Obsessive-compulsive symptoms and cigarette smoking: an initial cross-sectional test of mechanisms of co-occurrence.
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ABSTRACT:
SUBMITTER: S Chasson G
PROVIDER: S-EPMC7483265 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVE:Sensory overresponsivity (SOR) is characterized by challenges in integrating and responding to everyday sensory experiences. Obsessive-compulsive disorder (OCD) is characterized by intrusive thoughts, ritualistic behaviors, and sensory phenomena. There is some evidence that individuals with co-occurring symptoms of SOR and OCD experience more severe anxiety than those with symptoms of OCD alone, but most studies employed small numbers of participants (typically with an OCD diagnosis) assessed at a single time point. Our 2-fold objective was to replicate previous research showing an association between OCD symptoms and SOR symptoms concurrently and to extend these analyses longitudinally in a large, birth-register-based sample. METHOD:Twins (N = 1613) and their primary caregivers participated in a multimodal, multimethod, longitudinal study. Primary caregivers completed the SOR inventory for their offspring at the age of 8 years, and twins completed the adult sensory profile at the age of 13 years. Parents completed the OCD module of the Diagnostic Interview Schedule for Children-IV when twins were 8 years; twins completed the same module at 13 years. Linear regression models tested for the concurrent and longitudinal associations between SOR and OCD controlling for socioeconomic status. RESULTS:Concurrently, participants' likelihood of exhibiting OCD symptoms increased with each symptom of tactile or auditory overresponsivity at 8 years and 13 years (odds ratio = 1.1-2.7). However, SOR measured at age 8 years was unrelated to adolescent OCD symptoms at 13 years and vice versa. CONCLUSION:SOR symptoms, although significantly related to concurrent OCD symptoms, do not appear to precede OCD symptoms, suggesting that SOR symptoms may reflect another type of OCD sensory phenomenon rather than a comorbid condition.
| S-EPMC6579637 | biostudies-literature
Project description:BackgroundThe relationships between obsessive-compulsive symptoms and distinct forms of impulsivity and compulsivity are unclear. Such examination would be relevant in terms of how best to classify psychiatric disorders and in understanding candidate 'traits' that extend across a continuum between normalcy and clinical disorders.Method515 young adults (aged 18-29years) completed the Padua Inventory and undertook detailed clinical and neurocognitive assessments. Relationships between obsessive-compulsive symptoms and distinct types of impulsivity and compulsivity were evaluated using linear regression modeling.ResultsObsessive-Compulsive symptoms were significantly predicted by female gender, lower quality of life, psychiatric disorders in general (but not impulse control disorders), and worse extra-dimensional set-shifting. Obsessive-Compulsive symptoms were not significantly predicted by alcohol/nicotine consumption, stop-signal reaction times, or decision-making abilities.ConclusionThese data indicate that obsessive-compulsive symptoms are more related to certain forms of compulsivity than to impulsivity. These findings have important implications for diagnostic conceptualizations and neurobiological models.
| S-EPMC5330431 | biostudies-literature
Project description:Aim: The network model suggests that the comorbidity of obsessive–compulsive disorder (OCD) and depression is due to direct interactions between OCD and depression symptoms. The study investigates the network structure of OCD and depressive symptoms in patients with OCD and explores the pathways that connect the OCD and depression symptoms. Materials and Methods: The items of Yale-Brown Obsessive–Compulsive Symptom (Y-BOCS) Scale and the Depression Self-Rating Scale of 445 patients with OCD were analyzed by network model. Statistical analysis and visualization of the network were conducted using R software. Results: Two bridge edges “uneasiness” and “time consumed by obsessions” and “low spirit” and “distress caused by obsessions” connected the OCD symptoms to depressive symptoms. Two closely related edges were between “interference due to obsessions” and “interference due to compulsions” and between “difficulty resisting obsessions” and “difficulty resisting compulsions.” The symptoms “interference due to compulsions,” “distress caused by obsessions,” “time consumed by compulsions,” and “uneasiness” had the highest expected influence centrality. Conclusions: This study highlighted the relationship between “uneasiness” and “time consumed by obsessions” and between “low spirit” and “distress caused by obsessions.” In addition, “interference due to compulsions” is found as the core symptom in the network. Targeting these symptoms may help prevent and treat the comorbidity of obsession–compulsion and depression in patients with OCD.
