Depressive symptoms and psoriasis: Domain-specific associations in national cohorts.

Total, somatic, and cognitive-affective depressive symptoms trajectories and urinary incontinence: Evidence from two national longitudinal cohorts.

Prior literature suggests a dose-response relationship between physical activity (PA) and depressive symptoms. The intensity and domain of PA are suggested to be critical to its protective effect against depression; however, existing literature has shown mixed results. The purpose of this population-based study is to examine the associations between depressive symptoms and weekly duration of (1) total PA and (2) PA subset by intensity, domain, or both. A cross-sectional analysis of National Health and Nutrition Examination Survey data from 2007 to 2018 was conducted using multivariable logistic and linear regression models and survey weights. Participants (N=29,730) were 20 years and older and completed the Physical Activity Questionnaire and Depression Screener. The primary outcome was the presence of depressive symptoms, and the secondary outcomes were cognitive-affective and somatic symptoms of depression. Participants (N=29,730) had a weighted mean age of 47.62 (SD 16.99) years, and 15,133 (51.34%) were female. On average, participants without depressive symptoms engaged in 10.87 hours of total PA per week, whereas participants with depressive symptoms engaged in 8.82 hours (P<.001). No significant associations were seen between the weekly duration of total PA and depressive symptom odds, somatic, or cognitive-affective symptoms (all P>.05). Participants with an increased weekly duration of recreational PA had decreases in depressive symptom odds (adjusted odds ratio [aOR] 0.965, 95% CI 0.944-0.986) and in somatic (adjusted coefficient [aβ]=-0.016, 95% CI -0.022 to -0.009) and cognitive-affective (aβ=-0.015, 95% CI -0.023 to -0.007) symptoms. When recreational PA was subset by intensity, participants with an increased weekly duration of vigorous-intensity recreational PA had decreases in depressive symptom odds (aOR 0.926, 95% CI 0.883-0.972) and in somatic (aβ=-0.021, 95% CI -0.032 to -0.010) and cognitive-affective (aβ=-0.022, 95% CI -0.035 to -0.009) symptoms. However, significant associations were not seen for the weekly duration of work-related, moderate- or vigorous-intensity PAs (all P>.05). Findings suggest that recreational, not work-related PA is associated with reduced symptoms of depression. Future studies should explore the impact of the different types and contexts of PA on depressive symptomatology.

BACKGROUND Prior literature suggests a dose-response relationship between physical activity (PA) and depressive symptoms. The intensity and domain of PA are suggested to be critical to its protective effect against depression; however, existing literature has shown mixed results. OBJECTIVE The purpose of this population-based study is to examine the associations between depressive symptoms and weekly duration of (1) total PA and (2) PA subset by intensity, domain, or both. METHODS A cross-sectional analysis of National Health and Nutrition Examination Survey data from 2007 to 2018 was conducted using multivariable logistic and linear regression models and survey weights. Participants (N=29,730) were 20 years and older and completed the Physical Activity Questionnaire and Depression Screener. The primary outcome was the presence of depressive symptoms, and the secondary outcomes were cognitive-affective and somatic symptoms of depression. RESULTS Participants (N=29,730) had a weighted mean age of 47.62 (SD 16.99) years, and 15,133 (51.34%) were female. On average, participants without depressive symptoms engaged in 10.87 hours of total PA per week, whereas participants with depressive symptoms engaged in 8.82 hours (&lt;i&gt;P&lt;/i&gt;&amp;lt;.001). No significant associations were seen between the weekly duration of total PA and depressive symptom odds, somatic, or cognitive-affective symptoms (all &lt;i&gt;P&lt;/i&gt;&amp;gt;.05). Participants with an increased weekly duration of recreational PA had decreases in depressive symptom odds (adjusted odds ratio [aOR] 0.965, 95% CI 0.944-0.986) and in somatic (adjusted coefficient [aβ]=–0.016, 95% CI –0.022 to –0.009) and cognitive-affective (aβ=–0.015, 95% CI –0.023 to –0.007) symptoms. When recreational PA was subset by intensity, participants with an increased weekly duration of vigorous-intensity recreational PA had decreases in depressive symptom odds (aOR 0.926, 95% CI 0.883-0.972) and in somatic (aβ=–0.021, 95% CI –0.032 to –0.010) and cognitive-affective (aβ=–0.022, 95% CI –0.035 to –0.009) symptoms. However, significant associations were not seen for the weekly duration of work-related, moderate- or vigorous-intensity PAs (all &lt;i&gt;P&lt;/i&gt;&amp;gt;.05). CONCLUSIONS Findings suggest that recreational, not work-related PA is associated with reduced symptoms of depression. Future studies should explore the impact of the different types and contexts of PA on depressive symptomatology.

