Impaired Fasting Blood Sugar

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Prediabetes, also called impaired fasting glucose, has a new, lower diagnostic cutpoint according to the American Diabetes Association (ADA). The new level is a blood glucose of 100 mg/dl, instead of the former 110 mg/dl. A level of 126 or above is the diagnosing criterion for diabetes. The ADA estimates there are about 16 million Americans with prediabetes, but the new cut-off point will increase that to more than 20 million. The majority of those with prediabetes will progress to type 2 diabetes within 5 to 10 years.

However, this progression is far from inevitable. The Diabetes Prevention Program Trial showed that a lowfat diet, along with moderate weight loss (7% of initial body weight) and 150 minutes of aerobic exercise a week, could cut the number of people with prediabetes progressing to diabetes by nearly 60% over 3 years.1

 

Earlier intervention with exercise, a healthier diet and weight loss can prevent the development of type 2 diabetes and cardiovascular disease (CVD). Prediabetes usually starts with a condition called insulin resistance (IR). While IR may not initially raise blood sugar levels, it leads to a host of metabolic disturbances called the metabolic syndrome. At first the beta-cells of the pancreas compensate by making extra insulin which keeps glucose levels within the normal range. However, over time, the beta-cells begin to fail and the loss of beta-cell function leads to higher blood glucose levels. Once blood glucose levels become high enough for a diagnosis of prediabetes, one is already well on the way to developing type 2 diabetes. Most people who have prediabetes and type 2 diabetes die from CVD. The National Cholesterol Education Program should follow the lead of the ADA and lower their cutpoint for impaired fasting glucose since it is still set at 110. This would help identify people with the metabolic syndrome sooner, when diet, exercise and weight loss can reverse the metabolic syndrome.

 

By James Kenney, PhD, RD, LD, FACN.

 

Reference:

 

1. N Engl J Med 2002;346:393-403

 

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