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Non-Alcoholic Fatty Liver Disease (NAFLD)

Fat Overload, Liver Damage, and the Inflammatory Storm

NAFLD is defined as deposition of fat in the liver cells of patients with minimal or no alcohol intake and with no other known cause.7 The term “NAFLD” refers to a group of related and progressive conditions closely associated with overweight and obesity.2

NAFLD starts off as a low-level disturbance characterized by dull right upper-quadrant abdominal discomfort and fatigue in most patients, but it is hardly benign.8 Early NAFLD can ultimately progress to a more serious condition, non-alcoholic steatohepatitis or NASH.9 About a third of people with NAFLD will develop NASH,8 and about 20% of people with NASH will go on to liver fibrosis and cirrhosis, with its accompanying risk of liver failure and even liver cancer.2,8,10 Overall, people with NAFLD stand a 12% increased risk of liver-related death over 10 years.8

NAFLD has multiple interrelated causes. Primary mechanisms include obesity leading to steadily increasing insulin resistance coupled with an overabundance of circulating fatty acids. These factors fuel one another in a destructive cycle.4 Together with advanced glycation end-products (AGEs), these events lead to increased oxidant stress and ultimately inflammation, cell death, and fibrous destruction of liver tissue.3,4,8

An overload of fatty acids and abnormal lipid profiles factor so heavily in the onset of NAFLD that they’re now referred to as “lipotoxicity” because of the ways they directly poison liver tissue.9,11,12 And as fat builds inside liver cells, they begin churning out a storm of fat-related cytokines known as adipokines, which fan the inflammatory flames of the metabolic syndrome and NAFLD.1

Of course, what we eat is as important as the calories it contains. One of the major bad actors in today’s world is fructose, found in high quantities in high-fructose corn syrup.13 Fructose promotes formation of new fat molecules in the liver, blocks breakdown of existing fats, stimulates free radical production, and promotes insulin resistance.14 An increasing number of studies are linking increased fructose consumption with NAFLD, and even with its deadlier consequence, non-alcoholic steatohepatitis (NASH).15 Patients with NAFLD consume 2‒3 times as much fructose as do control patients, even corrected for body weight.16