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Background Alcohol consumption contributes to excess morbidity and mortality in part through the development of alcohol-related medical conditions (AMCs, including alcoholic cardiomyopathy, hepatitis, cirrhosis, etc.). The current study aimed to clarify the extent to which risk for these outcomes differs as a function of socioeconomic position (SEP), as discrepancies could lead to exacerbated health disparities. Methods and findings We used longitudinal Swedish national registries to estimate the individual and joint associations between 2 SEP indicators, educational attainment and income level, and risk of AMC based on International Classification of Diseases codes, while controlling for other sociodemographic covariates and psychiatric illness. We conducted Cox proportional hazards models in sex-stratified analyses (N = 1,162,679 females and N = 1,196,659 males), beginning observation at age 40 with follow-up through December 2018, death, or emigration. By the end of follow-up, 4,253 (0.37%) females and 11,183 (0.93%) males had received an AMC registration, corresponding to overall AMC incidence rates among females and males of 2.01 and 5.20, respectively. In sex-stratified models adjusted for birth year, marital status, region of origin, internalizing and externalizing disorder registrations, and alcohol use disorder (AUD) registration, lower educational attainment was associated with higher risk of AMC in both females (hazard ratios [HRs] = 1.40 to 2.46 for low- and mid-level educational attainment across 0 to 15 years of observation) and males (HRs = 1.13 to 1.48). Likewise, risk of AMC was increased for those with lower income levels (females: HRs = 1.10 to 5.86; males: HRs = 1.07 to 6.41). In secondary analyses, we further adjusted for aggregate familial risk of AUD by including family genetic risk scores for AUD (FGRS.sub.AUD ), estimated using medical, pharmacy, and criminal registries in extended families, as covariates. While FGRS.sub.AUD were associated with risk of AMC in adjusted models (HR = 1.17 for females and HR = 1.21 for males), estimates for education and income level remained largely unchanged. Furthermore, FGRS.sub.AUD interacted with income level, but not education level, such that those at higher familial liability to AUD were more susceptible to the adverse effect of low income. Limitations of these analyses include the possibility of false negatives for psychiatric illness registrations, changes in income after age 40 that were not accounted for due to modeling restrictions, restriction to residents of a high-income country, and the inability to account for individual-level alcohol consumption using registry data. Conclusions Using comprehensive national registry data, these analyses demonstrate that individuals with lower levels of education and/or income are at higher risk of developing AMC. These associations persist even when accounting for a range of sociodemographic, psychiatric, and familial risk factors. Differences in risk could contribute to further health disparities, potentially warranting increased screening and prevention efforts in clinical and public health settings., Author(s): Alexis C. Edwards 1,*, Sara Larsson Lönn 2, Karen G. Chartier 1,3, Séverine Lannoy 1, Jan Sundquist 2,4,5, Kenneth S. Kendler 1, Kristina Sundquist 2,4,5 Introduction Excessive alcohol use [...]

Background Men with prostate cancer (PC) may experience significant psychosocial distress from physical symptoms, treatment side effects, or fear of recurrence. However, little is known about the long-term risk of anxiety disorders in men with PC. Methods A national cohort study was conducted of 180 189 men diagnosed with PC during 1998-2017 and 1 801 890 age-matched population-based control men in Sweden. Anxiety disorders were ascertained from nationwide outpatient and inpatient records through 2018. Cox regression was used to estimate hazard ratios (HRs) while adjusting for sociodemographic factors and prior psychiatric disorders. Subanalyses explored differences by PC treatment during 2005-2017. Results In 7.8 million person-years of follow-up, 94 387 (5%) men were diagnosed with anxiety disorders. Men with high-risk PC had a nearly 2-fold higher risk of anxiety disorders than control men without PC (adjusted HR = 1.96, 95% CI = 1.87 to 2.05). This risk was highest in the first 3 months after PC diagnosis (adjusted HR = 2.99, 95% CI = 2.49 to 3.59) but remained significantly elevated 10 or more years later (adjusted HR = 1.53, 95% CI = 1.35 to 1.74). Those treated only with androgen deprivation therapy (ADT) had the highest risk of anxiety disorders (adjusted HR = 2.08, 95% CI = 1.93 to 2.25). Men with low- or intermediate-risk PC had a modestly increased risk (adjusted HR = 1.39, 95% CI = 1.34 to 1.44). Conclusions In this large national cohort, men with PC had substantially increased risk of anxiety disorders, especially those with high-risk PC and treated only with ADT. Men with PC need close monitoring for timely detection and treatment of anxiety symptoms, particularly shortly after PC diagnosis. [ABSTRACT FROM AUTHOR]

