Non-alcoholic fatty liver disease

are also associated with a greater risk of NAFLD and NASH at any given body mass index, and preliminary evidence suggests greater liver fat content in certain ethnicities that are also known to be at increased risk of type 2 diabetes. Preliminary evidence suggests a genetic predisposition to hepatic accumulation of fat in some people through the PNP3A gene. Such people may not necessarily display the usual metabolic associations with NAFLD, but genetic screening for PNP3A is not currently recommended. Strictly speaking, NAFLD should only be diagnosed in people who consume no or only modest amounts of alcohol (daily intake <20 g (2.5 units) in women and <30 g (3.75 units) in men), although the clinical reality is that in many people both obesity and alcohol will contribute to their level of liver fat and risk of progressive liver disease. Uncommon causes of fatty liver also should be considered (drugs including amiodarone, diltiazem, steroids, synthetic oestrogens, tamoxifen, and highly active antiretroviral therapy; refeeding syndrome and total parenteral nutrition; severe weight loss after jejunoileal or gastric bypass; lipodystrophy and other rare disorders) by taking an appropriate medical history.