Medical news I find interesting

Here is research shared by Dr. John McDougall in his December, 2012 newsletter.  I have been reading that fat intake is as important, or more so, than carb intake in diabetes control.  This article explains that dietary fat decreases insulin activity/efficiency, that diabetics should be fat-counting rather than carb counting, and that most type-II diabetics could be cured by following a strict low fat diet with it's associated weight loss.

Fat Paralyzes Insulin, Making Diabetes Worse

Dietary fat acutely increases glucose concentrations and insulin requirements in patients with type 1 diabetes: Implications for carbohydrate-based bolus dose calculation and intensive diabetes management by Howard A. Wolpert, published November 2012 in the online issue of Diabetes Care, found that “this evidence that dietary fat increases glucose levels and insulin requirements highlights the limitations of the current carbohydrate-based approach to bolus dose calculation…and suggest(s) that dietary fat intake is an important nutritional consideration for glycemic control in individuals with type 1 diabetes.”

Comment: In most people’s minds (including medical doctors), carbohydrate (sugar and starch) is the cause of diabetes. One result is that diabetics manage their disease and medications by “carbohydrate counting.” According the American Diabetic Association this meal planning technique is used to keep your blood sugar in control by keeping track of how many carbohydrates are consumed. Although carbohydrate calories do count in the sense that the blood sugar goes up right after eating a meal, this effect does not make the underlying disease of diabetes worse.

Diabetes (both type-1 and type-2) is due to the reduction of the metabolic effects of the hormone, insulin. Insulin is released from the pancreas after eating and causes body cells to take up carbohydrate and fat cells to take up fat (triglycerides). When the actions of insulin become insufficient the blood sugar rises and diabetes is diagnosed. This ineffectiveness is caused by lack of insulin production (as in classic type-1 diabetes) or is due to insulin resistance (as in type-2 diabetes). This study shows that dietary fat reduces insulin activity. (In this case the insulin injected by a person with type-1 diabetes, but the same is true for insulin produced by the pancreas, as in a person with type-2 diabetes.)

Contrary to popular belief, refined sugars actually make the body’s insulin work more efficiently. When the refined sugar content of an experimental diet of people with mild diabetes was doubled from 45 percent sugar to 85 percent sugar, every measurement of their diabetic condition, including fasting blood sugar, fasting insulin levels, and the oral glucose tolerance, showed that their diabetes improved.² The researchers concluded, “These data suggest that the high-carbohydrate diet increased the sensitivity of peripheral tissues to insulin.” The increase in insulin’s sensitivity (efficiency) counteracted any blood sugar-raising effects from consuming more carbohydrates and calories.

Therefore, diabetics should be “fat-counting,” not “carbohydrate counting” in order to improve their underlying disease. Almost all type-2 diabetics can be cured of their disease by strictly avoiding fat (and the weight loss that follows eating starches, vegetables and fruits). Type-1 diabetics will find their insulin needs decreasing by about 30% when they avoid the fat and add the carbohydrate. All people, with or without diabetes, will find great improvements in their health from this simple dietary change.

1) Wolpert HA, Atakov-Castillo A, Smith SA, Steil GM. Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes: Implications for carbohydrate-based bolus dose calculation and intensive diabetes management. Diabetes Care. 2012 Nov 27

2) Brunzell JD, Lerner RL, Hazzard WR, Porte D Jr, Bierman EL. Improved glucose tolerance with high carbohydrate feeding in mild diabetes. N Engl J Med. 1971 Mar 11;284(10):521-4.