Objectives: Experimental and small human studies have indicated that high total adiponectin levels have beneficial cardiometabolic effects. In contrast, however, high total adiponectin levels are also associated with higher all‐cause and cardiovascular mortality in thoroughly adjusted epidemiological studies. To gain further insight into these seemingly contradictory results, we report results on total adiponectin from the indigenous Melanesian population of Kitava, Trobriand Islands, Papua New Guinea, where an apparent absence of cardiometabolic disease has been previously reported. Methods: Fasting levels of serum total adiponectin were measured cross‐sectionally in ≥40‐year‐old Kitavans (n = 102) and Swedish controls matched for age and sex (n = 108). Multivariable linear regression was used for the analysis of associations with total adiponectin when controlled for group, sex, smoking, hypertension and/or type 2 diabetes, age, and body mass index. Results: Total adiponectin was lower for Kitavans compared to Swedish controls (Median [Mdn] 4.6 μg/mL, range 1.0–206 μg/mL and Mdn 9.7 μg/mL, range 3.1–104 μg/mL, respectively, r =.64, p <.001). Lower total adiponectin was associated with Kitavan group, male sex (only in Swedish controls), smoking (only in Kitavans and Swedish controls combined), younger age (not in Swedish controls), higher BMI, lower total, low‐density lipoprotein, high‐density lipoprotein (HDL) (only in Kitavans and Swedish controls combined), and non‐HDL cholesterol, and higher anti‐PC IgG (only in Kitavans and Swedish controls combined). Conclusion: Total adiponectin in Kitavans was significantly lower than in Swedish controls. [ABSTRACT FROM AUTHOR]

Background: Beneficial effects from practising a Paleolithic diet as compared to a diabetes diet on weight, waist circumference, satiety, leptin, HbA1c and glucose control in randomised controlled trial participants with type 2 diabetes could be due to lower leptin resistance. Support for this hypothesis comes from an in vitro experiment that showed that digested wheat gluten, which is excluded from a Paleolithic diet, inhibits leptin from binding to its receptor, thus indicating a possible dietary cause of leptin resistance. However, the clinical relevance of the latter finding is unclear since removal of enzyme activity from the gluten digest by heat treatment also abolished leptin binding inhibition. Assessment of leptin binding inhibition in vivo is possible by comparison of total leptin levels with those of 'biologically active' leptin bound to its receptor (bioLep). Objectives: To assess the effects of a Paleolithic diet compared to a diabetes diet on leptin binding inhibition and to replicate our in vitro study. Methods: BioLep and total leptin levels were measured in secondary analysis of fasting plasma samples from our open label random order three plus three-month long cross-over trial performed in 2005–2007, that compared a Paleolithic diet with a diabetes diet in participants with type 2 diabetes without insulin treatment (per protocol). BioLep was also measured in vitro for known recombinant leptin concentrations incubated with a series of concentrations of 10 kDa spin-filtered digested wheat gluten, with or without prior heat treatment, at 100ºC for 30 min and centrifugation. Results: There was no difference between diets when comparing differences between bioLep and total leptin levels and their ratio in the 13 participants, three women and 10 men, aged 52–74 years with a mean BMI of 30 kg/m2 and a mean diabetes duration of eight years. We found no carry-over or period effect for bioLep and total leptin. In vitro, wheat gluten digest inhibited leptin binding in a dose-dependent manner but not after heat treatment. Conclusions: We found no leptin binding inhibition after the Paleolithic or diabetes diet, possibly due to its abolishment from cooking-related heat treatment of wheat gluten. Trial registration: Registered on 14/02/2007 at ClinicalTrials.gov Identifier: NCT00435240. [ABSTRACT FROM AUTHOR]

