Deadly Duo: Fat & Disease
- 08-29-2007, 12:20 PM
Deadly Duo: Fat & Disease
Deadly Duo: Fat & Disease
The epidemic continues to sweep our nation: obesity. According to the CDC’s National Center for Health Statistics, the U.S. has the “highest prevalence of obesity among the developed nations.” In fact, stats are nearly double that of a decade ago with approximately 300,000 obesity-related deaths annually.
Aesthetics aside, being overweight or obese puts you in a higher-risk category for chronic conditions, from insulin resistance, Type-2 (adult onset) diabetes, high blood pressure, high cholesterol, stroke, heart attack, congestive heart failure, gallstones, gout, osteoarthritis, sleep apnea and—according to current research—a liver disease called nonalcoholic fatty liver disease (NAFLD).
Silent and deadly. NAFLD has no symptoms. Typically, it is detected via routine blood test, when liver enzymes (ALT and AST) appear elevated. However, it also may be detected through ultrasounds performed on the abdomen for other reasons.
The stages of NAFLD range from a fatty liver (a buildup of fat in the liver, common in all stages) to liver inflammation (caused by fat in the liver called NASH, nonalcoholic steatohepatitis) and cirrhosis (irreparable scarring of liver resulting from chronic inflammation).
The initial fatty liver stage can exist without affecting liver function, but further “hits” to the liver can lead to the inflammation stage, NASH. Approximately 20% of NASH patients develop cirrhosis over time. These additional injuries to the liver may come from hormonal imbalance, oxidative stress or mitochondrial abnormalities.
The common denominator in all NAFLD stages is insulin resistance—thought to be the root cause of NAFLD.
According to an April 2007 article in Alimentary Pharmacology & Therapeutics, called “GI Epidemiology: nonalcoholic fatty liver disease” by P. Angulo, “insulin resistance and oxidative stress play an important role in NAFLD development and progression.”
Insulin resistance and being overweight/obese go hand in hand. Insulin resistance renders your body ineffective for burning food. Ideally, the pancreas responds to your food intake by secreting enough insulin throughout the day to keep blood sugar (glucose) levels normal. Insulin is a hormone that acts on cell receptors, triggering complex biochemical reactions to control glucose. For the most part, these cells are liver cells, fat cells and muscle cells.
But the American lifestyle often disrupts this ideal. A rich diet filled with sugars, fat, high calories and refined foods compounded by a sedentary lifestyle creates a recipe for health disaster, upping the rate for weight gain, obesity, insulin resistance and diabetes.
When you eat these types of foods, your body responds to the sugar. Your pancreas cranks out increasing levels of insulin to maintain blood glucose levels. Eventually, cell receptors become resistant, turning a deaf ear to the flood of insulin, which causes the insulin to lose its effectiveness. As a result, blood glucose is out of control and fasting blood glucose levels drift upward.
The high-insulin environment, created after a high-carb meal, locks up body fat so it can’t be used as fuel. When the body is low on fuel, it slowly turns to burning fat. But in the presence of insulin, it can’t do that because the fat is locked away and in storage mode.
When body fat is locked up, the only thing the body can do for fuel is eat again . . . which instigates food cravings. However, it’s not true hunger; it’s hormonal hunger caused by the high insulin. And on the cycle goes as you continue to not only overeat, but eat a highly refined diet, which catapults insulin levels even more.
Insulin resistance affects not only the metabolism of glucose, but also fat in the liver, muscles and fat cells. Your liver is the hub of your body activities, acting as the detoxifying center. Excess calories force your liver to pack away a lot of fat—ultimately compromising your liver functions. Triglyceride fat is taken in from the diet, abdominal fat and peripheral muscles, then stored inside the liver cells, where it produces a fatty liver.
The BMI factor. As you probably are beginning to see, controlling your weight is critical to avoiding NAFLD and insulin resistance. In discussions about insulin resistance, obesity and NAFLD, the body mass index (BMI) is often mentioned.
This quick calculator based on height and weight groups people into four categories: underweight = <18.5; normal weight = 18.5-24.9; overweight = 25-29.9 and obesity = BMI of 30 or greater.
But there’s a problem with relying on this generic approach to calculating body mass index. It’s missing a factor: What comprises that weight? For example, BMI calculators put a 5’9” male, 190 pounds, at 28.1. However, this same individual over the years gained 17 pounds of muscle and lost 23 pounds of fat. His body has totally transformed, but the BMI remained the same.
So in terms of “disease risk,” an insurance underwriter using the sole BMI table would put this person in the overweight, teetering toward the lower-end obese category, labeling him as high risk.
In the previous example, the added weight was muscle and bone, which are heavy. Most athletes would be considered obese because they have extra muscle mass. There’s a major shift in health consequences for the person carrying around 20 pounds of leg muscle versus 20 pounds of fat.
You need a certain amount of body fat for cellular functions. An ideal goal would be having less than 20% body fat. Some statistics label any woman with over 30% body fat and any man with over 25% body fat as obese.
Source: Cenegenics, ATL
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