The varying burden of depressive symptoms across adulthood: Results from six NHANES cohorts.

BACKGROUND: Depressive symptoms differ from each other in the degree of functional impairment they cause. The incidence of depression varies across the adult lifespan. We examined whether age moderates the impairment caused by depressive symptoms. METHODS: The study sample (n = 21,056) was adults drawn from six multistage probability samples from the National Health and Nutrition Examination Survey series (NHANES, years 2005-2016) conducted in the United States using cross-sectional, representative cohorts. Depressive symptoms were assessed with the nine-item Patient Health Questionnaire (PHQ-9). We used regression models to predict high functional impairment, while controlling for sociodemographic variables and physical disorders. RESULTS: Age moderated the association between depressive symptoms and functional impairment: middle-aged adults perceived moderate and severe symptoms as more impairing than did others. Older adults reported slightly higher impairment due to mild symptoms. The individual symptoms of low mood, feelings of worthlessness and guilt, and concentration difficulties were more strongly related to high impairment in mid-adulthood as compared to early and late adulthood. LIMITATIONS: Cross-sectional data allows only between-person comparisons. The PHQ-9 is brief and joins compound symptoms into single items. There was no information available concerning comorbid mental disorders. Co-occurring physical disorders were self-reported. CONCLUSIONS: Symptoms of depression may imply varying levels of impairment at different ages. The results suggest a need for age adjustments when estimating the functional impact of depression in the general population. Additionally, they show a need for more accurate assessments of depression-related impairment at older ages. Evidence-based programs may generally benefit from symptom- and age-specific findings.

Education as a moderator of genetic risk for higher body mass index: prospective cohort study from childhood to adulthood.

OBJECTIVES: The life-course development of body mass index (BMI) may be driven by interactions between genes and obesity-inducing social environments. We examined whether lower parental or own education accentuates the genetic risk for higher BMI over the life course, and whether diet and physical activity account for the educational differences in genetic associations with BMI. SUBJECTS/METHODS: The study comprised 2441 participants (1319 women, 3-18 years at baseline) from the prospective, population-based Cardiovascular Risk in Young Finns Study. BMI (kg/m2) trajectories were calculated from 18 to 49 years, using data from six time points spanning 31 years. A polygenic risk score for BMI was calculated as a weighted sum of risk alleles in 97 single-nucleotide polymorphisms. Education was assessed via self-reports, measured prospectively from participants in adulthood and from parents when participants were children. Diet and physical activity were self-reported in adulthood. RESULTS: Mean BMI increased from 22.6 to 26.6 kg/m2 during the follow-up. In growth curve analyses, the genetic risk score was associated with faster BMI increase over time (b=0.02, (95% CI, 0.01-0.02, P<0.001)). The association between the genetic risk score and BMI was more pronounced among those with lower educational level in adulthood (b=-0.12 (95% CI, -0.23-0.01); P=0.036)). No interaction effect was observed between the genetic risk score and parental education (b=0.05 (95% CI, -0.09-0.18; P=0.51)). Diet and physical activity explained little of the interaction effect between the genetic risk score and adulthood education. CONCLUSIONS: In this prospective study, the association of a risk score of 97 genetic variants with BMI was stronger among those with low compared with high education. This suggests lower education in adulthood accentuates the risk of higher BMI in people at genetic risk.

Symptom severity and disability in psychiatric disorders: The U.S. Collaborative Psychiatric Epidemiology Survey.

