PubMed · 1135339
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J Pionkowski, I Wojdytawska, E Patura. [Pathological alcohol intoxication].. https://pubmed.ncbi.nlm.nih.gov/1135339/
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CONTEXT: During the last few decades, mortality from drowning has decreased in the United States for unknown reasons. It has been hypothesized that this decline may be due to decreased use of alcohol in and around water or improved medical treatment after a submersion. OBJECTIVES: To estimate changes in unintentional mortality due to submersion, estimate trends in drownings attributable to alcohol use, and assess the role of medical care in these mortality trends. DESIGN: A 21-year longitudinal study of case findings, from January 1, 1975, through December 31,1995. SETTING AND PARTICIPANTS: All residents of King County, Washington, who died unintentionally from submersion and 284 persons hospitalized for submersion who survived. MAIN OUTCOME MEASURES: Changes in submersion-related mortality incidence over time, proportion of this mortality that could be attributed to alcohol use, changes over time in the case-fatality rate of treated patients, and estimate of deaths prevented in 1995 compared with projected estimates had there been no change in incidence since 1975. RESULTS: There were 539 deaths due to drowning in King County during 21 years. Mortality rates during this period declined by 59% (95% confidence interval [CI], -70% to -46%). The incidence of death attributable to alcohol use decreased by 81% (95% CI, -91% to -57%); this could account for 51% of deaths prevented in 1995. Among 249 comatose patients who received prehospital care, 205 died; the odds of survival decreased 40% over 21 years (P = .40). Among 101 comatose patients who were hospitalized, 63 died; the odds of survival decreased 29% (P = .75). The incidence of survival of comatose hospital patients decreased by 29% from 1975 to 1995 (95% CI, -78% to +125%). We found no evidence that trends in medical treatment prevented any deaths due to drowning in 1995. CONCLUSIONS: Drowning incidence in King County, Washington, declined because of a decrease in severe submersion episodes rather than an increase in success of medical interventions. Our data support the theory that less use of alcohol around water prevents some deaths. About half of the decrease was unexplained.
This paper reviews the law related to voluntary intoxication and criminal responsibility in the 50 United States, the District of Columbia, the US Virgin islands, and Puerto Rico. Statutory and case law citations are provided which govern the use of intoxication evidence in each jurisdiction to negate mens rea (i.e., to establish diminished capacity), to support an insanity defense, and to mitigate criminal sentencing. Factors that courts typically focus on when deciding whether to admit this evidence in a particular case are discussed, and these factors are related to clinically relevant criteria.
This study addresses the role of the lipid peroxidation product, 4-hydroxynonenal (HNE), in ethanol-related damage of cytochrome c oxidase (COX) in vivo. It utilizes an animal model with acute ethanol exposure in which HNE levels in liver mitochondria are strikingly increased. Pregnant female Sprague-Dawley rats were administered 5 doses of ethanol (4 gm/kg, po at 12-hour intervals) beginning on day 17 of gestation and were sacrificed on day 19. Controls were pair-fed and received dextrose isocaloric to ethanol. Mitochondria were isolated from maternal and fetal livers and COX activities were measured spectrophotometrically. Compared with the pair-fed controls, COX activity was decreased with exposure to ethanol by 25% in maternal rats and 43% in fetal rats (P<.05). Western Blot with an HNE-Histidine antibody showed enhanced formation of HNE adducts with COX from ethanol-exposed rats, which was more pronounced in fetal than in adult livers. The HNE adducts were mainly with subunit IV of COX. The cause and effect relationship between HNE adduct formation and COX inhibition was examined in vitro by incubating purified COX with HNE. COX inhibition was accompanied by concentration-dependent HNE adduct formation that was consistent with those found in in vivo ethanol-exposed samples. These results suggest that the ethanol-related decreases in COX activity found in liver mitochondria could be attributable to HNE adduct formation with the enzyme complex. This could be an important mechanism by which modification of proteins occur in in vivo oxidative stress.