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The role of mental illness in the aetiology of suicide is well-recognised whereas the importance of personality and other enduring psychological characteristics has received relatively little attention in prospective studies.
Prospective cohort study of men and women aged 20+ years who participated in the Nord- Trøndelag Health Study, Norway, in 1984-86 (HUNT 1, n=74,977) and 1995-97 (HUNT II, n=66,140). State and trait psychological measures (personality traits, self-esteem and sense of coherence) along with sociodemographic, life style and physical health factors known to influence mental health and suicide risk were self reported by participants. Study members were followed up until 31st of December 2004.
There were 153 suicides amongst the study members included in the analyses. Traits of neuroticism and conscientiousness (dutifulness) were associated with a modest (30-80%) increased risk of suicide. Low self-esteem (hazard ratio 5.22 95% CI 0.90 to 30.42) and low sense of meaning in life (hazard ratio 4.88 95% CI 1.86 to 12.82) were associated with an increased suicide risk in the fully adjusted models even after controlling for common mental disorder.
Our results suggest that simple questions relating to markers of personality, self-esteem and meaningfulness (SOC) might be useful tools in clinical suicide risk assessment. However, findings need replication in future large scale prospective studies.
There have been conflicting reports on the relationship between thyroid function and mood between studies in subjects on thyroxine and the general population not on thyroxine. We investigated this relationship in a large population study.
We analysed data on serum TSH levels and Hospital Anxiety and Depression Scale (HADS) scores from the HUNT 2 study (age ≥ 40 years). Following a test for interaction, analyses were performed separately in females on thyroxine (n=1,265) and in people not on thyroxine (males n=9,319 and females n=17,694).
More females on thyroxine had high depression and anxiety scores than females not on thyroxine (depression 18.4% vs 13.0%, p< 0.001, anxiety 23.4% vs 18.7% p< 0.001). In those not on thyroxine there was an inverse association between serum TSH and depression score in males (B coefficient = -0.61, 95% CI -0.91 to -0.24, p=0.001) though not in females (B coefficient = -0.07, -0.33 to 0.19), and an inverse association between TSH and anxiety score in both sexes (B coefficient for males = -0.68, 95% CI -1.04 to -0.32, p< 0.001; females -0.37, -0.67 to -0.08, p=0.01). By contrast, in females on thyroxine, TSH was positively associated with both depression (B coefficient = +0.27, 95% CI 0.02 to 0.51, p< 0.05) and anxiety (B coefficient = +0.29, 0.01 to 0.56, p< 0.05).
There is a different relationship between thyroid function and depression and anxiety in females on thyroxine compared to individuals with no thyroid disease.
Depression is reported to be associated with increased mortality, but underlying mechanisms are uncertain. Associations between anxiety and mortality are also uncertain. In a large population study, we investigated associations between anxiety, depression and mortality over a 3-6 year period. We utilized a unique link between a large regional community survey and a comprehensive national mortality database.
Baseline information on mental and physical health was collected in a population-based health study (n=61,349) (the HUNT-2 study) of adults aged 20 years and over. Anxiety and depressive symptoms were ascertained using the Hospital Anxiety and Depression Scale (HADS). Records were linked with the Norwegian national mortality database.
Case-level depression was a risk-factor for mortality, but case-level anxiety was not (having adjusted for confounding factors). The association between anxiety symptoms and mortality was U-shaped, and anxiety comorbid with depression was associated with lower mortality compared to depression alone. Associations between depression and mortality were partly but not entirely explained by somatic symptoms and conditions, and also physical impairment, but not by smoking, obesity, cholesterol level or blood pressure.
Depression predicted general mortality after adjustment for multiple potential confounding factors. Associations between anxiety symptoms and mortality were U-shaped. Lower mortality was found in comorbid anxiety and depression than in depression alone.
Study prospectively the effect of sleep-related complaints and sleep duration on all cause mortality in a general population sample.
The data were gathered from the adult population from the County of Nord-Trøndelag as part of a general health survey whichhad a participation rate of 71.2%. Data included self-reported somatic disorders, somatic symptoms,health related behaviour, impairment, public benefits, medication use, anxiety and depression as well as anthropometric measures, blood pressure and cholesterol level.
Main outcome measure:
Mortality during a 4-year period following the general health survey as recorded in the Norwegian Death register.
An ordinal five point scale of sleep disturbance predicted mortality in the observation period, even in the probable over-adjusted model including all available confounders. The variables that most strongly accounted for the effects of the sleep disturbance were (in order of magnitude) somatic diagnoses, health related behaviour, anxiety and depression, subjectively reported physical impairment, educational and social differences, blood-pressure, cholesterol level, and BMI. Time in bed was strongly associated with mortality, and the association was U-shaped. Compared to the median value of 7 hours, spending either less or more time in bed predicted death.