| S-EPMC10309257 | biostudies-literature
Project description:Obsessive-compulsive symptoms (OCS) in the population have been linked to obsessive-compulsive disorder (OCD) in genetic and epidemiological studies. Insulin signaling has been implicated in OCD. We extend previous work by assessing genetic overlap between OCD, population-based OCS, and central nervous system (CNS) and peripheral insulin signaling. We conducted genome-wide association studies (GWASs) in the population-based Philadelphia Neurodevelopmental Cohort (PNC, 650 children and adolescents) of the total OCS score and six OCS factors from an exploratory factor analysis of 22 questions. Subsequently, we performed polygenic risk score (PRS)-based analysis to assess shared genetic etiologies between clinical OCD (using GWAS data from the Psychiatric Genomics Consortium), the total OCS score and OCS factors. We then performed gene-set analyses with a set of OCD-linked genes centered around CNS insulin-regulated synaptic function and PRS-based analyses for five peripheral insulin signaling-related traits. For validation purposes, we explored data from the independent Spit for Science population cohort (5,047 children and adolescents). In the PNC, we found a significant shared genetic etiology between OCD and 'guilty taboo thoughts'. In the Spit for Science cohort, we additionally observed genetic sharing between 'symmetry/counting/ordering' and 'contamination/cleaning'. The CNS insulin-linked gene-set also associated with 'symmetry/counting/ordering' in the PNC. Further, we identified genetic sharing between peripheral insulin signaling-related traits: type 2 diabetes with 'aggressive taboo thoughts', and levels of fasting insulin and 2?h glucose with OCD. In conclusion, OCD, OCS in the population and insulin-related traits share genetic risk factors, indicating a common etiological mechanism underlying somatic and psychiatric disorders.
| S-EPMC7186226 | biostudies-literature
Project description:Purpose: The purpose of this study was to examine associations between postpartum obsessive-compulsive (OC) symptoms, infant care and feeding worries, and breastfeeding experiences in a sample of postpartum women. Materials and Methods: Women were recruited via an online U.S. research volunteer database and were eligible if they were aged 18-47 years, their primary language was English, they had an infant 2-6 months old, and tried breastfeeding the infant at least once. Participants completed a survey to assess breastfeeding experiences and practices, OC symptoms and other mental health conditions, and demographics. Modified Poisson regression and linear regression were used to estimate associations between clinically elevated OC symptoms, reported thoughts or worries about infant feeding and care, and breastfeeding experiences, problems, and duration. Results: Of 232 participants, 32 (14%) had clinically elevated OC symptoms. These women had more perinatal OC symptoms (scoring 3.6 points higher on perinatal OC symptoms score [95% confidence interval {CI}: 0.4 to 6.9]), including symptoms specific to infant care and feeding [e.g., adjusted relative risk(repeated washing of baby's bottles, bowl, or plate) = 2.37, 95% CI:1.55 to 3.64], and more breastfeeding problems (adjusted β = 0.3, 95% CI: 0.0 to 0.2) than women with fewer OC symptoms. However, they did not report an overall worse breastfeeding experience (adjusted β = 0.4, 95% CI: -9.3 to 10.1). Adjusted models controlled for depressive symptoms. Conclusions: Obsessive thoughts and compulsions were common in this sample and extended to infant feeding activities. These symptoms were associated with more breastfeeding problems. Interactions in mother-infant dyads are critical because of lasting impacts on parent-child relationships and child development. Treating OC symptoms may foster healthier mother-infant relationships.
