Depression is not caused by a lack of serotonin.
https://healthselfdefense.substack.com/p/depression-is-not-caused-by-a-lack
WHAT IS THE “SEROTONIN HYPOTHESIS”?
The serotonergic hypothesis posits that one of the main causes of depression (depressive responses) is related to a significant deficiency or absence of the neurotransmitter/biomolecule serotonin in the brain. The context of the monoamine hypothesis (dopamine, serotonin, norepinephrine, etc.) emerged in 1963 when Carlsson and Lindqvist discovered that neuroleptic drugs tested for the treatment of schizophrenia increased the turnover and quantity of dopamine in the brains of rodents.
However, despite serotonin being a chemical neurotransmitter traditionally associated with mood regulation in the nervous system, and despite the significant scientific advancements in its research, all efforts to empirically validate the serotonin hypothesis for depression have failed.
THE CONSEQUENCES OF PSYCHOLOGISTS’ LACK OF SELF-CRITICISM
Supporting a disease-centered model, and the biological alteration of serotonin as the cause of “depressive” behaviors, does not help students and professionals critically review the full range of theoretical approaches, while ignoring vast areas of theory and research and contradicting the principles of social work ethics and practice, including the crucial role of families and culture, client strengths and empowerment, and the individualized approach to each case.
The only certainty we have about the “serotonin hypothesis” is that things are always happening in the brain, no matter what we do. Interestingly, in many psychology and psychiatry clinics, they simply use questions and descriptions about our behavior, about whether we have been suffering excessively in recent months, to diagnose “depression,” without performing biological tests that demonstrate brain deficits of serotonin, which is supposedly where “depression” originates and resides. “An explanation is not more scientific simply because it is expressed in neurobiological terms.”
GENETIC STUDIES DISMANTLE THE “SEROTONIN THEORY”
If there truly were a lack of serotonin (or if serotonin receptors were less sensitive), genetic studies of serotonin-related biomolecules should demonstrate an alteration associated with high levels of homovanillic acid in cerebrospinal fluid, which has not been demonstrated in any conclusive study. Similarly, hormonal studies are inconclusive, having shown no abnormalities or differences in growth hormone and prolactin levels in subjects diagnosed with “depression.”
And most importantly, there are no conclusive studies linking an imbalance between serotonin 5-HT1A receptors and SERT (serotonin transporter) levels. As an explanation for these failures, we can say that, at the outset of the hypothesis, it was probably not foreseen that we would currently possess the tools to detect imbalances in the genes involved in serotonin production.
THE PHILOSOPHY OF SCIENCE DISMANTLES THE “SEROTONIN HYPOTHESIS”
According to Popper, the “serotonin hypothesis” has low falsifiability due to its lack of specificity (even abstraction). In this case, if one prediction about serotonin was not confirmed, another easily took its place, making it almost indestructible. According to Kuhn, we can assume that the “serotonin paradigm” has endured because a sufficiently prominent and more successful alternative hypothesis was never developed, so there has never been a real crisis that would incentivize an update and conversion of that paradigm.
According to Lakatos, the “serotonin hypothesis” is more accurately described as a degenerative than a progressive research program, due to its numerous failed predictions and many ad hoc alterations to the main hypothesis, resulting in the hypothesis’s core being excessively distorted.
WHY IS THE “SEROTONIN HYPOTHESIS” STILL SO SUCCESSFUL?
In the 1960s, linking psychiatry with the high prestige of neurochemistry and psychopharmacology fulfilled the medical desire to “bring psychiatry back into the mainstream of medicine.” This desire has persisted due to the simplicity, low cost of professional intervention, and high economic interest behind the “one neurotransmitter, one disease” model—a perfect marketing concept for pharmaceutical companies, and in this case, for selling SSRI drugs.
We routinely assume that the accumulation of studies on a topic is strong evidence supporting its validity, when in reality it indicates the opposite: it indicates that no definitive study on the subject yet exists. This medical view of “depression” reduces therapeutic empathy and increases the stigma surrounding “mental disorders.” Unfortunately, it is very appealing, as it allows for the evasion of responsibility, blaming people for their own problems, and “chronicizing” depression to extract economic benefits for longer.
WHAT WOULD THE “SEROTONIN HYPOTHESIS” HAVE NEEDED TO BE RIGOROUS AND RESPECTED?
For the “serotonin hypothesis” to have been empirically validated during its 60-year history, it would have needed to devise alternative hypotheses. It would have needed to design one or more crucial experiments with possible alternative outcomes, each of which would have ruled out one or more of the hypotheses. It would also have needed to obtain a clean and definitive result, while recycling the procedure, and formulate “sub-hypotheses” or sequential hypotheses, to refine the possibilities that remain to be verified.
Psychiatry needs theories with higher levels of specificity and falsifiability. Science works best when diverse theories with different predictions compete with each other, but in this case, the “serotonin hypothesis” has been defended with a fervor that cannot be justified by the available evidence. Therefore, in conclusion, psychiatry is probably not ready for “grand” unitary theories like the “serotonin hypothesis” as a cause of “depression.”
Decolonizing also means letting go of bioessentialism:
"As I began to see the structural and systemic roots of our distress, I increasingly moved away from “born this way” thinking. The more I prioritized intentional community building and reconnecting to my cultural roots, the more impossible it became to see my pain as separate from other people’s struggles. It’s all interconnected and psychiatric labels simply failed to capture these nuances that collectivist communities are built on.
Decolonizing also means letting go of bioessentialism
Maybe we shouldn’t assume anything of people who do or don’t carry a neurodivergent label. Maybe someone identifying as neurodivergent or NOT won’t help you understand much about them or circumvent the process of getting to know them with care, over time. Maybe we should let people open our world to new worlds. Maybe we shouldn’t covertly or overtly force people to turn to a colonial tool like the DSMV to figure out “what they have” or “who they are”. Maybe we don’t need to push people into categories excessively to make them comprehensible.
If terms under the umbrella of neurodivergence are important to you, then know that I’m not asking you to abandon them, nor am I framing them unilaterally as “bad”. I’m asking you to look beyond them, to be aware of how they can be leveraged for harm and to recognize that there are other ways for communities to make sense of their distress without these labels. I’m asking you to embrace complexity and create space for it. The rest of the world should not have to speak this precise language. The language of colonial psychiatry should never have been forced upon the global south and it shouldn’t be today, including any reclaimed version within the neurodiversity framework."
Psychiatric diagnoses & bioessentialism will not liberate us, Ayesha Khan, Ph.D.
https://wokescientist.substack.com/p/psychiatric-diagnoses-and-bioessentialism







