Тактика лечения эректильной дисфункции у мужчин без партнерши

Обосновывается актуальность проблемы оказания помощи мужчинам с эректильной дисфункцией, не имеющим сексуальной партнерши. Описаны предложенные автором подходы к коррекции нарушения сексуального здоровья мужчин и лечебные тактики.The importance of the issue of rendering the aid to the men with erectile dysfunction who do not have a female partner is substantiated. The author describes the original approaches to correction of the sexual health in the men and therapeutic tactics

Examining the independent and joint effects of molecular genetic liability and environmental exposures in schizophrenia : results from the EUGEI study

Schizophrenia is a heritable complex phenotype associated with a background risk involving multiple common genetic variants of small effect and a multitude of environmental exposures. Early twin and family studies using proxy-genetic liability measures suggest gene-environment interaction in the etiology of schizophrenia spectrum disorders, but the molecular evidence is scarce. Here, by analyzing the main and joint associations of polygenic risk score for schizophrenia (PRS-SCZ) and environmental exposures in 1,699 patients with a diagnosis of schizophrenia spectrum disorders and 1,542 unrelated controls with no lifetime history of a diagnosis of those disorders, we provide further evidence for gene-environment interaction in schizophrenia. Evidence was found for additive interaction of molecular genetic risk state for schizophrenia (binary mode of PRS-SCZ above 75% of the control distribution) with the presence of lifetime regular cannabis use and exposure to early-life adversities (sexual abuse, emotional abuse, emotional neglect, and bullying), but not with the presence of hearing impairment, season of birth (winter birth), and exposure to physical abuse or physical neglect in childhood. The sensitivity analyses replacing the a priori PRS-SCZ at 75% with alternative cut-points (50% and 25%) confirmed the additive interaction. Our results suggest that the etiopathogenesis of schizophrenia involves genetic underpinnings that act by making individuals more sensitive to the effects of some environmental exposures

Estimating Exposome Score for Schizophrenia Using Predictive Modeling Approach in Two Independent Samples : The Results From the EUGEI Study

Exposures constitute a dense network of the environment: exposome. Here, we argue for embracing the exposome paradigm to investigate the sum of nongenetic "risk" and show how predictive modeling approaches can be used to construct an exposome score (ES; an aggregated score of exposures) for schizophrenia. The training dataset consisted of patients with schizophrenia and controls, whereas the independent validation dataset consisted of patients, their unaffected siblings, and controls. Binary exposures were cannabis use, hearing impairment, winter birth, bullying, and emotional, physical, and sexual abuse along with physical and emotional neglect. We applied logistic regression (LR), Gaussian Naive Bayes (GNB), the least absolute shrinkage and selection operator (LASSO), and Ridge penalized classification models to the training dataset. ESs, the sum of weighted exposures based on coefficients from each model, were calculated in the validation dataset. In addition, we estimated ES based on meta-analyses and a simple sum score of exposures. Accuracy, sensitivity, specificity, area under the receiver operating characteristic, and Nagelkerke's R2 were compared. The ESMeta-analyses performed the worst, whereas the sum score and the ESGNB were worse than the ESLR that performed similar to the ESLASSO and ESRIDGE. The ESLR distinguished patients from controls (odds ratio [OR] = 1.94, P < .001), patients from siblings (OR = 1.58, P < .001), and siblings from controls (OR = 1.21, P = .001). An increase in ESLR was associated with a gradient increase of schizophrenia risk. In reference to the remaining fractions, the ESLR at top 30%, 20%, and 10% of the control distribution yielded ORs of 3.72, 3.74, and 4.77, respectively. Our findings demonstrate that predictive modeling approaches can be harnessed to evaluate the exposome

Smoking, symptoms, and quality of life in patients with psychosis, siblings, and healthy controls : a prospective, longitudinal cohort study

