In 2003, psychiatrists Vikram Patel and Arthur Kleinman suggested that there is a correlation between poverty and depression, as well as other common mental illness, in developing countries. They argued that the “experience of insecurity and hopelessness, rapid social change and the risks of violence and physical ill-health” explain why impoverished people are so vulnerable to mental illnesses such as depression.
In the United States, as of 2011, 30.9 percent of people in poverty are depressed. While this isn’t a global statistic, it does illuminate the relationship between the global depression phenomenon and global stressors, such as insecurity, violence, etc. These external factors are crucial to the development of depression, but so are internal or hereditary ones; a combination of the two is what neuroscientists now believe causes the neurological disorder.
Studies of the neurology of depression center around the neurotransmitter serotonin, a chemical messenger found in the brain associated with feelings of well-being, mood regulation, memory and cognition. Neurons release serotonin into the synaptic cleft, the space in-between neurons, and receptors on adjacent neurons receive it.
Different receptors have specialized effects. The two most important serotonin receptors in depression research are 5-hydroxytryptamine receptor 1A (5HT1A) and 2A (5HT2A.) The former is associated with increased activity, while the latter is associated with decreased activity.
One theory is that depression is caused by an uneven ratio of 5HT1A to 5HT2A receptors, with an excess of 5HT2A. This is an hereditary occurrence that leaves one more prone to depression, though not necessarily depressed. If there is insecurity, violence, etc. in this person’s environment, however, he or she is likely to develop symptoms of depression.
Another theory suggests that people suffering from depression naturally produce less serotonin than those who do not. This is, again, genetic and will only ever make one vulnerable to depression; it’s most likely a combination of genetic predisposition and external influences from one’s environment that cause this mental illness.
To counteract genetic predispositions to depression, neurologists, commonly use an antidepressant medication called selective serotonin re-uptake inhibitor (SSRI) drugs. They block what is called re-uptake, a process during which neurotransmitter transporters limit the amount of a neurotransmitter – in this case serotonin – in the synaptic cleft by taking it from receptors and driving it to other areas of the brain. Blocking re-uptake increases one’s serotonin levels where it counts, in the synaptic cleft where neurons communicate.
The effects of this medication may seem counter intuitive.
“Regardless of the emotion being happy or sad it would seem SSRI drugs dampens the experienced intensity of the emotion,” said Albert Gjedde, a neuroscientist who studies antidepressant SSRI drugs. “People in treatment with SSRI dugs describe it as if the peak of their emotions are cut away.”
Drugs such as SSRIs can help people with innate biases toward depression, but until poverty and its consequences are reduced, there will always be those at risk. Neuroscientists and philanthropists must work in tandem to mitigate the effects of depression and, eventually, to annihilate it.
– Adam Kaminski