BackgroundPrior research has established a link between depressive symptoms and the incidence of hip fractures, with most studies relying on a single assessment and failing to differentiate among symptom subtypes. This study utilized repeated measurements to construct symptom trajectories and separately examined the cognitive-emotional and physical dimensions to elucidate their relationship with the risk of hip fractures.MethodsWe analyzed data from individuals aged 45 and older participating in the Health and Retirement Study (HRS, USA) and the English Longitudinal Study of Ageing (ELSA, UK), excluding those with a history of hip fractures. Depressive symptoms were assessed biennially using the Center for Epidemiological Studies Depression Scale (CES-D) over a span of eight consecutive years. Participants were categorized into five trajectory groups based on their CES-D scores: consistently low, decreasing, fluctuating, increasing, and consistently high. Over the subsequent 10 years, the incidence of hip fractures was ascertained through self-reported physician diagnoses. The Cox proportional hazards model was employed to calculate the hazard ratio (HR) and 95% confidence interval (CI) to examine the association between the trajectory of depressive symptoms and the risk of hip fractures, while controlling for sociodemographic factors, health behaviors, and overall health status.ResultsAmong 7,014 participants (mean age 64.4 years, 61.2% female), 382 incident hip fractures occurred during follow-up. In the fully adjusted model, participants with increasing total depressive symptoms (HR = 1.53, 95% CI: 1.12–2.09) and consistently high total depressive symptoms (HR = 1.70, 95% CI: 1.12–2.56) had elevated hip fracture risk compared with those with consistently low symptoms. Decreasing (HR = 0.81, 95% CI: 0.53–1.22) and fluctuating trajectories (HR = 1.13, 95% CI: 0.85–1.51) were not significantly associated with hip fracture risk. Regarding symptom subtypes, consistently high cognitive-affective symptoms were associated with increased hip fracture risk (HR = 1.71, 95% CI: 1.09–2.69). For somatic symptoms, both increasing (HR = 1.61, 95% CI: 1.17–2.20) and consistently high trajectories (HR = 1.72, 95% CI: 1.06–2.81) were associated with increased hip fracture risk.ConclusionElevated hip fracture risk is linked to increasing and consistently high total depressive symptom trajectories, whereas decreasing and fluctuating patterns do not significantly differ from consistently low levels. Greater fracture risk is indicated by consistently high cognitive-affective symptoms and both increasing and consistently high somatic symptoms. These findings imply that monitoring depressive symptom trajectories and their subtypes may help identify individuals at elevated fracture risk and inform targeted prevention strategies. Additional research on underlying mechanisms and approaches to identify and address high-risk populations is necessary.

