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DIETARY CARBOHYDRATE RESTRICTION AS THE FIRST APPROACH IN DIABETES MANAGEMENT: CRITICAL REVIEW AND EVIDENCE BASE

In this 2015 review, a team comprising Richard Feinman, Eugene Fine, Eric Westman, and others summarizes the evidence supporting carbohydrate restriction as the first approach in the treatment and management of Type 2 diabetes.

The authors provide the following definitions for different calorically restricted diets:

  • Very low-carbohydrate ketogenic diet (VLCKD): 20-50 g/d of carbohydrate
  • Low-carbohydrate diet: <130 g/d or <26% of calories from carbs
  • Moderate-carbohydrate diet: 26%-45% of calories from carbs
  • High-carbohydrate diet: >45% of calories from carbs

For context, the authors note that the average American diet is estimated to be 49% carbohydrate, the Dietary Guidelines for Americans recommend a 45-65% carbohydrate diet, and the American Diabetes Association recommends, by the authors’ definition, a high-carbohydrate diet for diabetics.

They summarize the evidence in 12 points as follows:

  1. Hyperglycemia is the most salient feature of diabetes. Dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels.
    The most characteristic feature of diabetes (both Type 1 and Type 2) is an excessive glucose response to food; other effects, such as impacts on insulin, are downstream of this primary defect. It is uncontroversial that dietary carbohydrate intake is the main determinant of blood glucose levels. A 2012 trial showed that a very low-calorie ketogenic diet led to greater suppression of fasting glucose and HbA1c than caloric restriction over 24 weeks.
  2. During the obesity and Type 2 diabetes epidemics, caloric increases have been due almost entirely to increased carbohydrate intake.
    Between 1971 and 2000, the observed increase in the average American’s caloric intake (6.8% in men, 21.7% in women) was almost entirely accounted for by an increase in carbohydrate consumption, which increased 23.4% in men and 38.4% in women. Mechanistically, the sustained hyperinsulinemia consequent to chronic carbohydrate overconsumption increases liver fat and hepatic insulin resistance, which then leads to increased fasting glucose, increased fat storage in other tissues, and impaired pancreatic beta-cell function.
  3. Benefits of carbohydrate restriction do not require weight loss.
    A 2010 trial showed that a diet that moderately reduced carbohydrate intake to 30% improved glycemic control even in the absence of weight loss. Thus, while carbohydrate restriction can be an important tool to induce weight loss, a low-carb diet does not need to result in weight loss to improve blood glucose control.
  4. Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss.
    Two recent trials (Figure 4) randomized diabetic subjects to a low-carbohydrate or low-fat diet. In both cases, carbohydrate restriction led to more consistent weight loss. This is particularly important given the ineffectiveness of low-fat diets in inducing weight loss, as is shown in the Women’s Health Initiative and elsewhere. Additionally, most popular low-carb diets are delivered ad libitum, and induce weight loss without any deliberate caloric restriction.
  5. Adherence to low-carbohydrate diets in people with Type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.
    In 19 clinical trials, similar adherence rates were shown for low-carb and low-fat diets. Widespread anecdotal evidence, collected in the Active Low-Carber Forum, suggests low-carbohydrate diets induce more consistent satiety and reduce hunger, improving ease of compliance.
  6. Replacement of carbohydrate with protein is generally beneficial.
    Most low-carb diets replace carbohydrate with fat. However, those studies that analyze the impact of high-protein, low-carb diets have been associated with greater weight loss and greater preservation of fat-free mass than higher-carb diets.
  7. Dietary total and saturated fat do not correlate with risk for cardiovascular disease.
    A large volume of literature has documented the failure of the diet-heart hypothesis, which links saturated fat consumption to heart disease risk. Recent meta-analyses have reinforced this observation, demonstrating that if there are any cardiovascular benefits associated with a reduction in saturated fat (and there may not be), they are very small.
  8. Plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary lipids.
    While dietary saturated fats are not correlated with heart disease, plasma saturated fats are. Increased plasma saturated fats, however, are associated with increased net triglyceride production, which is itself associated with increased carbohydrate, not saturated fat, consumption.

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