What is non-alcoholic fatty liver disease (NAFLD) and is it related to visceral fat?

Non-alcoholic fatty liver disease (NAFLD), fat deposition in liver cells in men who drink little or no alcohol, is driven primarily by visceral fat and insulin resistance through the portal fat delivery mechanism: free fatty acids and inflammatory adipokines from visceral fat flood the liver via the portal vein, promoting hepatic triglyceride synthesis and impairing insulin signaling, producing a spectrum from simple steatosis (benign fat deposition) to NASH (non-alcoholic steatohepatitis, with active inflammation) to cirrhosis, affecting approximately 25% of US adults, most undiagnosed (Younossi et al., Hepatology, 2019).

For men, NAFLD is both a consequence of visceral fat and an independent cardiovascular risk factor: men with NAFLD have significantly higher rates of cardiovascular events independent of traditional risk factors, through increased hepatic VLDL production (raising ApoB and triglycerides), systemic inflammatory cytokine secretion, and impaired fibrinogen metabolism. An elevated ALT on routine blood work in a man with a large waist is almost certainly reflecting hepatic steatosis, not a random lab variation, and deserves further evaluation.

Honesty Scale: Solid (1) for the visceral fat-NAFLD-cardiovascular risk chain.

What to do: If your routine ALT is elevated (above 40 U/L) and you drink little alcohol, ask your physician about a liver ultrasound to assess for hepatic steatosis. Visceral fat reduction through diet and exercise is the primary treatment for NAFLD, there is no approved pharmacological treatment except the recently approved resmetirom (Rezdiffra) for MASH.

For the full picture, read The Visceral Fat Deep Dive