Not a member? Sign Up!
Enter Username or Email to reset.
By the time we reach full maturity, our bodies contain, on average, 75 trillion cells, which share a single, unified goal: achieving a state of natural order within our bodies by controlling the chemical reactions that power them. Like diligent cogs in an assembly line, our cells are grouped together according to function and we, as their hosts, are barely even conscious of their presence until something goes terribly wrong.
Depression, like any other mental illness, signals malfunctions in our brain cells, or neurons, which communicate with each other by virtue of electrical impulses in the form of chemicals. Many of these neurons are responsible for producing one chemical in particular called serotonin, which is linked to feelings of well-being and happiness. Thus, it has been posited that starving the brain of serotonin can contribute to feelings of hopelessness, apathy, and therefore depression.
Naturally, in an epoch that values quick fixes, the medical community and pharmaceutical industry latched on to the idea that raising serotonin levels in the brain could proportionately increase energy levels, mitigate despondency, and hopefully one day eliminate depression. This led to the rise of drug giants, such as Celexa, Lexapro, and Zoloft, which are classified as selective serotonin reuptake inhibitors, or SSRIs. Put simply, these drugs inhibit serotonin-emitting neurons from snatching back the serotonin they have just released, thus increasing the chemical’s presence in the brain. While their introduction signaled a scientific breakthrough and led millions to imbibe their brand names, the efficacy of SSRIs has been hotly contested.
Like any other class of drugs, SSRIs come neatly pre-packaged with a warning label detailing a litany of side effects, including an increased risk of suicide. This is not to be taken lightly, as critics have contended that because SSRIs increase energy levels before alleviating feelings of general depression (which usually takes up to six weeks), individuals are left feeling as they always did except with a newfound sense of ability, which, many argue, gives them the strength to actually carry out their own deaths.
Furthermore, it seems common sense that a multifaceted illness such as depression cannot be cured through drugs alone. Rather, treatment must include some form of talk therapy supplemented by practical application outside of an analyst’s office in order to achieve long-term results. One frequent recommendation is to engage in some form of physical activity, which for many patients is no easy feat, as depression saps energy, leaving people sluggish and unmotivated.
In addition, it has been relatively unclear how exercise can mitigate depression until a few weeks ago when a group of Scandinavian mice demonstrated that physical activity can serve as an emotional bulwark. Although rodents lack the ability to communicate with humans, Swedish scientists were able to discern several symptoms that could indicate whether a mouse was depressed, such as refusing simple pleasures like treats, weight loss, and an apparent lack of motivation to escape dangerous scenarios like being trapped in an underwater maze.
Thus, the researchers divided the mice into two groups. The first group did not engage in preliminary physical activity and was subjected to low levels of stress, such as small electric shocks and physical restraints. Predictably, these mice stopped eating and soon displayed little resilience to being repeatedly placed in unpleasant scenarios. In essence, they became depressed.
The second group of mice were exposed to the same treatments but with one difference: they were genetically bred to have an abundance of a protein called PGC-1alpha1, a catalyst that the body naturally produces as a result of aerobic exercise. Afterwards, while the mice seemed mildly anxious and suffered some weight loss, they did not demonstrate other signs consistent with depression; they sought out treats and attempted to extricate themselves from the underwater maze. They also exhibited decreased levels of kynurenine, a chemical the body produces after being repeatedly subjected to high levels of stress.
Through later observations, the scientists learned that PGC-1alpha1 signals the brain to produce another protein, which breaks down kynurenine. As a substance, kynurenine causes inflammation the brain, leading, it is suspected, to depression. However, as the second group of mice demonstrated, bodies rich in PGC-1alpha1 have the capability to resist the build-up of kynurenine before it can inflict serious damage.
So what does this call mean? For starters, the experiments illustrate that people who exercise may develop a chemical resiliency to depression; conversely, those who do not participate in aerobic respiration may be putting themselves at emotional risk. Finally, while it has yet to be proven that exercise can work in similar ways for people who are already depressed, scientists are hopeful and have already set out recruiting future rodents.
Chaya Himelfarb is a frequent contributor to Painted Brain News.