Preventing Obesity-Related Fatty Liver Damage

November 30, 2012 | Byron J. Richards, Board Certified Clinical Nutritionist

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 Preventing Obesity-Related Fatty Liver Damage
Your liver is the metabolic brain of your body, the workhorse that processes, stores, and distributes every calorie you consume. Your liver must also work right for you to clear toxins of any kind, as well as make bile for digestive purposes. As liver function deteriorates, so goes health in general. 

As you gain weight your body looks for various places to store extra fat, because your white adipose tissue is being strained and inflamed too much. Your body's goal is to find some place to put the extra fat so that it doesn't clog arteries and organs, and make them not work. Our bodies have two or more backup systems for almost every issue.

In this case, the body will start storing extra fat in liver cells. This is called simple fatty liver or steatosis. It is invariably happening as your waistline expands. This is actually a natural system to help your body deal with calorie abuse, it's not harmful in and of itself. As you lose weight you will deplete the extra fat in your liver as this backup system is no longer needed.

However, as your waistline continues to expand your liver's back up storage system is progressively overwhelmed with too much fat. This starts to occur at the point your waistline is more than half your height in inches. The larger your waist, the greater the risk for problems. This sets a cascade of problems in motion, marked by inflammation and free radical damage, leading to a problem called NASH (nonalcoholic steatohepatitis). NASH means that liver cells are being damaged, losing functional capacity, and scar tissue is forming. If NASH progresses it can eventually become cirrhosis, meaning advanced scarring and severe liver damage.

Following The Leptin Diet and regular exercise will of course reduce fatty accumulation in your liver.

Referenced Studies

  1. ^ NAC, Obesity, and Liver Health  Journal of Nutrition  January N. Baumgardner, Kartik Shankar, Leah Hennings, Emanuele Albano, Thomas M. Badger, and Martin J. J. Ronis.

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