To examine antidepressant use before and after the diagnosis of diabetes.
This study was a longitudinal analysis of diabetic and nondiabetic groups selected from a prospective cohort study of 151,618 men and women in Finland (the Finnish Public Sector Study, 1995-2005). We analyzed the use of antidepressants in those 493 individuals who developed type 2 diabetes and their 2,450 matched nondiabetic control subjects for each year during a period covering 4 years before and 4 years after the diagnosis. For comparison, we undertook a corresponding analysis on 748 individuals who developed cancer and their 3,730 matched control subjects.
In multilevel longitudinal models, the odds ratio for antidepressant use in those who developed diabetes was 2.00 (95% CI 1.57-2.55) times greater than that in nondiabetic subjects. The relative difference in antidepressant use between these groups was similar before and after the diabetes diagnosis except for a temporary peak in antidepressant use at the year of the diagnosis (OR 2.66 [95% CI 1.94-3.65]). In incident cancer case subjects, antidepressant use substantially increased after the cancer diagnosis, demonstrating that our analysis was sensitive for detecting long-term changes in antidepressant trajectories when they existed.
Awareness of the diagnosis of type 2 diabetes may temporarily increase the risk of depressive symptoms. Further research is needed to determine whether more prevalent use of antidepressants noted before the diagnosis of diabetes relates to effects of depression, side effects of antidepressant use, or a common causal pathway for depression and diabetes.
Mental disorders have been associated with increased mortality, but the evidence is primarily based on hospital admissions for psychoses. The underlying mechanisms are unclear.
To investigate whether the risks of death associated with mental disorders diagnosed in young men are similar to those associated with admission for these disorders and to examine the role of confounding or mediating factors.
Prospective cohort study in which mental disorders were assessed by psychiatric interview during a medical examination on conscription for military service at a mean age of 18.3 years and data on psychiatric hospital admissions and mortality during a mean 22.6 years of follow-up were obtained from national registers.
A total of 1,095,338 men conscripted between 1969 and 1994.
All-cause mortality according to diagnoses of schizophrenia, other nonaffective psychoses, bipolar or depressive disorders, neurotic and adjustment disorders, personality disorders, and alcohol-related or other substance use disorders at conscription and on hospital admission.
Diagnosis of mental disorder at conscription or on hospital admission was associated with increased mortality. Age-adjusted hazard ratios according to diagnoses at conscription ranged from 1.81 (95% CI, 1.54-2.10) (depressive disorders) to 5.55 (95% CI, 1.79-17.2) (bipolar disorders). The equivalent figures according to hospital diagnoses ranged from 5.46 (95% CI, 5.06-5.89) (neurotic and adjustment disorders) to 11.2 (95% CI, 10.4-12.0) (other substance use disorders) in men born from 1951 to 1958 and increased in men born later. Adjustment for early-life socioeconomic status, body mass index, and blood pressure had little effect on these associations, but they were partially attenuated by adjustment for smoking, alcohol intake, intelligence, educational level, and late-life socioeconomic status. These associations were not primarily due to deaths from suicide.
The increased risk of premature death associated with mental disorder is not confined to those whose illness is severe enough for hospitalization or those with psychotic or substance use disorders.
Associations between body mass index (BMI) and attempted (nonfatal) suicide have recently been reported. However, the few existing studies are relatively small in scale, the majority cross-sectional, and results contradictory. The authors have explored BMI-attempted suicide associations in a large cohort of 1,133,019 Swedish men born between 1950 and 1976, with BMI measured in early adulthood. During a mean follow-up of 23.9 years, a total of 18,277 (1.6%) men had at least 1 hospital admission for attempted suicide. After adjustment for confounding factors, there was a stepwise, linear decrease in attempted suicide with increasing BMI across the full BMI range (per standard deviation increase in BMI, hazard ratio = 0.93, 95% confidence interval: 0.91, 0.94). Analyses excluding men with depression at baseline were essentially identical to those based on the complete cohort. In men free from depression at baseline, controlling for subsequent depression slightly attenuated the raised risk of attempted suicide, particularly in lower weight men. This study suggests that lower weight men have an increased risk of attempted suicide and that associations may extend into the "normal" BMI range.
RefSource: Am J Epidemiol. 2010 Oct 15;172(8):900-4; discussion 905-6
Studies have suggested both adverse and protective associations of obesity with depressive symptoms. We examined the contribution of environmental and heritable factors in this association. Participants were same-sex twin pairs from two population-based twin cohort studies, the Older Finnish Twin Cohort (n = 8,215; mean age = 44.1) and the US Midlife Development in the United States (MIDUS; n = 1,105; mean age = 45.1). Body mass index (BMI) was calculated from self-reported height and weight. Depressive symptoms were assessed using Beck's Depression Inventory (BDI; Finnish Twin Cohort), and by negative and positive affect scales (MIDUS). In the Finnish Twin Cohort, higher BMI was associated with higher depressive symptoms in monozygotic (MZ) twins (B = 2.01, 95% CI = 1.0, 3.0) and dizygotic (DZ) twins (B = 1.17, 0.5, 1.9) with BMI >22. This association was observed in within-pair analysis in DZ twins (B = 1.47, CI = 0.4, 2.6) but not in within-pair analysis of MZ twins (B = 0.03, CI = -1.9, 2.0). Consistent with the latter result, a bivariate genetic model indicated that the association between higher BMI and higher depressive symptoms was largely mediated by genetic factors. The results of twin-pair analysis and bivariate genetic model were replicated in the MIDUS sample. These findings suggest an association between obesity and higher depressive symptoms, which is largely explained by shared heritable biological mechanisms.
