There is an extensive body of literature linking ADHD to overweight and obesity. Research indicates that impulsivity features of ADHD account for a degree of this overlap. The neural and polygenic ...correlates of this association have not been thoroughly examined. In participants of the IMAGEN study, we found that impulsivity symptoms and body mass index (BMI) were associated (r = 0.10, n = 874, p = 0.014 FWE corrected), as were their respective polygenic risk scores (PRS) (r = 0.17, n = 874, p = 6.5 × 10
FWE corrected). We then examined whether the phenotypes of impulsivity and BMI, and the PRS scores of ADHD and BMI, shared common associations with whole-brain grey matter and the Monetary Incentive Delay fMRI task, which associates with reward-related impulsivity. A sparse partial least squared analysis (sPLS) revealed a shared neural substrate that associated with both the phenotypes and PRS scores. In a last step, we conducted a bias corrected bootstrapped mediation analysis with the neural substrate score from the sPLS as the mediator. The ADHD PRS associated with impulsivity symptoms (b = 0.006, 90% CIs = 0.001, 0.019) and BMI (b = 0.009, 90% CIs = 0.001, 0.025) via the neuroimaging substrate. The BMI PRS associated with BMI (b = 0.014, 95% CIs = 0.003, 0.033) and impulsivity symptoms (b = 0.009, 90% CIs = 0.001, 0.025) via the neuroimaging substrate. A common neural substrate may (in part) underpin shared genetic liability for ADHD and BMI and the manifestation of their (observable) phenotypic association.
The association between attention-deficit/hyperactivity disorder (ADHD) and shorter height is unclear. This study examined the risk of shorter height in individuals with ADHD, and the influence of ...prenatal factors, ADHD medication, psychiatric comorbidity, socioeconomic factors, and familial liability.
We drew on Swedish National Registers for 2 different study designs. First, height data for 14,268 individuals with ADHD and 71,339 controls were stratified into 2 groups: (1) before stimulant treatment was introduced in Sweden, and (2) after stimulant treatment was introduced in Sweden. Second, we used a family-based design including 833,172 relatives without ADHD with different levels of relatedness to the individuals with ADHD and matched controls.
ADHD was associated with shorter height both before (below-average height: OR = 1.31, 95% CI = 1.22-1.41) and after (below-average height: OR = 1.21, 95% CI = 1.13-1.31) stimulants for ADHD were introduced in Sweden, and was of similar magnitude in both cohorts. The association between ADHD and shorter height attenuated after adjustment for prenatal factors, psychiatric disorders, and socioeconomic status. Relatives of individuals with ADHD had an increased risk of shorter height (below-average height in full siblings: OR = 1.14, 95% CI = 1.09-1.19; maternal half siblings: OR = 1.10, 95% CI = 1.01-1.20; paternal half siblings: OR = 1.15, 95% CI = 1.07-1.24, first full cousins: OR = 1.10, 95% CI = 1.08-1.12).
Our findings suggest that ADHD is associated with shorter height. On a population level, this association was present both before and after ADHD medications were available in Sweden. The association between ADHD and height was partly explained by prenatal factors, psychiatric comorbidity, low socioeconomic status, and a shared familial liability for ADHD.
Growing evidence suggests that ADHD, an early onset neurodevelopmental disorder, is associated with poor somatic health in adulthood. However, the mechanisms underlying these associations are poorly ...understood. Here, we tested whether ADHD polygenic risk scores (PRS) are associated with mid-to-late life somatic health in a general population sample. Furthermore, we explored whether potential associations were moderated and mediated by life-course risk factors. We derived ADHD-PRS in 10,645 Swedish twins born between 1911 and 1958. Sixteen cardiometabolic, autoimmune/inflammatory, and neurological health conditions were evaluated using self-report (age range at measure 42-88 years) and clinical diagnoses defined by International Classification of Diseases codes in national registers. We estimated associations of ADHD-PRS with somatic outcomes using generalized estimating equations, and tested moderation and mediation of these associations by four life-course risk factors (education level, body mass index BMI, tobacco use, alcohol misuse). Results showed that higher ADHD-PRS were associated with increased risk of seven somatic outcomes (heart failure, cerebro- and peripheral vascular disease, obesity, type 1 diabetes, rheumatoid arthritis, and migraine) with odds ratios ranging 1.07 to 1.20. We observed significant mediation effects by education, BMI, tobacco use, and alcohol misuse, primarily for associations of ADHD-PRS with cardiometabolic outcomes. No moderation effects survived multiple testing correction. Our findings suggests that higher ADHD genetic liability confers a modest risk increase for several somatic health problems in mid-to-late life, particularly in the cardiometabolic domain. These associations were observable in the general population, even in the absence of medical treatment for ADHD, and appear to be in part mediated by life-course risk factors.