BACKGROUND: While most psychiatric diagnoses are based on simple counts of symptoms, some symptoms may be sign of a more severe mental syndrome than others. This calls for validated estimates of the relative severity specific symptoms imply within a disorder. We focused on four diagnostic disorders: Manic Episode (ME), Major Depressive Episode (MDE), Post-traumatic Stress Disorder (PTSD) and Generalized Anxiety Disorder (GAD). Symptom-specific severity parameters were estimated, and validated by examining their association with levels of self-reported disability in daily activities over and above the number of symptoms. METHODS: Data from the cohort study of the U.S. Collaborative Psychiatric Epidemiology Surveys (CPES) was used, which comprises the National Comorbidity Survey Replication, National Survey of American Life, and the National Latino and Asian American Study. The four analytic datasets included respondents who endorsed disorder-specific pre-screening symptoms according to the World Mental Health Survey Initiative's version of the Composite International Diagnostic Interview. Disability was measured using the WHO Disability Assessment Schedule. Item Response Theory and Tobit models were implemented. RESULTS: For ME, PTSD, and GAD (not MDE) symptom severity based on psychometric Item Response Theory predicted disability outcomes after adjusting for symptom count. For PTSD, symptom count was not associated with disability. LIMITATIONS: The analytic sample for each psychiatric disorder was based on a pre-selection stemming from index criteria (e.g. sadness or pleasure loss for MDE), which implies that our results are only generalizable to those individuals at risk rather than for the entire population. Additionally, we acknowledge that the use of unidimensional models is only one of the several options to model psychopathological constructs. CONCLUSIONS: The same number of symptoms may be related to different levels of disability, depending on the specific symptoms from which the person suffers. Diagnostic procedures and treatment decisions may benefit from such additional information without extra costs.

Job strain as a risk factor for clinical depression: systematic review and meta-analysis with additional individual participant data.

BACKGROUND: Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression. METHOD: We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol. RESULTS: We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47-2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04-1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94-1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81-1.32). CONCLUSIONS: Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.

Psychosocial factors associated with work disability in men and women with diabetes: a pooled analysis of three occupational cohort studies.

AIMS: To examine the extent to which adverse psychosocial factors, such as living alone, psychological distress, job strain and low support from supervisor, increase the risk of work disability (sickness absence and disability pension) among employees with diabetes. METHODS: In this pooled analysis of individual-participant data from three occupational cohort studies (the Finnish Public Sector Study, the British Whitehall II study, and the French GAZEL study), 1088 women and 949 men with diabetes were followed up to determine the duration (number of days) and frequency (number of spells) of work disability. The mean follow-up periods were 3.2 years in the GAZEL study, 4.6 years in the Whitehall II study and 4.7 years in the Finnish Public Sector Study. Psychosocial factors and potential confounding factors were assessed at baseline using standard questionnaires. Study-specific estimates were pooled using fixed-effects meta-analysis. RESULTS: In analysis adjusted for sociodemographic factors, health behaviours and comorbidities, participants with psychological distress had longer (rate ratio 1.66; 95% CI 1.31-2.09) and more frequent absences (rate ratio 1.33; 95% CI 1.19-1.49) compared with those with no psychological distress. Job strain was associated with slightly increased absence frequency (rate ratio 1.19 95% CI 1.05-1.35), but not with absence duration. Living alone and low supervisor support were not associated with absence duration or frequency. We observed no sex differences in these associations. CONCLUSIONS: Psychological distress was associated with increased duration and frequency of work disability among employees with diabetes. Job strain was associated with increased absence frequency but not with absence duration.

Job strain and risk of obesity: systematic review and meta-analysis of cohort studies.

Job strain, the most widely used indicator of work stress, is a risk factor for obesity-related disorders such as cardiovascular disease and type 2 diabetes. However, the extent to which job strain is related to the development of obesity itself has not been systematically evaluated. We carried out a systematic review (PubMed and Embase until May 2014) and meta-analysis of cohort studies to address this issue. Eight studies that fulfilled inclusion criteria showed no overall association between job strain and the risk of weight gain (pooled odds ratio for job strain compared with no job strain 1.04, 95% confidence interval (CI) 0.99-1.09, NTotal=18 240) or becoming obese (1.00, 95% CI 0.89-1.13, NTotal=42 222). In addition, a reduction in job strain over time was not associated with lower obesity risk (1.13, 95% CI 0.90-1.41, NTotal=6507). These longitudinal findings do not support the hypothesis that job strain is an important risk factor for obesity or a promising target for obesity prevention.

