Major depressive disorder signals increased risk for onset of type II diabetes. Limitations of the findings arise from the difficulty in determining temporal order with two chronic conditions, even when the temporal order of measurement is clear. In addition, even though control variables were introduced for the use of health services, it is possible that the treatment for depression led to an earlier diagnosis of diabetes in this sample.

These data suggest that a history of dysphoria and a major depressive episode increase the risk of MI. The association between psychotropic medication use and MI is probably a reflection of the primary relationship between depression and MI.

Abdominal aortic aneurysms (AAAs) have historically been considered to be a manifestation of atherosclerosis. However, there are epidemiologic and biochemical differences between occlusive atherosclerotic disease and aneurysmal disease of the aorta. A case-control study was performed to investigate risk factors for AAA at the two tertiary care hospitals in Winnipeg, Manitoba, Canada, between June 1992 and December 1995 to investigate risk factors for AAA. Newly diagnosed cases of AAA (n = 98) were compared with non-AAA controls (n = 102), who underwent ultrasound for indications similar to those of the cases. Compared with that for never smokers, the adjusted odds ratio (OR) was 2.75 (95% confidence interval (CI): 0.85, 8.91) for 1-19 pack-years, 7.31 (95% CI: 2.44, 21.9) for 20-34 pack-years, 7.35 (95% CI: 2.40, 22.5) for 35-49 pack-years, and 9.55 (95% CI: 2.81, 32.5) for 50 or more pack-years. Other factors significantly associated with AAA were male gender (OR = 2.68, 95% CI: 1.26, 5.73), diastolic blood pressure (OR per 10 mmHg = 1.88, 95% CI: 1.31, 2.69), and family history of AAA (OR = 4.77, 95% CI: 1.26, 18.1). There was an inverse association between diabetes mellitus and AAA (OR = 0.32, 95% CI: 0.12, 0.88). Neither clinical hypercholesterolemia nor serum levels of total cholesterol, low density lipoprotein cholesterol, and high density lipoprotein cholesterol was associated with AAA. The results of this study suggest that the risk factors for AAA differ from those for atherosclerosis and that atherosclerosis per se is not an adequate explanation as the cause of AAAs.

Based on this large population sample, we believe that early support to survivors with high levels of loss may reduce PTSD following earthquakes.

To assess the relation of increased mortality and morbidity to personal loss and damage following the 1988 earthquake in Armenia, the authors conducted a prospective study of mortality and a nested case-control analysis of incident morbidity. Employees of the Armenian Ministry of Health and their immediate families (n = 35,043) who survived the disaster formed the study population. Two sets of interviews with the employees, carried out over a period of 4 years of follow-up, were used as the primary source of data for this study. The highest numbers of deaths from all causes and from heart disease were observed within the first 6 months following the earthquake. The nested case-control analysis of 483 cases of newly reported heart disease and 482 matched non-heart-disease controls revealed that people with increasing levels of loss of material possessions and family members had significant increases in heart disease risk (odds ratios for "loss scores" of 1, 2, and 3 were 1.3, 1.8, and 2.6, respectively). The findings were similar with regard to the relation of damage and loss to newly reported hypertension, diabetes mellitus, and arthritis. The findings of this study support the hypothesis that longer term increased rates of heart disease and chronic disease morbidity following an earthquake are related to the intensity of exposure to disaster-related damage and losses. People sustaining such losses should be closely monitored for increased long term morbidity.

No abstract

Most studies of psychopathology following disasters are concerned with posttraumatic stress disorder (PTSD).

To determine Kaposi's sarcoma (KS) risk related to timing of human immunodeficiency virus type 1 (HIV-1) and human herpesvirus type 8 (HHV-8) infections, stored longitudinal sera from 400 homosexual men with known dates of HIV-1 seroconversion (+/-4.5 months) were tested for HHV-8 antibody. Times from HHV-8 seroconversion to KS were compared for the 69 men who became infected with HHV-8 after acquiring HIV-1 to the 182 men who were HHV-8 seropositive before their HIV-1 infection. None developed KS before coinfection. HHV-8 seroconversion after HIV-1 infection increased the risk of KS (risk ratio, 2.55; 95% confidence interval, 1.06-6.10) compared with those infected with HHV-8 before HIV-1. The KS hazards in HHV-8-infected men increased by 60% (P<.001) for each year of HIV-1 infection. Faster CD4 cell loss and higher HIV-1 RNA levels significantly predicted KS. The quicker development of KS in men acquiring HHV-8 after HIV-1 and its association with CD4 slope argues that KS is more likely if HHV-8 infection occurs in an immunocompromised person.