Aims: To examine whether vulvovaginal candidiasis (VVC) precedes type 2 diabetes and to quantify the possible time period between VVC and subsequent diabetes. Material and Methods: We conducted a nationwide retrospective primary healthcare study including 1 838 929 women aged 35–65 years in Sweden (2007–2018). Cox regression models were used to examine associations between VVC and type 2 diabetes, while controlling for possible confounders. Propensity‐score‐weighted analysis was also conducted. Results: The incidence rate of diabetes per 1000 person‐years was 3.06 (95% confidence interval [CI] 3.05–3.08) in women without preceding VVC and 4.05 (95% CI 3.86–4.24) in women with preceding VVC. The incidence rate was particularly high in women aged 55 years and older with VVC: 9.56 (95% CI 8.01–11.11). Women with VVC had a hazard ratio (HR) of 1.41 (95% CI 1.28–1.55) for diabetes compared to women without VVC in the multivariable‐adjusted model. The corresponding HR was 1.63 (95% CI 1.53–1.74) in propensity‐score‐weighted analysis. Women with prior VVC also seemed to have a stronger risk of diabetes with older age, particularly after the age of 55 years. The mean (range) time between VVC and subsequent diabetes was 0.57 (0–2) years, depending on the age of the woman. Conclusion: We found temporal associations between VVC and diabetes. The findings demonstrate that the presence of VVC may indicate a future diagnosis of diabetes, especially in women aged 55 years and older. This knowledge could be valuable for clinicians when treating women with VVC. [ABSTRACT FROM AUTHOR]

A diet with low content of fermentable oligo-, di-, and monosaccharides and polyols (FODMAP) is established treatment for irritable bowel syndrome (IBS), with well-documented efficiency. A starch- and sucrose-reduced diet (SSRD) has shown similar promising effects. The primary aim of this randomized, non-inferiority study was to test SSRD against low FODMAP and compare the responder rates (RR = ∆Total IBS-SSS ≥ −50) to a 4-week dietary intervention of either diet. Secondary aims were to estimate responders of ≥100 score and 50% reduction; effects on extraintestinal symptoms; saturation; sugar craving; anthropometric parameters; and blood pressure. 155 IBS patients were randomized to SSRD (n = 77) or low FODMAP (n = 78) for 4 weeks, with a follow-up 5 months later without food restrictions. The questionnaires Rome IV, IBS-severity scoring system (IBS-SSS), and visual analog scale for IBS (VAS-IBS) were completed at baseline and after 2 and 4 weeks and 6 months. Weight, height, waist circumference, and blood pressures were measured. Comparisons were made within the groups and between changes in the two groups. There were no differences between groups at baseline. The responder rate of SSRD was non-inferior compared with low FODMAPs at week 2 (79.2% vs. 73.1%; p = 0.661;95% confidence interval (CI) = −20–7.2) and week 4 (79.2% vs. 78.2%; p = 1.000;95%CI = −14–12). Responder rate was still high when defined stricter. All gastrointestinal and extraintestinal symptoms were equally improved (p < 0.001 in most variables). SSRD rendered greater reductions in weight (p = 0.006), body mass index (BMI) (p = 0.005), and sugar craving (p = 0.05), whereas waist circumference and blood pressure were equally decreased. Weight and BMI were regained at follow-up. In the SSRD group, responders at 6 months still had lowered weight (−0.7 (−2.5–0.1) vs. 0.2 (−0.7–2.2) kg; p = 0.005) and BMI (−0.25 (−0.85–0.03) vs. 0.07 (−0.35–0.77) kg/m2; p = 0.009) compared with baseline in contrast to non-responders. Those who had tested both diets preferred SSRD (p = 0.032). In conclusion, a 4-week SSRD intervention was non-inferior to low FODMAP regarding responder rates of gastrointestinal IBS symptoms. Furthermore, strong reductions of extraintestinal symptoms were found in both groups, whereas reductions in weight, BMI, and sugar craving were most pronounced following SSRD. [ABSTRACT FROM AUTHOR]