Higher effort-reward imbalance and lower job control predict exit from the labour market at the age of 61†years or younger: evidence from the English Longitudinal Study of Ageing.

BACKGROUND: We examined whether higher effort-reward imbalance (ERI) and lower job control are associated with exit from the labour market. METHODS: There were 1263 participants aged 50-74 years from the English Longitudinal Study on Ageing with data on working status and work-related psychosocial factors at baseline (wave 2; 2004-2005), and working status at follow-up (wave 5; 2010-2011). Psychosocial factors at work were assessed using a short validated version of ERI and job control. An allostatic load index was formed using 13 biological parameters. Depressive symptoms were measured using the Center for Epidemiologic Studies Depression Scale. Exit from the labour market was defined as not working in the labour market when 61 years old or younger in 2010-2011. RESULTS: Higher ERI OR=1.62 (95% CI 1.01 to 2.61, p=0.048) predicted exit from the labour market independent of age, sex, education, occupational class, allostatic load and depression. Job control OR=0.60 (95% CI 0.42 to 0.85, p=0.004) was associated with exit from the labour market independent of age, sex, education, occupation and depression. The association of higher effort OR=1.32 (95% CI 1.01 to 1.73, p=0.045) with exit from the labour market was independent of age, sex and depression but attenuated to non-significance when additionally controlling for socioeconomic measures. Reward was not related to exit from the labour market. CONCLUSIONS: Stressful work conditions can be a risk for exiting the labour market before the age of 61 years. Neither socioeconomic position nor allostatic load and depressive symptoms seem to explain this association.

Personality change associated with chronic diseases: pooled analysis of four prospective cohort studies.

BACKGROUND: Common chronic conditions, such as heart disease and cancer, are associated with increased psychological distress, functional limitations and shortened life expectancy, but whether these diseases alter aspects of personality remains unclear. METHOD: To examine whether the onset of heart disease, stroke, diabetes, cancer, hypertension, arthritis and respiratory disease is associated with subsequent changes in personality traits of the five-factor model, we pooled data from the Health and Retirement Study, the Midlife in the United States Survey, and the graduate and sibling samples of the Wisconsin Longitudinal Study for an individual-participant meta-analysis (total n=17,493; mean age at baseline 55.8 years). RESULTS: After adjustment for age, we observed consistent decreases in extraversion [-0.25 T-scores per one disease; 95% confidence interval (CI) -0.40 to -0.10], emotional stability (-0.40, 95% CI -0.61 to -0.19), conscientiousness (-0.44, 95% CI -0.57 to -0.30) and openness to experience (-0.25, 95% CI -0.37 to -0.13) but not in agreeableness (-0.05, 95% CI -0.19 to 0.08) after the onset of chronic diseases. The onset of each additional chronic disease accelerated the average age-related personality change by 2.5 years in decreasing extraversion, 5.5 years in decreasing conscientiousness, and 1.6 years in decreasing openness to experience, and attenuated the increasing levels of emotional stability by 1.9 years. Co-morbid conditions were associated with larger changes than single diseases, suggesting a dose-response association between morbidity and personality change. CONCLUSIONS: These results support the hypothesis that chronic diseases influence personality development in adulthood.

Is personality associated with cancer incidence and mortality? An individual-participant meta-analysis of 2156 incident cancer cases among 42,843 men and women.

