DISCUSSION
Antidepressant and anxiolytic effects of smoking are known to the smoking population, despite the popular belief that smoking has a positive mood affects. The evidence established in Boden, Fergusson, & Horwood (2010) and other literature that have linked smoking to depression assert that the smoking population may actually be vindicated. Regardless of the direction of the causal relationship; it is still a statistically significant relationship with important practical implications. It is possible that the relationship could even be bidierectional, which effectively marries the research findings from both extremes, with infrequenet or acute smoking leading to a reduction in the negative mood affect, while chronic tobacco use exacerbates the situation. It is also possible that both smoking and depressive symptoms are caused by similar risk factors, and thus there really is no causal relationship between them, but their concurrence causes a perception of a causal relationship (Munafò & Araya, 2010).
There is equally compelling evidence that genetic predisposition to smoking, with the fibndings in the above research findings leading to conclusions to this end. The collected data is consistent with multiple causal relationship between different fcators, which cannot be exclusively explained by a single causal relationship. The reliance on the symptoms as against the actual diagnoses in the mainstream literature supporting the possibility of smoking causing depression is puzzlling, and especially because the Composiite International Diagnostic Interview was developed as a diagnostic instrument. The authors in in Boden, Fergusson, & Horwood (2010); Kahler, Spillane, Busch, & Leventhal (2011) and Perkins, Karelitz, Conklin, Sayette, & Giedgowd (2010) for instance carried out additional tests that used ordinal variables that included diagniostic categories that resulted in similar conclusions. The symptoms of depressions are unlike clinical depression, despite the fact that a dimensional measure of the symptoms allows for increased power of statistical testing of the associations and negative affectivity. Choosing the symptoms to assess smoking behavior is not usual, since the number of cigarettes smoked a day is a good pointer to exposure.
The paradox remains in the face of mounting empirical evidence suggesting that smoking causes depressive symptoms, while smokers insist that they get an emotional lift from smoking. It is possible according to Munafò & Araya (2010) may be explained by the fact that nicotine has a short half-life and the withdrawal symptoms speed in heavy smokers who have abstained for hours. The withdrawal syndromes associated with severe abstinance from smoking helps to better the heighten the withdrawal symptoms. The subjective experiences that have largely been captured in successive studies are likely to be of negative affects that can be mitigated through smoking. This assertion is supported by the fact that withdrawal symptoms are usually followed by positive improvements in the mood.
It is however critical to point out that empirical data cannot unequivocally offer causation evidence, not least because experimental studies are impossible due to ethical reasons. The possibility of resolving the causation direction lies in the passibility of applying Mendelian Randomization principle, in which the geneticn information forms a central part of the tests to confirm the causal relationships/hypotheses. The [isolation of the genetic factors that predispose individuals to depresion and/or smoking will offer the solution or narrow down the search. In addition, it will allow for the easier identification of the environemental factors that lead tpo the same result, which should ultimately facilitate the establihment of the true causal link between the two variables. Genetics has alaredy been exploredf in Lewis, et al. (2010), which resulted in inconclusive evidence on the genetic predisposition and the role of enviornmental factors to causing both smoking and depression.
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