Nutrients, Genetic Factors, and Their Interaction in Non-Alcoholic Fatty Liver Disease and Cardiovascular Disease

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in Western countries and expose patients to increased risk of hepatic and cardiovascular (CV) morbidity and mortality. Both environmental factors and genetic predisposition contribute to the risk. An inappropriate diet, rich in refined carbohydrates, especially fructose, and saturated fats, and poor in fibers, polyunsaturated fats, and vitamins is one of the main key factors, as well as the polymorphism of patatin-like phospholipase domain containing 3 (PNPLA3 gene) for NAFLD and the apolipoproteins and the peroxisome proliferator-activated receptor (PPAR) family for the cardiovascular damage. Beyond genetic influence, also epigenetics modifications are responsible for various clinical manifestations of both hepatic and CV disease. Interestingly, data are accumulating on the interplay between diet and genetic and epigenetic modifications, modulating pathogenetic pathways in NAFLD and CV disease. We report the main evidence from literature on the influence of both macro and micronutrients in NAFLD and CV damage and the role of genetics either alone or combined with diet in increasing the risk of developing both diseases. Understanding the interaction between metabolic alterations, genetics and diet are essential to treat the diseases and tailoring nutritional therapy to control NAFLD and CV risk.

Overview of Non-Alcoholic Fatty Liver Disease (NAFLD) and the Role of Sugary Food Consumption and Other Dietary Components in Its Development

“…Fructose is present in natural foods (fruits, vegetables, honey) and in processed foods (juices, nectars, other beverages) [ 71 ]. In addition, fructose is a primary component in the most widely used sweeteners (sucrose or high fructose corn syrup [HFCS]).…”

“…Similar results were also obtained in a subgroup of 6613 US adults participating in the National Health and Nutrition Examination Survey [ 132 ]. However, it is not fully known whether the protective effect of fibre against NAFLD is due to an indirect action through modulation of the microbiome or if it is a result of the direct anti-inflammatory properties of fibre [ 71 ].…”

Lentinan Protects against Nonalcoholic Fatty Liver Disease by Reducing Oxidative Stress and Apoptosis via the PPARα Pathway

“…NAFLD covers a spectrum of liver damage ranging from simple steatosis to more severe forms of liver injury, including nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma [4,5]. Furthermore, NAFLD is a strong risk factor for cardiovascular disease, atherosclerosis, Type 2 diabetes, and chronic kidney disease [3,6]. Currently, there are limited therapeutic options.…”

Nonalcoholic Fatty Liver Disease and the Kidney: A Review

“…Both diseases share main risk factors, mostly represented by obesity and metabolic syndrome. Insulin resistance [19,46], systemic low-grade inflammation [47,48] and increased oxidative stress [49,50], induced by visceral obesity and metabolic dysregulation, can promote both NAFLD and CKD. Western diet, rich in added sugars and saturated fats, promotes insulin resistance and visceral obesity [51].…”