Experts report that the number of Americans currently taking antidepressant medications has increased by 65% between 1999 and 2014, with approximately 1 in every 8 Americans today currently taking some form of antidepressant, according to the Centers for Disease Control and Prevention.
Furthermore, of those that reported taking antidepressants in the previous month, 1/4 confirmed that they had been taking their medications for 10 years or more. Despite this high level of antidepressant use, the rates both of depression and suicide in the United States have been on a rise. So, what are we missing?
A new study published online in the journal ‘Neuroscience’ may hold the answer to these questions and more. The research team led by Hiroshima University (HU) focused their attention on a potential new cause for the disease, specifically the role of a protein marker called RGS8 in our depressive moods and behaviors. What they discovered may provide a new direction for the treatment of those who are suffering from depression around the world.
The currently accepted theory regarding the cause of depression focuses on two chemicals within the brain, serotonin, and norepinephrine (NE). The theory states that those who are depressed are lacking in these two chemicals, and modern antidepressants are designed to counteract this deficiency. However, mental health professionals are reporting a large number of people who are not getting the relief that they seek from this approach to treatment.
Yumiko Saito and Yuki Kobayashi, two neuroscientists in HU’s Graduate School of Integrated Arts and Sciences and members of the research team explained, “Thirty percent of people on these drugs do not experience an effect. Obviously, we need a new drug! We need another explanation for what could cause depression.” This was the basis for their research.
The study involved the use of a number of mice, putting them through a swim test. This a common method that researchers use to assess depressive behaviors in animals, as it triggers the same areas or brain causing a similar response. After each swim test, the researchers would subtract the time that the mouse was active from the total test time, providing them with a clear measurement of how long they were immobile. These tests were completed both without medication and after having been given an antidepressant to balance out the two identified chemicals in the brain. They then compared these immobility times to tests measuring the levels of hormones and protein markers in the body, searching for a pattern.
Surprisingly, they found that the antidepressant didn’t help the mice, but there was a pattern involving the RGS8. The protein marker plays an important role in controlling the hormone receptor MCHR1, which works to regulate feeding, sleep and mood responses in the body. The mice with an increased amount of RGS8 in their body showed shorter immobility periods than those that had normal levels. After being given the antidepressants, those with higher RGS8 levels saw even shorter times. The team then gave the mouse a drug targeting MCHR1, stopping it from working, and noticed that the immobility times stayed common across all tested.
While is only the initial testing, and the phenomenon has not been tested in human subjects, it certainly opens up the discussion for improved treatment options for those suffering from depression. If MCHR1 and RGS8 levels are found to be a better predictor of and solution to depressive episodes, then this may lead to the development of a more effective medication. Further studies are still required.