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  #1   ^
Old Tue, Jan-14-03, 12:28
rustpot's Avatar
rustpot rustpot is offline
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Default Are all Carbs equal?

This is a technical article but gives a boost to the relationship between insulin resistance and the glycemic index


Dr Gary Frost, Head of Nutitional and Dietetics/Senior Lecturer, Hammersmith Hospital, London



Are all carbohydrates equal?

Coronary heart disease (CHD) remains the major cause of premature death in the Western world(1). In Europe modest improvements in CHD mortality have occurred during the last decade(2). It is likely that some of this reduction in CHD mortality is a result of health strategies first introduced in the 1960s that targeted modifiable CHD risk factors(2). These included reducing smoking levels and treating hypertension and raised cholesterol concentrations. Despite modest falls in CHD mortality during this period in the general population, no improvement in CHD has occurred within the diabetic population(3). The prevalence of cardiovascular disease in type 2 diabetes is extremely high and has been attributed to the multiple metabolic risk factors associated with type 2 diabetes(4). Central to the high prevalence of CHD risk factors associated with type 2 diabetes is increased insulin resistance(4). Ethnic groups known to have a genetic predisposition for insulin resistance, have a high prevalence of coronary heart disease. Current treatments for type 2 diabetes have little impact on reducing insulin resistance and this may explain why treating diabetes has only marginal benefit on reducing CHD mortality(5). It is hoped that this may change with the introduction of the thiazolidinedones, a novel class of oral agents that reduce insulin resistance and other associated metabolic cardiac risk factors(6).

Insulin resistance has emerged as the most important metabolic contributor to CHD so far identified(7). The term insulin resistance syndrome encompasses the phenotypic and metabolic changes that accompany a decreased sensitivity to insulin action(4). Many of the metabolic changes occur as a consequence of insulin resistance and are themselves independent CHD risk factors. Examples include lipoprotein changes, with reduced HDL cholesterol and increases in small dense LDL cholesterol, and an increase in the thrombotic tendency due to changes in the fibrinolytic pathways(4). Other CHD risk factors, such as increased abdominal fat exert their detrimental effect by contributing to the pathogenesis of insulin resistance(8).

To date the public health campaigns to reduce premature coronary heart disease have focused on diets to lower total cholesterol rather than diets to reduce the many metabolic disturbances attributed to insulin resistance(4). The diets that are currently advocated emphasise low fat, high carbohydrate foods with five or more portions of fruit and vegetables(9). Despite the strong observational epidemiological evidence of Keyes in the 1960s relating dietary fat intake with serum cholesterol and CHD risk(10;11) and supported by migrant population studies(12), reducing dietary cholesterol and fat has produced only modest benefits on CHD morbidity and mortality(13). That low cholesterol diets provide little CHD protection may reflect their inability to reduce insulin resistance(14). Theoretically greater benefit in CHD prevention would be anticipated from diets that improve the underlying insulin resistance syndrome. Diets in which the majority of carbohydrates are derived from low glycaemic index foods, reduce insulin resistance and improve a number of important metabolic risk factors. We hypothesise that diets that incorporate both traditional dietary advice and low glycaemic index foods would have a greater effect on reducing CHD risk.

The glycaemic index of each dietary carbohydrate provides a measure of its ability to raise post-prandial blood glucose values. High glycaemic index foods give higher post-prandial blood glucose levels than low glycaemic index foods when compared to a standard of white bread or glucose(15). It has been demonstrated that the glycaemic index of a carbohydrate provides a good predictor of the insulin response to that food(16). The nutritional branch of the WHO endorses the use of the glycaemic index as a method of categorising carbohydrates as this provides information on the likely metabolic effects of that carbohydrate(17). Low glycaemic index diets have been shown by ourselves and others to reduce fasting and post-prandial insulin, glucose, tryglyceride and non-esterified fatty acid concentrations(17). In addition these diets increase HDL-cholesterol and decrease fasting total cholesterol, while improving in-vivo and in-vitro insulin mediated glucose uptake(17). Prospective studies have demonstrated that low glycaemic carbohydrates improve insulin sensitivity in subjects with diabetes, obesity and CHD, as well as those at risk of CHD(18-21). Intervention studies using low glycaemic index diets have shown VLDL concentrations are lowered and one recent study has reported an increase in HDL concentrations in a small cohort of type 2 diabetic subjects(22). From the above studies we conclude that low glycaemic index diets have been associated with a wide range of benefits on the established metabolic risk factors for CHD.

