There is little doubt that alcohol-related disorders in humans are genetically based. The influence of environmental factors, however, remains unclear. Given that studies of humans are complicated by a multitude of cultural and day-to-day-living factors, researchers in the March issue of Alcoholism: Clinical & Experimental Research use rhesus monkeys to examine genetic and environmental influences on alcohol consumption. Results indicate that, just as with humans, both genetic and environmental factors contribute to variation in alcohol consumption among the non-human primates.
"Rhesus macaques provide a good model for many human diseases due in part to their phylogenetic closeness," said Joseph G. Lorenz, research associate at the Coriell Institute for Medical Research and corresponding author for the study. "Also, like humans, they are highly social, which is important for diseases like alcoholism where there are social factors affecting alcohol consumption. And, finally, because we can control their social environment and precisely measure their exposure to alcohol, whereas human studies often rely on self-reported consumption patterns."
Researchers examined data drawn from an ongoing longitudinal study of genetic and environmental factors affecting the neurobiology, behavior and alcohol consumption among rhesus macaques. For this particular analysis, study authors investigated factors that may have contributed to variation in alcohol consumption among 156 monkeys during a period of 10 years when they were considered adolescents (between 2 and 4 years of age). All belonged to a single extended pedigree, and received identical early rearing backgrounds and subsequent treatments. Alcohol consumption was measured during unfettered and simultaneous access to both aspartame-sweetened (8.4% v/v) alcohol-water solution as well as water for one hour each day during early afternoon for a period of five to seven weeks.
"This study demonstrates that additive genetic factors contribute to the observed inter-individual variation in the consumption of alcohol in rhesus," said Lorenz. The term "additive genetic factors" refers to that portion of total genetic effects that is solely due to the presence or absence of a gene's given alleles. For example, additive genetic variance accounts for the genetic component of resemblance or non-resemblance that may exist among relatives.
"Additive genetic effects account for 20 percent of the total variation, leaving 20 percent of the variance attributable to 'residual environmental effects' not accounted for by the experimental treatments and covariates identified in the study," said Lorenz.
In earlier research, Lorenz and his colleagues had discovered that early rearing experiences (mother- versus peer-reared) during the first several months of life among infant rhesus monkeys had later effects on alcohol consumption. "Two percent of the total variation in alcohol consumption depended on whether the monkeys had been reared by their mothers or not," he said, "with mother-reared animals drinking significantly less than others." This more recent study, added Lorenz, shows that this effect -- while statistically significant -- is much smaller than additive genetic effects.
"Identifying a genetic component to alcohol consumption in this important animal model is a precursor to searching for the specific regions of the genome for genes that influence alcohol consumption," said Lorenz. "Many of these linkage studies have been carried out in human groups, but there is always the problem of precise measurement of phenotype and controlling for environmental variation in human studies -- which is not as great an issue in animal studies."
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Genetic and Other Contributions to Alcohol Intake in Rhesus Macaques (Macaca mulatta)," were: Jeffrey C. Long of the Department of Human Genetics, and the Center for Statistical Genetics, at the University of Michigan Medical School; Markku Linnoila (deceased); David Goldman of the Laboratory of Neurogenetics at the National Institute on Alcohol Abuse and Alcoholism; Stephen J. Suomi of the Laboratory of Comparative Ethology at the National Institute of Child Health and Human Development; and J. Dee Higley of the Section for the Study of Primate Models of Psychopathology in the Laboratory of Clinical and Translational Studies at the National Institute on Alcohol Abuse and Alcoholism. The study was funded by the National Institute of Child Health and Human Development and the National Institute on Alcohol Abuse and Alcoholism.
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