BackgroundEarlier research has documented an association between depressive symptomatology and heightened stroke risk. However, prior work largely assessed depressive manifestations at isolated time points and failed to differentiate symptom subtypes. This investigation seeks to characterize the longitudinal progression of depressive symptoms via repeated measurement and explore their link to stroke risk by considering total depressive symptoms alongside cognitive-affective and somatic dimensions.MethodsThis prospective cohort study included individuals aged ≥ 45 years from the Health and Retirement Study (HRS) in the United States and the English Longitudinal Study of Ageing (ELSA) in the United Kingdom, excluding those with a history of stroke during the exposure period. Depressive symptoms were measured using the 8-item Center for Epidemiologic Studies Depression Scale (CES-D) across four biennial assessments. Individuals were categorized into five distinct depressive symptom trajectories: consistently low, decreasing, fluctuating, increasing, and consistently high, based on assessment scores. Over a subsequent decade of follow-up, incident strokes were identified through self-reported physician diagnoses. The analyses incorporated adjustments for demographic factors (sex, age, etc.), health-related behaviors (smoking, drinking, etc.), and health status covariates (hypertension, diabetes, etc.). Cox proportional hazards regression models generated hazard ratios (HRs) and 95% confidence intervals (CIs) to evaluate links between trajectories of total depressive symptoms, cognitive-affective and somatic subtypes, and stroke occurrence.ResultsThe final cohort included 10,011 participants (63.3% female; mean age 60.2 years). During the 10-year follow-up, 720 incident strokes were recorded. Analyses demonstrated that, after adjusting for the aforementioned demographic and health-related confounders, relative to the consistently low trajectory, participants with fluctuating (HR = 1.24, 95% CI: 1.01–1.52), increasing (HR = 1.31, 95% CI: 1.03–1.67), and consistently high (HR = 1.42, 95% CI: 1.03–1.97) total depressive symptom trajectories exhibited significantly elevated stroke risk. Conversely, the decreasing trajectory (HR = 1.11, 95% CI: 0.85–1.45) did not significantly impact stroke risk. Furthermore, an increasing trajectory of cognitive-affective depressive symptoms (HR = 1.43, 95% CI: 1.13–1.82), alongside fluctuating (HR = 1.27, 95% CI: 1.03–1.55) and consistently high (HR = 1.97, 95% CI: 1.42–2.74) somatic depressive symptom trajectories, were each significantly associated with heightened stroke risk. Critically, the consistently high somatic trajectory demonstrated the most robust association with stroke.ConclusionTrajectories of total depressive symptoms marked by escalation, instability, or sustained elevation exhibited significantly elevated stroke risk. In contrast, individuals displaying decreasing depressive symptoms exhibit stroke risk comparable to those maintaining consistently low levels. Specifically, an ascending trajectory of cognitive-affective symptoms, alongside unstable and persistently elevated trajectories of somatic symptoms, are linked to increased stroke risk. These findings emphasize the clinical importance of monitoring dynamic changes in depressive symptoms and their subtypes for stroke prevention. Future investigations should elucidate underlying mechanisms to refine identification and intervention strategies for high-risk populations.

Race/ethnicity moderates the relationship between depressive symptom severity and C-reactive protein: 2005-2010 NHANES data.

In this study, we analyzed pooled data from two prospective population-based cohorts—the Health Retirement Study (HRS) and the English Longitudinal Study of Ageing (ELSA)—to explore the association between trajectories of depressive symptoms and the risk of cardiac events. Depressive symptoms were assessed using the 8-item CES-D scale and categorized into somatic and cognitive-affective subtypes. Trajectories were tracked for four surveys from baseline. Heart disease was identified based on self-reported physician-diagnosed conditions. Hazard ratios and 95% confidence intervals were calculated with Cox proportional risk models that adjusted for potential confounders. In total, 17,787 subjects (59.7% female, median age 63 years) were enrolled at baseline. During a 10-year follow-up, 2409 cases of heart disease were identified. Participants with fluctuating (HR = 1.13, 95% CI: 1.06–1.20), increasing (HR = 1.43, 95% CI: 1.25–1.64), and consistently high (HR = 1.64, 95% CI: 1.45–1.84) depressive symptom trajectories exhibited an increased risk of heart disease compared to those with consistently low depressive symptoms, while a decreasing (HR = 1.07, 95% CI: 0.96–1.19) depressive symptom trajectory did not significantly affect the risk of heart disease. Moreover, the association between heart disease and somatic depressive symptoms was found to be stronger than with cognitive-affective symptoms. These findings suggest a significant link between depressive symptom trajectories and heart disease, with particular emphasis on stronger associations with somatic symptoms. It is recommended that the identification and management of depressive symptoms be incorporated into heart disease prevention strategies.

