The Most Popular SSRI Antidepressants Don't Work the Way Big Pharma Claims

One of the most popular classes of drugs is SSRIs, or selective serotonin reuptake inhibitors. The first blockbuster SSRI was Prozac (fluoxetine), which came on the market in 1987 as a treatment for depression. Some other often-prescribed SSRIs are:

• Celexa (citalopram)

• Lexapro (escitalopram)

• Paxil (paroxetine)

• Zoloft (sertraline)

Depression is associated with a spectrum of negative emotions
Depression is associated with a spectrum of negative emotions

Pharmaceutical companies needed a scientific rationale for the “mechanism of action” of these drugs in the body. They proposed the theory that SSRIs work by increasing the amount of serotonin—usually considered a “feel good neurotransmitter”—available in the brain.

To send a signal, a nerve cell has to release serotonin into a synapse, the space between it and the next nerve cell. The serotonin attaches to receptors on the next cell, completing the signal transmission. The serotonin molecules are then released by the receptor cells and jump back across the synapse to the original nerve cell.

There are over 100,000 different molecules synthesized by our cells
There are over 100,000 different molecules synthesized by our cells

 SSRIs are believed to work by blocking the receptor sites for serotonin molecules on the receptor cells (reuptake), thus increasing the availability of serotonin in the brain’s synapses.

The molecular theory of SSRIs fit neatly into the concept that perplexing mental health problems like anxiety, depression, PTSD and phobias were biomedical problems that could be solved by finding the right drug combination.

At the same time, psychiatry was captivated by the idea that most mental illness is due to defective brain chemistry. A prominent psychiatric textbook declared that “The cause of mental illness is now considered an aberration of the brain, a chemical imbalance” (reviewed in Deacon & Lickel, 2009). From this followed the prescribing of medications like SSRIs to correct those imbalances.

Yet these medications have serious side effects. A study found that among middle-aged women, bone fractures increased by over 70%, indicating compromised cell repair (Sheu et al., 2015). Other studies link SSRIs to memory loss and premature death, while the risk of cancer rises 35%.

While these side effects might be justified if SSRIs were dramatically reducing the rate of depression, this is not the case. Over the past two decades, the number of people treated for depression has doubled, with one in ten Americans now taking antidepressants (Olfson & Marcus, 2009).

A study published in JAMA Psychiatry used PET scans to find out what’s happening to serotonin levels in the brains of subjects with social phobias, who are usually treated with SSRIs (Frick et al., 2015). The goal of the study was to find out if the “low serotonin” theory is scientifically valid.

A large research team at Uppsala University used a tracer within the brain to measure the level of serotonin signal transmission. Led by Andreas Frick of the Department of Psychology, the team used a PET camera to obtain visual images of the tracer to determine which brain regions were active, and which neurotransmitters were dominant.

They showed that within the amygdala, a part of the brain’s fear center that I call the “fire alarm” because when activated it sends the signals of stress to the rest of the body, serotonin production spiked. There was a significant link between higher anxiety and higher serotonin.

Lead investigator Frick said: “Not only did individuals with social phobia make more serotonin than people without such a disorder, they also pump back more serotonin. We were able to show this in another group of patients using a different tracer which itself measures the pump mechanism. We believe that this is an attempt to compensate for the excess serotonin active in transmitting signals.”

This discovery is in direct conflict with the underlying theory of how SSRIs work. While it was previously known that nerve activity within the amygdala was higher for patients with social phobia, and that their brain’s fear centers were overly sensitive, this study demonstrates that it is an excess of serotonin and not a deficiency that is part of the problem.

Frick commented that: “Serotonin can increase anxiety and not decrease it as was previously often assumed.”

Fortunately, there are many drug-free alternatives to SSRIs that have been proven to reduce the symptoms of anxiety, depression and phobias in dozens of studies. These include Mindfulness Meditation, EFT (Emotional Freedom Techniques), Cognitive Behavioral Therapy, the Relaxation Response, and others. As the physiological basis of drug therapies for these mental health issues comes into question, increasing numbers of patients are seeking non-drug alternatives.


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