Objective: There is growing interest in how peers' genotypes may influence health (i.e., peer social genetic effects). The authors sought to clarify the nature of peer social genetic effects on risk for drug use disorder, alcohol use disorder (AUD), major depression, and anxiety disorder. Method: Cox models were used with data from a population-based Swedish cohort (N=655,327). Outcomes were drug use disorder, AUD, major depression, and anxiety disorder registrations between ages 17 and 30 from medical, criminal, and pharmacy registries. The authors indexed peer social genetic effects with peers' family genetic risk scores (FGRSs) for the same disorders, which are personalized measures of genetic risk inferred from diagnoses in first- to fifth-degree relatives. Results: Across disorders, peer FGRSs predicted increased risks of proband registration (hazard ratio range, 1.01–1.59), with stronger effects for drug use disorder and AUD than for major depression and anxiety disorder. Peer social genetic effects were stronger for school classmates than for geographically proximal peers, and for peers from upper secondary school (ages 16–19) versus peers from lower secondary school (ages 7–16). Peer social genetic effects remained significant following statistical control for sociodemographic confounders, whether peers were affected, and peers' FGRS for educational attainment. Peer social genetic effects were more pronounced for probands at higher genetic risk. Conclusions: The genetic makeup of adolescents' peers has long-reaching consequences on risks for drug use disorder, AUD, major depression, and anxiety disorder. Individuals at high genetic risk are more sensitive to social genetic effects. Alternative hypotheses such as sociodemographic stratification, exposure to affected peers, and genetic predispositions for educational attainment did not explain the risk associated with peer social genetic effects for substance use and psychiatric disorders. [ABSTRACT FROM AUTHOR]

Background: There is increasing evidence implicating hemoglobin/heme and their scavengers in oxidative stress-mediated pathologies, but information is limited in abdominal aortic aneurysm (AAA). Methods and results: In this case-control study, we assessed heme/heme-related markers in 142 men with AAA and 279 men with a normal aortic diameter consecutively recruited from an ultrasound screening program in Sweden. Enzyme-linked immunosorbent assays (ELISAs) were used to measure heme oxygenase-1 (HO-1) and hemopexin (Hpx) plasma levels, colorimetric assays for cell-free heme and whole blood hemoglobin (Hb) levels, and droplet digital PCR (ddPCR) and real-time PCR to determine haptoglobin (Hp) (pheno)type and genotype, respectively. Hpx and heme plasma levels at baseline were elevated, while HO-1 levels were lower in men with AAA (p < 0.001) and were significantly associated with AAA prevalence independently of potential confounders. A combination of heme and HO-1 showed the best diagnostic potential based on the area under the curve (AUC): 0.76, sensitivity: 80%, specificity: 48%. Additionally, when previously described inflammatory biomarker interleukin-6 (IL-6), was added to our model it significantly improved the diagnostic value (AUC: 0.87, sensitivity: 80%, specificity: 79%) compared to IL-6 alone (AUC: 0.73, sensitivity: 80%, specificity: 49%). Finally, Hb (positively) and Hpx (negatively) levels at baseline were associated with AAA growth rate (mm/year), and their combination showed the best prognostic value for discriminating fast and slow-growing AAA (AUC: 0.76, sensitivity: 80%, specificity: 62%). Conclusions: This study reports the distinct disruption of heme and related markers in both the development and progression of AAA, underscoring their potential in aiding risk stratification and therapeutic strategies. [ABSTRACT FROM AUTHOR]

Background: The concept of schizotypal personality disorder (SPD) emerged from observations of personality characteristics common in relatives of schizophrenic patients. While often studied in family designs, few studies and none with genetic measures, have examined SPD in epidemiological samples. Methods: We studied individuals born in Sweden 1940–2000 with an ICD-10 diagnosis of SPD with no prior schizophrenia (SZ) diagnosis (n = 2292). Demographic features, patterns of comorbidity, and Family Genetic Risk Scores (FGRS) were assessed from multiple Swedish registries. Prediction of progression to SZ was assessed by Cox models. Results: SPD was rare, with a prevalence of 0.044%, and had high levels of comorbidity with autism spectrum disorder (ASD), OCD, ADHD, and major depression (MD), and increased rates of being single, unemployed and in receipt of welfare. Affected individuals had elevated levels of FGRS for SZ (+0.42), ASD (+0.30), MD (+0.29), and ADHD (+0.20). Compared to cases of schizophrenia, they had significantly lower rates of FGRSSZ, but significantly elevated rates of genetic risk for ASD, MD, and ADHD. Over a mean follow-up of 8.7 years, 14.6% of SPD cases received a first diagnosis of SZ, the risk for which was significantly increased by levels of FGRSSZ, male sex, young age at SPD diagnosis and an in-patient SPD diagnosis and significantly decreased by comorbidity with MD, ASD, and ADHD. Conclusions: Our results not only support the designation of SPD as a schizophrenia spectrum disorder but also suggest potentially important etiologic links between SPD and ASD and, to a lesser extent, ADHD, OCD, and MD. [ABSTRACT FROM AUTHOR]