Aims/hypothesisInsulin resistance and inflammation are components of a biological framework that is hypothesised to be shared by type 2 diabetes and depression. However, depressive symptoms include a large heterogeneity of somatic and cognitive-affective symptoms, and this may obscure the associations within this biological framework. Cross-sectional and longitudinal data were used to disentangle the contributions of insulin resistance and inflammation to somatic and cognitive-affective symptoms of depression.MethodsThis secondary analysis used data from the Emotional Distress Sub-Study of the GRADE trial. Insulin resistance and inflammation were assessed using the HOMA-IR estimation and high-sensitivity C-reactive protein (hsCRP) levels, respectively, at baseline and at the study visits at year 1 and year 3 (HOMA-IR) and every 6 months (hsCRP) for up to 3 years of follow-up. Depressive symptoms were assessed at baseline using the Patient Health Questionnaire (PHQ-8), and a total score as well as symptom cluster scores for cognitive-affective and somatic symptoms were calculated. For the cross-sectional analyses, linear regression analyses were performed, with inflammation and insulin resistance at baseline as dependent variables. For the longitudinal analyses, linear mixed-effect regression analyses were performed, with inflammation and insulin resistance at the various time points as dependent variables. In all analyses, depressive symptoms (total score and symptom cluster scores) were the independent variables, controlled for important demographic, anthropometric and metabolic confounders. For the analysis of insulin resistance (HOMA-IR), data from 1321 participants were analysed. For the analysis of inflammation (hsCRP), data from 1739 participants were analysed.ResultsIn cross-sectional analysis and after adjustment for potential confounders, a one-unit increase in PHQ-8 total score was significantly associated with a 0.8% increase in HOMA-IR (p=0.007), but not with hsCRP (0.6% increase, p=0.283). The somatic symptom score was associated with a 5.8% increase in HOMA-IR (p=0.004). Single-item analyses of depressive symptoms showed that fatigue (3.6% increase, p=0.002) and increased/decreased appetite (3.5% increase, p=0.009) were significantly associated with HOMA-IR cross-sectionally. The cognitive-affective symptom score was not significantly associated with HOMA-IR at baseline. In longitudinal analyses, a one-unit increase in PHQ-8 total score was significantly associated with a 0.8% increase in hsCRP over time (p=0.014), but not with HOMA-IR over time (0.1% decrease, p=0.564). Again, only the somatic symptom cluster was significantly associated with hsCRP over time (5.2% increase, p=0.017), while the cognitive-affective symptom score was not.Conclusion/interpretationThe results highlight the associations of depressive symptoms with markers of inflammation and insulin resistance, both cross-sectionally and longitudinally, in individuals with type 2 diabetes. In particular, somatic symptoms of depression appear to be the driver of these associations, even after controlling for concomitant conditions, with a potential role for fatigue and issues with appetite.Trial registration: ClinicalTrials.gov NCT01794143Graphical

Association between depressive symptom clusters and food attentional bias

BACKGROUNDDepressive symptoms differ from clinical depression. However, the relationship between depressive symptom trajectories and stroke risk across diverse geographic regions remains unclear.AIMTo address the gap in the existing understanding of the relationship between depressive symptom trajectories and stroke risk, the current study utilized three representative cohorts.METHODSIn this study, we used three representative cohorts from Asia, Europe, and the Americas: China Health and Retirement Longitudinal Study (CHARLS), English Longitudinal Study of Ageing (ELSA), and Health and Retirement Study (HRS). Depressive symptoms were assessed using the 8-item Center for Epidemiological Studies Depression scale and categorized into somatic and cognitive-affective subtypes. The trajectories of depressive symptoms were monitored over four surveys starting from baseline and classified into five distinct states: persistently low, decreasing, fluctuating, increasing, and consistently high. Self-reported physician diagnoses were used to evaluate the subsequent stroke events. Hazard ratios (HRs) and 95% confidence intervals (95%CIs) were computed using Cox proportional-risk models adjusted for potential confounding factors.RESULTSA total of 7990 participants from CHARLS (females: 52.3%, mean age: 63.4 years), 5642 participants from ELSA (females: 56.2%, mean age: 63.7 years), and 12260 participants from HRS (females: 61.4%, mean age: 64.7 years) participated in this study. The median follow-up periods were 5 years for CHARLS, 8 years for ELSA, and 10 years for HRS. In comparison with the persistently low trajectory, consistently high and fluctuating trajectories of total depressive symptoms increased the risk of stroke in all three cohorts (CHARLS: HR = 1.80, 95%CI: 1.36-2.38; ELSA: HR = 1.50, 95%CI: 1.02-2.21; HRS: HR = 1.45, 95%CI: 1.29-1.62 for consistently high; CHARLS: HR = 1.47, 95%CI: 1.14-1.90; ELSA: HR = 1.44, 95%CI: 1.17-1.77; HRS: HR = 1.26, 95%CI: 1.13-1.41 for fluctuating). Increasing trajectories enhanced the risk in the European cohort (ELSA: HR = 1.71, 95%CI: 1.06-2.74), while decreasing trajectories did not increase stroke risk in any cohort. For somatic depressive symptoms, consistently high and fluctuating trajectories increased the risk of stroke across all cohorts (CHARLS: HR = 2.16, 95%CI: 1.67-2.79; ELSA: HR = 1.94, 95%CI: 1.34-2.81; HRS: HR = 1.79, 95%CI: 1.49-2.15 for consistently high; CHARLS: HR = 1.35, 95%CI: 1.20-1.62; ELSA: HR = 1.56, 95%CI: 1.27-1.92; HRS: HR = 1.33, 95%CI: 1.20-1.46 for fluctuating). Increasing trajectories only increased the risk in the European cohort (ELSA: HR = 1.95, 95%CI: 1.11-3.43), while decreasing trajectories did not increase stroke risk in the European and American cohorts. For cognitive-affective depressive symptoms, consistently high and fluctuating trajectories increased the risk in the Asian and European cohorts (CHARLS: HR = 2.06, 95%CI: 1.52-2.81; ELSA: HR = 1.25, 95%CI: 1.02-1.54 for consistently high; CHARLS: HR = 1.63, 95%CI: 1.23-2.16; ELSA: HR = 1.58, 95%CI: 1.11-2.24 for fluctuating). Increasing trajectories increased the risk only in the American cohort (HRS: HR = 14.67, 95%CI: 1.87-114.91).CONCLUSIONConsistently high and fluctuating trajectories of total and somatic depressive symptoms were associated with an increased risk for stroke across all populations. Consistently high, fluctuating, and increasing trajectories of cognitive-affective symptoms pose a risk for certain populations. These findings highlight the importance of targeted interventions for managing depressive symptoms as potential strategies for stroke prevention, particularly in regions where specific symptom trajectories are prevalent.