| S-EPMC8972019 | biostudies-literature
Project description:We investigated whether obsessive-compulsive (OC) symptoms from a population-based sample could be analyzed to detect genetic variants influencing obsessive-compulsive disorder (OCD). We performed a genome-wide association studies (GWAS) on the obsession (rumination and impulsions) and compulsion (checking, washing, and ordering/precision) subscales of an abbreviated version of the Padua Inventory (N = 8,267 with genome-wide genotyping and phenotyping). The compulsion subscale showed a substantial and significant positive genetic correlation with an OCD case-control GWAS (r G = 0.61, p = .017) previously published by the Psychiatric Genomics Consortium (PGC-OCD). The obsession subscale and the total Padua score showed no significant genetic correlations (r G = -0.02 and r G = 0.42, respectively). A meta-analysis of the compulsive symptoms GWAS with the PGC-OCD revealed no genome-wide significant Single-Nucleotide Polymorphisms (SNPs combined N = 17,992, indicating that the power is still low for individual SNP effects). A gene-based association analysis, however, yielded two novel genes (WDR7 and ADCK1). The top 250 genes in the gene-based test also showed a significant increase in enrichment for psychiatric and brain-expressed genes. S-Predixcan testing showed that for genes expressed in hippocampus, amygdala, and caudate nucleus significance increased in the meta-analysis with compulsive symptoms compared to the original PGC-OCD GWAS. Thus, the inclusion of dimensional symptom data in genome-wide association on clinical case-control GWAS of OCD may be useful to find genes for OCD if the data are based on quantitative indices of compulsive behavior. SNP-level power increases were limited, but aggregate, gene-level analyses showed increased enrichment for brain-expressed genes related to psychiatric disorders, and increased association with gene expression in brain tissues with known emotional, reward processing, memory, and fear-formation functions.
| S-EPMC7317414 | biostudies-literature
Project description:ImportanceNeurobiological models have postulated shared neural mechanisms between obsessive-compulsive disorder (OCD) and substance use disorders, but results from clinical and epidemiological studies are conflicting or even suggest that OCD may be protective against substance misuse.ObjectiveTo investigate whether OCD and obsessive-compulsive symptoms are associated with substance misuse and the extent to which shared genetic and/or environmental factors account for this association.Design, setting, and participantsIn this cohort study, individuals in the general population of Sweden born between January 1, 1932, and December 31, 1997 (population cohort), were followed up through Swedish nationwide registers from January 1, 1997, to December 31, 2013. The second cohort included twin participants in the Child and Adolescent Twin Study in Sweden (CATSS) followed up from ages 18 to 24 years. Data were analyzed from March 1, 2021, to March 31, 2022.ExposuresLifetime International Statistical Classification of Diseases and Related Health Problems, Tenth Revision, diagnosis of OCD in the National Patient Register (population cohort 1), and self-reported obsessive-compulsive symptoms at 18 years of age (CATSS cohort).Main outcomes and measuresSubstance misuse was defined as registered substance use-related disorder, criminal conviction, or death (population cohort), and self-reported alcohol and drug dependence symptoms at 18 and 24 years of age (CATSS cohort).ResultsThe general population cohort included 6 304 188 individuals (48.9% women and 51.1% men; median baseline age, 30.5 [IQR, 15.0-46.4] years), of whom 27 342 had an OCD diagnosis. Obsessive-compulsive disorder was associated with an elevated risk of substance misuse (hazard ratio, 3.68 [95% CI, 3.52-3.85]). In the 9230 individuals in the CATSS cohort (5551 women [60.1%] and 3679 men [39.9%]), obsessive-compulsive symptoms at 18 years of age were associated with increased symptoms of alcohol dependence (concurrent [n = 9219], β = 0.18 [95% CI, 0.16-0.20]; longitudinal [n = 3381], β = 0.10 [95% CI, 0.06-0.14]) and drug dependence (concurrent [n = 749], β = 0.19 [95% CI, 0.11-0.27]; longitudinal [n = 452], β = 0.15 [95% CI, 0.04-0.25]). Comorbid anxiety and depression did not entirely explain the associations in either cohort. Using data from full siblings and maternal half-siblings (population cohort) and monozygotic and dizygotic twins (CATSS cohort) provided estimates of the relative contribution of genetic and environmental influences to the covariance between OCD and obsessive-compulsive symptoms and substance misuse or dependence. The associations were explained by genetic (56%-68%) and nonshared environmental (32%-44%) factors.Conclusions and relevanceThe findings of this Swedish population-based cohort study challenge the notion that OCD is protective against developing substance misuse. The association of OCD and obsessive-compulsive symptoms with substance misuse was largely explained by shared genetics but was also compatible with partial environmental mediation.
