Plain language summary
Non-alcoholic fatty liver disease (NAFLD) and heart disease are influenced by diet and genetics. NAFLD cannot be managed with drugs and so lifestyle modification is the main recommendation, which is also advised in heart disease. The aim of this large review of 176 papers was to discuss the role of nutrients and genetics in NAFLD and heart disease. Amongst the main nutrients, excess fructose (a simple sugar) and high saturated and trans-fats were all shown to contribute to the development of both diseases. The influence of protein on NAFLD is controversial. Animal studies suggest that protein can be of benefit, but studies on humans have failed to support this. This is similar for heart disease where large scale trials in humans are not definitive. The role of fibre in NAFLD and heart disease appears to be beneficial. Several micronutrients were also reviewed including vitamins D, K, curcumin, plant chemicals and caffeine. The complex interplay involving genetics was also discussed and although fairly new science, evidence is mounting in support of genetic considerations when making dietary recommendations. It was concluded that diet and genetics influence the development of NAFLD, and heart disease and dietary recommendations need to reflect this. This study could be used by health care professionals to understand the interaction between diet and genetics and the importance of making personalised nutrition recommendations to individuals with NAFLD or heart 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.
Methodological quality
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