Wednesday, September 13, 2006

Diabetic Complications Inevitable? Not So Fast...

In the September issue of Diabetes Care, a study published - Treating Postprandial Hyperglycemia Does Not Appear to Delay Progression of Early Type 2 Diabetes - had an ominous conclusion:

"Ameliorating postprandial hyperglycemia did not appear to delay progression of early type 2 diabetes. Factors other than postprandial hyperglycemia may be greater determinants of progression of diabetes. Alternatively, once FPG exceeds 126 mg/dl, ß-cell failure may no longer be remediable."

Now how is that for a conclusion? Pretty depressing if you ask me!

But this conclusion is totally understandable if you consider the perspective of those doing the research. They believe the dietary intervention used in this study was a proper diet for those with type II diabetes. The conclusion is that it's a losing battle to try to slow progression in those with diabetes who follow the dietary intervention with or without including acrabose. For those not aware of what acrabose is - it's a starch blocker designed to slow carbohydrate digestion and absorption. From my understanding, it effectively can block about 10-15g of carbohydrate when taken before a meal.

So, after five years of following the two groups, both given the same dietary intervention - with one group, the treatment group, given acrabose and the control group given a placebo - there was no statistically significant differences between the groups in rates of progression to "frank fasting hyperglycemia."

Some background on the study - the researchers investigated whether an intervention with acarbose in subjects with early diabetes (fasting plasma glucose greater than 140mg/dl and two-hour postprandial glucose of greater than 200mg/dl) would prevent or delay progression to "frank fasting hyperglycemia."

To understand why both groups experienced a continued progression, the researchers didn't consider the diet - 55% carbohydrate, 30% fat and 15% protein - as a potential problem in the equation. Why should they? It is, after all, the recommended diet for those with type II diabetes!

In fact, while the researchers did include the potential of the dietary intervention as a possible confounder in the results, it wasn't because the diet was problematic and raised blood sugars too high, but because "the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function."

The researchers simply could not wrap their heads around the idea the diet itself is the problem, so they totally failed to consider the negative effect the diet itself had on glycemic control (or lack thereof). Here is the paragraph the researchers included in their full-text paper:

It is possible that the dietary suggestions provided to both groups were potent and overwhelmed any effects of acarbose on ß-cell function. However, postprandial glucose was significantly lower in the acarbose group, and acarbose lowered A1C slightly but significantly over the first several years, suggesting that the drug itself had a superior effect on glycemia. In addition, the dietary intervention was no more potent than that provided to the placebo arms in studies such as the DPP and STOP-NIDDM.

To give you some perspective here, the diet was the standard carbohydrate:fat: protein ratio of 55:30:15. So, if a meal is 55% carbohydrate, 30% fat and 15% protein and provides 600-calories, it would provide 83g of carbohydrate. If acrabose is taken and actually reduces absorption of carbohydrate in the meal by 15g, the meal still provides 68g of carbohydrate that will be converted to glucose by the metabolism. Such a meal is not unreasonable if one is consuming 2,000-calories a day with three meals at 600-calories and two snacks at 100-calories each.

How great is the difference between a carbohydrate load of 83g versus 68g?

Quite frankly, not much when one considers each gram of carbohydrate converts to blood glucose and that rise in blood glucose must be reduced as much as the body can do with its insulin and medications. In those with type II diabetes, the ability to lower blood sugars is impaired and blood sugars stay elevated longer than they should. Basically their metabolism is doing the best it can with what it has and dietary carbohydrate strongly influences how high blood sugars rise since all carbohydrates (expect fiber) are converted to glucose - the more you consume carbohydrate, the higher blood sugars rise and over time, the less the body is able to reduce them effectively.

As Dr. Richard K. Bernstein illustrates this in what he calls the Laws of Small Numbers for controlling blood sugars - in type II diabetics, who still make insulin, it's common for a gram of carbohydrate to potentially raise blood glucose by 3mg/dl. I'll be clear here - how high blood sugars do rise is highly individual and based on insulin and insulin sensitivity. I'm going to use the 3mg/dl as an example to highlight how the current dietary recommendations can potentially raise blood sugars in someone with type II diabetes.