BACKGROUNDDepression is a significant risk factor for diabetes, particularly type 2 diabetes. However, depressive symptoms differ from clinical depression. Previous research has not fully considered the relationship between the trajectory of depressive symptoms and the risk of developing diabetes over time.AIMTo investigate the association between depressive symptoms, their trajectories, and the risk of developing diabetes in two prospective cohort studies.METHODSIn the first phase we analyzed the association between depressive symptoms and the risk of developing diabetes separately using the Health and Retirement Study (HRS). Depressive symptom trajectories were assessed by examining changes in depressive symptoms at baseline and again 8 years later. We then identified specific depressive symptom trajectories that increased the risk of diabetes in the second phase. Finally, we confirmed the association between depressive symptoms and their trajectories with diabetes risk using the English Longitudinal Study of Ageing (ELSA) as a validation study. Depressive symptom trajectories were categorized into five states based on changes in the modified 8-item Center for Epidemiological Studies-Depression scores: Persistently high; increasing; fluctuating; decreasing; and persistently low. Diabetes mellitus was defined as self-reported, physician-diagnosed diabetes. Cox proportional hazards models were used to assess hazard ratios (HR) and 95% confidence intervals (CI), adjusting for potential confounders.RESULTSIn the first phase a total of 27658 participants were included (HRS: 18633, ELSA: 9025), among whom 6582 had depressive symptoms (HRS: 4547, ELSA: 2035), 6407 had somatic depressive symptoms (HRS: 4414, ELSA: 1993), and 26415 had cognitive-affective depressive symptoms (HRS: 17755, ELSA: 8660). We found that overall depressive symptoms (HRS: HR = 1.14, 95%CI: 1.07-1.22; ELSA: HR = 1.18, 95%CI: 1.03-1.34) and somatic depressive symptoms (HRS: HR = 1.14, 95%CI: 1.07-1.22; ELSA: HR = 1.25, 95%CI: 1.10-1.42) increased the risk of diabetes, while cognitive depressive symptoms were not associated with diabetes risk. Over an 8-year follow-up we identified 19729 trajectories of overall, somatic, and cognitive-affective depressive symptoms (HRS: 13918, ELSA: 5811). In the second phase we found that persistently high (HRS: HR = 1.22, 95%CI: 1.06-1.40, ELSA: HR = 1.54, 95%CI: 1.16-2.05 in total and HRS: HR = 1.24, 95%CI: 1.07-1.43, ELSA: HR = 1.79, 95%CI: 1.36-2.35 in somatic) and fluctuating (HRS: HR = 1.09, 95%CI: 1.01-1.17, ELSA: HR = 1.33, 95%CI: 1.14-1.55 in total and HRS: HR = 1.10, 95%CI: 1.02-1.18, ELSA: HR = 1.31, 95%CI: 1.13-1.53 in somatic) trajectories of overall and somatic depressive symptoms increased the risk of diabetes, while increasing trajectories may also raise diabetes risk. However, decreasing trajectories were not associated with diabetes risk. Cognitive-affective depressive symptoms showed no association with diabetes risk regardless of trajectory changes. Sensitivity analyses confirmed the reliability of the findings.CONCLUSIONPersistently high and fluctuating trajectories of overall and somatic depressive symptoms increased the risk of diabetes, while decreasing trajectories were not associated with diabetes risk. In contrast trajectories of cognitive-affective depressive symptoms show no relationship with diabetes risk. Focusing on depressive symptom trajectories, particularly those of somatic depressive symptoms, represented a viable strategy for future diabetes prevention.

