Study sheds light on why antidepressants only do so much

Chronic dejection is a normal (and in my opinion, intelligent) reaction to being alive so there needs to be some sort of categorical demarcation that warrants poking around the wet stuff in our skull. Neurologically speaking, what is depression?

Some people rely on one’s ability to function day to day as a measure for when to consider clinical consultation. This is a fine way to gauge severity but not the presence of the mood disorder itself.  Individuals suffering from crippling depression and persistent depressive disorder (high-functioning) are more imperatively linked by a critical neurotransmitter deficiency.

Monoamine neurotransmitters like serotonin govern several important psychological functions, from modulating cognition, to dreaming to overall disposition. Its depletion, therefore, sees moods become deaf to the court of reason and beholden to precarious and unreliable predictors; both of which are defining characteristics of a clinical depressive state. Left unattended circumstance loses all of its powers of persuasion, meaning sufferers will begin to feel impossibly miserable for no reason at all.

Anit-depressants work by revitalizing communication between presynaptic neurons and postsynaptic neurons — the space between the two is what’s known as a synapse. When a normal brain gets the sads, a nerve impulse will travel down the axon terminal to the nerve ending of the presynaptic neuron, and call upon the help of neurotransmitters to release serotonin into the synapse. By and by, the postsynaptic neuron harvests some of that serotonin, improving mood in the process. In a depressed brain, there isn’t enough serotonin to be received by the postsynaptic neuron.

Enter SSRIs, short for selective serotonin reuptake inhibitors, and their most popular manifestation, Sertraline.

The chemical hyperbole

Sertraline, more commonly known as Zoloft, first came into use back in 1992, to varying effect.  For users under the age of 25, the drug carries an increased risk for suicide among a litany of more comical side effects, like diarrhea and E.D.  As the tools to address mental health become more and more refined, researchers at University College London Psychiatry conducted the largest placebo-controlled trial of an antidepressant in medical history. The findings, which were free from the burden of pharmaceutical funding, were published in the Journal Lancet Psychiatry. 

From the report: “Antidepressants are now used in a much wider group of people than in previous regulatory trials. We investigated the clinical effectiveness of sertraline in patients in primary care with depressive symptoms ranging from mild to severe and tested the role of severity and duration in treatment response.”

The 653 participants involved in the study were all between the ages of 18 and 74. Although all of the subjects expressed some degree of depressive symptoms their recruitment was based on their agnosticism toward clinical treatment. Half of these were administered sertraline and the other half were given an inactive placebo. After six weeks, the participants were again assessed.

While there seemed to be no discernible improvement to the depressive symptoms cited before the drug trial began, like loss of pleasure, anhedonia, and lack of concentration from either group, the patients that were given sertraline were twice as likely to feel less anxious. Positive effects on depressive symptoms took longer to manifest and were much more modest when they did. This implies that perhaps antidepressants work by eliminating some of the symptoms associated with the disorder, but not the presence of the disorder itself (not to imply that the efficiency of pharmaceutical treatment has ever been uniformly celebrated.)

The authors note early on in the new report that their interest was partly authored by papers written by colleagues motioning against the purported efficiency of antidepressants, namely as they pertain to the four-week window canonized by physicians.

“It appears that people taking the drug are feeling less anxious, so they feel better overall, even if their depressive symptoms were less affected,” Commented corresponding study author Gemma Lewi in a press release. “We hope that we have cast new light on how antidepressants work, as they may be primarily affecting anxiety symptoms such as nervousness, worry and tension, and taking longer to affect depressive symptoms.”

As it stands, if your roughest days meet the criteria required for clinical attenuation, make sure there are other mechanisms in place to mitigate symptoms. The disorder is famously adaptable and persuasive. Addressing the neurophysiology is never enough. Develop grounding techniques to remind yourself that episodes do eventually come to an end. They return too, of course, which is why it’s important that we do everything we can to keep our chemical militia up too speed in-between seasons.