Non-alcoholic fatty liver disease (NAFLD) is a condition is increasingly being linked to poor diet. In particular, increased consumption of fructose may overload the liver with energy, and this increases the rate of fatty acid synthesis through the de novo lipogenesis pathway. These fatty acids accumulate in the liver and lead to the development of NAFLD, which can deteriorate into cirrhosis of the liver. In this respect NAFLD is similar in aetiology to alcoholic fatty liver disease, although while the latter is caused by the over consumption of ethanol, the former is caused by the over consumption of fructose. The similar metabolic fates of fructose and alcohol explain the similarity in the pathologies of NAFLD and alcoholic fatty liver disease. A genetic predisposition to NAFLD may exist in some individuals, and in particular the sterol regulatory element-binding factor gene, that codes for the sterol regulatory element-binding protein may be involved in predisposing people to the development of NAFLD.
For example, in one study1 researchers measured the polymorphisms in the sterol regulatory element-binding factor gene in a group of healthy subjects without and clinical signs of NAFLD, type 2 diabetes or metabolic syndrome. In addition, the researchers recorded the subjects lifestyle habits such as diet and exercise as well as known biochemical markers of the metabolic syndrome such as circulating levels of adipokine and C-reactive protein, as well as markers of endothelial dysfunction. These subjects were then followed for 7 years to assess changes in their biochemistry and clinical development of NAFLD. The results showed that polymorphisms in the sterol regulatory element-binding factor gene predicted the 7 year elevation in C-reactive protein and endothelial dysfunction in the healthy subjects. In particular, the presence of one particular version (allele) of the sterol regulatory element-binding factor gene (SREBF-1c) predicted the development of NAFLD.
The researchers then analysed the polymorphisms in a group of subjects who had developed NAFLD. These results showed that the presence of the SREBF-1c allele increased the risk of developing severe liver steatosis, non-alcoholic steatosis, steatohepatitis, insulin resistance and pancreatic β-cell dysfunction. Carriers of the SREBF-1c gene had an impaired oral fat tolerance, a postprandial accumulation of triglyceride rich lipoproteins (very low density lipoproteins (VLDL)), increased oxidised low density lipoprotein (LDL), lower high density lipoprotein (HDL) cholesterol levels and lower adiponectin levels. The SREBF-1c allele of the sterol regulatory element-binding factor gene is therefore associated with an increase risk of developing NAFLD and metabolic syndrome. However, this does not detract from the fact that for this gene to predispose to an increased risk of disease, a typical Western low quality diet is required to provide the correct environmental conditions for the condition to develop.
Dr Robert Barrington’s Nutritional Recommendation: everyone has a unique biochemical individuality that is a reflection of the unique genes that we carry. While this predisposes some to particular conditions, it should be remembered that in many cases these genes contribute to disease only if the correct environmental conditions are available. While some individuals can undoubtedly consume a poor diet and remain healthy, most cannot. Blaming genes for a particular disease is not helpful, because often it is poor lifestyle choices that are the deciding factor. And we all have those choices.
RdB
