeneous condition like depression can be caused by a deficit in a single neurotransmitter is not accepted by mental health professionals”.

Some scientific work has even ventured to dismiss the role of serotonin in depression. Notably, an “umbrella review” published in 2022 by Moncrieff et al. concluded “there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity”^[2], results that were met with widespread media attention.

However, other scientists advised caution in interpreting the review’s conclusions, emphasizing that it was premature to say serotonin had no role in depression. Indeed, the review was criticized by other scientists for its flawed methodology and misinterpretation of certain studies, as a follow-up comment in the journal Molecular Psychiatry^[3] and this article in Psychiatric Times show.

The media attention triggered by the umbrella review illustrated the gulf between the current scientific consensus on depression and the public’s understanding of depression, highlighting the need for more nuance and better communication when it comes to explaining depression to the public.

But the bottom line here is that the current scientific understanding of serotonin’s role in depression rests somewhere in the middle of “low serotonin causes depression” and “serotonin has no role in depression”. Most scientists consider serotonin to play a key role in depression—just not the only factor to have a role.

In summary, Brecka’s claims that depression is defined as low serotonin and that low serotonin alone is the cause of depression are inaccurate and incorrect.

Serotonin in the gut doesn’t make it into the brain

Brecka’s claim that the gut makes 90% of serotonin in the body is more or less accurate, but where he erred is in claiming that serotonin travels up the vagus nerve to the brain, and in implying that gut serotonin levels have a significant effect on serotonin levels in the brain.

“There is a lot of serotonin in the gut, but it does not travel up the vagus nerve to the brain. Serotonin is unable to penetrate the blood-brain barrier,” Cowen said.

In some TikTok videos, Brecka can also be seen claiming that tryptophan is methylated into serotonin.

Serotonin is made from the essential amino acid tryptophan, which we obtain from our diet, but methylation isn’t involved. Instead the biosynthesis of serotonin from tryptophan involves the enzymes tryptophan hydroxylase and aromatic amino acid decarboxylase (see Figure 1 below).

Neither tryptophan hydroxylase nor aromatic amino acid decarboxylase perform methylation. 

A hydroxylase enzyme adds a hydroxyl group (a chemical group comprising one oxygen and one hydrogen atom) to a compound, and a decarboxylase enzyme removes a carboxyl group (a chemical group comprising one carbon, one hydrogen, and two oxygen atoms) from a compound.

Methylation, on the other hand, adds a methyl group (a chemical group consisting of one carbon atom and three hydrogen atoms) to a compound. This makes it a chemical process distinct from those that occur with tryptophan hydroxylase and aromatic amino acid decarboxylase.

Overall, Brecka’s claim that serotonin in the gut can travel to the brain is inaccurate, as is his claim that serotonin is made from the methylation of tryptophan.

SSRIs are effective in treating depression for many patients, but not all

Brecka also claimed that SSRIs, or selective serotonin reuptake inhibitors, are ineffective in treating depression since they don’t raise serotonin levels.

This is misleading but is in line with a narrative propagated by some, including U.S. Congresswoman Marjorie Taylor Greene, former Fox News host Tucker Carlson, and current U.S. health secretary Robert F. Kennedy Jr., that antidepressants like SSRIs are ineffective, unnecessary, and even unsafe.

SSRIs are a class of drugs that work by blocking the serotonin transporter on neurons, preventing serotonin from being reabsorbed by neurons. This increases the amount of serotonin that’s available in the space between neurons, also known as the synaptic cleft or junction, thereby increasing serotonin activity in the place where communication between neurons takes place.

That said, whether SSRIs work simply because they increase serotonin activity in the brain or because of a different mechanism is still unclear.

“In both depressed people and healthy participants, serotonin-enhancing antidepressants increase serotonin function,” said Cowen. “This leads to changes in synaptic plasticity and emotional processing, which in some depressed people facilitate recovery.”

“Serotonin-enhancing antidepressants do not alter mood in non-depressed people”, however, which suggests that increased serotonin activity alone doesn’t explain the recovery seen in people with depression who take SSRIs.

It’s true that SSRIs don’t work for all patients with depression, but this doesn’t mean SSRIs aren’t useful for treating depression. It’s important to keep in mind that there are many drugs that work in some patients but not in others, and this phenomenon isn’t limited to SSRIs. For example, there are forms of anesthesia that work in some people but not others. There are also certain cancer treatments that work better for some patients compared to others.

Therefore, to dismiss SSRIs entirely because they don’t work on a subset of people with depression is flawed logic. Evidence from randomized clinical trials show that SSRIs work better than placebo in treating depression^[5].

More research is still needed to better understand how SSRIs work, which could also help clinicians learn about which group of people are most likely to benefit from SSRIs.

Finally, experts have stated that while there are some side effects associated with antidepressants—as with any medical intervention—on the whole these drugs provide significant benefits.

Gail Saltz, a clinical associate professor of psychiatry at Weill Cornell Medical College, told CNN: “The reality is that for some people, these are lifesaving medications — literally, they keep them from killing themselves or harming themselves. Or maybe they wouldn’t kill themselves, but they would destroy their lives”.

Conclusion

In the TikTok videos reviewed, Brecka promoted a now-outdated theory about the causes of depression, attributing depression solely to low serotonin. In fact, most mental health professionals don’t define depression as having low serotonin, nor do they consider low serotonin to be the cause of depression. Depression is a highly complex mental health disorder that manifests in diverse ways from individual to individual. It’s unlikely that such a heterogeneous disorder can be explained solely by the quantity of one neurotransmitter.

Furthermore, Brecka’s advice on treating depression is based on this outmoded view of depression and on an inaccurate understanding of serotonin biosynthesis and transport in the human body. While roughly 90% of serotonin is made in the gut, it cannot reach the brain as it doesn’t pass through the blood-brain barrier. Therefore, even if one could change serotonin levels in the gut, there’s no evidence that this will have any meaningful impact on serotonin levels in the brain.

Finally, Brecka’s claim that SSRIs don’t treat depression is inaccurate and misleading. Evidence from randomized clinical trials have shown that SSRIs can be helpful for many people with depression.

References:

1. Klein et al. (2012) Personality and Depression: Explanatory Models and Review of the Evidence. Annual Reviews of Clinical Psychology.
2. Moncrieff et al. (2022) The serotonin theory of depression: a systematic umbrella review of the evidence. Molecular Psychiatry.
3. Jauhar et al. (2023) A leaky umbrella has little value: evidence clearly indicates the serotonin system is implicated in depression. Molecular Psychiatry.
4. aan het Rot et al. (2009) Neurobiological mechanisms in major depressive disorder. CMAJ.
5. Cipriani et al. (2018) Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. Lancet.