Psychiatric disorders are common among autistic children and adults. Little is known about sex differences in psychiatric disorders and hospitalization in early adulthood.
To examine sex differences ...in psychiatric diagnoses and hospitalizations in autistic compared with nonautistic young adults.
This population-based cohort study assessed all individuals born in Sweden between 1985 and 1997. A total of 1 335 753 individuals, including 20 841 autistic individuals (7129 34.2% female individuals), were followed up from age 16 through 24 years between 2001 and 2013. Analysis took place between June 2021 and August 2022.
Autism was defined as having received at least 1 clinical diagnosis of autism based on the International Classification of Diseases.
The cumulative incidence of 11 psychiatric diagnoses up until age 25 years was estimated, and birth year-standardized risk difference was used to compare autistic female and male individuals directly. Sex-specific birth year-adjusted hazard ratios (HRs) with 95% CIs were calculated using Cox regression. Analyses were repeated for inpatient diagnoses to assess psychiatric hospitalization.
Of 1 335 753 individuals included in this study, 650 314 (48.7%) were assigned female at birth. Autism was clinically diagnosed in 20 841 individuals (1.6%; 7129 34.2% female) with a mean (SD) age of 16.1 (5.1) years (17.0 4.8 years in female individuals and 15.7 5.2 years in male individuals) for the first recorded autism diagnosis. For most disorders, autistic female individuals were at higher risk for psychiatric diagnoses and hospitalizations. By age 25 years, 77 of 100 autistic female individuals and 62 of 100 autistic male individuals received at least 1 psychiatric diagnosis. Statistically significant standardized risk differences were observed between autistic female and male individuals for any psychiatric disorder (-0.18; 95% CI, -0.26 to -0.10) and specifically for anxiety, depressive, and sleep disorders. Risk differences were larger among autistic than nonautistic individuals. Compared with nonautistic same-sex individuals, autistic female individuals (HR range 95% CI, 3.17 2.50-4.04.-20.78 18.48-23.37) and male individuals (HR range 95% CI, 2.98 2.75-3.23-18.52 17.07-20.08) were both at increased risk for all psychiatric diagnoses. Any psychiatric hospitalization was statistically significantly more common in autistic female individuals (32 of 100) compared with autistic male individuals (19 of 100). However, both autistic female and male individuals had a higher relative risk for psychiatric hospitalization compared with nonautistic female and male individuals for all disorders (female individuals: HR range 95% CI, 5.55 4.63-6.66-26.30 21.50-32.16; male individuals: HR range 95% CI, 3.79 3.22-4.45-29.36 24.04-35.87).
These findings highlight the need for profound mental health services among autistic young adults. Autistic female individuals, who experience more psychiatric difficulties at different levels of care, require increased clinical surveillance and support.
Attention-deficit/hyperactivity disorder (ADHD) and obesity are 2 frequent conditions that co-occur, which has implications for the management of both conditions. We hypothesized that ADHD symptoms ...predict BMI and vice versa from late childhood (10-12 years) up to early adulthood (20-22 years).
Participants were adolescents in the Netherlands (
= 2773, 52.5% male, mean age = 11 years at baseline, 5 waves up to mean age 22) from the Tracking Adolescents' Individual Lives Survey cohort. We examined bidirectional relationship between ADHD symptoms (hyperactivity/impulsivity and inattention) and BMI using the random intercept cross-lagged panel model. Time-varying covariates were pubertal status, stimulant use, depressive symptoms, and family functioning, and socioeconomic status was a time-invariant covariate.
We found a time-invariant association of BMI with hyperactivity and impulsivity, but not with inattention, which was slightly stronger in female adolescents (female:
= 0.102; male:
= 0.086,
< .05). No longitudinal direct effects were found between ADHD symptoms and BMI during this period.
