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Smoking, Diabetes and HyperlipidaemiaDepartment of Chemical Pathology & Human Metabolism, Royal Free Hospital & School of Medicine (Univ. of London) Pond Street London NW3 2QG United Kingdom
Department of Chemical Pathology & Human Metabolism Royal Free Hospital & School of Medicine (Univ. of London) Pond Street London NW3 2QG United Kingdom
Department of Chemical Pathology & Human Metabolism Royal Free Hospital & School of Medicine (Univ. of London) Pond Street London NW3 2QG United Kingdom The epidemiological evidence linking smoking with insulin resistance is considerable. This evidence is even more convincing because there is a dose response relationship between smoking and the risk of non-insulin dependent diabetes (NIDDM). Similarly, there is a time-dependent decrease in risk of NIDDM for those who quit smoking. Insulin resistance (in the form of impaired glucose tolerance, IGT) may precede the development of NIDDM. There is a biochemical basis for the smoking- IGT / NIDDM relationship. Smoking increases the risk of developing diabetic complications like nephropathy, neu ropathy and retinopathy. Smoking is also an independent risk factor for myocardial infraction and all-cause mortality in NIDDM. Smokers are both insulin resistant and lipid intolerant. Smoking cessation increases circulating high density lipoprotein (HDL) and reduces low density lipoprotein (LDL) levels, despite weight gain. Those providing advice or treatment to improve cardiovascular risk factors should be aware of these smoking-related harmful effects. This is especially true if IGT is underdiag nosed despite the fact that this condition increases the risk of vascular events. Explaining that smoking increases the chance of developing diabetes as well as raising 'blood fat' levels may convince more smokers to quit.
Key Words: Cardiovascular risk diabetes hyperlipidaemia insulin resistance smoking
The Journal of the Royal Society for the Promotion of Health, Vol. 118, No. 2,
91-93 (1998) |
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