Depression is thought to affect more than 300 million people worldwide and, if the latest studies are anything to go by, rates of depression and suicide are only increasing.
A number of external factors are involved – diet, exercise, social media, politics, and even lighting can all take their toll or help improve mental health. But much of it is physiological.
The overwhelming consensus is that depression arises because of something called the monoamine hypothesis. That is, people with depression have a shortage of two particular chemicals, serotonin and norepinephrine. Therefore, it makes sense that the vast majority of treatment options focus on fixing this imbalance.
The problem is that it doesn’t always work.
“Thirty percent of people on these drugs do not experience an effect,” Yumiko Saito and Yuki Kobayashi, neuroscientists at HU’s Graduate School of Integrated Arts and Sciences, said in a statement.
“Obviously, we need a new drug! We need another explanation for what could cause depression.”
And that is what they have found. The results of a new study have been published in the journal Neuroscience.
It comes down to a very specific protein called RGS8, which is involved in movement and mood regulation and is responsible for controlling the hormone receptor MCHR1. When MCHR1 is active and working as it should, it helps regulate sleep, feeding, and emotional responses.
Previous studies have suggested that low levels of RGS8 can increase depressive behavior but until now, this theory has not been tested on living organisms. So the researchers had mice complete a forced swim test, which is a method often used to test depressive behavior in animals. They worked out each critter’s total immobility time, ie the amount of time they spent not swimming.
Those with added levels of RGS8 in their nervous system had shorter immobility times than those with normal levels, suggesting lower levels of depressive behavior. When given anti-depressants that work on monoamines, they had even shorter immobility times. However, when they were given drugs to stop MCHR1 from working, the immobility times remained steady, suggesting higher levels of depressive behavior.
“These mice showed a new type of depression,” Saito added. “Monoamines appeared to not be involved in this depressive behavior. Instead, MCHR1 was.”
Next, the team looked at the mice brains under a microscope. The mice with added levels of RGS8 didn’t just act more depressed, they also had longer cilia (hair-like structures involved in cellular communication) in the regions of the brain where RGS8 concentrations are at their highest. Abnormal cilia have been linked to physical conditions, including obesity, retinal disease, and kidney disease, but this appears to be the first time it has been linked to a mood disorder.
This is significant because it could explain why antidepressants work better for some people than they do for others – and there is overwhelming evidence to show that for most people they do work. The hope is that the findings here will lead to new and more effective drugs for the people who are left behind.
If you think this could apply to you, please don’t stop taking your antidepressants until you have spoken to a medical professional.