References

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1 He J, Gu D, Wu X, et al: Major causes of death among men and women in China. N Engl J Med

2005;353:1123-1134.

2 Chen C, Lu FC, Department of Disease Control, Ministry of Health, PR China: The guidelines for prevention and control of overweight and obesity in Chinese adults. Biomed Environ Sci 2004;17(suppl):1-36.

3 Franz MJ, Bantle JP, Beebe CA, et al: Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care 2002;25:148-198.

4 Knowler WC, Barrett-Connor E, Fowler SE, Diabetes Prevention Program Research Group: Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393-403.

5 Mann JI, De Leeuw I, Hermansen K, et al: Evidence-based nutritional approaches to the treatment and prevention of diabetes mellitus. Nutr Metab Cardiovasc Dis 2004;14:373-394.

6 Kraus RM, Eckel RH, Howard B, et al: American Heart Association Scientific Statement: AHA Dietary Guidelines. Circulation 2000;102:2284-2299.

7 Leosdottir M, Nilsson PM, Nilsson J-A, et al: Dietary fat intake and early mortality patterns -data from the Malmö Diet and Cancer Study. J Intern Med 2005;258:153-165.

8 Trichopoulou A, Orfanos P, Norat T, et al: Modified Mediterranean diet and survival: EPIC-elderly prospective cohort study. BMJ 2005;330:991.

9 Knowler WC, Pettitt DJ, Savage PJ, Bennett PH: Diabetes incidence in Pima Indians: contributions of obesity and parental diabetes. Am J Epidemiol 1981;113:144-156.

10 Pan X-R, Li G-W, Wang J-X, et al: Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: the Da Qing IGT and Diabetes Study. Diabetes Care 1997;20: 537-544.

11 Tuomilehto J, Lindstrom J, Eriksson JG, et al: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med 2001;344: 1343-1350.

12 Diabetes Prevention Program Research Group: The Diabetes Prevention Program (DPP): description of the lifestyle intervention. Diabetes Care 2002;25:2165-2171.

13 Ratner R, Goldberg R, Haffner S, Diabetes Prevention Program Research Group: Impact of intensive lifestyle and metformin therapy on cardiovascular disease risk factors in the diabetes prevention program. Diabetes Care 2005;28:888-894.

14 Salmeron J, Ascherio A, Rimm EB, et al: Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care 1997;20:545-550.

15 Dansinger ML, Gleason JA, Griffith JL, et al: Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction. JAMA 2005;293:43-53.

16 Bray GA, Nielsen SJ, Popkin BM: Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004;79:537-543.

17 Schultze MB, Manson JE, Ludwig DS, et al: Sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women. JAMA 2004;292:927-934.

Discussion

Dr. T. Wilkin: The difficulty you had with your conclusions may reflect the initial slides which are very challenging. You showed us the exponential increase in type-2 diabetes with body mass index and the lack of effect of various amounts of fat in the diet, at least in one study. If you are looking at the problem as to whether it is dietary content or body mass, then the issue is surely one of tolerance. If you can tolerate the fats and if you can tolerate the glucose, and that by and large is related to body mass and adipocyte capacity, then you could probably get away with a healthy and a varied diet or what some might consider an unhealthy diet, whereas if you have gained the weight and lost the adipocyte capacity and lost the glucose tolerance, then your ability to tolerate becomes narrower and narrower. So what I took from your talk was a far stronger emphasis on body mass than on what the diet actually contains.

Dr. Knowler: That is also my feeling, but I might add that this is in terms of type-2 diabetes, not necessarily of dyslipidemia. In terms of risk of diabetes, the body weight or body mass index is by far the most important. As long as people can limit their weight or overweight people can reduce their weight then the specific dietary components may be less important. An important question for diabetes prevention is: what is the best approach to loosing weight? Unfortunately there is no easy answer for that question.

Dr. Hill: One of the mistakes I think we make in the US is basing general recommendations on results from weight loss studies. For example Dr. Golay demonstrated that if you fix calories during food restriction the dietary composition is not an important determinant of the amount of weight loss. However, in most cases calorie intake is not fixed when people try to lose weight. Many people who go on the Atkins diet lose a lot of weight probably because they eat less. For dietary fat, lots of data suggest that the higher fat in the diet the more energy you are likely to consume. So it is dangerous to base population recommendations on short-term weight loss results. My question is whether or not you think that the optimum diet should vary with physical activity? Is the optimum diet for a sedentary person different than for someone who gets regular physical activity?

Dr. Knowler: That is very likely but I actually don't know how I would change the recommendation for the very active person. A person can be very active comsuming either a high fat or high carbohydrate diet.

Dr. Hill: If you are very physically active and are burning a lot of fat, the optimum amount of fat in the diet could be higher than for a sedentary person.

Dr. Knowler: It could be, but I don't know what it is.

