Obesity is defined as an excess amount of body fat. The normal amount of body fat (expressed as a percentage of body weight) is between 25-30% in women and 18-23% in men. Women with over 30% body fat and men with over 25% body fat are considered obese. Another easier way of defining obesity is by calculating the body mass index (BMI). The BMI is a mathematical formula that takes into account both a person's weight and height in calculating the degree of obesity. In adults, normal weight is defined as a BMI between 20 and 25 BMI units, overweight from 25 to 30, obesity from 30 to 35, significant obesity from 35 to 40, morbid obesity from 40 to 45, super obesity from 45 to 50, and super-morbid obesity greater than 50. Eighty percent of deaths related to obesity occurs in obese individuals with a BMI greater than 30. To find out what your BMI is, please refer to the Body Mass Index (BMI) Table for Adults, and the Body Mass Index (BMI) Index Table for Teens.
What is nonalcoholic fatty liver disease (NAFLD)?
Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases ranging from the most common, fatty liver (accumulation of fat in the liver, also known as steatosis), to Nonalcoholic steatohepatitis (NASH, fat in the liver causing liver inflammation), to cirrhosis (irreversible, advanced scarring of the liver as a result of chronic inflammation of the liver). All of the stages of Nonalcoholic fatty liver disease are now believed to be due to insulin resistance, a condition closely associated with obesity. In fact, the BMI correlates with the degree of liver damage, that is, the greater the BMI the greater the liver damage.
The term Nonalcoholic is used because liver disease due to alcohol can show the same spectrum of liver disease as nonalcoholic fatty liver disease; however, patients with nonalcoholic fatty liver disease do not consume excessive amounts of alcohol.
In most patients nonalcoholic fatty liver disease causes no symptoms. Nonalcoholic fatty liver disease often is discovered when routine blood tests show slightly elevated levels of liver enzymes (ALT and AST) in the blood. Another way in which nonalcoholic fatty liver disease is discovered is whenultrasound examination of the abdomen is done for other purposes, say for looking for gallstones, and fat is found in the liver. In the late stages of non alcoholic fatty liver disease, the development of cirrhosis can lead to failure of the liver, swelling of the legs (edema, accumulation of fluid in the abdomen (ascites), bleeding from veins in the esophagus (varices), and mental confusioN (hepatic encephalopath Patients with cirrhosis caused by Nonalcoholic fatty liver disease also may be at risk of developingliver cancer (hepatocellular carcinoma HCC).
One common cause of liver failure (and thus a common reason for transplantation of the liver) is cryptogenic cirrhosis (cryptogenic meaning that the cause of the cirrhosis is unknown). Doctors now believe that a large number of patients with cryptogenic cirrhosis are actually patients in the late stages of nonalcoholic fatty liver disease. Doctors and public health officials project that obesity related liver diseases (cryptogenic cirrhosis and liver cancer) will become the leading cause of liver failure and liver transplantation in the not too distant future.
How are nonalcoholic fatty liver disease and nonalcoholic steatohepatitis treated?
Losing excess weight is the cornerstone of treatment of nonalcoholic fatty liver disease. One retrospective study (that is, a study that looks back in time) found that among obese individuals with elevated transaminases, weight gain led to a further increase in the level of the liver enzymes. In contrast, a 10% loss of weight leads to a significant decrease in the levels of the enzymes, and the enzymes even may become normal. The decrease in enzymes occurred at the rate of 8% per 1% loss of body weight. In studies of patients undergoing stomach (gastric) reduction operations for morbid obesity, substantial weight loss is accompanied by a marked reduction in transaminases and a regression (improvement) of non alcoholic fatty liver disease.
Doctors also are using medications to treat nonalcoholic fatty liver disease. For example, insulin-sensitizing agents, such as the thiazolidinediones, pioglitazone (Actos) and rosiglitazone (Avandia), and metformin (Glucophage) not only help to control blood glucose in patients with diabetes, but they also improve enzyme levels in patients with Nonalcoholic fatty liver disease. Medications in the statin class of drugs (for example, atorvastatin/Lipitor) decrease the bad LDL cholesterol and, improve enzyme levels among patients with atorvastatin. More studies are necessary to determine whether these medications also reduce the amount of fat and inflammation in the liver.
Early uncontrolled studies (not the strongest type of studies) suggested possible benefit of ursodiol (Actigall, Urso) and vitamin E in treating atorvastatin, but more recent studies showed no benefit of either of these medications in treating atorvastatin.
The bottom line, however, is that the single most effective treatment for obese people with Nonalcoholic steatohepatitis is to simply lose weight through diet and exercise. Unfortunately, this is no easy task in a society dominated by a sedentary lifestyle and high-calorie, high-carbohydrate, high-fat diets. With great effort, however, weight loss is achievable. Furthermore, in view of the possible detrimental effects of fat in other liver diseases, weight loss might be added to the treatment of other liver diseases that are not primarily due to fat, such as hepatitis C. Ultimately, non alcoholic steatohepatitis probably can be largely prevented and eliminated by promoting healthy eating habits and active lifestyles in children, where it all begins.
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