The biochemical imbalance theory is dead. Someone should tell your doctor.
For many years, I've been writing articles about the frauds perpetrated on the public by the field of psychiatry, aided and abetted by the pharmaceutical industry. I’ve discussed in great depth the total lack of evidence for the ‘biochemical imbalance’ theory of depression, the total lack of validity of diagnostic criteria for so-called mental illnesses such as depression and anxiety, and the disease-mongering activities of serially criminal pharmaceutical corporations which either invent so-called mental disorders out of thin air, or expand diagnostic boundaries so far that virtually everyone will be encompassed by them at some point in their lives.
You can imagine my frustration then, at the continued rampant overprescription of antidepressant medication in Australia. With 106.7 doses of antidepressant taken per thousand Australians per day in 2016, only Icelanders pop more of these mind-altering drugs than us.
And that was before the devastation unleashed on people's lives by non-evidence-based COVID-19 policies that devastated lives and livelihoods across the nation, which helped to propel sertaline (sold as Zoloft) into the top ten most-prescribed drugs in Australia for the first time ever in 2020. Only statins and blood pressure drugs are taken by more Australians than Zoloft. Let that sink in for a moment.
Yet while doctors continue to write prescriptions for antidepressant drugs that work no better than placebos, scientific research is unravelling the giant tapestry of fraud that constitutes psychiatry, thread by thread. One of these unravelling threads recently caught my eye.
Yet more proof that the serotonin hypothesis is bunkum
Swedish researchers recently discovered that serotonin transporter levels increased in people whose depression lifted after completing a course of internet-based cognitive behavioural therapy.
What does this mean, and why does it matter?
The serotonin transporter protein, 5-HTT, pumps serotonin away from synapses (the tiny gaps between brain cells), thus lowering the amount of active serotonin in the brain. The serotonin hypothesis, which blames depression on low levels of serotonin activity in the brain, has been the dominant pathophysiological model of depression for decades - despite a remarkable lack of supporting evidence. The most commonly prescribed antidepressant drugs, including Zoloft, inhibit the serotonin transporter (5-HTT), thus increasing the concentration of serotonin in the synapses.
If the serotonin hypothesis were true, we would expect to see higher levels of 5-HTT in the brains of depressed people than non-depressed people, since the function of 5-HTT is to reduce the concentration of serotonin in synapses. We would also expect that as depression remits, the levels of 5-HTT would decrease (allowing serotonin activity to increase).
But the Swedish researchers noted that previous studies had found lower levels of 5-HTT in the brains of depressed people - the exact opposite of what the serotonin hypothesis predicts. This observation sparked a question: are aberrations in the serotonin system a trait (i.e. a fixed characteristic of depression-prone people), or a state (i.e. present only around the time of the depressive episode)?
Using positron emission tomography (PET), a brain imaging technique which allows scientists to quantify levels of different substances in the brain using radioactive tracers, the researchers assessed the levels of 5-HTT in the brains of depressed people both before and after they undertook a course of internet-based cognitive behavioural therapy (CBT).
The CBT program focused on helping people understand why they were feeling bad, getting them to engage in enjoyable activities and connect with other people, and equipping them with tools to challenge the thinking patterns that reinforced their depression.
After 3 months of treatment, the majority of participants reported significant improvement in their depression, and their 5-HTT levels were on average 10% higher than at baseline. This strongly argues in favour of the state, rather than trait, hypothesis. In an interview, lead researcher Johan Lundberg stated
"Our results suggest that changes to the serotonin system are part of the biology of depression and that this change is related to the episode rather than a static feature — a state rather than a trait."
This conclusion would be no surprise to George Ashcroft, the psychiatrist who first advanced the serotonin theory of depression in the late 1950s, then abandoned it due to lack of evidence by 1970. He wrote:
“What we believed was that 5‐HIAA [a metabolite of serotonin] levels were probably a measure of functional activity of the systems and not a cause. It could just as well have been that people with depression had low activity in their system and that 5‐HIAA was mirroring that and then when they got better it didn't necessarily go up.”
In other words, rather than causing depression, alterations in the serotonin system are a response to it. Furthermore, these changes may actually be adaptive, which implies that pharmaceutically meddling with them might be harmful and counterproductive. Another member of the Swedish team speculated that
"One possible interpretation is that the serotonin system doesn’t cause depression but is part of the brain’s defence mechanism for protecting itself against depression. One might hypothesize, for example, that the level of 5-HTT drops when an individual is subjected to stress, such as during a depressive state, and that the level rises or normalises when this stress goes away."
Or, to put it more plainly, what's going on in your life affects what goes on in your brain. Your brain adapts to difficult life circumstances by altering its activity. When the difficulty passes, whether due to your own actions or merely due to a change in external circumstances, the brain's activity returns to normal - exactly as any other system of the body that is perturbed by stress, such as your heart rate or digestive function, returns to normal when the stress subsides.
Depression is real, it is really distressing, and people suffering from it need and deserve real help to overcome it. However, the pharmaceutical-medical complex has, for over half a century, aggressively pushed a flawed narrative of depression which has levied enormous financial, social and psychological tolls on everyone directly and indirectly affected by it - which is pretty much all of us.
The serotonin hypothesis should have been consigned to the dustbin of history fifty years ago, when its originator, George Ashcroft, disavowed it. It's now suffering the death of a thousand cuts, as study after study disproves its propositions. It's time to put the serotonin hypothesis out of its misery once and for all, and focus on rational approaches to alleviating depression.