Sleep disturbances as well as spending either short or long time in bed are predictors of mortality. Both predictors are robust for adjustment for multiple confounding factors.
Depression is reported to increase general mortality. For cause-specific mortality, there is evidence for the effect of depression on cardiac mortality and suicide. Less is known as to other mortality diagnoses. The literature on anxiety in relation to mortality is scarce and conflicting. This study investigates empirically the association between anxiety/depression and cause-specific mortality with particular attention to underlying mechanisms and causes of death.
Employing a historical cohort design we utilized a unique link between a large epidemiological cohort study and a comprehensive national mortality database. Baseline information on physical and mental health (HADS) was gathered from the population based health study (N=61349). Causes of death were registered with ICD-10 diagnoses during 4.4 year follow-up.
Case-level depression increased mortality for all major disease-related causes of death, whereas case-level anxiety and comorbid anxiety/depression did not. The effect of depression was equal in cardiac mortality compared to all other causes combined, and confounding factors were also markedly similar. Accidents and suicide was predicted by comorbid anxiety depression.
Depression is a risk factor for all major disease-related causes of death, and is not limited to cardiac mortality or suicide. Case-level anxiety imposes no increased disease-related mortality, but comorbid anxiety depression predicts external causes of death. As the association between depression and cardiac mortality was comparable to the other causes of death combined, and confounding and mediating factors are markedly similar, future investigation as to mechanisms underlying the effect of depression on mortality should not be limited to CVD mortality.
Previous studies on the relationship between blood pressure (BP) and psychological morbidity are conflicting. To resolve this confusing picture we examined the hypothesis that there is a non-linear relationship between panic and systolic BP (SBP) and explored the association of generalized anxiety symptoms with SBP.
We used data from the population-based Nord-Trøndelag health study (HUNT) in which all 92 936 individuals aged ⩾20 years residing in one Norwegian county were invited to participate. Panic was assessed using one item from the anxiety subscale of the Hospital Anxiety and Depression Scale (HADS) and generalized anxiety with the remaining six items of this subscale. SBP was the mean of two measurements by an automatic device.
A total of 64 871 respondents had SBP recorded (70%). Both unadjusted (n=61 408) and adjusted analyses provided evidence for a non-linear relationship between panic and SBP, represented by a U-shaped curve with a minimum prevalence of panic at around 140 mmHg. The relationship was strengthened after adjustment for confounders, with the quadratic term significantly associated with panic (p=0.03). Generalized anxiety symptoms were associated only with low SBP.
The U-shaped relationship between SBP and panic provides a unifying explanation for the separate strands of published literature in this area. The results support the hypothesis that high BP and panic disorder could share brainstem autonomic and serotonergic abnormalities. By contrast, generalized anxiety symptoms were more common only at lower BPs, suggesting that any biological link between panic and high BP does not extend to generalized anxiety.
Elevated levels of circulating C-reactive protein (CRP) have been associated with coronary heart disease and, in some studies, depression. Most studies have been of populations selected by age and/or gender. We investigate these associations with depression, myocardial infarction (MI), or both, in a large general population sample.
A cross-sectional population study of 9258 women and men aged ⩾20 years. The study included clinical examination, self-report of MI and depression and factors known to confound their associations. The Hospital Anxiety and Depression Scale was used to assess severity of depressive symptoms. Elevated high sensitive-CRP was defined as values >2.2 mg/l.
The association of elevated CRP with depression was attenuated towards the null [from odds ratio (OR) 1.28, p=0.001 to OR 1.08, p=0.388] following extensive adjustment, while associations with MI (adjusted OR 1.42, p=0.032) and co-morbid MI and depression (adjusted OR 2.66, p=0.003) persisted. Confounders associated with elevated CRP levels were smoking (OR 1.66; p<0.001), chronic physical illness (OR 1.34, p<0.001), BMI ⩾30 (OR 1.13, p<0.001), employment (OR 0.70, p<0.001) and high coffee consumption (OR 0.83, p=0.017). Interaction tests indicated a lower effect of old age (OR 0.54, p<0.001) and smoking (OR 0.63, p<0.001) on elevated CRP levels in women compared with men.
CRP levels were raised in those with MI and co-morbid MI and depression; the positive association with depression was explained by confounding factors. We found new evidence that might help understand gender-specific patterns. Future studies should explore the neurobiological mechanisms underpinning these interrelations and their relevance for treatment of these conditions.
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