Over the course of adolescence, the link between ADHD and BMI is stable and is predominantly with hyperactive and impulsive symptoms rather than inattention. There was no direct effect of ADHD symptoms on BMI increase nor of BMI on enhanced ADHD symptoms during this developmental period. The findings point to a shared genetic or familial background and/or potential causal effects established already earlier in childhood, thus suggesting that intervention and prevention programs targeting overweight and obesity in children with ADHD should be implemented in early childhood.
Post-traumatic stress disorder (PTSD) has been linked to violent crime in veteran populations. However, whether there is a link between PTSD and violent crime in the general population is not known. ...This study aimed to investigate the hypothesised association between PTSD and violent crime in the Swedish general population and to investigate the extent to which familial factors might explain this association using unaffected sibling control individuals.
This nationwide, register-based cohort study assessed individuals born in Sweden in 1958–93 for eligibility for inclusion. Individuals who died or emigrated before their 15th birthday, were adopted, were twins, or whose biological parents could not be identified were excluded. Participants were identified and included from the National Patient Register (1973–2013), the Multi-Generation Register (1932–2013), the Total Population Register (1947–2013), and the National Crime Register (1973–2013). Participants with PTSD were matched (1:10) with randomly selected control individuals from the population without PTSD by birth year, sex, and county of residence in the year of PTSD diagnosis for the matched individual. Each participant was followed up from the date of matching (ie, the index person's first PTSD diagnosis) until violent crime conviction or until being censored at emigration, death, or Dec 31, 2013, whichever occurred first. Stratified Cox regressions were used to estimate the hazard ratio of time to violent crime conviction ascertained from national registers in individuals with PTSD compared with control individuals. To account for familial confounding, sibling analyses were conducted, comparing the risk of violent crime in a subsample of individuals with PTSD with their unaffected full biological siblings.
Of 3 890 765 eligible individuals, 13 119 had a PTSD diagnosis (9856 75·1% of whom were female and 3263 24·9% of whom were male), were matched with 131 190 individuals who did not, and were included in the matched cohort. 9114 individuals with PTSD and 14 613 full biological siblings without PTSD were also included in the sibling cohort. In the sibling cohort, 6956 (76·3%) of 9114 participants were female and 2158 (23·7%) were male. Cumulative incidence of violent crime convictions after 5 years was 5·0% (95% CI 4·6–5·5) in individuals diagnosed with PTSD versus 0·7% (0·6–0·7) in individuals without PTSD. At the end of follow-up (median follow-up time 4·2 years, IQR 2·0–7·6), cumulative incidence was 13·5% (11·3–16·6) versus 2·3% (1·9–2·6). Individuals with PTSD had a significantly higher risk of violent crime than the matched control population in the fully-adjusted model (hazard ratio HR 6·4, 95% CI 5·7–7·2). In the sibling cohort, the risk of violent crime was also significantly higher in the siblings with PTSD (3·2, 2·6–4·0).
PTSD was associated with increased risk of violent crime conviction, even after controlling for familial effects shared by siblings and in the absence of SUD or a history of violent crime. Although our results might not be generalisable to less severe or undetected PTSD, our study could inform interventions that aim to reduce violent crime in this vulnerable population.
None.
Background
Attention‐deficit/hyperactivity disorder (ADHD) frequently co‐occurs with other psychiatric disorders. Twin studies have established that these co‐occurrences are in part due to shared ...genetic risks. However, the strength of these genetic overlaps and the potential heterogeneity accounted for by type of psychiatric symptoms, age, and methods of assessment remain unclear. We conducted a systematic review to fill this gap.
Methods
We searched PubMed, PsycINFO, Embase, and Web of Science until March 07, 2019. Genetic correlations (rg) were used as effect size measures.
Results
A total of 31 independent studies fulfilled the inclusion criteria. The pooled estimates showed that the associations between ADHD and other psychiatric symptoms were partly explained by shared genetic factors, with a pooled genetic correlation of 0.50, 95% confidence interval: 0.46–0.60. The genetic correlations (rg) between ADHD and externalizing (rg = .49 0.37–0.61), internalizing (rg = .50 0.39–0.69), and neurodevelopmental (rg = .56 0.47–0.66) symptoms were similar in magnitude. The genetic correlations in childhood and adulthood were rg = .53 (0.43–0.63) and rg = .51 (0.44–0.56), respectively. For methods of assessment, the genetic correlations were also similar in strength, self‐reports rg = .52 (0.47–0.58), other informants rg = .55 (0.41–0.69), and combined raters rg = .50 (0.33–0.65).