Background: The self-medication hypothesis postulates that the high prevalence of smoking in patients with psychosis can be explained by the ameliorating effect of smoking on symptoms. However, there are few large prospective studies testing this hypothesis. We aimed to examine the multi-cross-sectional and prospective associations of changes in smoking behaviour with symptoms and quality of life. Methods: In this prospective cohort study we recruited patients with a non-affective psychosis (n=1094), unaffected siblings (n=1047), and healthy controls (n=579). Patients aged between 16 and 50 years and diagnosed with a non-affective psychosis according to DSM-IV were recruited by clinicians from four university medical centres and 36 associated mental health-care institutions in the Netherlands and Belgium between Jan 13, 2004, and March 6, 2014. Smoking status and number of cigarettes per day were assessed at baseline, and at 3-year and 6-year follow-up using the Composite International Diagnostic Interview (CIDI). Symptom frequency was self-rated with the Community Assessment of Psychotic Experience (CAPE), and quality of life was assessed by the WHO Quality of Life (WHOQOL) schedule. Multiple linear mixed-effects regression analyses were done accounting for multiple confounders. Findings: At baseline, 729 (67%) of 1094 of patients smoked (mean 17·5 cigarettes per day, SD 8·8) compared with 401 (38%) of 1047 siblings and 145 (25%) of 579 healthy controls. Multi-cross-sectional results of linear mixed-effects analyses showed that smoking in patients and siblings was associated with more frequent positive symptoms (estimate 0·14, SE 0·02, p<0·0001 in patients; 0·03, 0·01, p=0·0019 in siblings), negative symptoms (0·15, 0·03, p<0·0001 in patients; 0·09, 0·02, p<0·0001 in siblings), and depressive symptoms (0·12, 0·03 p<0·0001 in patients; 0·08, 0·02 p<0·0001 in siblings) and lower quality of life (−0·59, 0·11, p<0·0001 in patients; −0·31, 0·09, p=0·0002 in siblings) than non-smokers. In controls, smoking was associated with significantly higher frequency of subclinical positive symptoms (0·03, 0·01, p=0·0016) and depressive symptoms (0·05, 0·03, p=0·0432) than in participants who did not smoke. Patients who started to smoke during follow-up showed a significant increase in self-reported symptoms, particularly positive symptoms (0·161, 0·077, p=0·0381), whereas smoking cessation was not associated with changes in symptoms or quality of life compared with those who showed no change in smoking behaviour. Similar results were obtained for the changes in the number of cigarettes smoked. Interpretation: Our findings do not empirically support the self-medication hypothesis. The absence of long-term symptomatic relief from smoking should encourage clinicians to help patients with psychosis to quit smoking. Funding: Dutch Health Research Council, Lundbeck, AstraZeneca, Eli Lilly, Janssen Cilag, Academic Psychiatric Center of the Academic Medical Center, GGZ inGeest, Arkin, Dijk en Duin, GGZ Rivierduinen, Erasmus Medical Center Amsterdam, GGZ Noord Holland Noord, University Medical Center Groningen, Lentis, GGZ Friesland, GGZ Drenthe, Dimence, Mediant, GGNet Warnsveld, Yulius Dordrecht, Parnassia Psycho-medical Center, Maastricht University Medical Center, GGzE, GGZ Breburg, GGZ Oost-Brabant, Vincent van Gogh voor Geestelijke Gezondheid, Mondriaan, Virenze riagg, Zuyderland GGZ, MET GGZ, Universitair Centrum Sint-Jozef Kortenberg, CAPRI University of Antwerp, PC Ziekeren Sint-Truiden, PZ Sancta Maria Sint-Truiden, GGZ Overpelt, OPZ Rekem, University Medical Center Utrecht, Altrecht, GGZ Centraal, and Delta

Expressive suppression in psychosis: The association with social context.

As emotion regulation deficits have been implicated in psychotic disorders, it is imperative to investigate not only the effect of regulation strategies but also how they are used. One such strategy is expressive suppression, the inhibition of emotion-expressive behavior, which may be influenced by social context. Therefore, this study aimed to investigate whether the use of expressive suppression was associated with social context and affect in daily life and if this differed between patients with psychosis and controls. Multilevel models using experience sampling method (ESM) data of 34 patients with psychotic disorders and 53 controls from the Genetic Risk and Outcome in Psychosis (GROUP) project were conducted. Expressive suppression and social context were assessed once a day for six days and daily affect was averaged per participant per day. Social context was significantly associated with the use of expressive suppression in daily life, so that the use of expressive suppression differed when in the presence of familiar versus non-familiar company when receiving negative feedback. This finding did not differ between patients and controls. This demonstrates that taking the situation into account when studying expressive suppression, and emotion regulation in general, may improve our understanding of how regulation takes place

Developmental course of subclinical positive and negative psychotic symptoms and their associations with genetic risk status and impairment

