Unsupported guidelines

9 September 2006

In Drs. Marshall and Flyvbjerg’s review of diabetes treatment1 one of their major points was pharmaceutical lowering of  blood lipids. No doubt statin treatment may reduce the risk of cardiovascular disease in diabetic patients, but the  absolute effect is small; in secondary prevention less than  6 % and in primary prevention less than 2 %.2 Crucial is also that no significant effect has been seen on total mortality and the question is therefore if the small reduction  of non-fatal events is sufficient to balance the risks of side effects. Of particular interest for diabetic patients is peripheral neuropathy.  According to a large population study the odds ratio for that risk in patients treated with statins for longer than two years was 26.4 (17.8-45.4).3 Other researchers found polyneuropathy in five of 50 cardiology clinic patients after 28 months of statin treatment.4 Most likely the risk is larger in diabetic patients and such symptoms may be seen as a complication to the primary disease and not to the treatment preventing their alleviation by discontinuation of the drug.
     The authors also stressed the importance of reducing total and LDL-cholesterol below a certain level. This advice is not supported by scientific evidence. Several studies have shown that high cholesterol is not a risk factor in diabetic patients,5-7 and no statin trial has shown association between baseline total or LDL-cholesterol, or between individual degree of cholesterol lowering, and outcome8 indicating that the benefit from the statins has nothing to do with cholesterol lowering. To govern statin treatment by its effect on the blood lipids is therefore meaningless.

     Also surprising is that the authors´ only dietary advice was to “eat healthily” referring to a multifactorial trial that included a low-fat diet ignoring the promising results from a steadily increasing number of succesful, controlled low-carbohydrate trials. A general finding from these experiments is that a low-carb diet is more effective for weight reduction than a low-fat diet,9-10 most of all in overweight patients with decreased insulin sensitivity.11 A reduction of dietary carbohydrates also leads to a substantial lowering of  HbA1c and improvement of insulin sensitivity.9-12 As a consequence many patients with type 2 diabetes were able to stop or reduce their antidiabetic treatment. Most interesting is that in spite of high intakes of saturated fat no adverse effects on serum lipids were seen. On the contrary HDL-cholesterol increased in some of the trials and in all of them triglycerides went down substantially.

     A common argument against the lowcarb diet is that we have not yet tested its effect on hard end-points in long-term, unifactorial trials. True, but the lowfat diets have been tested that way and have failed.13 Considering the many short-term benefits on important risk factors a lowcarb diet appears at least as a promising alternative when other treatments have failed. 

  1. Marshall SM, Flyvbjerg A. Prevention and early detection of vascular complications of diabetes. BMJ 2006;333:475-80.
  2. Costa J, Borges M, David C, Vaz Carneiro A. Efficacy of lipid lowering drug treatment for diabetic and non-diabetic patients: meta-analysis of randomised controlled trials. BMJ 2006;332:1115-24.
  3. Gaist D, Jeppesen U, Andersen M, Garcia Rodriguez LA, Hallas J, Sindrup SH. Statins and risk of polyneuropathy: a case-control study. Neurology 2002;58:1333-7.
  4. Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA. Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation. BioFactors 2005;25:147–52.
  5. Fontbonne A, Eschwege E, Cambien F, Richard JL, Ducimetiere P, Thibult N et al. Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study. Diabetologia 1989;32:300-4.
  6. Laakso M, Lehto S, Penttila I, Pyorala K. Lipids and lipoproteins predicting coronary heart disease mortality and morbidity in patients with non-insulin-dependent diabetes. Circulation 1993;88:1421-30.
  7. Liu J, Sempos C, Donahue RP, Dorn J, Trevisan M, Grundy SM. Joint distribution of non-HDL and LDL cholesterol and coronary heart disease risk prediction among individuals with and without diabetes. Diabetes Care 2005;28:1916-21.
  8. Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM2002; 95: 397-403.
  9. Arora SK, McFarlane SI. The case for low carbohydrate diets in diabetes management. Nutr Metab 2005;2:16-24.
  10. Yancy WS Jr, Foy M, Chalecki AM, Vernon MC, Westman EC. A low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutr Metab 2005;2:34-40.
  11. Cornier MA, Donahoo WT, Pereira R, Gurevich I, Westergren R, Enerback S et al. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women.
    Obes Res 2005;13:703-9.
  12. Gannon MC, Nuttall FQ. Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metab 2006;3:16-23.
  13. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443-60.  

 

 

 

 

Competing interests: None declared

Competing interests: None declared

Uffe Ravnskov, independent researcher

Magle Stora Kyrkogata 9, 22350 Lund, Sweden

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