ReviewDiets and nonalcoholic fatty liver disease: The good and the bad
Introduction
The prevalence of nonalcoholic fatty liver disease (NAFLD) is rapidly increasing in the western countries and now affects about a third of the population.1 NAFLD is a spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) that occur mainly due to fat accumulation in the liver, but can ultimately lead to cirrhosis, which is not reversible and may progress to hepatocellular carcinoma. Therefore, NAFLD can be considered as a risk factor for cancer, but is now also recognized as a risk factor for cardiovascular diseases.2 Moreover, NAFLD is now considered to be the hepatic manifestation of the metabolic syndrome, which is characterized by insulin resistance, dyslipidemia, hypertension, type 2 diabetes and excess body weight.3, 4 In particular, patients presenting one of the metabolic syndrome features are at increased risk for the development of NAFLD compared to the unaffected ones. For instance, among morbidly obese patients, approximately 90% have NAFLD.5 The diagnosis of NAFLD is beyond the scope of this review and is discussed elsewhere.6 Because obesity strongly influences the development of NAFLD, weight loss appears as the main rational target to treat NAFLD. Indeed, to date no pharmacological therapy is approved for NAFLD, and lifestyle modifications are strongly recommended for patients with NAFLD.7 An important aspect of lifestyle is diet. The aim of this review is therefore to discuss the role of dietary interventions in the treatment, but also in the pathogenesis of NAFLD. We will first precise the pathophysiology of NAFLD and its nutritional implications will be summarized. Secondly, the potential role of some diets in the development of NAFLD will be outlined. Finally, we will examine the nutritional/dietary therapeutic approaches in the treatment of NAFLD.
Section snippets
Pathophysiology of NAFLD and nutritional implications
The pathophysiology of NAFLD is complex and multifactorial. It is mainly characterized by the accumulation of lipids. The latter may be due: 1) to excessive influx of fatty acids from endogenous fat depots (mostly white adipose tissue); 2) from excess dietary fat intake and 3) from de novo hepatic lipogenesis (Fig. 1). In animals, this net accumulation of fat in the liver, i.e. NAFLD, has been clearly linked to the development of hepatic insulin resistance.8, 9, 10, 11, 12, 13, 14, 15, 16, 17
Fatty acids
Several epidemiological studies have linked metabolic and cardiovascular diseases to altered lipid metabolism and dietary fat type, but data on the association between dietary type and fatty liver are scarce.21 A small sample size study has revealed that patients with NASH have an increased intake of saturated fat and cholesterol, and reduced dietary intake of polyunsaturated fatty acids.22 In line with these results, Toshimitsu and coworkers revealed that patients with fatty liver and NASH
Nutritional therapeutic approach: from theory to practice, effects on NAFLD
Dietary intake plays a very important role in the pathogenesis of NAFLD. Weight loss is an essential element in the therapy and treatment of this disease, although macronutrients composition seems to play an important role, as discussed above. To achieve weight loss, various approaches have been used resulting in either rapid and drastic or moderate weight loss. Historically, the very first trials experienced the effect of very low caloric diets and found that this type of diets drastically
Conclusion
NAFLD is the most frequent chronic liver disease and is mostly associated with the epidemic of obesity. NAFLD is associated with an increased risk of cardiovascular diseases and liver-related complications, such as liver cirrhosis or hepatocellular carcinoma. NAFLD is clearly associated with insulin resistance, which is a key risk factor for the development of type 2 diabetes. Current pharmacological options for NAFLD are disappointing and warrant further research. Weight loss is efficient and
Conflict of interest statement and statement of authorship
Each author has participated sufficiently, intellectually or practically, in the work to take public responsibility for the content of the article, including the conception, design, and for data interpretation. All authors have read and approved the final manuscript. MA and FRJ have no conflict of interest.
Acknowledgments
This work was supported by the Hjelt Foundation, the Olga Mayenfisch Foundation and the Fondation De Reuter.
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