Do depression symptoms predict early hypertension incidence in young adults in the CARDIA study? Coronary Artery Risk Development in Young Adults.

BACKGROUND: Hypertension has been linked to several psychological factors, including depression, but the relation between hypertension incidence and depressive symptoms has not been adequately examined. OBJECTIVE: To determine if depressive symptoms independently predict hypertension incidence. DESIGN AND SETTING: A prospective, multicenter, epidemiological cohort of young adults (aged 23-35 years at study entry) from the general community without hypertension followed up for 5 years. SUBJECTS: A sample of 3343 adults from 4 urban areas stratified for race (black and white) from the CARDIA (Coronary Artery Risk Development in Young Adults) study. MAIN OUTCOME MEASURE: Hypertension incidence, which was defined as blood pressure higher than 160/95 mm Hg (assessed on a single occasion) or the use of prescribed antihypertensive medication. RESULTS: Participants with high scores (> or = 16) on the Center for Epidemiological Studies Depression (CES-D) Scale were at significant risk for hypertension incidence compared with those with low CES-D scores (< or =7; odds ratio, 2.10; 95% confidence interval, 1.22-3.61) after adjustment for other hypertension risk factors (eg, age, resting systolic blood pressure at the 5-year examination, physical activity, daily alcohol use, parental history of hypertension, education, presence of diabetes mellitus or heart disease, sex, and race) in fixed logistic models. Those with intermediate depressive symptoms (CES-D scores 8-15) were also at significant risk (adjusted odds ratio, 1.78; 95% confidence interval, 1.06-2.98). These associations were significant in blacks alone but were not found in whites, who had a lower hypertension incidence (29 [2%] of 1806) than blacks (89 [6%] of 1537). CONCLUSIONS: Depressive symptoms were predictive of later hypertension incidence in young adults, and young blacks with depressive symptoms were at high risk of developing hypertension.

Negative mood and urban versus rural residence: using proximity to metropolitan statistical areas as an alternative measure of residence.

The purposes of this report is to describe the distribution of reported negative mood by place of residence focusing on proximity to metropolitan statistical areas (MSA's) as an alternative to the traditional urban versus rural residence variable using the 1991 National Health Interview Survey's Health Promotion and Disease Prevention (NHIS-HPDP) supplement. The self-report of negative mood comes from the negative affect items of the Bradburn Affect Balance Scale categorized as high and low presence. The proximity to MSA's is a county-based measure developed as a combination of the MSA/non-MSA residence variable from the NHIS-HPDP and the United States Department of Agriculture (USDA) adjacency code from the Area Resource File (ARF). The proximity to MSA's measure has four categories: 1. MSA central city 2. MSA not central city 3. non-MSA adjacent (contiguous) to MSA 4. non-MSA not adjacent to MSA The odds ratios for negative mood were 1.24 (95 percent confidence limits [CL] = 1.11,1.38) for MSA central city and 1.26 (95 percent CL = 1.05,1.52) for non-MSA not adjacent to MSA as compared with MSA not central city. The odds ratio for non-MSA adjacent to MSA was not significantly different from MSA not central city. Data are presented by age, sex, race, and education. Thus, the proximity measure demonstrated greater discrimination in rates of negative mood than did urban versus rural or other measures of place of residence.

A method to redefine stays on the 1985 National Nursing Home Survey.

This report describes a method for standardizing definitions of episodes of nursing home care in the 1985 National Nursing Home Survey. The method shows how the information on nursing home admissions and discharges collected on the Current and Discharged Resident Questionnaires can be used to redefine the endpoints of nursing home stays. The report also explains how errors caused by missing and inconsistent nursing home admission and discharge data were resolved.

Effects of unilateral brain damage on contralateral and ipsilateral upper extremity function in hemiplegia.

This article describes the long-term effects of unilateral penetrating hemispheric lesions on contralateral and ipsilateral upper extremity motor performance and functional outcome. Activities-of-daily-living skill and gross motor performance contralateral to the lesions were compared among 32 left-sided and 19 right-sided hemiplegic subjects using analysis of variance and chi-square techniques. Ipsilateral to the damaged hemisphere, fine motor tasks of simple visual motor reaction time, grip and pinch strength, finger tapping, and Purdue Pegboard performance were tested. Analysis of covariance compared each ipsilateral task to performance in the corresponding hand of 70 matched controls. Results indicate similar long-term functional ADL outcome in right and left hemisphere-damaged subjects, despite more severe contralateral functional motor deficits following lesions of the left hemisphere. Right hemisphere lesions led to ipsilateral decrements in reaction time, and lesions of either hemisphere diminished grip or pinch strength, finger tapping, and pegboard performance ipsilaterally. These results demonstrate that unilateral brain damage involving the motor areas of either hemisphere has detrimental effects on ipsilateral upper extremity motor function. Findings are discussed and related to the concept that the left hemisphere is specialized or has greater neuronal representation for bilateral motor processes. Physical therapists involved in the treatment of patients with hemiplegia should be aware that motor functions of the ipsilateral, nonparetic upper extremity may also be affected adversely by unilateral brain lesions.