Our most recent work has provided insight into the mechanisms by which low glycaemic diets improve insulin sensitivity. We have shown that low glycaemic index diets improve both adipocyte insulin-mediated glucose uptake(19) in-vitro and insulin sensitivity in-vivo as assessed by the post-prandial fall in non-esterified fatty acids (NEFA) levels(23). The literature suggests that a 10% fall in the glycaemic index of a diet will result in a 30% increase in insulin sensitivity. These observations support the commonly held hypothesis that reducing post-prandial NEFA levels optimises insulin stimulated glucose uptake in muscle, thereby increasing insulin sensitivity. Reducing post-prandial NEFA levels is important as their concentration has a rate-limiting effect on hepatic VLDL synthesis. High levels of VLDL production result in reduced HDL-cholesterol and increases in the formation of atherogenic small dense LDL(24). In a large cross-sectional study (2200 healthy adults) we have demonstrated that the glycaemic index of the diet is a greater determinant of HDL cholesterol than any other aspect of the diet, be it fat or dietary fibre(25). The Framingham study found that a 3% decrease in female and a 2% decrease in male cardiovascular morbidity was associated with a 0.026mmol/l increase in HDL-cholesterol. In our study, the HDL-cholesterol of the women in the lowest quintile for glycaemic index was 0.25mmol/l higher than for the women in the highest quintile. Extrapolating from published data this difference would translate to a 29% reduction in CHD morbidity. The corresponding potential decrease in male CHD morbidity would be 7% reflecting the 0.09 mmol/l difference in HDL-cholesterol between the lowest and the highest glycaemic index quintiles, this has been confimed recently by Willitts team(26). Also prospective evidence suggests that low glycaemic diets will lower total cholesterol(27;28), affect clotting through suppression of plasminogen activator inhibitor compound 1(29), reduce blood pressure(30) and induce weight loss(31).

As indicated above, dietary advice for lifestyle intervention for the secondary prevention of CHD has focused on low fat and high fibre diets(32). To date the results of healthy eating advice on both CHD and its risk factors have been disappointing. A recent meta-analysis of free living individuals given dietary advice to promote healthy lifestyle changes resulted in an average 5% reduction in total cholesterol(33). Poor compliance with low fat and high fibre diets prescribed for secondary prevention of CHD probable explains the modest falls in total cholesterol observed in these studies. We predict that emphasising low glycaemic dietary advice for secondary prevention of CHD will have additional advantages over the previously prescribed diet. The low glycaemic index diet is relatively simple to follow. It relies on exchanging different carbohydrate foods for each other, for example replacing cornflakes with Allbran, or potatoes with pasta or adding beans into stews. The low glycaemic index diet can be easily explained to subjects by this simple message of swapping different carbohydrate foods. In our hands, free living people with Type 2 diabetes given such advice have improved glycaemic control and achieved a 20% fall in total cholesterol over a 2 month period(28). Compliance with these diets has always been very good, possibly because of the simplicity of the dietary message.

Before any firm public health initiatives can be taken there is need of prospectice randomised control trial evidence of the role of low glycaemic carbohydrate in the prevention of CHD.

