Gambling disorder affects 0.5–2.4% of the population and shows strong associations with lifetime alcohol use disorder. Very little is known regarding whether lifetime alcohol use disorder can impact the clinical presentation or outcome trajectory of gambling disorder.

Data were pooled from previous clinical trials conducted on people with gambling disorder, none of whom had current alcohol use disorder. Demographic and clinical variables were compared between those who did versus did not have lifetime alcohol use disorder.

Of the 621 participants in the clinical trials, 103 (16.6%) had a lifetime history of alcohol use disorder. History of alcohol use disorder was significantly associated with male gender (relative risk [RR] = 1.42), greater body weight (Cohen’s D = 0.27), family history of alcohol use disorder in first-degree relative(s) (RR = 1.46), occurrence of previous hospitalization due to psychiatric illness (RR = 2.68), and higher gambling-related legal problems (RR = 1.50). History of alcohol use disorder was not significantly associated with other variables that were examined, such as severity of gambling disorder or extent of functional disability. Lifetime alcohol use disorder was not significantly associated with the extent of clinical improvement in gambling disorder symptoms during the subsequent clinical trials.

These data highlight that lifetime alcohol use disorder is an important clinical variable to be considered when assessing gambling disorder because it is associated with several untoward features (especially gambling-related legal problems and prior psychiatric hospitalization). The study design enabled these associations to be disambiguated from current or recent alcohol use disorder.

Social cognition impairments are a common feature of alcohol use disorders (AUD). However, it remains unclear whether these impairments are solely the consequence of chronic alcohol consumption or whether they could be a marker of vulnerability.

The present study implemented a family history approach to address this question for a key process of social cognition: theory of mind (ToM). Thirty healthy adults with a family history of AUD (FH+) and 30 healthy adults with a negative family history of AUD (FH−), matched for age, sex, and education level, underwent an fMRI cartoon-vignette paradigm assessing cognitive and affective ToM. Participants also completed questionnaires evaluating anxiety, depressive symptoms, childhood trauma, and alexithymia.

Results indicated that FH+ individuals differed from FH− individuals on affective but not cognitive ToM processing, at both the behavioral and neural levels. At the behavioral level, the FH+ group had lower response accuracy for affective ToM compared with the FH− group. At the neural level, the FH+ group had higher brain activations in the left insula and inferior frontal cortex during affective ToM processing. These activations remained significant when controlling for depressive symptoms, anxiety, and childhood trauma.

These findings highlight difficulties during affective ToM processing among first-degree relatives of AUD patients, supporting the idea that some of the impairments exhibited by these patients may already be present before the onset of AUD and may be considered a marker of vulnerability.

Marfan syndrome is a rare connective tissue disorder secondary to mutations in the FBN1 gene, characterised by skeletal, ocular, and cardiovascular manifestations. We present an extensive cohort of paediatric patients with Marfan syndrome highlighting the vital importance of promptly referring paediatric first-degree relatives of Marfan syndrome paediatric patients to a tertiary hospital as our results confirm that they are at higher risk of aortic dilatation.

Depression is associated with a high risk of suicidal thoughts (ST) and behaviour (SB). Suicidality and depression have partially shared genetic underpinnings and family history of mood disorders (FH) can reflect genetic impact on specific features of depression. Thus, in depressed patients, FH may affect suicidality and its associations with other risk factors, such as personality traits.

We conducted a cross-sectional study to test the impact of FH on the association between suicidality and personality traits in depressed patients.

200 depression in- and outpatients (64% (n=128) women, mean age (M(SD):36,21(15,09)) were enrolled. 28% (n=56) reported FH (“FH+” cohort), other patients comprised the “FH-” cohort. Columbia-Suicide Severity Rating Scale (C-SSRS) was used to assess ST and SB during the most suicidal period of life. Personality traits were assessed by Cloninger Temperament and Character Inventory (TCI-125). Information about FH and history of suicide attempts (SA) was obtained during the clinical interview.

Personality traits and suicidality characteristics (ST, SB, SA) did not differ between FH+ and FH- patients. In FH+, no differences in TCI-125 scores between suicide attempters and non-attempters were found, while in FH-, attempters had higher scores of TCI-125 “Novelty seeking” (p=0.002) and “Self-transcendence” (p=0.031) subscales. Multiple correlations between ST, SB and TCI-125 subscales were found only in FH-, In FH+, only one correlation (between ST and TCI-125 “Persistence” subscale (r=-0.288, p=0.038) was found.