Negative affect as a prospective risk factor for hypertension.

OBJECTIVE: The objective of this study was to test the hypothesis that negative affect is a prospective risk factor for hypertension among white and black persons. METHODS: A population-based cohort of 3310 initially normotensive and chronic disease-free persons in the NHANES I Epidemiologic Follow-up Study was tracked through four follow-up waves (maximum, 22 years). The association between hypertension and baseline negative affect was analyzed using Cox proportional hazards regression, adjusting for baseline age, sex, race, education, smoking, alcohol use, diastolic and systolic blood pressure, body mass index, and change in body mass index as a time-dependent covariate. Negative affect was based on combined symptoms of depression and anxiety. Hypertension end points included 1) self-reported, 2) treated (prescription of antihypertensive medications), and 3) incident (blood pressure > or =160/95 mm Hg or treated) hypertension. Blood pressure measurements were obtained only at baseline and the first follow-up examination (maximum, 13 years). RESULTS: Increased negative affect was associated with elevated risk for self-reported, treated, and incident hypertension at first follow-up. Through four waves of follow-up, high negative affect was associated with treated hypertension in baseline risk-adjusted models for white women (relative risk [RR] = 1.73, 95% confidence interval [95% CI] = 1.30-2.30), black women (RR = 3.12, 95% CI = 1.24-7.88), and all men (RR = 1.56, 95% CI = 1.08-2.25). Time-dependent covariate models produced similar RRs. CONCLUSIONS: Negative affect is predictive of development of hypertension. For treated hypertension, white women and all men with increased negative affect had similarly elevated RRs, whereas black women with increased negative affect had substantially higher RRs.

Symptoms of depression as a prospective risk factor for stroke.

OBJECTIVE: The objective of this study was to assess baseline levels of depression as a risk factor for stroke among white and black men and women. METHODS: A population-based cohort of 6095 stroke-free white and black men and women aged 25 to 74 years in the NHANES I Epidemiologic Followup Study were followed for an average of 16 years to a maximum of 22 years. The association between stroke and baseline self-reported depressive symptomatology was analyzed using Cox proportional hazards models adjusting for baseline age, race, sex, education, smoking status, body mass index, alcohol use, nonrecreational physical activity, serum cholesterol level, history of diabetes, history of heart disease, and systolic blood pressure. Hospital records and death certificates were used to identify stroke cases; a total of 483 cases were identified. RESULTS: In age-adjusted models for all persons, white men, white women, and black persons of both sexes, depression was predictive of stroke. In risk-adjusted models for all persons (relative risk (RR) = 1.73, 95% confidence interval (CI) = 1.30-2.31) and for white men (RR = 1.68, 95% CI = 1.02-2.75), depression remained predictive of stroke. For white women, depression (RR = 1.52, 95% CI = 0.97-2.38) reached borderline significance (p = .07). For black persons, depression (RR = 2.60, 95% CI = 1.40-4.80) demonstrated a higher risk of stroke. A series of supplemental analyses also supported the association between depression and stroke. CONCLUSIONS: Depression is predictive of stroke across all strata. This nationally representative study gives evidence of a prospective association between depression and stroke.

Perinatal events associated with maternal smoking during pregnancy.

To identify components of smoking-related increased perinatal mortality, detailed analyses of data from the Ontario Perinatal Mortality Study (50,000 births, 1,300 deaths, 1960-1961) measured the relationship of maternal smoking to birth weight, gestation, placental complications, and perinatal mortality. Cross-tabulations with other factors and multiple adjustment showed increases with amount smoked of birth weights less than 2500 gm, gestations less than 38 weeks, placenta previa, abruptio placentae, and perinatal mortality. These significant, smoking-related increases were independent of mother's height, weight, hospital status, age-parity group, birthplace, previous pregnancy history, weight gain, time of registration, and sex of child. Maternal smoking had the strongest effect on birthweight in the 8 factor regression, and birth less than 2500 gm increased directly with smoking level from 20% to 340% in 37 data subgroups. Births less than 38 weeks increased 20% and 50% and perinatal mortality increased 20% and 35% for less than 1 pack and 1 + pack smokers, respectively, adjusted for 7 other factors. Placental complications increased consistently with smoking level in all of 37 subgroups except for primiparous less than 1 pack smokers. Adjusted rates increased 25% and 92% for placenta previa, 23% and 86% for abruptions among smokers of less than 1 pack and 1 + packs, respectively. These complications carry high perinatal mortality risk, and account for one-third to one-half of the perinatal deaths attributable to maternal smoking.

