M J Klag

The Johns Hopkins Precursors Study, a long-term prospective study, was used to study the relation between self-reported sleep disturbances and subsequent clinical depression and psychiatric distress. A total of 1,053 men provided information on sleep habits during medical school at The Johns Hopkins University (classes of 1948-1964) and have been followed since graduation. During a median follow-up period of 34 years (range 1-45), 101 men developed clinical depression (cumulative incidence at 40 years, 12.2%), including 13 suicides. In Cox proportional hazards analysis adjusted for age at graduation, class year, parental history of clinical depression, coffee drinking, and measures of temperament, the relative risk of clinical depression was greater in those who reported insomnia in medical school (relative risk (RR) 2.0, 95% confidence interval (CI) 1.2-3.3) compared with those who did not and greater in those with difficulty sleeping under stress in medical school (RR 1.8, 95% CI 1.2-2.7) compared with those who did not report difficulty. There were weaker associations for those who reported poor quality of sleep (RR 1.6, 95% CI 0.9-2.9) and sleep duration of 7 hours or less (RR 1.5, 95% CI 0.9-2.3) with development of clinical depression. Similar associations were observed between reports of sleep disturbances in medical school and psychiatric distress assessed in 1988 by the General Health Questionnaire. These findings suggest that insomnia in young men is indicative of a greater risk for subsequent clinical depression and psychiatric distress that persists for at least 30 years.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the influence of race, sex, and other risk factors on the location of atherosclerotic occlusive lesions in cerebral vessels. Previous angiographic studies of patients with stroke or transient ischemic attack (TIA) suggest that extracranial atherosclerosis is more common in whites and intracranial disease is more common in blacks. Noninvasive techniques such as duplex ultrasound, transcranial Doppler (TCD), and magnetic resonance angiography (MRA) allow vascular assessment of a more representative proportion of patients than does conventional angiography alone. METHODS: Consecutive patients evaluated at a community hospital for stroke or TIA over a 2-year period were reviewed. Lesions were defined as a 50% or greater atherosclerotic stenosis by angiography, duplex ultrasound, or TCD, or a moderate stenosis by MRA. RESULTS: Whites were more likely than blacks to have extracranial carotid artery lesions (33% versus 15%, P = .001), but the proportion of patients with intracranial lesions was similar (24% versus 22%). Men were more likely to have intracranial lesions than women (29% versus 14%, P = .03). When multivariate logistic regression analysis was used, white race was the only predictor for extracranial carotid artery lesions, and male sex was the only predictor for intracranial lesions. The cause of stroke/TIA was extracranial carotid artery disease in 8% and intracranial disease in 8% of all patients in the study. CONCLUSIONS: The distribution of cerebral atherosclerosis is influenced by race and sex but not by other vascular risk factors. In our patient population, intracranial disease is as common a cause of cerebral ischemia as extracranial carotid disease.

BACKGROUND: An increased intake of magnesium might lower blood pressure (BP), yet evidence from clinical trials is inconsistent, perhaps as a result of small sample size or heterogeneity in study design. METHODS: We performed a meta-analysis of randomized trials that tested the effects of magnesium supplementation on BP. Twenty trials meeting the inclusion criteria were identified. Random effects models and meta-regression methods were used to pool study results and to determine the dose-response relationship of magnesium to BP. RESULTS: The 20 studies included 14 of hypertensive and 6 of normotensive persons totaling 1220 participants. The doses of magnesium ranged from 10 to 40 mmol/day (median, 15.4 mmol/day). Magnesium supplementation resulted in only a small overall reduction in BP. The pooled net estimates of BP change (95% confidence interval [CI]) were -0.6 (-2.2 to 1.0) mm Hg for systolic BP and -0.8 (-1.9 to 0.4) mm Hg for diastolic BP. However, there was an apparent dose-dependent effect of magnesium, with reductions of 4.3 mm Hg systolic BP (95% CI 6.3 to 2.2; P < .001) and of 2.3 mm Hg diastolic BP (95% CI 4.9 to 0.0; P = .09) for each 10 mmol/day increase in magnesium dose. CONCLUSIONS: Our meta-analysis detected dose-dependent BP reductions from magnesium supplementation. However, adequately powered trials with sufficiently high doses of magnesium supplements need to be performed to confirm this relationship.

BACKGROUND: In vitro, animal and epidemiological studies suggest that lipoprotein oxidation may play an important role in atherosclerosis. Antioxidants may protect against lipoprotein oxidation and in that way inhibit atherosclerosis and its clinical sequelae. To investigate this possibility, we examined the association between levels of several antioxidants and myocardial infarction using serum specimens collected 7 to 14 years before the onset of myocardial infarction. METHODS AND RESULTS: A nested case-control design was used. Cases and control subjects were selected from the 25,802 persons who had donated 15 mL of blood in 1974 for a serum bank. Cases comprised 123 persons with a subsequent first diagnosis of myocardial infarction who ranged from 23 through 58 years of age in 1974 and who had had their first diagnosis of myocardial infarction during 1981 to 1988. Two groups of control subjects matched to the cases for sex and age were selected from donors to the serum bank, one from those with hospital admissions during the same period and the other from the total group of donors. Sera were assayed for four carotenoids (beta-carotene, lycopene, lutein, and zeaxanthin), alpha-tocopherol, and cholesterol. Because associations with these serum nutrients showed similar trends whether based on hospital or community controls, the two control groups were combined. There was a significantly increasing risk for subsequent myocardial infarction with decreasing levels of beta-carotene in 1974 (P value for trend, .02) and a suggestive trend with decreasing levels of lutein (P = .09). When the results were stratified by smoking status, the excess risk of myocardial infarction associated with low serum levels of carotenoids was limited to smokers. A protective association with higher levels of alpha-tocopherol was suggested only among persons with high levels of serum cholesterol. CONCLUSIONS: Low serum levels of carotenoids were associated with an increased risk of subsequent myocardial infarction among smokers.