1 Murray, C. J. L. and Lopez, A. D. Mortality by cause for eight regions of the world: Global Burden of Disease. Lancet 349, 1269-1276. 1997. Ref Type: Abstract
2 Tunstall-Pedeo H, Kuulasma K, Mahonen M, Tolonen H, Ruokokoski E, Amouyel P. Contribution of trends in survival and coronary-event rates to changes in coronary heart disease mortality: 10-year results from 37 WHO MONICA project populations. Lancet 1999;353:1547-57.
3 Gu K, Cowie CC, Harris MI. Diabetes and decline in heart disease mortality in US adults. JAMA 1999;281:1291-7.
4 Reavan, G. M. Syndrome X: 6 years later. J.Intern.Med. 236(Supplement 736), 13-22. 1994.
5 Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group [see comments]. Lancet 1998;352(9131):837-53.
6 Ghazzi MN, Perez JE, Antonucci TK, Driscoll JH, Huang SM, Faja BW et al. Cardiac and glycemic benefits of troglitazone treatment in NIDDM. The Troglitazone Study Group. Diabetes 1997;46(3):433-9.
7 Despres, J-P., Lamarche, P., Mauriege, P., Cantin, B., Dagenais, G. R., Sital, M., and Lupien, P-J. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N.Engl.J.Med. 334(15), 952-957. 1996.
8 Reaven GM. Role of insulin resistance in human disease. Diabetes 1988;37:1595-607.
9 Cardiovascular Review Group, Committee on Medical Aspects of Food Policy. Nutritional Aspects of Cardiovascular disease. 46. 1994. London, HMSO.
10 Keys, A. Seven Countries: Multivariate analysis of death and coronary heart disease. 1980. Cambridge Massachusetts, Harvard University Ref Type: Report
11 Keys A, Anderson JT, Grande F. Serum cholestrol response to changes in diet. IV. Particularly saturated fatty acids in the diet. Metabolism Clinical And Experimental 1965;14:776-87.
12 Stamler I. Population studies. In: Levy RI, Rifkind BM, Dennis BH, Ernst N, editors. Nutrition, lipids and coronary heart disease. New York: Raven Press; 1979. p. 25-88.
13 Yu-Poth S, Zheo-G., Etherton T, Naglak M, Jonnalagadda S, Kris-Etherton PM. Effects of the National Cholesterol Education Program's Step I and Step II dietary intervension programs on cardiovascular disease risk factors: a meta-analysis. Am.J.Clin.Nutr. 1999;69:632-46.
14 Tremblay, A. Nutritional determinants of insulin resistance syndrom. Int.J.Obes. 19(Suppl1), S60-S68. 1995.
15 Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am.J.Clin.Nutr. 1981;34:362-6.
16 Bornet FR, Costagliola D, Rizkalla SW, Blayo A, Fontvieille AM, Haardt MJ et al. Insulinemic and glycemic indexes of six starch-rich foods taken alone and in a mixed meal by type 2 diabetics. Am.J.Clin.Nutr. 1987;45(3):588-95.
17 FAO/WHO. Carbohydrates in human nutrition. Report of a joint FAO/WHO report Rome 14-18 April 1997. Paper 66. 1998. FAO Food and Nutrition
18 Frost, G., Keogh, B., Smith, D., Akinsanya, K., and Leeds, A. The effect of low glycaemic carbohydrate on insulin and glucose response in vitro and in vivo in patients with coronary heart disease. Metabolism 45(6), 669-672. 1996
19 Frost, G., Leeds, A., Trew, G., Margara, R., and Dornhorst, A. Insulin sensitivity in women at risk of coronary heart disease and the effect of a low glycaemic index diet. Metabolism 47(10), 1245-1251. 1998.
20 Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effect of a low-insulin-response, energy restricted diet in weight loss and plasma insulin cincentrations in hyperinsulinemic obese females. Am J Clin Nutr 1994;60:48-53.
21 Wolever TM, Jenkins DJ, Vuksan V, Jenkins AL, Buckley GL, Wong GS et al. Beneficial effect of a low glycaemic index diet in type II diabetes. Diabetes Medicine 1992;9(5):451-8.
22 Luscombe ND, Noakes M, Clifton PM. Diets high and low in glycaemic index versus high monounsaturated fat diets: effects on glucose and lipid metabolism in NIDDM. Eur.J.Clin.Nutr. 1999;53:473-8.
23 Frost, G. S., Keogh, B., Smith, D., Leeds, A. R., and Dornhorst, A. Reduced Adipocyte Insulin sensitity in Caucasian and Asian Subjects with Coronary Heart Disease. Diabetes Medicine 15, 1003-1009. 1998.
24 Frayn, K. N., Williams, C. M., and Arner, P. Are increased plasma non-esterified fatty acid concentrations a risk marker for coronary heart disease and other chronic diseases? Clin.Sci. 90, 243-253. 1996.
25 Frost G, Leeds AA, Dore CJ, Madeiros S, Brading S, Dornhorst A. Glycaemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1999;353(9158):1045-8.
26 Liu S, Willett WC, Stampfer MJ, Hu FB, Franz M, Simpson L et al. A prospective study of dietary glycaemic load, carbohydrate intake and risk of coronary heart disease in US women. Am J Clin Nutr 2000;71(6):1455-61.
27 Jenkins DJ, Wolever TM, Kalmusky J, Guidici S, Giordano C, Patten R et al. Low-glycemic index diet in hyperlipidemia: use of traditional starchy foods. Am.J.Clin.Nutr. 1987;46:66-71.
28 Frost G, Wilding J, Beecham J. Dietary advice based on the glycaemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabetic Medicine 1994;11:397-401.
29 Jarvi, A. E., Karstrom, B. E., Granfeldt, Y., Bjorck, I., Asp, N. G., and Vessby, B. Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycaemic index diet in type 2 diabetes. Diabetes Care 22, 10-18. 1999.
30 Sciarrone SE, Strahan MT, Beilin LJ, Burke V, Rogers P, Rouse IR. Ambulatory blood pressure and heart rate responses to vegetarian meals. J.Hypertens. 1993;11(3):277-85.
31 Slabber M, Barnard H, Kuyl J, Dannhauser A, Schall R. Effect of a low-insulin-response, energy restricted diet in weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am J Clin Nutr 1994;60:48-53.
32 Tang JL, Armitage JM, Lancaster T, Silagy CA, Fowler GH, Neil HAW. Systematic review of dietary intervention trials to lower blood total cholesterol in free-living subjects. BMJ 1998;316(7139):1213-20.
33 Tang JL, Armitage JM, Lancaster T, Silagy CA, Fowler GH, Neil HAW. Systematic review of dietary intervension trials to lower blood total cholesterol in free-living subjects. BMJ 1998;316:1213-20.
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  #2   ^
Old Wed, Jan-15-03, 06:01
bluesmoke bluesmoke is offline
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good atticle, thanks for posting. DLB
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  #3   ^
Old Wed, Jan-15-03, 08:35
Sheldon's Avatar
Sheldon Sheldon is offline
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Default Re: Are all Carbs equal?