Conclusions
These findings indicate that the co‐occurrence of externalizing, internalizing, and neurodevelopmental disorder symptoms in individuals with ADHD symptoms in part is due to a shared genetic risk.
People with schizophrenia die prematurely, yet regional differences are unclear.
PRISMA 2020-compliant systematic review/random-effects meta-analysis of cohort studies assessing mortality relative ...risk (RR) versus any control group, and moderators, in people with ICD/DSM-defined schizophrenia, comparing countries and continents. We conducted subgroup, meta-regression analyses, and quality assessment. The primary outcome was all-cause mortality. Secondary outcomes were suicide-, /natural-cause- and other-cause-related mortality.
We included 135 studies from Europe (n = 70), North-America (n = 29), Asia (n = 33), Oceania (n = 2), Africa (n = 1). In incident plus prevalent schizophrenia, differences across continents emerged for all-cause mortality (highest in Africa, RR=5.98, 95 %C.I.=4.09–8.74, k = 1, lowest in North-America, RR=2.14, 95 %C.I.=1.92–2.38, k = 16), suicide (highest in Oceania, RR=13.5, 95 %C.I.=10.08–18.07, k = 1, lowest in North-America, RR=4.4, 95 %C.I.=4.07–4.76, k = 6), but not for natural-cause mortality. Europe had the largest association between antipsychotics and lower all-cause mortality/suicide (Asia had the smallest or no significant association, respectively), without differences for natural-cause mortality. Higher country socio-demographic index significantly moderated larger suicide-related and smaller natural-cause-related mortality risk in incident schizophrenia, with reversed associations in prevalent schizophrenia. Antipsychotics had a larger/smaller protective association in incident/prevalent schizophrenia regarding all-cause mortality, and smaller protective association for suicide-related mortality in prevalent schizophrenia. Additional regional differences emerged in incident schizophrenia, across countries, and secondary outcomes.
Significant regional differences emerged for all-cause, cause-specific and suicide-related mortality. Natural-cause death was homogeneously increased globally. Moderators differed across countries. Global initiatives are needed to improve physical health in people with schizophrenia, local studies to identify actionable moderators.
Accumulating evidence suggests a higher risk for cardiovascular diseases among individuals with mental disorders, but very little is known about the risk for overall and specific groups of ...cardiovascular diseases in people with attention‐deficit/hyperactivity disorder (ADHD). To fill this knowledge gap, we investigated the prospective associations between ADHD and a wide range of cardiovascular diseases in adults. In a nationwide population‐based cohort study, we identified 5,389,519 adults born between 1941 and 1983, without pre‐existing cardiovascular diseases, from Swedish registers. The study period was from January 1, 2001 to December 31, 2013. Incident cardiovascular disease events were identified according to ICD codes. Hazard ratios (HR) with 95% confidence intervals (CI) were calculated using Cox proportional hazards regression model, with ADHD as a time‐varying exposure. After an average 11.80 years of follow‐up, 38.05% of individuals with ADHD versus 23.57% of those without ADHD had at least one diagnosis of cardiovascular disease (p<0.0001). ADHD was significantly associated with increased risk of any cardiovascular disease (HR=2.05, 95% CI: 1.98‐2.13) after adjusting for sex and year of birth. Further adjustments for education level, birth country, type 2 diabetes mellitus, obesity, dyslipidemia, sleep problems and heavy smoking attenuated the association, which however remained significant (HR=1.84, 95% CI: 1.77‐1.91). Further adjustment for psychiatric comorbidities attenuated but could not fully explain the association (HR=1.65, 95% CI: 1.59‐1.71). The strongest associations were found for cardiac arrest (HR=2.28, 95% CI: 1.81‐2.87), hemorrhagic stroke (HR=2.16, 95% CI: 1.68‐2.77), and peripheral vascular disease/arteriosclerosis (HR=2.05, 95% CI: 1.76‐2.38). Stronger associations were observed in males and younger adults, while comparable associations were found among individuals with or without psychotropic medications and family history of cardiovascular diseases. These data suggest that ADHD is an independent risk factor for a wide range of cardiovascular diseases. They highlight the importance of carefully monitoring cardiovascular health and developing age‐appropriate and individualized strategies to reduce the cardiovascular risk in individuals with ADHD.
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