Genetic factors influence the susceptibility for advanced ALD. Monozygotic twins have a higher concordance rate for alcohol-related cirrhosis than dizygotic twins (23). Genetic factors may influence susceptibility to alcohol consumption or predisposition to development of ALD among those with AUD. Genes influencing the susceptibility for alcoholism include modifiers of neurotransmission such as γ-amino butyric acid and modifiers of alcohol metabolism such as alcoholic dehydrogenase and acetaldehyde dehydrogenase enzymes (24). The polymorphisms in these genes may be involved in an individual’s susceptibility to alcoholism, with wide allelic variation between different ethnic groups, but their role in the progression of ALD remains controversial. The second group of genes modifies the natural history of ALD through different mechanisms. Small candidate gene studies initially suggested a role for polymorphisms in genes encoding inflammatory mediators, endotoxin response and oxidative stress. However, larger studies including a recent genome-wide association study revealed that patatinlike phospholipase domain containing protein 3, may be the main genetic determinant of risk for and severity of ALD (25, 26). Phospholipase domain containing protein 3 is closely related with lipid metabolism and is also a risk factor for non-alcoholic fatty liver disease and HCC (26). The allele that negatively impacts disease progression (., rs738409) is more frequent within the Hispanic population, which is particularly sensitive to fatty liver diseases (25).
Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.
Tucker has always eaten Science Diet food and has been fairly healthy…he does have PRA which is hereditary where he has gone blind. He started vomiting so I took him to his vet and found out he was dehydrated and have high liver count. He’s been there over night two times and the vet has put him on Science Diet LD and Denosyl and another chewable tablet. He eats it fine and has gotten better. The problem i am having is when I take him outside…he finds anything he can to eat. Is he not getting enough to fill his belly from eating this food?