How Do You Fix a Fatty Liver?
Non-alcoholic fatty liver disease (NAFLD) comprises a wide range of disorders ranging from simple steatosis to steatohepatitis and cirrhosis.
The etiopathogenesis is unknown in part but the intervention of different factors that cause the accumulation of fatty acids in the hepatic parenchyma is known, producing a situation of oxidative stress, the formation of free oxygen radicals and the synthesis of an inflammatory cytokine cascade that determine the progression of the disease from steatosis to advanced fibrosis.
The diagnostic test of choice continues to be liver biopsy, although the development of different non-invasive techniques, both serological and imaging, has opened a new option for these patients.
How Do You Fix a Fatty Liver?
Modifications in lifestyle through diet and exercise are the main therapeutic bases. Weight loss, through caloric restriction, can itself improve transaminase levels, insulin resistance and, in some cases, biopsy data (steatosis and lobular inflammation, especially in patients with minimal fibrosis). The best way to lose weight in a maintained way is a change in eating behavior, reducing the caloric intake to 500-1000 kcal/day. The goal is a weight loss of 5 to 10% for 6 to 12 months, since a faster loss or a tighter diet mobilizes fatty acids from the liver and can cause an increase in portal inflammation.
The practice of medium intensity exercise, such as walking 30 to 45 min/day at a continuous rate, improves insulin sensitivity and glucose homeostasis, reduces the secretion of VLDL, apolipoprotein B and prevents steatosis, probably as a result of the stimulation of lipid oxidation and the inhibition of lipid synthesis in the liver through the activation of the AMPK pathway. These benefits of the exercise are independent of weight loss. By combining the weight loss maintained by the hypocaloric diet with the increase in physical activity, liver enzymes are significantly reduced in obese patients with NASH (Non-alcoholic steatohepatitis).
Bariatric surgery: It is one of the most effective options to achieve long-term weight loss in patients with severe obesity. It is indicated in patients with BMI (Body mass index) > 35 kg/m2 with associated comorbidity or BMI>40 kg/m2. Initially, cases of severe steatosis caused by rapid weight loss were described, especially with the jejuno-ileal bypass; however, currently the gastric-proximal bypass has alleviated this problem. Bariatric surgery in patients with NAFLD has shown the beneficial effects of weight loss on liver histology and enzymatic elevation of the liver.
Treatment of insulin resistance
Thiazolidinediones: It promotes the absorption of fatty acids in adipocytes and their accumulation in the form of triglycerides and, consequently, reduces the supply of free fatty acids to the liver.
Metformin: It is widely used in the treatment of type 2 diabetes mellitus. Transaminase levels and histological damage are reduced in patients with NAFLD treated with metformin.
Drugs that induce weight loss
Orlistat: produces a moderate weight loss by reducing fat absorption by 30% by inhibiting gastric and pancreatic lipases.
Sibutramine: is a serotonin and norepinephrine reuptake inhibitor in the central nervous system that increases satiety and induces weight loss; is associated with a decrease in transaminases.
Blockers of the Cannabinoid Receptor: Rimonabant
Rimonabant is a selective antagonist of the cannabinoid receptor type 1, located in the liver, adipocytes, musculoskeletal and pancreas. Endocannabinoids participate in the pathogenesis of NAFLD and its inactivation can decrease cell apoptosis (programmed cell death) in patients with fibrosis.
Lipid-lowering Drugs: Statins
They lead to a decrease in LDL (bad cholesterol) in the blood. Its therapeutic effects include a decrease in transaminases and steatosis.
Cytoprotective and Antioxidant Agents
Oxidative stress participates in the pathogenesis of NAFLD, so that antioxidants could reduce liver damage mediated by free radicals.
Among them are Pentoxifylline, Ursodeoxycholic acid, Tocopherol, N-acetylcysteine, Betaine and Angiotensin II receptor blockers.
The variety of therapeutic guidelines and modes of action mentioned here are not exclusive options. In the first place, the alcohol consumption should be avoided, as well as treatments with potentially hepatotoxic drugs.