Our results showed a weakened association between personality traits and suicidality in depressed patients with FH of mood disorders, although more data on larger samples are needed.

The study was supported by RSF grant # 20-15-00132

The age at onset of depression is not only an important clinical predictor of the further disease course, but also a robust marker, reflecting the genetic impact on depression risk.

This study aimed to find whether early-onset depression had an association with specific clinical symptoms, comorbid psychiatric disorders and family history of mood disorders.

This pilot cross-sectional, multicenter study was performed under the supervision of the Russian National Consortium for Psychiatric Genetics. Early-onset depression was defined as the first depressive episode before the median age of onset in the sample (Me=29 years). Logistic regression models were used to determine the independent association of early-onset depression, after adjusting for the effects of sex and age, with binary characteristics.

A total of 172 patients with depression were enrolled in the study (64.5% women; age - 40.9 (15.9) years). Early-onset depression was associated with psychomotor retardation (p=0,025; OR=2,3; 95%CI [1,1 - 4,9]), decreased libido (p=0,014; OR=2,8; 95%CI [1,2 - 6,2]), and lower prevalence of weight loss/decreased appetite (p=0,011; OR=0,4; 95%CI [0,2 - 0,8]). No associations were found with the history of comorbid psychiatric disorders and the family history of mood disorders.

Early-onset depression is associated with specific neurovegetative symptoms. Further clinical and genetic studies are needed to evaluate the specific effects of age at onset of depression on its clinical course.

Research is supported by an RSF grant №20-15-00132.

Recent well-powered genome-wide association studies have enhanced prediction of substance use outcomes via polygenic scores (PGSs). Here, we test (1) whether these scores contribute to prediction over-and-above family history, (2) the extent to which PGS prediction reflects inherited genetic variation v. demography (population stratification and assortative mating) and indirect genetic effects of parents (genetic nurture), and (3) whether PGS prediction is mediated by behavioral disinhibition prior to substance use onset.

PGSs for alcohol, cannabis, and nicotine use/use disorder were calculated for Minnesota Twin Family Study participants (N = 2483, 1565 monozygotic/918 dizygotic). Twins' parents were assessed for histories of substance use disorder. Twins were assessed for behavioral disinhibition at age 11 and substance use from ages 14 to 24. PGS prediction of substance use was examined using linear mixed-effects, within-twin pair, and structural equation models.

Nearly all PGS measures were associated with multiple types of substance use independently of family history. However, most within-pair PGS prediction estimates were substantially smaller than the corresponding between-pair estimates, suggesting that prediction is driven in part by demography and indirect genetic effects of parents. Path analyses indicated the effects of both PGSs and family history on substance use were mediated via disinhibition in preadolescence.

PGSs capturing risk of substance use and use disorder can be combined with family history measures to augment prediction of substance use outcomes. Results highlight indirect sources of genetic associations and preadolescent elevations in behavioral disinhibition as two routes through which these scores may relate to substance use.

A family history (FH) of mood disorders is an important clinical feature that affects the risk of depression and its clinical manifestations during the course of the disease.

To assess the impact of FH in patients with depression on the presence of concomitant psychiatric disorders.

This cross-sectional study included 172 patients with depression (64.5% women; age - 40,87±15,86 years). The M.I.N.I. was conducted to verify the diagnosis of psychiatric disorders. FH is based on indirect reports of patients.

The most prevalent concomitant psychiatric diagnoses in patients with depression were generalized anxiety disorder (GAD; 26,2%), panic disorder (24,4%) and social anxiety disorder (13,4%). FH was recorded in 52 (30.2%) patients with depression. Patients with depression and FH more often had concomitant GAD (with FH - 20 (38,5%), without FH - 25 (20,8%); p=0.016). Women with depression and FH showed a higher rate of early onset (before age 18) of depression (with FH - 10 (32,3%), without FH - 10 (12,5%); p=0.015). Men with depression and FH more often had concomitant GAD (with FH - 10 (47,6%), without FH - 8 (20%); p=0.025). Logistic regression revealed that FH was associated with GAD in patients with depression (p=0.019).

FH of mood disorders in patients with depression is associated with specific concomitant psychopathology. Further genetic studies are needed to explain this comorbidity.