Greater Hepatic Vulnerability after Alcohol Intake: DISCUSSION

9 Jan

alcohol consumption

In the present study, we analyzed racial differences in the most commonly used biomarkers of hepatic damage—AST, ALT, and GGT—and the extent to which alcohol consumption can explain racial differences. The findings show that hepatic enzyme mean values (especially GGT) may increase more markedly among African Americans than in whites in relation both to drinking status and amount of alcohol consumed. For GGT, racial differences exist even in non-drinkers. The most important differences were found for GGT: in all categories of drinking status (lifetime abstainers, former and current drinkers), average levels were significantly higher in African Americans compared to whites. Furthermore, among current drinkers differences in GGT mean values were larger than those observed either in lifetime abstainers or in former drinkers. In analyses based on tertiles of recent (past 30 days) alcohol consumption, differences in GGT mean values between the two ethnic groups tended to amplify with increasing tertiles of consumption.

The problem of disparities between U.S. white and nonwhite cirrhosis mortality rates is multifaceted and seems to originate from the interaction of several possible determinants, such as environmental, social, and genetic factors. Alcohol consumption has been speculated as the primary etiological agent for the observed pattern because of its high prevalence in the general population and its close relationship with potential liver damage. It has been suggested that among black people, the secular trends in cirrhosis mortality rates from the late 1950s may be a reflection of substantial changes in drinking habits initiated at the turn of the last century. Nevertheless, it is not still clear to what extent alcohol consumption may explain these cirrhosis-related mortality disparities between African Americans and Caucasians and which aspect of alcohol use may represent the major contributor to this phenomenon. Differences in drinking patterns and genetic vulnerability to alcohol-related damage have been speculated as the potential main determinants of these racial disparities, although the results in literature are still controversial. Several surveys have revealed similar probabilities of heavy drinking among various racial and ethnic groups, and a relatively higher proportion of abstainers in African Americans compared to other racial groups. Conversely, other studies have emphasized the importance of duration of heavy consumption as a major factor in cirrhosis etiology, underlining that mortality outcome represents the cumulative effects of past and current level of alcohol consumption. Moreover, several reports have found possible variations in the stability of heavy drinking during the lifetime among different racial groups as a potential explanation for the observed ethnic differences in liver damage. For example, in one study, Caetano has shown that age distribution of heavy drinking is substantially different between Caucasian and African-American men, with the African Americans more likely to be heavy drinkers at older ages. This different pattern of heavy drinking could increase the number of drinkers at risk for cirrhosis in the black population, despite the similarity of per-capita consumption of the two racial groups at a single point in time. Furthermore, in more recent analyses on changes in national drinking patterns among whites, blacks, and Hispanics, the same author has reported more stable rates of frequent heavy drinking over the life course among Hispanics and African Americans, compared to Caucasians. These results seem to point out that drinking among the two minority groups might reflect longer, heavier drinking careers and heavier consumption of alcohol, both in terms of quantity and frequency of drinking, relative to their white counterparts. In addition, a very large and detailed investigation on differentials in US drinking patterns by racial and ethnic subgroups has confirmed the substantial differences in drinking style between African Americas and Caucasians, with the former characterized by more extreme drinking habits (higher frequency of heavy drinking occasions, elevated intake of alcohol per drinking day, and major consumption of spirits). buy tadacip

These differences in drinking patterns might partially explain the higher death rates of alcoholic liver cirrhosis in the last decades among African Americans (and Hispanics) compared with Caucasians. However, other important determinants—such as socioeconomic status, diet, and genetic factors—might also contribute to these differences. Among them, a different racial sensitivity to the hepatotoxic effects of alcohol has been supported by a very recent study. In a cross-sectional analysis of adult subjects from the Third National Health and Examination Survey, the author found that, among current drinkers, black non-Hispanic and Mexican Americans experienced a higher risk for elevated AST and GGT levels (>95th percentile) compared to white non-Hispanic Americans with increasing risk for increasing frequency of alcohol consumption in the previous 30 days. Furthermore, the hypothesis of a different susceptibility to alcohol consumption among various racial and ethnic subgroups has been corroborated by several studies on genetic determinants of alcohol metabolism. Genetically determined variants in key enzymes for alcohol metabolism, such as alcohol dehydrogenase isozymes and acetaldehyde dehydrogenase, seem to play an important role in individual and racial differences in acute and chronic effects of alcohol drinking as well as towards vulnerability to organ damage after chronic alcohol abuse. In particular, alcohol dehydrogenase (ADH) polymorphisms are known to have different distributions for African Americans and Caucasians.
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Our study findings support the hypothesis of greater susceptibility to alcohol-related liver damage among African Americans, compared to Caucasians. It shows that at the highest levels of consumption, the more-specific enzymes of hepatocellular injury—such as AST and ALT—tend to be higher (though not significantly) in African Americans than in Caucasians. This finding is even more striking if we consider that the AST and ALT distributions in our sample were not significantly different between the two racial groups with very similar 95th percentiles for both enzymes. For GGT, the distribution was substantially different between the two races and the black participants exhibited significantly elevated mean values even among lifetime abstainers. This different racial distribution of GGT levels is not a new finding; it has been reported in other population-based studies. GGT is not a specific marker of alcohol consumption and alcohol-related hepatic injury, and its elevated average levels in African Americans even among lifetime abstainers might be due to hepatic vulnerability of this ethnic group.

Our study presents several limitations that need to be considered in the valuation of its results. First, the cross-sectional design doesn’t allow us to draw conclusions about cause-and-effect relationship. Further, we cannot rule out that the observed relationship might be explained by uncontrolled confounding by unknown confounders or by residual confounding. Furthermore, the suboptimal participation rate (59.5%) may influence the generalizabil-ity of the findings. Finally, the small sample size for African Americans might have affected the distribution of hepatic enzymes and does not allow us to provide detailed gender-specific analyses, as well as a detailed analysis of the potential effect of pattern of drinking on these markers of liver injury. On the other hand, the strength of this study consists of the very detailed information elicited on total and beverage specific alcohol consumption in the past 30 days as well as the examination of several covariates known to be related to hepatic enzymes.

In conclusion, our study corroborates the hypothesis of a racial-based difference in susceptibility to alcohol consumption as one of the potential contributors to disparities in cirrhosis-related mortality rates in the U.S. population. We found that even in nondrinkers, ethnic differences are present, suggesting the existence of other factors that may differentially affect liver metabolism and health. Our findings indicate the need to further investigate these factors as well as the complex interaction between race and alcohol use on liver function in additional population-based studies.