The proneness-persistence-impairment (PPI) model states that psychotic experiences are more likely to lead to impairment if their expression becomes persistent. Higher genetic risk for psychosis is known to affect proneness and persistence of subclinical positive symptoms. Less is known about potential effects of genetic risk on the course of subclinical negative symptoms, impairment, and their subsequent associations. The current study examined these issues in a large sample (n = 1131), consisting of individuals with higher genetic risk (siblings of patients with psychotic disorders, n = 703) and lower genetic risk (controls without a family member with lifetime psychosis, n = 428). Psychotic experiences were assessed with the CAPE questionnaire, at two time points three years apart. Participants were allocated to one of four groups representing developmental course: stable low, decreasing, increasing or persisting subclinical positive/negative symptoms. Lifetime clinical psychosis was an exclusion criterion at baseline. Higher genetic risk status was found to be associated with a persisting course of both subclinical positive and negative symptoms, symptom-related distress and functional impairment. There is no evidence for an effect of genetic risk status on the association between developmental course and impairment. The results of the current study underline the importance of assessing psychotic experiences in the context of genetic risk, multidimensional and over time. Additionally, the current findings both underscore and contribute to the PPI model: psychotic experiences are more likely to lead to impairment if their expression becomes persistent, both in individuals with higher and lower genetic risk for psychosis

Correction: Cognitive Performance and Long-Term Social Functioning in Psychotic Disorder: A Three-Year Follow-Up Study.

[This corrects the article DOI: 10.1371/journal.pone.0151299.]

Cognitive Performance and Long-Term Social Functioning in Psychotic Disorder: A Three-Year Follow-Up Study.

OBJECTIVE:Studies have linked cognitive functioning to everyday social functioning in psychotic disorders, but the nature of the relationships between cognition, social cognition, symptoms, and social functioning remains unestablished. Modelling the contributions of non-social and social cognitive ability in the prediction of social functioning may help in more clearly defining therapeutic targets to improve functioning. METHOD:In a sample of 745 patients with a non-affective psychotic disorder, the associations between cognition and social cognition at baseline on the one hand, and self-reported social functioning three years later on the other, were analysed. First, case-control comparisons were conducted; associations were subsequently further explored in patients, investigating the potential mediating role of symptoms. Analyses were repeated in a subsample of 233 patients with recent-onset psychosis. RESULTS:Information processing speed and immediate verbal memory were stronger associated with social functioning in patients than in healthy controls. Most cognition variables significantly predicted social functioning at follow-up, whereas social cognition was not associated with social functioning. Symptoms were robustly associated with follow-up social functioning, with negative symptoms fully mediating most associations between cognition and follow-up social functioning. Illness duration did not moderate the strength of the association between cognitive functioning and follow-up social functioning. No associations were found between (social) cognition and follow-up social functioning in patients with recent-onset psychosis. CONCLUSIONS:Although cognitive functioning is associated with later social functioning in psychotic disorder, its role in explaining social functioning outcome above negative symptoms appears only modest. In recent-onset psychosis, cognition may have a negligible role in predicting later social functioning. Moreover, social cognition tasks may not predict self-reported social functioning

Evidence for a Shared Etiological Mechanism of Psychotic Symptoms and Obsessive-Compulsive Symptoms in Patients with Psychotic Disorders and Their Siblings

The prevalence of obsessive-compulsive disorder in subjects with psychotic disorder is much higher than in the general population. The higher than chance co-occurrence has also been demonstrated at the level of subclinical expression of both phenotypes. Both extended phenotypes have been shown to cluster in families. However, little is known about the origins of their elevated co-occurrence. In the present study, evidence for a shared etiological mechanism was investigated in 3 samples with decreasing levels of familial psychosis liability: 987 patients, 973 of their unaffected siblings and 566 healthy controls. The association between the obsessive-compulsive phenotype and the psychosis phenotype c.q. psychosis liability was investigated. First, the association was assessed between (subclinical) obsessive-compulsive symptoms and psychosis liability. Second, in a cross-sib cross-trait analysis, it was examined whether (subclinical) obsessive-compulsive symptoms in the patient were associated with (subclinical) psychotic symptoms in the related unaffected sibling. Evidence was found for both associations, which is compatible with a partially shared etiological pathway underlying obsessive-compulsive and psychotic disorder. This is the first study that used a cross-sib cross-trait design in patients and unaffected siblings, thus circumventing confounding by disease-related factors present in clinical samples