Quote:
Originally posted by rustpot
Despite the strong observational epidemiological evidence of Keyes in the 1960s relating dietary fat intake with serum cholesterol and CHD risk....


Too bad this myth is repeated once again. Ravnskov shows that this is completely wrong. Keys presented no such evidence. What he did was cherry-pick the data and include only those that supported his hypothesis. He neglected an abundance of contrary findings, both across and within countries. Under the rules of scientific induction, one solid finding against a hypothesis is fatal. It matters not how many confirmations a researcher comes up with. In other words, it doesn't matter how many white swans you find. All it takes to destroy the proposition "All swans are white" is one black swan.

Sheldon

Last edited by Sheldon : Wed, Jan-15-03 at 08:36.
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  #4   ^
Old Thu, Jan-16-03, 10:44
rustpot's Avatar
rustpot rustpot is offline
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Posts: 1,110
 
Plan: atkins/protein power 1st
Stats: 269/278/210 Male 5 feet 10 ins.
BF:33%/30%/ ?
Progress: -15%
Location: Hertfordshire
Default

Thanks Sheldon,

The evidence from Ravnskov, clearly lends support to Frosts argument. Frost sites keyes as an aberration and this makes sense if later studies find no such correlation.

It seems clear to me in any event that the studies relating to fat and cholesterol were all done with significant carbohydrate in the diet.
I still await a definitive long study on low carb,cholesterol levels, and heart disease. Preliminary studies seem positive and helpful but none of the major heart associations around the world are prepared to stick their necks out and change their stance.
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  #5   ^
Old Thu, Jan-16-03, 11:04
Sheldon's Avatar
Sheldon Sheldon is offline
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Plan: Atkins
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Location: Conway, AR
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According to Ravnskov's book, serum cholesterol is not a good predictor of CHD. Neither is LDL. In the Framingham study, in men over 47, lower cholesterol was linked with a higher likelihood of death, and vice versa. Overall the correlation between cholesterol and CHD was 0.36, which is very weak. (1.0 is a perfect correlation.)

In the 1960s the famed heart surgeon Michael DeBakey found that a large number of people with CHD had normal cholesterol.

There is also evidence that cholesterol protects against stroke.

Sheldon

Last edited by Sheldon : Thu, Jan-16-03 at 11:12.
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