BACKGROUND: The putative role of personality in cancer risk has been controversial, and the evidence remains inconclusive. METHODS: We pooled data from six prospective cohort studies (British Household Panel Survey; Health and Retirement Study; Household, Income, and Labour Dynamics in Australia; Midlife in the United Survey; Wisconsin Longitudinal Study Graduate; and Sibling samples) for an individual-participant meta-analysis to examine whether personality traits of the Five Factor Model (extraversion, neuroticism, agreeableness, conscientiousness, and openness to experience) were associated with the incidence of cancer and cancer mortality in 42,843 cancer-free men and women at baseline (mean age 52.2 years, 55.6% women). RESULTS: During an average follow-up of 5.4 years, there were 2156 incident cancer cases. In random-effects meta-analysis adjusted for age, sex, and race/ethnicity, none of the personality traits were associated with the incidence of all cancers or any of the six site-specific cancers included in the analysis (lung, colon, breast, prostate, skin, and leukaemia/lymphoma). In the three cohorts with cause-specific mortality data (421 cancer deaths among 21,835 participants), none of the personality traits were associated with cancer mortality. CONCLUSIONS: These data suggest that personality is not associated with increased risk of incident cancer or cancer-related mortality.

Treatment of depression in diagnosed diabetes: common cause or detection bias?

BACKGROUND: This study examined two competing hypotheses concerning the association between diabetes and treatment for depression: (1) the detection/ascertainment bias hypothesis suggesting that those with diabetes are more likely to be diagnosed with and treated for depression because of increased medical attention and (2) a hypothesis assuming that diabetes and depression share common underlying pathophysiological pathways. METHOD: The study population included all persons aged 35-65 years in Finland with any record of type 2 diabetes in the national health and population registers from 1999 to 2002 and for whom register-based data on depression treatment (antidepressant medication use and hospitalizations for depression) were available at least 2 years before and after the diagnosis of diabetes (n = 18,217). Sociodemographic data were individually linked to the study population. Associations between diabetes diagnosis and time and indicators of depression care were assessed with population-averaged multilevel logistic models. RESULTS: Within the year following diagnosis diabetes, there was a 5% increase in antidepressant medication use but not in hospitalization for depression. The longitudinal change in antidepressant use over time was less steep after the diabetes diagnosis, and hospitalization risk decreased after the diagnosis. These associations between diabetes diagnosis and depression treatment were not modified by the participant's socio-economic position (SEP). CONCLUSIONS: These findings support the common cause hypothesis that treatment for diabetes is beneficial to the prevention of depression rather than the detection/ascertainment hypothesis that individuals with diabetes have higher rates of depression because they receive more medical attention in general.

Association of metabolically healthy obesity with depressive symptoms: pooled analysis of eight studies.

The hypothesis of metabolically healthy obesity posits that adverse health effects of obesity are largely avoided when obesity is accompanied by a favorable metabolic profile. We tested this hypothesis with depressive symptoms as the outcome using cross-sectional data on obesity, metabolic health and depressive symptoms. Data were extracted from eight studies and pooled for individual-participant meta-analysis with 30,337 men and women aged 15-105 years (mean age=46.1). Clinic measures included height, weight and metabolic risk factors (high blood pressure, high triglycerides, low high-density lipoprotein cholesterol, high C-reactive protein and high glycated hemoglobin). Depressive symptoms were assessed using clinical interview or standardized rating scales. The pooled sample comprised 7673 (25%) obese participants (body mass index ⩾30 kg m(-2)). Compared to all non-obese individuals, the OR for depressive symptoms was higher in metabolically unhealthy obese individuals with two or more metabolic risk factors (1.45; 95% confidence interval (CI)=1.30, 1.61) and for metabolically healthy obese with ⩽1 metabolic risk factor (1.19; 95% CI=1.03, 1.37), adjusted for sex, age and race/ethnicity. Metabolically unhealthy obesity was associated with higher depression risk (OR=1.23; 95% CI=1.05, 1.45) compared with metabolically healthy obesity. These associations were consistent across studies with no evidence for heterogeneity in estimates (all I(2)-values<4%). In conclusion, obese persons with a favorable metabolic profile have a slightly increased risk of depressive symptoms compared with non-obese, but the risk is greater when obesity is combined with an adverse metabolic profile. These findings suggest that metabolically healthy obesity is not a completely benign condition in relation to depression risk.

Childhood family factors predict developmental trajectories of hostility and anger: a prospective study from childhood into middle adulthood.

