Loneliness Induces Depression and Promotes Drinking Behavior
Long-term isolation is more likely to cause depression than work pressure. The social isolation caused during the COVID-19 pandemic has significantly increased the prevalence of depression and anxiety. The risk of suicide in patients with depression is 20 to 40 times that of normal people. To escape sadness and depression, people with depression tend to drink excessively. Clinical reports indicate that approximately 40.3% of patients with major depression suffer from alcohol use disorder. In turn, alcohol use increases the risk of suicide in patients with depression.
Even more frightening is that drinking behavior is considered to be a major obstacle in the treatment of depression: it leads to a decrease in the response to antidepressant drugs, which is as high as 70%. In addition, long-term heavy drinking gradually inactivates the function of the reward system, leading to an increase in the frequency and volume of drinking, becoming a patient with alcohol use disorder and becoming dependent on alcohol. Recently, the research team of Daejeon University in South Korea published a research paper titled: Social isolation-related depression accelerates ethanol intake via microglia-derived neuroinflammation in Science Advances.
The researchers used the social isolation model to find that the alcohol consumption of mice began to increase after the 8th day of rearing alone. In the conditional position preference experiment, it was further confirmed that social isolation promotes alcohol-seeking behavior. After social isolation, the mice's consumption of sugar and water decreased, and the time of forced swimming immobility increased and other depression-like behaviors.
In addition, social isolation promotes dopamine signals in the ventral tegmental area of the brain reward system, which in turn leads to increased alcohol use. This shows that alcohol use can aggravate the adverse effects of social isolation caused by the brain. Researchers found that the expression of synaptic proteins PSD95 and synaptophysin in the dorsal raphe nucleus of social isolation model mice was reduced. The expression of complement C1q and C3 related to synapse phagocytosis increased, the level of pro-inflammatory factor TNF-α increased, and the level of anti-inflammatory factor IL-10 decreased. After intraperitoneal injection of the microglia inhibitor minocycline can reduce the activation of microglia in socially isolated mice, the expression of complement C1q also returns to normal levels, and can relieve depression-like symptoms.
In general, this article finds that depression and anxiety-like behaviors caused by social isolation are further aggravated after alcohol use.
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Even more frightening is that drinking behavior is considered to be a major obstacle in the treatment of depression: it leads to a decrease in the response to antidepressant drugs, which is as high as 70%. In addition, long-term heavy drinking gradually inactivates the function of the reward system, leading to an increase in the frequency and volume of drinking, becoming a patient with alcohol use disorder and becoming dependent on alcohol. Recently, the research team of Daejeon University in South Korea published a research paper titled: Social isolation-related depression accelerates ethanol intake via microglia-derived neuroinflammation in Science Advances.
The researchers used the social isolation model to find that the alcohol consumption of mice began to increase after the 8th day of rearing alone. In the conditional position preference experiment, it was further confirmed that social isolation promotes alcohol-seeking behavior. After social isolation, the mice's consumption of sugar and water decreased, and the time of forced swimming immobility increased and other depression-like behaviors.
In addition, social isolation promotes dopamine signals in the ventral tegmental area of the brain reward system, which in turn leads to increased alcohol use. This shows that alcohol use can aggravate the adverse effects of social isolation caused by the brain. Researchers found that the expression of synaptic proteins PSD95 and synaptophysin in the dorsal raphe nucleus of social isolation model mice was reduced. The expression of complement C1q and C3 related to synapse phagocytosis increased, the level of pro-inflammatory factor TNF-α increased, and the level of anti-inflammatory factor IL-10 decreased. After intraperitoneal injection of the microglia inhibitor minocycline can reduce the activation of microglia in socially isolated mice, the expression of complement C1q also returns to normal levels, and can relieve depression-like symptoms.
In general, this article finds that depression and anxiety-like behaviors caused by social isolation are further aggravated after alcohol use.
At present, Wuxi Donglin Sci & Tech Development Co.,Ltd. has developed Elisa products for the proteins mentioned above. If you want to know information about them, you can directly visit the website:
C1q
http://www.dldevelop.com/Research-reagent/dl-c1qa-hu.html
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