Clinical Review

Prevention and early detection of vascular complications of diabetes

BMJ 2006; 333 doi: http://dx.doi.org/10.1136/bmj.38922.650521.80 (Published 31 August 2006) Cite this as: BMJ 2006;333:475

Unsupported guidelines

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: No competing interests
09 September 2006
Uffe Ravnskov
independent researcher
Magle Stora Kyrkogata 9, 22350 Lund, Sweden
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