My research emphasizes neurotransmitter metabolism, particularly serotonin and dopamine in relation to their nutrient precursors and diet composition. Our laboratory has successfully inhibited the craving for alcohol in addicted rats and prevented the major alcohol withdrawal symptoms through manipulation of brain neurotransmitters and nutrients such as tryptophan. Most recently we have been successful in sharply reducing blood alcohol and liver fat levels in rats consuming addictive amounts of alcohol These observations have led to an investigation of the intermediary metabolism of alcohol in relation to fat and carbohydrate. The accompanying table shows the effectiveness of a high-carbohydrate, ethanol- containing diet in reducing blood alcohol (not shown) and liver fat, compared to a high-fat diet.
Plasma ethanol and liver fat of rats fed high-carbohydrate or high-fat diets with or without ethanol.
| Ethanol Intake | 5-week Body Weight Gain | Liver Fat % of Weight Tissue |
|---|---|---|
| g/kg/diet | g | |
| High fat - | 169 ± 21 b | 6.4 ± 0.7 b |
| High fat 14.6 ± 0.8 | 109 ± 23 a | 10.2 ± 0.3 c |
| High CHO - | 177 ± 12 b | 3.9 ± 0.3 a |
| High CHO 15.2 ± 0. | 122 ± 17 a | 4.7 ± 1.0 a |
1Means ± SE for 10 rats/treatment.
2Means with different superscript letters are significantly different from each other (P < 0.05) Fisher's PLSD test.
Our most recent findings show that high levels of dietary Vitamin E and of Selenium, in the presence of alcohol, significantly worsen fatty liver concentrations. On the other hand, DPPD, a synthetic antioxidant, in the presence of caffeine, significantly reduces the alcoholic fatty liver.