Gender Differences in Gambling Disorder: Results from an Italian Multicentric Study.

Objective: Although gender-specific evidence on Gambling Disorder (GD) is still limited, some studies reported specific differences, mainly in psychopathological profiles, gambling behavior patterns, and pathogenesis. In order to further examine the role of gender in GD, we conducted a multicenter investigation in a sample of Italian outpatients. Method: One hundred-four outpatients with a diagnosis of GD based on DSM-5 criteria were consecutively recruited at two clinics based in Milan. Socio-demographic and clinical variables were collected for the whole sample and analyzed for the effect of gender. The severity of illness was assessed using the Canadian Problem Gambling Index and the Gambling Attitudes and Beliefs (GABS). Results: Among females, a significantly higher mean age (52.23 ± 10.95 vs. 40.96 ± 15.76; p=0.005) and older age at illness onset emerged (43.5 ± 11.92 vs. 29.22 ± 14.26; p<0.001). Females showed a significantly higher rate of psychiatric comorbidities, lifetime suicide ideation, stressful events at GD onset, and positive family history for GD compared to males. A predictive effect of male gender was found for the GABS questionnaires by performing a linear regression model, with males showing a higher risk to reach higher scores compared to females (B= 11.833; t=2.177; p=0.034). Conclusions: Our study seems to confirm the hypotheses that gender in GD may influence psychopathological profiles, course, and comorbidity. GD in female gender is frequently a comorbid condition with other specific clinical characteristics compared to males. Identifying specific clinical factors by gender may prompt more focus on the public health of women in relation to gambling, while still recognizing that males are at-risk of earlier gambling problems. These findings should be considered in therapeutic perspectives.

The effects of cocaine exposure in adolescence: Behavioural effects and neuroplastic mechanisms in experimental models.

Drug addiction is a devastating disorder with a huge economic and social burden for modern society. Although an individual may slip into drug abuse throughout his/her life, adolescents are at higher risk, but, so far, only a few studies have attempted to elucidate the underlying cellular and molecular bases of such vulnerability. Indeed, preclinical evidence indicates that psychostimulants and adolescence interact and contribute to promoting a dysfunctional brain. In this review, we have focused our attention primarily on changes in neuroplasticity brought about by cocaine, taking into account that there is much less evidence from exposure to cocaine in adolescence, compared with that from adults. This review clearly shows that exposure to cocaine during adolescence, acute or chronic, as well as contingent or non-contingent, confers a vulnerable endophenotype, primarily, by causing changes in neuroplasticity. Given the close relationship between drug abuse and psychiatric disorders, we also discuss the translational implications providing an interpretative framework for clinical studies involving addictive as well as affective or psychotic behaviours. LINKED ARTICLES: This article is part of a themed issue on New discoveries and perspectives in mental and pain disorders. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.17/issuetoc.

Anhedonic-like behavior and BDNF dysregulation following a single injection of cocaine during adolescence.

We have previously demonstrated that a single exposure to cocaine during adolescence causes several behavioural and neurobiological changes, highlighting the unique vulnerability of this period of life. The purpose of our work was to investigate whether a single exposure to cocaine during brain development is sufficient to shape a negative emotional state in adolescent rats. A single injection of cocaine during adolescence followed by measurement of sucrose consumption, a measure of anhedonia, identifies two separate groups of rats, i.e. anhedonic (AN) and non anhedonic (NON-AN) rats. AN rats show reduced ability to synthesize, traffic and translate the neurotrophin BDNF at synaptic level, reduced activation of hippocampal BDNF signaling, reduced BDNF plasma levels and a steep rise of corticosterone secretion. Conversely, NON-AN rats exhibit reduced trafficking of BDNF while up-regulating hippocampal BDNF synthesis and stabilizing its downstream signaling with no changes of BDNF and corticosterone plasma levels. Adult rats exposed to cocaine showed no signs of anhedonia, an increase of BDNF both in hippocampus and plasma and decreased levels of corticosterone. In conclusion, our findings reveal a complex central and peripheral dysregulation of BDNF-related mechanisms that instead are preserved in NON-AN rats, suggesting that BDNF modulation dictates behavioural vulnerability vs. resiliency to cocaine-induced anhedonia, a profile uniquely restricted to adolescent rats.

Circadian activity rhythm abnormalities in ill and recovered bipolar I disorder patients.

OBJECTIVES: Most physiological indicators of bipolar disorder (BPD) reflect current acute illness, and rarely have proved to be state-independent. Activity rhythms are highly abnormal in acute phases of BPD; we compared circadian activity rhythms in BPD I patients during ill and recovered states to those of normal controls to test the hypothesis that some abnormalities may persist. METHODS: We compared 36 adult DSM-IV BPD I patients during acute mania or mixed states, and during full and sustained clinical recovery, to 32 healthy controls of similar age and sex distribution, using wrist-worn, piezoelectric actigraphic monitoring for 72 h and computed cosinor analysis of circadian activity rhythms. RESULTS: We verified expected major differences between manic or mixed-state BPD I patients and matched normal controls, including phase advances averaging 2.1 h in ill BPD I patients and 1.8 h in recovered patients. Moreover, recovered BPD patients differed highly significantly from controls in several measures, including acrophase advance, higher percentage of nocturnal sleep, and lower average daily activity (mesor). Actigraphic measures among recovered BPD patients were independent of ratings of mania (on the Young Mania Rating Scale), depression (on the Hamilton Depression Rating Scale), or rating-scale scored subjective distress, as well as the type and dose of concurrent psychotropic medication. CONCLUSIONS: These findings suggest that abnormal activity rhythms, including sustained phase advances, may represent enduring (trait) characteristics of BPD patients even during clinical recovery. If verified, such indices may be useful in supporting diagnoses and as an objective phenotype for genetic or other biological studies.