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Background People with severe mental illness (SMI) have an elevated risk of obesity but the causes and mechanisms are unclear. We explored the familial association between parental SMI and body mass index (BMI) in middle-aged offspring. Our objective was to determine if the offspring of either parent with SMI have an increased risk for obesity. Methods The Northern Finland Birth Cohort 1966 is a cohort study of offspring with expected date of birth in 1966. The data include originally 12 068 mothers and 12 231 children from the provinces of Lapland and Oulu in Finland. The final study sample included 5050 middle-aged offspring. Parental SMI was used as exposure in the study. BMI measured at the age of 46 years was used as a primary outcome. Results Risk for obesity was elevated in the offspring of mothers with SMI [overweight: adjusted odds ratio (OR) 1.93 (1.29–2.90), obese class I: 1.97 (1.20–3.25), obese classes II–III: 2.98 (1.67–5.33)]. For the offspring of either parent with SMI, statistically significant results were found in obese class I and obese classes II–III [overweight: adjusted OR 1.21 (0.94–1.54), obese class I: 1.52 (1.03–1.08), obese classes II–III: 1.53 (1.01–2.32)]. Conclusions We found an elevated risk of obesity in the middle-aged offspring of either parent with SMI, especially in the offspring of mothers with SMI. Thus, there might be a common familial pathway leading to the co-occurrence of obesity and SMI.

Objective: The elevated prevalence of cardiometabolic disorders is consistently reported in patients with severe mental illness (SMI). We explored the association between parental SMI and offspring cardiometabolic morbidity. Our hypothesis was that offspring of people with SMI have increased morbidity risk. Method: The Northern Finland Birth Cohort 1966 is a study of offspring whose date of birth was expected in 1966. The follow-up lasted until 2015 (49 years). The final study sample included 11,175 children. We used parental SMI as the exposure in the study. The following cardiometabolic disorders were used as outcome measures: diabetes mellitus, hypertension, hyperlipidemia, coronary artery disease, obesity, and cerebrovascular disorders. Results: There were 139 (14.7%; hazard ratios [HR] = 1.63; 95% confidence interval [CI] = 1.36–1.94) children of parents with SMI who developed cardiometabolic disorder during follow-up and 957 (9.4%) in the comparison cohort. Statistically significant HRs were found in males (HR = 1.95; 95% CI =1.56–2.44), but not in females (HR = 1.29; 95% CI = 0.96–1.73). Conclusions: Having a cardiometabolic disorder was associated with male offspring of parents with SMI. Our findings suggest that there is an elevated risk of coronary artery disease, hyperlipidemia, obesity, and hypertension in the male offspring of parents with SMI. Our results suggest that the somatic health of offspring of parents with SMI should also be considered in addition to their mental health in clinical practice.

PurposeThe lifespan of people with severe mental illness (SMI) is shorter compared to the general population. There might be common familial pathway leading to a high co-occurrence of somatic disorders and SMI. To study this we explored the long-term mortality for natural causes in the offspring of people with SMI.MethodsParticipants were members of the Northern Finland Birth Cohort 1966 (NFBC1966;N = 11,325). The data on cause of deaths of the members were obtained from the Population Register Center until year 2015. The data on hospital-treated psychiatric disorders of parents were obtained from nationwide Care Register for Health Care. Cumulative incidences by age were calculated in the NFBC1966 members having a parent with SMI and those who did not have. We were able to take into account multiple confounders.ResultsOf the total sample of 11,325 offspring, 853 (7.4%) died during the follow-up period, 74 (8.7%) from the study cohort and 779 (91.3%) from the comparison group. These numbers included 160 stillborn children. There were 557 cases of deaths from diseases and medical conditions and 296 deaths from external causes. The adjusted risk ratio for offspring of mothers with SMI was 1.08 (0.72–1.64), and for offspring of fathers with SMI 0.58 (0.36–0.93).ConclusionsThis was the first long-term follow-up study (up to age 49) of all-cause mortality in offspring of parents with SMI. Our findings were contrary to expectations. Offspring of parents with SMI had no increased risk for dying. In fact, the risk for dying in the group of offspring of fathers with SMI was lower than in the comparison group. This study does not support the assumption of common familial pathway leading to a high co-occurrence of somatic disorders and SMI.

This is the first study to assess antiviral activity against human influenza virus A/Aichi/2/68 and bird influenza virus A/chicken/Kurgan/05/2005 and phytochemical characteristics of an ethanol extract of Cacalia hastata L. from wild populations growing in the vicinity of Tomsk, Russia (mixed forest). A log10 neutralization index—an indicator of inhibition of virus replication by the extract from C. hastata leaves—was ≤2 lg for each influenza virus. The extract reduced the infectivity of the human influenza virus by 1.5-fold and that of the avian influenza virus by 1.7-fold. The phytochemical characterization of C. hastata (its various organs) showed that the largest amount of the tested biologically active substances is present in leaves and rhizomes.

Background The prevalence of obesity is increasing public health problem with significant costs. Elevated risk for obesity is reported in patients with severe mental illness. People with obesity have an increased risk for a number of common medical conditions, including type 2 diabetes, cardiovascular disease, coronary heart disease, dyslipidemia and hypertension. The increased physical illness may be associated with unhealthy lifestyles such as smoking, substance use, often with inadequate access to health services. Still, very is known about the comorbidity of SMI and obesity in families. We explored the association between parental severe mental illness and BMI in middle-aged offspring. Our hypothesis was that offspring of people with severe mental illness have increased risk for obesity. Methods The Northern Finland Birth Cohort 1966 is cohort study of offspring with expected date of birth in 1966. The final study sample included 5,467 middle-aged offspring. We used parental severe mental illness as exposure in the study. BMI measured.at the age of 46 years was classified in for categories: underweight (BMI below 18.5), normal range (BMI 18.5–24.9), overweight (BMI 25.0–29.9), obese class I (BMI 30.0–34.9) and obese class II-III (BMI 35 or more). We used mothers’ marital status, smoking, educational level and offspring’ place of birth as confounders. Results Risk for obesity was elevated in offspring of mothers with SMI (overweight: adjusted OR 1.81 (1.25–2.63), obese class I: 1.71 (1.08–2.73), obese class II-III: 2.36 (1.35–4.13)). For offspring of fathers with SMI the results were not statistically significant (overweight: adjusted OR 0.94 (0.70–1.26), obese class I: 1.42 (1.00–2.00), obese class II-III: 0.89 (0.51–1.56)). Discussion According to our knowledge, this is the first study of BMI in adult offspring of parents with severe mental illness. We found an elevated risk of obesity in the middle-aged offspring of mothers with SMI. The findings support our hypothesis of higher morbidity from obesity in offspring of parents with SMI. We found an elevated risk of substantially increased BMI in the middle-aged offspring of mothers with SMI. However, we did not find elevated risk of increased BMI in the middle-aged offspring of fathers with SMI and when examining the offspring of either parent with SMI. This means that there might be a common familial pathway leading to co-occurrence of obesity and SMI.