Premature Aging in Male Alcoholics: “Accelerated Aging” or “Increased Vulnerability”?

This study involved an evaluation of two versions of the "premature aging" theory of chronic alcoholism: the accelerated aging and increased vumerabHty versions. The major dependent measures used were the tests included in Reitan's brain age quotient (BAO), a series of neuropsychological tests known to be sensitive to the effects of alcoholism and aging. Subjects were 40 chronic alcoholic inpatients and 40 matched controls, divided into age groups by; decade, ranging from the 30s to the 60s. It was proposed that an j interaction between age and presence or absence of alcoholism, with BAO test differences between alcoholics and controls widening as age increases, would support the increased vulnerability version, while the absence of such aw interaction would support the accel-] erated aging version. The results dearty favored the accelerated aging version, with merited BAO test differences between alcoholics, and controls appearing even in the 30-year-old groups. It was concluded that chronic ateohoftcs tend to perform at levels found for nonalconoiics 10 years their senior, but the discrepancy between, alcoholics and nonalcohoics does not increase with age.     

Cellular Immune Functions, Endorphins, and Alcohol Consumption in Males

The effects of alcohol abuse on cellular immune functions were measured by various levels of alcohol use in adult men. Total lifelong abstainers were used as controls. Previous abusers, current abusers, and patients with alcoholic cirrhosis or pancreatitis were age-matched to controls. T-lymphocyte mitogenesis stimulated by phytohemagglutinin and concanavalin A was generally reduced in peripheral blood lymphocytes of current and previous alcohol consumers, although the decrease was not statistically significant. B-cell mitogenesis stimulated by pokeweed mitogen was not changed by previous alcohol consumption. The number of T-cells was not changed by either previous or current alcohol abuse. T-helper cells were significantly increased and T-suppressor cells increased only in the patients with alcoholic cirrhosis or pancreatitis. The percentage of T-lymphocytes with T-suppressor characteristics in controls was 27% while in alcoholic cirrhosis or pancreatitis subjects it was 16%. Plasma corticosteroid levels were significantly increased in people currently consuming alcohol (12.1 +/- 1.1 mg/dl) compared to controls (7.7 +/- 1.1). The corticosteroid levels were also higher in previous alcohol abusers although not statistically significant. Plasma endorphin levels were increased by severe alcohol abuse in the patients with cirrhosis or pancreatitis to 25.03 +/- 6.74 from 11.85 +/- 2.48 pg/ml in controls.     

Usefulness of high-dose anticoagulants in preventing left ventricular thrombus in acute myocardial infarction

Fifty-three patients with a suspected first anterior wall acute myocardial infarction (AMI) were randomized to intervention with intravenous heparin followed by oral warfarin (26 patients) or matching placebo (27 patients). The regimen was started within 12 hours after the onset of AMI. Anticoagulation was maintained at a therapeutic level (for heparin, activated partial thromboplastin time 70 to 140 seconds; for warfarin, thrombotest 5 to 10%) for 10 days, and no bleeding episodes occurred. The baseline characteristics of the 2 study groups were well matched. In 7 patients in the placebo group and in none in the anticoagulant group, left ventricular thrombus developed during the study, as detected by serial 2-dimensional echocardiography. Early intervention with high-dose anticoagulant drugs may prevent the development of left ventricular thrombus in anterior wall AMI.     

Lipid accumulation in jejunal and colonic mucosa following chronic cholestyramine (Questran) feeding

The hypolipidemic agent, cholestyramine (Questran), when fed to rats inhibits intestinal absorption of cholesterol and triglycerides and causes significant epithelial cell damage in both small and large intestine. In this study, we report significant accumulation of lipids in the mucosal layer of both jejunum and colon in rats administered 2% cholestyramine for a four-week period, when compared to a control group maintained on regular chow. The total lipid increment with cholestyramine was 4.7-fold in the jejunum and 3.7-fold in the colon. The triglyceride fraction increased substantially in the small but not the large intestine. Relative phospholipid levels decreased in the treated jejunum but not in the colon. The biochemical data were reflected in morphological evidence of lipid-laden enterocytes obtained by light and transmission electron microscopy. Since cholestyramine has been shown to sequester 99.8% of micellar phospholipidin vitro, it is concluded that the presence of cholestyramine in the intestinal lumen may interefere with phospholipid availability for chylomicron synthesis and serosal lipid exit from the epithelium. This unusual deposition of lipid within the mucosal layer may also be correlated with the known cocarcinogenic effect of this resin in experimentally induced intestinal cancer.Supported by USDA grants 82CRCR 1071 and 82 CRCR 1001.