Page Changed: Research Connecting Blood Sugar Levels to Complications
Changes: Added the highlighted text to the following sections to explain that it isn't the fasting or post-glucose tolerance test reading that is causing complications but the blood sugar highs that are associated with these readings:
Beta Cell Destruction Begins at Levels Over 100 mg/dl (5.6 mmol/L)When a team of Italian researchers led by A Gastardelli started examining beta cell response to glucose in people with normal blood sugars, they discovered that a small amount of beta cell dysfunction began to be detectable in people whose blood sugar rose only slightly over 100 mg/dl on a 2-hour glucose tolerance test. The beta cells are the cells in the pancreas that produce the insulin your body uses to control your blood sugar.
Analyzing their data further, they found that with every small increase in the 2-hour glucose tolerance test result, there was a corresponding increase in how much beta cell failure was detectable. The higher a person's blood sugar rose within "normal" range, the more beta cells were failing.
It is important to remember, though, that the 100 mg/dl here is a value taken 2 hours after drinking the 70 or 75 g of glucose administered in the glucose tolerance test. What really does the damage isn't that 100 mg/dl, it's the much higher blood sugars that were present during the previous 2 hours while the glucose was in the bloodstream. It is also important to remember that glucose is metabolized much more quickly than the carbs in food which need time to be digested, so a person who ends up with a 100 mg/dl reading 2 hours after a glucose tolerance test may see readings of 130 to 150 at two hours after eating a high carb meal containing the same amount of carbohydrate.
Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study. Gastaldelli A; Ferrannini E; Miyazaki Y; Matsuda M; De Fronzo RA;Diabetologia 2004 Jan;47(1):31-9
Beta Cells Die Off in People Whose Fasting Blood Sugar is Over 110 mg/dl (6.1 mmol/L)An intriguing study shows the severe organ damage experienced by people whose blood sugar falls into a range most doctors consider to be near-normal. A team of researchers autopsied the pancreases of deceased patients who were known to have had fasting blood sugars that tested between 110 mg/dl and 125 mg/dl within two years of their deaths. The researchers found that these patients, whose blood sugar was not high enough for them to be diagnosed as diabetic, had already lost, on average, 40% of their insulin-producing beta cells.
Since the American Diabetes Association believes that a fasting blood sugar level of 100 mg/dl to 125 mg/dl corresponds to a 2-hour glucose tolerance levels of 140 mg/dl to 199 mg/dl, this suggests that patients whose post-meal blood sugars rise only to the non-diabetic "impaired" level may be well on the way to losing as much as 40% of their beta cell mass. It also suggests that people with abnormal glucose tolerance who wish to avoid further beta cell loss should try to keep their blood sugars under 140 mg/dl at all times.
However, it is important to understand that in any study that measures only fasting blood sugar and finds a correlation with complications, it isn't the fasting blood sugars that are doing the damage when they are under 140 mg/dl. The reason slightly elevated fasting blood sugars correlate with beta cell destruction is that people with slightly elevated fasting blood sugars who eat high carbohydrate meals are experiencing high, and often long lasting, blood sugar spikes after each meal they eat. A 210 lb person whose fasting blood sugar is 110 needs to eat only 12 grams of carbohydrate to raise their blood sugar to 150, and most of them are likely to be eating 50 to 60 grams of carbohydrate per meal, ensuring that their blood sugars are well over 150 for several hours after each meal.
It is those high post meal readings that go along with elevated fasting levels that cause the glucose toxicity that damages organs and causes complications.
Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC.Diabetes. 2003;52:102-110.