Background: Pain is associated with falls, disability and a poor quality of life among older adults. It is highly prevalent in many societies, and studies have shown that pain could be preventable or managed more effectively at the population level. However, few studies have investigated who is at higher risk of pain in the general population, which is important for development of effective interventions. The purpose of this study was to investigate, by using nationally representative samples in Sweden, whether neighbourhood socioeconomic status (SES) is associated with pain among older adults after considering other important risk factors. Methods: The study used the Statistics on Income and Living Conditions (EU‐SILC), which is a nationwide annual survey of the living conditions of residents in Sweden. We used the data of individuals who were over 65 years of age between 2008 and 2013. Multivariable logistic regression was conducted to investigate the association between neighbourhood SES and severe pain. Results: Those who resided in low SES neighbourhoods had a 30% higher odds of having severe pain than those who resided in high SES neighbourhoods after controlling for individual risk factors, such as the sex, age, individual SES, smoking, exercise habits and body mass index. Exercise was protective against severe pain. Conclusion: Given the high prevalence of pain across populations, interventions targeting geographic areas (such as those in the current study) in combination with individual risk factors could be effective to reduce the burden of pain at the population level. Significance: Those who reside in neighbourhoods with low SES may have higher risks of pain due to a lack of health‐promoting resources as well as psychological stress. Further studies identifying the specific mechanisms behind the association between neighbourhood SES and pain would be useful in order to develop effective interventions. [ABSTRACT FROM AUTHOR]

Background: One potential cause of comorbidity is the direct causal effect of one disorder – A – on risk for subsequent onset of disorder B. Could genetic risk scores be utilized to test for such an effect? If disorder A causally impacts on risk for disorder B, then genetic risk for disorder A should be lower in cases of disorder A with v. without a prior onset of B. Methods: In all individuals (n = 905 736) born in Sweden from 1980 to 1990, from six psychiatric and drug use disorders (major depression, anxiety disorders, alcohol use disorder, drug use disorder, bipolar disorder, and schizophrenia), we formed 14 pairs of disorders A and B. In these pairs, we compared, using Cox proportional hazards models, the predictive effect of the familial-genetic risk score (FGRS) for disorder B in those who had v. had not had a prior onset of disorder A. Results: In all pairs, the impact of the FGRS for disorder B was significantly stronger in cases without v. with a prior history of disorder A. These effects were similar across sex, stable across levels of FGRS and not likely due to clinician bias. In many of our disorder pairs, previous clinical studies suggest a mechanism for a causal effect of disorder A on B. Conclusions: Our findings provide indirect evidence that the occurrence of one psychiatric or substance use disorder often has a causal effect on risk for subsequent disorders. This mechanism may substantially contribute to the widespread comorbidity among psychiatric conditions. [ABSTRACT FROM AUTHOR]

Background: To determine whether genetic risk factors for major depression (MD) and alcohol use disorder (AUD) interact with a potent stressor – death of spouse, parent, and sibling – in predicting episodes of, respectively, MD and AUD. Methods: MD and AUD registrations were assessed from national Swedish registries. In individuals born in Sweden 1960–1970, we identified 7586, 388 459, and 34 370 with the loss of, respectively, a spouse, parent, and sibling. We started following subjects at age 18 or the year 2002 with end of follow-up in 2018. We examined time to event – a registration for MD within 6 months or AUD within a year – on an additive scale, using the Nelson–Aalen estimator. Genetic risk was assessed by the Family Genetic Risk Score (FGRS). Results: In separate models controlling for the main effects of death of spouse, parent, and sibling, FGRS, and sex, significant interactions were seen in all analyses between genetic risk for MD and death of relative in prediction of subsequent MD registration. A similar pattern of results, albeit with weaker interaction effects, was seen for genetic risk for AUD and risk for AUD registration. Genetic risk for bipolar disorder (BD) and anxiety disorders (AD) also interacted with event exposure in predicting MD. Conclusions: Genetic risk for both MD and AUD act in part by increasing the sensitivity of individuals to the pathogenic effects of environmental stressors. For prediction of MD, similar effects are also seen for genetic risk for AD and BD. [ABSTRACT FROM AUTHOR]