BACKGROUND: Low socio-economic status (SES), and a conflictive, cold and unsupportive family environment in childhood have been associated with early adulthood hostility. However, it is unknown whether this association changes in magnitude with age from childhood to adulthood. We investigated whether childhood family factors (SES and parental child-rearing style) predicted differential development of offspring hostility and anger from early to middle adulthood. METHOD: Between 2041 and 2316 participants (age range 3-18 years at baseline) were selected from the longitudinal Young Finns study. The participants were followed for 27 years between 1980 and 2007. Childhood SES and parent's self-reported child-rearing style were measured twice: at baseline and 3 years after baseline. Hostility and anger were assessed with self-report questionnaires at 12, 17, 21 and 27 years after baseline. RESULTS: Low parental SES and hostile child-rearing style at baseline predicted higher mean levels of offspring anger and hostility. Low parental SES and one of the hostile child-rearing style components (strict disciplinary style) became more strongly associated with offspring hostility with age, suggesting an accumulating effect. CONCLUSIONS: Childhood family factors predict the development of hostility and anger over 27 years and some of these family factors have a long-term accumulating effect on the development of hostility.

Ageing and the prevalence and treatment of mental health problems.

BACKGROUND: Ageing is an important factor in the development of mental health problems and their treatment. We assessed age trajectories of common mental disorders (CMDs) and psychotherapy utilization from adolescence to old age, and examined whether these trajectories were modified by time period or birth cohort effects. METHOD: British Household Panel Survey (BHPS) with an 18-year follow-up between 1991 and 2009 (n=30 224 participants, aged 15­100 years, with an average 7.3 person-observations per person). CMDs were assessed with the 12-item version of the General Health Questionnaire (GHQ). Psychotherapy treatment utilization during the past year was self-reported by the participants. The modifying influences of time period and cohort effects were assessed in a cohort-sequential longitudinal setting. RESULTS: Following a moderate decrease after age 50, the prevalence of GHQ caseness increased steeply from age 75. This increase was more marked in the 2000s (GHQ prevalence increasing from 24% to 43%) than in the 1990s (from 22% to 34%). Psychotherapy utilization decreased after age 55, with no time period or cohort effects modifying the age trajectory. These ageing patterns were replicated in within-individual longitudinal analysis. CONCLUSIONS: Old age is associated with higher risk of CMDs, and this association has become more marked during the past two decades. Ageing is also associated with an increasing discrepancy between prevalence of mental disorders and provision of treatment, as indicated by lower use of psychotherapy in older individuals.

Longitudinal course of depressive symptoms in adulthood: linear stochastic differential equation modeling.

BACKGROUND: Although many studies have addressed the topic of stability versus change in depressive symptoms, few have further decomposed the change to continuous accumulation versus non-systematic state fluctuations or measurement errors. This further step requires a longitudinal follow-up and an appropriate stochastic model; it would, for example, evaluate the hypothesis that women accumulate more susceptibility events than men. Method A linear stochastic differential equation model was estimated for a 16-year longitudinal course of depressive symptoms in the Young Finns community sample of 3596 participants (1832 women, 1764 men). This model enabled us to decompose the variance in depression symptoms into a stable trait, cumulative effects and state/error fluctuations. RESULTS: Women showed higher mean levels and higher variance of depressive symptoms than men. In men, the stable trait accounted for the majority [61%, 90% confidence interval (CI) 48.9-69.2] of the total variance, followed by cumulative effects (23%, 90% CI 9.9-41.7) and state/error fluctuations (16%, 90% CI 5.6-23.2). In women, the cumulative sources were more important than among men and accounted for 44% (90% CI 23.6-58.9) of the variance, followed by stable individual differences (32%, 90% CI 18.5-54.2) and state fluctuations (24%, 90% CI 19.1-27.3). CONCLUSIONS: The results are consistent with previous observations that women suffer more depression than men, and have more variance in depressive symptoms. We also found that continuously accumulating effects are a significant contributor to between-individual differences in depression, especially for women. Although the accumulating effects are often confounded with non-systematic state fluctuations, the latter are unlikely to exceed 27% of the total variance of depressive symptoms.

