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Smoking contributed to the development of schizophrenia and depression

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Manish Saini
Manish works as a Journalist and writer at Revyuh.com. He has studied Political Science and graduated from Delhi University. He is a Political engineer, fascinated by politics, and traditional businesses. He is also attached to many NGO's in the country and helping poor children to get the basic education. Email: Manish (at) revyuh (dot) com

British geneticists have found a causal link between smoking and the risk of developing schizophrenia and depression. Using a full-genome analysis of associations, they showed that smokers had a 2.27-fold risk of developing schizophrenia and 1.99 times higher than depression. In this case, the feedback was also observed – but only for depression.

There are more smokers among people with mental disorders than among a healthy population. Due to the additional health problems that smoking causes (e.g. lung disease and cardiovascular disease), their lifespan can be significantly reduced, so the nature of the link between smoking and mental disorders needs to be understood accurately. It is not always obvious, and it cannot be established precisely even by studying biochemical mechanisms.

It is known, for example, that substances contained in tobacco inhibit the production of monoamine oxidase, an enzyme that breaks down monoamine neurotransmitters, such as dopamine. Related effects have antidepressants from the group of inhibitors monoamine oxidase, from which it can be concluded that in depression smoking could be used as self-medication.

On the other hand, dopamine itself at high concentrations of nicotine in the body begins to produce more strongly. Increased activity of dopaminergic neurons, in turn, is one of the clear biomarkers of schizophrenia: that is why most drugs that buy the symptoms of the disease, “antipsychotics – act on dopamine. Show the link between smoking and the development of mental disorders through the effect on the work of neurotransmitters of the brain, so it is possible, but it will remain bilateral; in addition, smoking may well be a side variable.

Robin Wotton, from the University of Bristol, and his colleagues tried to find a causal link between smoking and the risk of developing mental disorders with using a genome-wide association search. To do this, they used the results of a recent study on genetic markers associated with smoking as a binary variable: in it, on the samples of more than 1.3 million people, 378 single-nucleotide polymorphisms were detected.

After that, they conducted their own research on the genomes of 462,690 people who provided information about how much they smoke, how often and about their attempts to quit. As a result, scientists managed to detect 126 polymorphisms related to the duration of smoking, the number of cigarettes smoked and whether people tried to stop (and whether they managed to).

Then, scientists used the already known single-nucleotide polymorphisms associated with the development of depression and schizophrenia (40 and 114, respectively). Scientists conducted a statistical analysis of the relationship between smoking and the development of mental disorders using Mendelian randomization methods – they evaluate the influence of genetic markers on the development of a trait as instrumental variables and help determine a cause-effect relationship (with an eye to the fact that genetic factors are a variable random).

The analysis showed that smoking (both a binary variable and all the studied parameters) is a risk factor for the development of schizophrenia and depression (both p <0.001): smokers have a 2.27-fold higher risk of schizophrenia and a 1.99 times higher depression. Feedback was found only for depression (p = 0.005), but not for schizophrenia – while there was a weak connection between the presence of this disease and the onset of smoking.

The authors concluded that the link between smoking and the development of depression and schizophrenia is causal. At the same time, they specify that this is true only for a part of the studied population: because of the fact that there was also feedback, but only for depression (this seems to be due self-medication hypothesis), it is necessary to transfer the results to the entire population with caution. The biochemical mechanism of such a link has yet to be studied: the authors, however, note that it is most likely to involve the work of monoamine neurotransmitters (not only dopamine but also serotonin).

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