Background: Prior research has reported an association between divorce and suicide attempt. We aimed to clarify this complex relationship, considering sex differences, temporal factors, and underlying etiologic pathways. Methods: We used Swedish longitudinal national registry data for a cohort born 1960–1990 that was registered as married between 1978 and 2018 (N = 1 601 075). We used Cox proportional hazards models to estimate the association between divorce and suicide attempt. To assess whether observed associations were attributable to familial confounders or potentially causal in nature, we conducted co-relative analyses. Results: In the overall sample and in sex-stratified analyses, divorce was associated with increased risk of suicide attempt (adjusted hazard ratios [HRs] 1.66–1.77). Risk was highest in the year immediately following divorce (HRs 2.20–2.91) and declined thereafter, but remained elevated 5 or more years later (HRs 1.41–1.51). Divorcees from shorter marriages were at higher risk for suicide attempt than those from longer marriages (HRs 3.33–3.40 and 1.20–1.36, respectively). In general, HRs were higher for divorced females than for divorced males. Co-relative analyses suggested that familial confounders and a causal pathway contribute to the observed associations. Conclusions: The association between divorce and risk of suicide attempt is complex, varying as a function of sex and time-related variables. Given evidence that the observed association is due in part to a causal pathway from divorce to suicide attempt, intervention or prevention efforts, such as behavioral therapy, could be most effective early in the divorce process, and in particular among females and those whose marriages were of short duration. [ABSTRACT FROM AUTHOR]

Background A diagnosis of prostate cancer (PC) may cause psychosocial distress not only in a man but also in his intimate partner. However, long-term risks of depression, anxiety, or suicide in partners of men with PC are largely unknown. Methods A national cohort study was conducted of 121 530 partners of men diagnosed with PC during 1998-2017 and 1 093 304 population-based controls in Sweden. Major depression, anxiety disorder, and suicide death were ascertained through 2018. Cox regression was used to compute hazard ratios (HRs) while adjusting for sociodemographic factors. Results Partners of men with high-risk PC had increased risks of major depression (adjusted HR = 1.34, 95% confidence interval [CI] = 1.30 to 1.39) and anxiety disorder (adjusted HR = 1.25, 95% CI = 1.20 to 1.30), which remained elevated 10 or more years later. Suicide death was increased in partners of men with distant metastases (adjusted HR = 2.38, 95% CI = 1.08 to 5.22) but not other high-risk PC (adjusted HR =1.14, 95% CI = 0.70 to 1.88). Among partners of men with high-risk PC, risks of major depression and anxiety disorder were highest among those 80 years of age or older (adjusted HR = 1.73; 95% CI = 1.53 to 1.96; adjusted HR = 1.70, 95% CI = 1.47 to 1.96, respectively), whereas suicide death was highest among those younger than 60 years of age (adjusted HR = 7.55, 95% CI = 2.20 to 25.89). In contrast, partners of men with low- or intermediate-risk PC had modestly or no increased risks of these outcomes. Conclusions In this large cohort, partners of men with high-risk PC had increased risks of major depression and anxiety disorder, which persisted for 10 or more years. Suicide death was increased 2-fold in partners of men with distant metastases. Partners as well as men with PC need psychosocial support and close follow-up for psychosocial distress. [ABSTRACT FROM AUTHOR]

Patients with bipolar disorder have higher rates of type 2 diabetes (T2D) compared to the general population. Neighbourhood deprivation is associated with T2D and bipolar disorder. The aim of this study was to explore the potential effect of neighbourhood deprivation on incident T2D in patients with bipolar disorder. This nationwide open cohort study (1997–2018) included adults in Sweden ≥20 years with bipolar disorder (90,780 patients) to examine the subsequent risk of T2D. The association between neighbourhood deprivation and T2D was explored using Cox regression analysis, with hazard ratios (HRs) and 95% confidence intervals (95% CIs). All models were conducted in both men and women and adjusted for individual‐level sociodemographic factors and comorbidities. Neighbourhood deprivation was significantly associated with T2D in patients with bipolar disorder. The HRs were 1.61 (95% CI 1.40–1.86) for men and 1.83 (1.60–2.10) for women living in high deprivation neighbourhoods compared to those from low deprivation neighbourhoods. After adjustment, these results remained significant: 1.35 (1.17–1.56) in men and 1.39 (1.20–1.60) in women living in high deprivation neighbourhoods. The suggested graded association of higher incident T2D among patients with bipolar disorder, observed when levels of neighbourhood deprivation increased, raises important clinical and public health concerns. The results may help develop a contextual approach to prevention of T2D in patients with bipolar disorder that includes the neighbourhood environment. [ABSTRACT FROM AUTHOR]