Association of personality with the development and persistence of obesity: a meta-analysis based on individual-participant data.

Personality is thought to affect obesity risk but before such information can be incorporated into prevention and intervention plans, robust and converging evidence concerning the most relevant personality traits is needed. We performed a meta-analysis based on individual-participant data from nine cohort studies to examine whether broad-level personality traits predict the development and persistence of obesity (n = 78,931 men and women; mean age 50 years). Personality was assessed using inventories of the Five-Factor Model (extraversion, neuroticism, agreeableness, conscientiousness and openness to experience). High conscientiousness - reflecting high self-control, orderliness and adherence to social norms - was associated with lower obesity risk across studies (pooled odds ratio [OR] = 0.84; 95% confidence interval [CI] = 0.80-0.88 per 1 standard deviation increment in conscientiousness). Over a mean follow-up of 5.4 years, conscientiousness predicted lower obesity risk in initially non-obese individuals (OR = 0.88, 95% CI = 0.85-0.92; n = 33,981) and was associated with greater likelihood of reversion to non-obese among initially obese individuals (OR = 1.08, 95% CI = 1.01-1.14; n = 9,657). Other personality traits were not associated with obesity in the pooled analysis, and there was substantial heterogeneity in the associations between studies. The findings indicate that conscientiousness may be the only broad-level personality trait of the Five-Factor Model that is consistently associated with obesity across populations.

Body mass index and depressive symptoms: instrumental-variables regression with genetic risk score.

The causal role of obesity in the development of depression remains uncertain. We applied instrumental-variables regression (Mendelian randomization) to examine the association of adolescent and adult body mass index (BMI) with adult depressive symptoms. Participants were from the Young Finns prospective cohort study (n = 1731 persons, 2844 person-observations), with repeated measurements of BMI and depressive symptoms (modified Beck's Depression Inventory). Genetic risk score of 31 single nucleotide polymorphisms previously identified as robust genetic markers of body weight was used as a proxy for variation in BMI. In standard linear regression analysis, higher adult depressive symptoms were predicted by higher adolescent BMI (B = 0.33, CI = 0.06-0.60, P = 0.017) and adult BMI (B = 0.47, CI = 0.32-0.63, P < 0.001). These associations were replicated in instrumental-variables analysis with genetic risk score as instrument (B = 1.96, CI = 0.03-3.90, P = 0.047 for adolescent BMI; B = 1.08, CI = 0.11-2.04, P = 0.030 for adult BMI). The association for adolescent BMI was significantly stronger in the instrumented analysis compared to standard regression (P = 0.04). These findings provide additional evidence to support a causal role for high BMI in increasing symptoms of depression. However, the present analysis also demonstrates potential limitations of applying Mendelian randomization when using complex phenotypes.

Late-onset lower motor neuronopathy: a new autosomal dominant disorder.

OBJECTIVE: Characterization of a new type of late-onset autosomal dominant lower motor neuron disease. METHODS: Patients from 2 families underwent detailed neurologic, electrophysiologic, muscle biopsy, and laboratory investigations. MRI of lower limbs was performed in selected patients. DNA samples from leukocytes were used for molecular genetic linkage studies. RESULTS: First symptoms were muscle cramps and fasciculations after age 25-30, followed by a slowly progressive proximal and distal weakness without overt atrophy during the first decades of symptoms. Nerve conduction velocities were within normal range and EMG showed widespread neurogenic alterations. Muscle biopsy revealed characteristic neurogenic findings: fiber type grouping and group atrophy. MRI showed diffuse fatty-degenerative changes, marked in medial gastrocnemius. CONCLUSION: Exactly the same clinical phenotype has not previously been described, and linkage studies showed exclusion of known chromosomal loci for hereditary motor neuropathies, suggesting the disease we report may represent a new disorder.