Research suggests that moderate intakes of ethanol in the form of wine, beer, cider, spirits or other alcoholic drinks are beneficial to the health. Although their polyphenol content has been shown to contribute a certain degree of this protective effect, research clearly shows a positive health benefit for the ethanol component. However, excessive intakes of ethanol cause metabolic disruption and lead to deleterious health consequences because ethanol can only be oxidised in the liver. In particular, ethanol consumption can induce liver dysfunction when hepatocytes become overloaded with the quantity of ethanol delivered for metabolic processing. The ethanol can change the metabolic balance of the liver by increasing flux through the de novo lipogenesis pathway, with the result that fatty acid production increases. Concomitantly, ethanol also decreases the oxidation of fatty acids through competitive substrate oxidation, with hepatocytes favouring the ethanol rather than fatty acids.
The over production and under utilisation of lipids therefore causes a metabolic disturbance in the liver that leads to the formation of fatty liver disease. If left untreated this disorder can eventually progress to cirrhosis of the liver. Ethanol overconsumption therefore gradually destroys the liver through the deposition of fatty acids, that interfere with cell function to the detriment of overall health. Like ethanol most ingested fructose in metabolised in the liver (actually around 90%), and over consumption can also overload the liver with energy. As with ethanol, this overconsumption results in an increased flux through the de novo lipogenesis pathway, resulting in the production of fatty acids that accumulate in the liver and cause non-alcoholic fatty liver. Until recently the similarities in the aetiology of alcohol induced fatty liver and fructose induced fatty liver had not been considered, but recently research has begun to highlight the shared characteristics.
It is interesting to consider the wider implications of the fructose induced fatty liver because understanding this can increase understanding of the current diet and exercise paradigm of ‘weight loss’. Fatty acids produced in the liver through fructose overconsumption causes the accumulation of lipids in body tissues. These lipids interfere with the insulin signal cascade and this reduces insulin sensitivity. Excess lipids in combination with insulin resistance cause the accumulation of adipocytes in the viscera which leads to central adiposity and obesity. To suggest that an alcoholic could reverse hepatic dysfunction and its associated metabolic abnormalities through physical exercise or calorie restriction would rightly be seen with derision amongst medical ‘experts’. However, in essence this is exactly what is being suggested with our forced energy restriction paradigm that supposes that fructose induced abdominal obesity and liver dysfunction can be ‘worked’ off.
Abdominal obesity is therefore an outward manifestation of a metabolic dysfunction to hepatocytes. To suggest that physical activity or forced calorie restriction could reverse such a metabolic dysfunction, once established, is plainly absurd. By extension the current diet exercise paradigm of weight loss is also flawed, and this explains its poor record in treating abdominal obesity. In reality, those that over consume fructose are metabolically similar to those who over consume alcohol, and yet they are not treated in a similar fashion. Logically the only way that fructose induced fatty liver, abdominal obesity and hepatic dysfunction can be reversed is through changes to the quality of nutrition. In particular, removal of the low quality fructose containing foods and replacement with high quality foods containing a low fructose to fibre ratios is paramount. Fructose and ethanol are indeed brothers in disease, and should therefore be considered metabolically similar when treatment is administered.
RdB