While recent studies have reported an inverse relation between childhood intelligence test scores and all-cause mortality in later life, the link with disease-specific outcomes has been rarely examined. Furthermore, the potential confounding effect of birthweight and childhood social circumstances is unknown. We investigated the relation of childhood intelligence with coronary heart disease (CHD) and stroke risk in a cohort of 6910 men born in 1953 in the Copenhagen area of Denmark. Events were ascertained from 1978 to 2000 using a cause-of-death register and hospital discharge records. There were 150 CHD (19 fatal; 131 non-fatal) and 93 stroke (4 fatal; 89 non-fatal) events during follow-up into mid-life. Childhood intelligence was inversely related to CHD with the highest rate apparent in adults with low childhood test scores (HR(lowest vs. highest quartile), 2.70; 95% confidence interval: 1.60, 4.57; P(trend) = 0.0001). After adjustment for paternal social class and birthweight, this association was attenuated only marginally. There was little evidence of a IQ-stroke relationship. The cognitive characteristics captured by IQ testing in the present study, such as communication and problem solving ability, appear to be associated with risk of CHD. Health promotion specialists and clinical practitioners may wish to consider these skills in their interactions with the general public. Replication of these results using studies which hold data on intelligence and socio-economic position across the life course is required.
Although low pre-morbid IQ is an established risk factor for severe mental illness, its association with personality disorder (PD) is unclear. We set out to examine whether there is a prospective association between childhood intelligence and PD in adulthood. Using a population-based prospective cohort study, we linked childhood IQ scores to routinely collected hospital discharge records in adulthood. Lower IQ scores were related to higher risk of being hospitalized with a PD across the full range of IQ scores, (odds ratio per one SD increase in IQ was 0.60; 95% CI: 0.49-0.75; p(trend) = 0.001). Adjusting for potential confounding variables had virtually no impact. We conclude that low childhood IQ predicts hospitalization with PD and may be an important factor in the development of PD.
Studies examining the relationship between early-life IQ and the risk of subsequent psychiatric disorder in adulthood are scarce. In the present investigation, the childhood IQ scores of 7022 singleton-born Danish males were linked to psychiatric hospital discharge records in adulthood. IQ scores were inversely related to the risk of total psychiatric illness, with the highest levels apparent in the lowest scoring IQ group (HRlowest quintile v. highest=1.70, 95% CI 1.34-2.14). Adjusting for paternal occupational social class and birth weight had only a small attenuating effect. Low childhood IQ may have an aetiological role in the development of adult total psychiatric disorder.
Work disability affects quality of life, earnings, and opportunities to contribute to society. Work characteristics, lifestyle and sociodemographic factors have been associated with the risk of work disability, but few multifactorial algorithms exist to identify individuals at risk of future work disability. We developed and validated a parsimonious multifactorial score for the prediction of work disability using individual-level data from 65,775 public-sector employees (development cohort) and 13,527 employed adults from a general population sample (validation cohort), both linked to records of work disability. Candidate predictors for work disability included sociodemographic (3 items), health status and lifestyle (38 items), and work-related (43 items) variables. A parsimonious model, explaining?>?99% of the variance of the full model, comprised 8 predictors: age, self-rated health, number of sickness absences in previous year, socioeconomic position, chronic illnesses, sleep problems, body mass index, and smoking. Discriminative ability of a score including these predictors was high: C-index 0.84 in the development and 0.83 in the validation cohort. The corresponding C-indices for a score constructed from work-related predictors (age, sex, socioeconomic position, job strain) were 0.79 and 0.78, respectively. It is possible to identify reliably individuals at high risk of work disability by using a rapidly-administered prediction score.
ErratumIn: Sci Rep. 2018 Nov 16;8(1):17224 PMID 30442992
More education is associated with healthier smoking and drinking behaviors. Most analyses of effects of education focus on mean levels. Few studies have compared variance in health-related behaviors at different levels of education or analyzed how education impacts underlying genetic and environmental sources of health-related behaviors. This study explored these influences. In a 2002 postal questionnaire, 21,522 members of the Danish Twin Registry, born during 1931-1982, reported smoking and drinking habits. The authors used quantitative genetic models to examine how these behaviors' genetic and environmental variances differed with level of education, adjusting for birth-year effects. As expected, more education was associated with less smoking, and average drinking levels were highest among the most educated. At 2 standard deviations above the mean educational level, variance in smoking and drinking was about one-third that among those at 2 standard deviations below, because fewer highly educated people reported high levels of smoking or drinking. Because shared environmental variance was particularly restricted, one explanation is that education created a culture that discouraged smoking and heavy drinking. Correlations between shared environmental influences on education and the health behaviors were substantial among the well-educated for smoking in both sexes and drinking in males, reinforcing this notion.
BACKGROUND: Greater education is associated with better physical health. This has been of great concern to public health officials. Most demonstrations show that education influences mean levels of health. Little is known about the influence of education on variance in health status, or about how this influence may impact the underlying genetic and environmental sources of health problems. This study explored these influences. METHODS: In a 2002 postal questionnaire, 21 522 members of same-sex pairs in the Danish Twin Registry born between 1931 and 1982 reported physical health in the 12-item Short Form Health Survey. We used quantitative genetic models to examine how genetic and environmental variance in physical health differed with level of education, adjusting for birth-year effects. RESULTS: and Conclusions As expected, greater education was associated with better physical health. Greater education was also associated with smaller variance in health status. In both sexes, 2 standard deviations (SDs) above mean educational level, variance in physical health was only about half that among those 2 SDs below. This was because fewer highly educated people reported poor health. There was less total variance in health primarily because there was less genetic variance. Education apparently reduced expression of genetic susceptibilities to poor health. The patterns of genetic and environmental correlations suggested that this might take place because more educated people manage their environments to protect their health. If so, fostering the personal charactieristics associated with educational attainment could be important in reducing the education-health gradient.