PIP: To identify components of smoking-related increased perinatal mortality, detailed analyses of data from the Ontario Perinatal Mortality Study (50,000 births, 1300 deaths, 1960-1961) measured the relationship of maternal smoking to birth weight, gestation, placental complications, and perinatal mortality. Cross-tabulations with other factors and multiple adjustment showed increases with amount smoked of birth weights 2500 gm, gestations 38 weeks, placenta previa, abruptio placentae, and perinatal mortality. These significant, smoking-related increases were independent of mother's height, weight, hospital status, age-parity group, birthplace, previous pregnancy history, weight gain, time of registration, and sex of child. Maternal smoking had the strongest effect on birthweight in the 8 factor regression, and birth 2500 gm increased directly with smoking level from 20 to 340% in 37 data subgroups. Births 38 weeks increased 20 and 50% and perinatal mortality increased 20 and 35% for 1 pack and 1 + pack smokers, respectively, adjusted for 7 other factors. Placental complications increased consistently with smoking level in all of 37 subgroups except for primiparous 1 pack smokers. Adjusted rates increased 25 and 92% for placenta previa, 23 and 86% for abruptions among smokers of 1 pack and 1 + packs, respectively. These complications carry high perinatal mortality risk, and account for 1/3 to 1/2 of the perinatal deaths attributable to maternal smoking.

Are symptoms of anxiety and depression risk factors for hypertension? Longitudinal evidence from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study.

OBJECTIVE: To test the hypothesis that symptoms of anxiety and depression increase the risk of experiencing hypertension, using the National Health and Nutrition Examination I Epidemiologic Follow-up Study. DESIGN: A cohort of men and women without evidence of hypertension at baseline were followed up for 7 to 16 years. The association between 2 outcome measures (hypertension and treated hypertension) and baseline anxiety and depression was analyzed using Cox proportional hazards regression adjusting for hypertension risk factors (age; sex; education; cigarette smoking; body mass index; alcohol use; history of diabetes, stroke, or coronary heart disease; and baseline systolic blood pressure). Analyses were stratified by race and age (white persons aged 25-44 years and 45-64 years and black persons aged 25-64 years). SETTING: General community. PARTICIPANTS: A population-based sample of 2992 initially normotensive persons. MAIN OUTCOME MEASURES: Incident hypertension was defined as blood pressure of 160/95 mm Hg or more, or prescription of antihypertensive medications. Treated hypertension was defined as prescription of antihypertensive medications. RESULTS: In the multivariate models for whites aged 45 to 64 years, high anxiety (relative risk [RR], 1.82; 95% confidence interval [CI], 1.30-2.53) and high depression (RR, 1.80; 95% CI, 1.16-2.78) remained independent predictors of incident hypertension. The risks associated with treated hypertension were also increased for high anxiety (RR, 2.36; 95% CI, 1.73-3.23) and high depression (RR, 1.89; 95% CI, 1.25-2.85). For blacks aged 25 to 64 years, high anxiety (RR, 2.74; 95% CI, 1.35-5.53) and high depression (RR, 2.99; 95% CI, 1.41-6.33) remained independent predictors of incident hypertension. The risks associated with treated hypertension were also increased for high anxiety (RR, 3.24; 95% CI, 1.59-6.61) and high depression (RR, 2.92; 95% CI, 1.37-6.22). For whites aged 25 to 44 years, intermediate anxiety (RR, 1.62; 95% CI, 1.18-2.22) and intermediate depression (RR, 1.60; 95% CI, 1.17-2.17) remained independent predictors of treated hypertension only. CONCLUSION: Anxiety and depression are predictive of later incidence of hypertension and prescription treatment for hypertension.

Psychologic factors as precursors to hypertension.

The possibility that certain psychologic factors lead to hypertension has been considered by many investigators over the past 60 years, but prospective studies with suitable methods to evaluate this hypothesis were not available for analysis until the 1990s. There are now five large longitudinal studies demonstrating a relation between symptoms of anxiety or depression and subsequent hypertension incidence. Anger expression, long considered a major psychologic factor in hypertension, has been studied less extensively, and the findings to date are less consistent. While some evidence supports the biological plausibility of psychologic factors as risk factors for hypertension, biobehavioral mechanisms explaining the relationship have not been adequately explored. The results of these recent studies may lead to new intervention trials specifically selecting hypertensive patients with anxiety or depression for treatment with stress reduction or other appropriate psychologic therapies. Such studies would further contribute to the evaluation of anxiety and depression as risk factors for hypertension.

Intellectual function following penetrating head injury in Vietnam veterans.

The extent to which intellectual processes are preserved as a function of preinjury 'intelligence' and of size and location of the brain lesions was evaluated in Vietnam war veterans who survived penetrating missile wounds. With regard to an overall postinjury intelligence test score, preinjury intelligence was most predictive, size of lesion was next most predictive and lesion location was least important. For subtest scores from the same intelligence test, lesion location assumed much greater predictive value. Specifically, left temporal and occipital lesions impaired performance on subtests assessing vocabulary and object-function matching ability.