| S-EPMC9171556 | biostudies-literature
Project description:Astrocytes and neurons extensively interact in the brain. Identifying astrocyte and neuron proteomes is essential for elucidating the protein networks that dictate their respective contributions to physiology and disease. Here we used cell-specific and subcompartment-specific proximity-dependent biotinylation1 to study the proteomes of striatal astrocytes and neurons in vivo. We evaluated cytosolic and plasma membrane compartments for astrocytes and neurons to discover how these cells differ at the protein level in their signalling machinery. We also assessed subcellular compartments of astrocytes, including end feet and fine processes, to reveal their subproteomes and the molecular basis of essential astrocyte signalling and homeostatic functions. Notably, SAPAP3 (encoded by Dlgap3), which is associated with obsessive-compulsive disorder (OCD) and repetitive behaviours2-8, was detected at high levels in striatal astrocytes and was enriched within specific astrocyte subcompartments where it regulated actin cytoskeleton organization. Furthermore, genetic rescue experiments combined with behavioural analyses and molecular assessments in a mouse model of OCD4 lacking SAPAP3 revealed distinct contributions of astrocytic and neuronal SAPAP3 to repetitive and anxiety-related OCD-like phenotypes. Our data define how astrocytes and neurons differ at the protein level and in their major signalling pathways. Moreover, they reveal how astrocyte subproteomes vary between physiological subcompartments and how both astrocyte and neuronal SAPAP3 mechanisms contribute to OCD phenotypes in mice. Our data indicate that therapeutic strategies that target both astrocytes and neurons may be useful to explore in OCD and potentially other brain disorders.
| S-EPMC10132990 | biostudies-literature
Project description:Visual stimuli are often used for obsessive-compulsive (OC) symptom provocation in research studies. We tested the induction of anxiety and OC checking symptoms across different types of checking provocation stimuli in three populations: individuals with obsessive compulsive disorder (OCD), individuals with checking symptoms but without a diagnosis of OCD, and control individuals with neither checking symptoms nor a clinical diagnosis. One set of provocative images depicted objects that are commonly associated with checking anxiety. Another set ('enhanced provocative images') depicted similar objects but also included contextual cues suggesting a specific harmful scenario that could occur. As expected, the enhanced provocative images were more effective at inducing anxiety and OC symptoms than the standard provocative images. Future studies requiring checking symptom provocation should therefore consider incorporating similarly suggestive images. Individuals with clinical OCD reported the greatest provocation in response to these images, followed by those with nonclinical checking, followed by control individuals. Thus, these stimuli are able to provoke OC checking symptoms and anxiety differentially across groups, with the intensity of provocation reflecting diagnostic status. All groups demonstrated a similar qualitative pattern of provocation across images. Finally, in all groups, reported anxiety closely tracked intrusive thoughts and checking urges.
| S-EPMC6063514 | biostudies-literature
Project description:BackgroundUntil recently, hoarding was considered an obsessive-compulsive symptom (OCS). However, current evidence suggests that these two phenotypes may be clinically, and perhaps etiologically, distinct. Both hoarding and OCS have a genetic etiology, but the degree of unique and shared genetic contributions to these phenotypes has not been well studied.MethodPrevalence rates were assessed for hoarding and OCS in a sample of adult twin pairs (n = 7906 twins) and their family members from The Netherlands Twin Register (total sample = 15,914). Using Mplus, genetic analyses using liability threshold models were conducted for both phenotypes, for their co-morbidity, and for specific hoarding symptoms (cluttering, discarding and acquiring).ResultsOf the total sample, 6.7% met criteria for clinically significant hoarding; endorsement of all three hoarding symptoms was > or = 79%. Men had slightly higher rates than women. Also, 5.7% met criteria for clinically significant OCS; rates were similar in males and females. Genetic factors accounted for 36% of the variance for hoarding and 40% of the variance for OCS. The genetic correlation between hoarding and OCS was 0.10. There was no evidence of sex-specific genetic contributions for hoarding or OCS. There was evidence for a genetic contribution to all hoarding symptom subtypes. Only cluttering showed evidence of a contribution from the shared environment.ConclusionsOCS and hoarding are common in this population-based sample, have prevalence rates similar to those previously reported, and show significant heritability. Genetic factors contributed to the co-morbidity of both traits, although the genetic correlation between them was low.
| S-EPMC4429876 | biostudies-literature