The association between depressive symptoms and respiratory health remains inconclusive, with limited research exploring dynamic changes in overall and symptom-specific depression. This study aimed to investigate the relationship between depressive symptom trajectories and the risk of chronic lung diseases (CLDs) as well as pulmonary function. We used data from two prospective cohorts: the China Health and Retirement Longitudinal Study (CHARLS) and the Health and Retirement Study (HRS). Depressive symptoms were assessed using the 10-item and 8-item CES-D scales, respectively, at three time points (CHARLS: wave1-3; HRS: wave 5-7), and classified into five trajectories: consistently low, decreasing, fluctuating, increasing, and consistently high. Incident CLDs were identified by self-reported physician diagnoses (CHARLS: wave 4-5; HRS: wave 8-12), and pulmonary function was evaluated by peak expiratory flow (PEF, CHARLS: wave 3; HRS: wave 8). Cox proportional hazards and linear regression models were used to estimate hazard ratios (HRs), beta coefficients (β), and 95% confidence intervals (CIs), adjusting for potential confounders. At baseline, individuals with depressive symptoms had a higher risk of Incident CLDs and lower PEF values. Compared to the consistently low group, the fluctuating (CHARLS: HR = 1.56, 95% CI: 1.33, 1.84; HRS: HR = 1.52, 95% CI: 1.30, 1.77), increasing (CHARLS: HR = 2.39, 95% CI: 1.86, 3.07; HRS: HR = 1.62, 95% CI: 1.13, 2.31), and consistently high (CHARLS: HR = 2.59, 95% CI: 2.16, 3.11; HRS: HR = 1.66, 95% CI: 1.30, 2.13) trajectories were associated with significantly increased CLDs risk. These trajectories were also significantly associated with lower PEF. The decreasing trajectory showed no significant association with CLDs risk or PEF. Total and somatic depressive symptoms demonstrated stronger associations with adverse respiratory outcomes. Depressive symptom trajectories characterized by fluctuation, increase, or persistent elevation are associated with higher CLDs risk and poorer pulmonary function. In contrast, symptom remission appears unrelated to respiratory outcomes. Total and somatic symptoms may serve as more sensitive indicators for predicting respiratory health.

Specific types of depressive symptoms trajectories and risk of chronic lung diseases events in middle-aged and older adults: Result from two prospective cohort studies.

Depression is an independent predictor of adverse outcomes in patients with heart failure (HF). However, the effect of changes in cognitive-affective and somatic symptoms on mortality of HF patients is not known. The purpose of this study was to examine whether changes in cognitive-affective and somatic depressive symptoms over time were associated with mortality in HF. In this secondary analysis of data from the Rural Education to Improve Outcomes in Heart Failure clinical trial, we analyzed data from 457 HF patients (39% female, mean [standard deviation] age = 65.6 [12.8] years) who survived at least 1 year and repeated the Patient Health Questionnaire at 1 year. Cognitive-affective and somatic depression scores were calculated, respectively, based on published Patient Health Questionnaire factor models. Using Cox proportional hazards regression analyses, we evaluated the effect of changes in cognitive-affective and somatic symptoms from baseline to 1 year on cardiac and all-cause deaths. Controlling for baseline depression scores and other patient characteristics, the change in somatic symptoms was associated with increased risk of cardiac death during the subsequent 1-year period (hazard ratio = 1.24, 95% confidence interval = 1.07-1.44, p = .005), but the change in cognitive-affective symptoms was not (hazard ratio = 0.94, 95% confidence interval = 0.81-1.08, p = .38). Similar results were found for all-cause mortality. Worsening somatic depressive symptoms, not cognitive-affective symptoms, are independently associated with increased mortality of HF patients. The findings suggest that routine and ongoing assessment of somatic depressive symptoms in HF patients may help clinicians identify patients at increased risk for adverse outcomes. ClinicalTrials.gov NCT00415545.

Depression and markers of inflammation as predictors of all-cause mortality in heart failure