Nicotine withdrawal may be one potential cause of depression in people predisposed to getting depression, via nicotine sharing several biological pathways with depression. While depressed people may be more likely to smoke (e.g., Edwards et al., 2011), smoking may also cause depression, via nicotine withdrawal. There are several neurological pathways that depression and nicotine are associated with, such as hypothalamic–pituitary–adrenal (HPA) axis, dopamine, acetylcholine, and serotonin related pathways. Nicotine withdrawal affecting these shared pathways may be one potential cause of depression. Nicotine might be a potential cause of depression since mice can start to exhibit anxiety and depression symptoms, in addition to HPA axis activation
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Cinciripini et al. (2013) had participants receive smoking cessation counseling, and Varenicline, bupropion, or a placebo for 12 weeks. Varenicline is a selective partial agonist of the α4 β 2 acetylcholine receptor. It stimulates dopamine release from the nucleus accumbens, but less than nicotine does (e.g., Cinirpini et al., 2013). It likely works similar to a nicotine patch, allowing for a gradual withdrawal from stimulation of the reward system. Bupropion is an atypical antidepressant. The study found that, at the 3-month follow up, both medications were more effective than placebo at reducing depression and smoking reward symptoms. At the 6-month follow-up, only Varenicline significantly reduced symptoms. Since an antidepressant helped with smoking symptoms, this might suggest that reducing depression may have caused participants to experience a reduction in smoking reward symptoms. However, the opposite may also be true, since Varenicline helped reduce both kinds of symptoms. While both drugs reduced smoking reward symptoms, they may have potentially reduced nicotine withdrawal symptoms as well if they reduced the effects of nicotine in general. However, this is uncertain. Thus, depression and nicotine withdrawal may both exacerbate each other, and there does seem to be a connection between nicotine and depression in affecting an acetylcholine
Cinciripini et al. (2013) had participants receive smoking cessation counseling, and Varenicline, bupropion, or a placebo for 12 weeks. Varenicline is a selective partial agonist of the α4 β 2 acetylcholine receptor. It stimulates dopamine release from the nucleus accumbens, but less than nicotine does (e.g., Cinirpini et al., 2013). It likely works similar to a nicotine patch, allowing for a gradual withdrawal from stimulation of the reward system. Bupropion is an atypical antidepressant. The study found that, at the 3-month follow up, both medications were more effective than placebo at reducing depression and smoking reward symptoms. At the 6-month follow-up, only Varenicline significantly reduced symptoms. Since an antidepressant helped with smoking symptoms, this might suggest that reducing depression may have caused participants to experience a reduction in smoking reward symptoms. However, the opposite may also be true, since Varenicline helped reduce both kinds of symptoms. While both drugs reduced smoking reward symptoms, they may have potentially reduced nicotine withdrawal symptoms as well if they reduced the effects of nicotine in general. However, this is uncertain. Thus, depression and nicotine withdrawal may both exacerbate each other, and there does seem to be a connection between nicotine and depression in affecting an acetylcholine