Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 5, 9

Dietary Carbohydrate Restriction in Type 2 Diabetes Mellitus and Metabolic Syndrome: Time for a Critical Appraisal

Affiliations

Dietary Carbohydrate Restriction in Type 2 Diabetes Mellitus and Metabolic Syndrome: Time for a Critical Appraisal

Anthony Accurso et al. Nutr Metab (Lond).

Abstract

Current nutritional approaches to metabolic syndrome and type 2 diabetes generally rely on reductions in dietary fat. The success of such approaches has been limited and therapy more generally relies on pharmacology. The argument is made that a re-evaluation of the role of carbohydrate restriction, the historical and intuitive approach to the problem, may provide an alternative and possibly superior dietary strategy. The rationale is that carbohydrate restriction improves glycemic control and reduces insulin fluctuations which are primary targets. Experiments are summarized showing that carbohydrate-restricted diets are at least as effective for weight loss as low-fat diets and that substitution of fat for carbohydrate is generally beneficial for risk of cardiovascular disease. These beneficial effects of carbohydrate restriction do not require weight loss. Finally, the point is reiterated that carbohydrate restriction improves all of the features of metabolic syndrome.

Figures

Figure 1
Figure 1
Glucose and Insulin response for patients with type 2 diabetes on low carbohydrate diet vs. control. Data (means ± SE) are for 9 patients with type 2 diabetes after seven days on their usual high-carbohydrate diet (control) and after 2 weeks) on a low-carbohydrate diet. Medication was reduced in 4 patients and discontinued in one during the low-carbohydrate diet. Figure redrawn from Boden, et al. [8].
Figure 2
Figure 2
Comparison of low and high carbohydrate diets at 6 and 12 months. Results from a multi-center trial in which 63 obese men and women were randomly assigned to either diet. Data from Foster, et al. [26]. Figure from Volek & Feinman [24], used with permission. DBP, diastolic blood pressure; TAG, triglycerides.
Figure 3
Figure 3
Effect of dietary interventions on reduction in triglycerides. Eucaloric diets of indicated carbohydrate content were begun at time 0. At week 3, a 1000 kcal reduction in energy was implemented and at week 9, dieters were put on maintenance diet. Combined effect of calorie reduction and maintenance are reported at week 12. Solid Lines: data from Krauss, et al. [58] were converted from reported log values in their Table 2 and per cent of baseline was calculated. Dashed line: data from Sharman, et al [56]: A eucaloric ketogenic diet was instituted for six weeks (no weight loss phase). Points were recorded at week 3 and 6. Figure modified from Feinman & Volek [57]. Similar results were found for HDL, apoB/apoA1 and other markers of CVD [57, 58]

Similar articles

See all similar articles

Cited by 59 PubMed Central articles

See all "Cited by" articles

References

    1. American Diabetes Association Nutrition Recommendations and Interventions for Diabetes-2007. Diabetes Care. 2007;30:S48–S65. doi: 10.2337/dc07-S048. - DOI - PubMed
    1. American Diabetes Association Nutrition Recommendations and Interventions for Diabetes-2008. Diabetes Care. 2008;31:S61–S78. doi: 10.2337/dc08-S061. - DOI - PubMed
    1. Mann JI, De Leeuw I, Hermansen K, Karamanos B, Karlstrom B, Katsilambros N, Riccardi G, Rivellese AA, Rizkalla S, Slama G, et al. Evidence-based nutritional approaches to the treatment and prevention of diabetes mellitus. Nutr Metab Cardiovasc Dis. 2004;14:373–394. doi: 10.1016/S0939-4753(04)80028-0. - DOI - PubMed
    1. Draznin B. Molecular mechanisms of insulin resistance: serine phosphorylation of insulin receptor substrate-1 and increased expression of p85alpha: the two sides of a coin. Diabetes. 2006;55:2392–2397. doi: 10.2337/db06-0391. - DOI - PubMed
    1. Reusch JE, Draznin BB. Atherosclerosis in diabetes and insulin resistance. Diabetes Obes Metab. 2007;9:455–463. doi: 10.1111/j.1463-1326.2006.00620.x. - DOI - PubMed

LinkOut - more resources

Feedback