Objective Comorbid mental disorders in anorexia nervosa during long‐term course require detailed studies. Method This matched cohort study was based on nationwide Danish register data of all patients born 1961–2008 with a first‐time ICD‐10 diagnosis of anorexia nervosa (AN) between 1994 and 2018 at age 8–32 and matched controls taken from all individuals without an eating disorder (ED). For nine categories of non‐eating mental disorders, time from date of first AN‐diagnosis (inclusion date) to time of first diagnosis, accounting for censoring, was studied by use of time‐stratified Cox models. Results A total of 9,985 patients with AN (93.5% females) and 49,351 matched controls were followed for a median (IQR) of 9.0 (4.4–15.7) years. For patients, there was about 25% and 55% risk of receiving any non‐ED disorder during the first 2 years and two decades after inclusion, respectively. A hazard ratio (HR) of seven for any non‐ED was found for the first 12 months after inclusion, a ratio that reduced to two at five or more years after inclusion. During the first years, large HRs ranging in 6–9 were found for affective, autism spectrum, personality, and obsessive–compulsive disorders with the latter displaying the highest continuous increased risk. The HR at 12 months after inclusion was highest for any non‐ED disorder and affective disorders in patients aged 8–13 at diagnosis. Discussion Comorbid mental disorders in AN are most frequently diagnosed in the first years after diagnosis of AN and on longer terms imply a double immediate risk.

Objective Familial and genetic factors seem to contribute to the development of depression but whether this varies with age at diagnosis remains unclear. We examined the influence of familial factors on the risk of depression by age at first diagnosis. Methods We included 23 498 monozygotic and 39 540 same‐sex dizygotic twins from the population‐based Danish Twin Registry, followed from 1977 through 2011 in nationwide registers. We used time‐to‐event analyses accounting for censoring and competing risk of death to estimate cumulative incidence, casewise concordance, relative recurrence risk, and heritability of first depression by age using monozygotic and same‐sex dizygotic twin pairs. Results During follow‐up, a total of 1545 twins were diagnosed with depression. For twins at age 35 or younger at first depression, heritability was estimated to be 24.8% (95% confidence interval [CI], 4.6–43.1%), whereas at age 90 it was 14.7% (95% CI, 3.1–26.3%). The relative recurrence risk was higher at younger ages: At age 35, the risk was 27.7‐fold (95% CI, 20.0–35.5) and 6.9‐fold (95% CI, 3.9–9.8) higher than the population risk for monozygotic and same‐sex dizygotic twins, respectively, while the corresponding numbers were 3.0 (95% CI, 2.3–3.6) and 1.8 (95% CI, 1.3–2.2) at age 90. Heritability seemed similar for male and female twins. Conclusion Familial risk of depression, caused either by genes or shared environment, seemed to slightly decrease with age at diagnosis and an elevated concordance risk for monozygotic over same‐sex dizygotic pairs suggested a genetic contribution to the development of depression.

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Objective To assess the risk of somatic diseases in connection with anorexia nervosa (AN). Method This matched cohort study was based on Danish registries of all patients born 1961–2008 with a first‐time diagnosis of AN in 1994–2018 at age 8–32 and matched controls without an eating disorder. For 13 somatic disease categories, time from inclusion date to time of first somatic diagnosis, accounting for censoring, was studied by use of time‐stratified Cox models. Results A total of 9985 AN patients born 1961–2008 and 49,351 controls were followed for a median (interquartile range) of 9.0 (4.4–15.7) years. During the first 2 years after entry there was a 60% higher hazard for any somatic disease among patients with AN than among controls, while the ratio from three to 11 years was reduced to 1.18. Regardless of age at diagnosis, the hazard among patients and controls were no different at approximately a decade after diagnosis of AN and the cumulative risk for patients for 12 of 13 disease categories was always higher or no less that for controls. For all disease categories, the hazard ratio (HR) was higher when close to entry. For most disease categories, age at diagnosis of AN did not modify the effect. Discussion While around 90% of all individuals had any somatic disease at the end of follow‐up, the cumulative incidence over time was higher for patients with AN than for controls. Large HRs were seen in the early years after diagnosis during which patients require extensive medical interventions. Public Significance Based on Danish registries, a large sample of almost 10,000 patients with AN born 1961–2008 and almost 50,000 matched controls were followed for a median of 9 years. While around 90% of all individuals had any somatic disease at the end of follow‐up, the cumulative incidence over time was higher for patients with AN than for controls.

Aim: Our aim was to explore whether familial factors influence the risk of ischemic heart disease, stroke, and their co-occurrence. Methods: In total, 23,498 monozygotic and 39,540 same-sex dizygotic twins from the Danish Twin Registry were followed from 1977 to 2011 in the Danish National Patient Registry for ischemic heart disease and stroke. Time-to-event analyses accounting for censoring and competing risk of death were used to estimate familial risk (casewise concordance relative to the cumulative incidence) and heritability of ischemic heart disease, stroke, and the co-occurrence by age. Results: During follow-up, we observed 5561 and 4186 twin individuals with ischemic heart disease and stroke respectively, with 936 twin pairs concordant for ischemic heart disease and stroke. Familial risks were significant for both, with higher cumulative risks in monozygotic than in dizygotic twins. Estimates for heritability were significant for ischemic heart disease as well as for stroke diagnosed after the age of 80. The casewise concordance of ischemic heart disease in twins whose co-twin was diagnosed with stroke did not differ for monozygotic and dizygotic twins; however, from age 55 it was 10% higher than the cumulative risk in the overall twin cohort and was 25% higher at age 90. A similar pattern was seen for stroke following the co-twin’s ischemic heart disease. Conclusions: As in previous studies, we found a higher heritability of ischemic heart disease than of stroke. There was a significant familial risk but no heritability for the co-occurrence of ischemic heart disease and stroke. The co-occurrence is therefore likely due to other shared familial than genetic factors, highlighting that preventive initiatives should target families rather than individuals.