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Seasonal Affective Disorder and Premenstrual Dysphoric Disorder a psychopathological continuum: the role of serotonin

Seasonal Affective Disorder and Premenstrual Dysphoric Disorder a psychopathological continuum: the role of serotonin

Chronobiology studies in the psychiatric field have highlighted numerous aspects that unite seasonal affective disorder and premenstrual dysphoric disorder. Today there is the hypothesis that these two disorders could be manifestations of the same pathology.

 

Advertising message Since ancient times it has been observed that climatic variations influence the state of health and mood. Hippocrates in 400 BC. C. described a depression related to the seasons. His writings and those of Pliny and Aristotle in the classical period testify that a number of symptoms that afflicted women in the premenstrual period were also known. Chronobiology currently studies periodic phenomena in living organisms and describes the molecular mechanisms linked to dark-light cycles, to the alternation of seasons and moon phases. It is now proven that the production of numerous hormones and various neurotransmitters is influenced by these facts. Numerous chronobiological psychiatric studies have been conducted over the past twenty years.

There are two mood disorders, the seasonal affective disorder and the premenstrual dysphoric disorder, which in addition to having the periodicity in manifestation in common, seem to share some etiopathogenetic aspects.

Seasonal Affective Disorder is an atypical chronic depressive disorder whose symptoms can occur with a winter periodicity, with onset in the autumn season, or summer with spring onset. From a clinical point of view, the atypical nature of the disorder is linked to the fact that the mood is depressed but reactive. This means that those who suffer from it have a drop in mood, but are able to rejoice in the face of positive events. Other symptoms are hyperphagia, with preference for carbohydrate ingestion, fatigue, hypersomnia and weight gain. There are several etiopathogenetic hypotheses for SAD, all of which have a common denominator represented by the duration of exposure to sunlight. The amount of light affects the endogenous production of melatonin and serotonin. Melatonin, also called sleep hormone, it could be produced in excess in the absence of sunlight. Too high levels generate hypersomnia and could predispose to depression. According to the results of a study by researchers at the University of Copenhagen, presented at the XII International Conference on Neuropsychopharmacology in London (2014), people who develop SAD have altered SERT levels, which is the serotonin transporter molecule.

Advertising message It is a mood disorder that occurs among the symptoms of premenstrual syndrome. It is characterized not only by depressed mood but also by irritability and emotional lability. The intensity of these symptoms can be such as to significantly affect work activity and social interactions. There are several etiological factors called into question to explain the origin of this disorder. Rojanski et al. (1991) in one study reported an overall reduction in serotonin plasma levels in the luteinic phase of the ovarian cycle in women with PMS. Serotonin convolution is also demonstrated by the ex-juvantibus criterion, in fact in 60% of women with PMS, the symptoms regress with the administration of serotonergic antidepressants (Steiner M. et al. 1995, Freeman Ew. 2005).

In 2006, the results of a study were published in the Italian Journal of Psychopathology which aimed to evaluate the prevalence of SAD and PMS in a population of women without psychiatric disorders and to determine the prevalence of PMS in women who presented with a diagnosis of SAD. The results of the study allow us to affirm that SAD and PMS have an overlapping epidemiological profile and a similar symptomatology. The therapeutic efficacy of serotonergic antidepressants is recognized for both disorders. In the Italian female population SAD and PMS occur frequently in association. All these data lead to suppose a common neurobiological basis, the two disorders could be manifestations of the same pathology.