With that in mind, in this study, if 83g were consumed in the control group with an average fasting blood sugar of 126mg/dl, after the meal with 83g of carbohydrate their blood glucose would rise to 249mg/dl; those in the treatment group taking acrabose with absorption reduced to 68g would have blood sugars rise to 204mg/dl.

Lower? Yes.

Normal? No.

And it's because blood sugars were not normalized by the diet or the addition of the acrabose, the researchers really did reach the only logical conclusion one could reach when the perspective is that the dietary approach was a correct dietary intervention for those with diabetes - progression happens, not much we can do, life goes on.

Can we do better? Absolutely!

To do better we must evaluate interventions that specifically result in a normalization of blood sugars naturally.

In this study we find that the data speaks volumes of the inability of the current dietary recommendations with or without acrabose to normalize blood sugars. Both groups continued to deteriorate and it wasn't because that's what happens with diabetes - it was because they were consuming too many carbohydrates which kept blood sugars too high!

Is there a better way to use diet as an intervention?

From numerous studies we find that carbohydrate restriction can reduce blood sugars more effectively than the current dietary guidelines offered by the American Diabetes Association.

In this study the researchers truly missed a golden opportunity in the five years of time spent following these folks. They failed to discuss the very real problem their data shows clearly - the dietary intervention held near and dear is ineffective at normalizing blood sugars in those with type II diabetes. Even adding acrabose had little effect in the long-term. It did lower postprandial blood sugars, but not enough to reduce risks or slow progression. The reason is because neither the diet nor the diet and acrabose effectively reduced blood sugars to the normal range. Simply reducing blood sugars isn't enough - reduction must bring blood sugars back into the normal range!

It's only when we carefully consider the implications of this data that we see it tell us an important piece of the puzzle - progression is inevitable if control of post-prandial blood sugars is not normalized.

Over the long term, this continuous hyperglycemia leads to progression and is damaging and deadly to beta-cell function, kidneys, cardiovascular system, eyes and nerves.

The problem isn't that the diet and acrabose are ineffective to slow progression thus we just have to accept the inevitable - the problem is that the diet isn't restricting the very foods that are producing hyperglycemia after each meal, day after day after day.

The diet includes too many carbohydrates for the metabolism of those with type II diabetes to effectively deal with each day.

So, while the take home message to many physicians and healthcare professionals reading this study will be "reducing postprandial hyperglycemia doesn't slow progression in those with type II diabetes" the real finding here is that unless postprandial glucose is NORMALIZED one will continue to experience progressively worse deterioration as hyperglycemia takes its toll throughout the body and damages nerves, the cardiovascular system, kidneys, retinas and more.

What this study tells us is that simply lowering fasting and post prandial sugars is not good enough - we must establish dietary recommendations with the goal to normalize blood sugars as much as possible in those with type II diabetes if we are to have any hope of slowing progression and possibly reversing damage from hyperglycemia.


  1. Please explain to me the logic of telling someone to eat carbs and then give them a drug that prevents those carbs frombeing absorbed!?!?!?

    I can see the fat blockers.....after all, we're not supposed to eat fat so any that we do eat should be blocked.....but they say we should eat carbs, then block them?????

    More insanity, huh?

  2. They were fed an calorically nuetral diet with no interventions other than the drug. Why would we expect that insulin sensitivity would improve without some type of dietary restriction, either carb or calorie, in the absense exercise prescription? Am I missing something here?

    1. Anonymous3:29 PM

  3. The answer is increased protein intake, increased MUFA and healthy PUFA intake, and moderate low-medium GI carbohydrate intake. Fruit/veggies should comprise the majority of carbs eaten as they will buffer the highly acidic qualities of protein consumption.

    Spreading the meals out will also allow for better post prandial control. The 3 square meals a day protocol is a product of the Indus. Revol. and should be kicked to the curb.

  4. hello good this acrobose wil be used as sustained release drug..