Dr. Field: The Diabetes Prevention Program (DPP) trial is our best evidence that diet influences outcome or prevention. An argument that is raised for the implementation of intensive lifestyle intervention for the prevention of type-2 diabetes is the considerable cost. Do you think that this approach is feasible based on the number of people at risk?

Dr. Knowler: When you are asking about feasibility and cost, are you referring to effort to prevent diabetes or treat diabetes, because the answer might be different?

Dr. Field: To prevent.

Dr. Knowler: Again I can't give you the answer for that for sure. Two economic analysis of the DPP have been published this year in the Annals of Internal Medicine, one by the DPP itself, one by an outside group, and they came to very different conclusions [1, 2]. The DPP analysis concluded that the DPP style intervention, specifically the intensive lifestyle intervention, did give good health value for money spent and, in terms of quality of life years improved, was comparable or favorable to many things that are standard medical practices. The other paper [2] came to very different conclusions that it was just not economically feasible at all. And the major differences I think, these were both exercises in modeling disease progression and cost. They projected well beyond the data in the DPP because they were projecting what would happen over 30 years, and whenever you are projecting out 30 years, obviously what you get depends on what you assume is going to happen in those 30 years.

Dr. Bantle: As we discuss diet, perhaps I can ask your thoughts about the growing body of evidence that suggests that energy intake, energy expenditure and body weight are all centrally regulated by the hypothalamus and under rigorous control. I am bothered by the thought that when we ask patients to override this control system by force of will, we are asking them to do something that is very difficult.

Dr. Knowler: I think that central control is also subject to external influences. The fact that there have been huge changes in obesity in virtually all countries of the world means that things are changing due to outside influences.

Dr. Huixia Yang: Some studies from Prof. Barker mentioned that birth weight is most important for diabetes and other chronic diseases. In the DPP study we don't know the patients' relation to birth weight. In the patients with low birth weight, meaning intrauterine growth retardation, perhaps diabetes also increases. I just want to know the relation of lifestyle changes in diabetes to the incidence of other things.

Dr. Knowler: Unfortunately I can't comment about that because we didn't have those data in the DPP.

Dr. Huixia Yang: I just wanted to confirm the Barker hypothesis because Prof. Barker mentioned that a lot of chronic diseases may be of fetal origin.

Dr. Knowler: I can't comment on that, regarding the DPP. In our studies of the Pima Indians, we do know the birth weight of many people and we could confirm that hypothesis in the people with very low birth weights had a higher risk of diabetes, but so did the people with a high birth weight, but for very different reasons. The infants who had very high birth weight tended to be born from mothers who had diabetes during the pregnancy, and that it puts them at very high risk. The infants with very low birth weight tended to be the offspring of diabetic fathers. Some of that effect may also be genetic, the people in the extremes of birth weight are inheriting different genetic susceptibility factors. But I think a very important thing is that the extremes of birth weight associated with greater diabetes risk included only about 10% of the population. Over about 90% of the range of birth weight there was no effect on subsequent risk of diabetes. Therefore the extremes of birth weight are very important for the individuals in those extremems, at least in our population but they are not frequent enough to explain diabetes in that population.

Dr. T. Wilkin: Could I just return to Dr. Bantle's question about the hypothalamus and setting, which I think is a very interesting one. I wonder whether the way in which our hypothalami are set relates to a far distant evolutionary period in which the exposure to food was very different than it is now. Perhaps the setting was far more related to carbohydrate content than to fat content, and as far as I understand, fat has very little anorexic effect in any case. So I wonder if our setting points are simply unrelated to the food type exposure that we have nowadays and therefore unresponsive to.

Dr. Ditschuneit: You mentioned the guidelines for an optimal diet and that two servings fish per week is optimal. I think that it has something to do with n-3 and n-6 fatty acids and that they may play a role in cardiovascular disease. I would like you to comment on the role of n-3 and n-6 fatty acids and the relation between these two fatty acids.

Dr. Knowler: As you point out I think the predominant evidence is that these fatty acids would be beneficial in terms of cardiovascular disease. I am not aware of data that they would have direct effects on either body weight or risk of diabetes. Certainly from the standpoint of cardiovascular health I think the evidence would favor the n-3 and n-6 fatty acids from fish and some vegetable sources, and that is why they are put on several groups' recommendations. An anecdotal observation, which is not very scientific is that two of the countries in the world that generally have the world's lowest mortality rates, are Japan and Sweden. Both have very high fish intakes, but very different diets in many other respects. The commonality of fish consumption is an interesting observation.

Dr. Gerasimidi-Vazeou: Is there any evidence about the impact of high fat-high protein diets on factors related to endothelial function like tumor necrosis factor-a, interleukin-6, C-reactive proteins, as the weight and the lipids have always been the endpoints of studies on the Atkins diet?

Dr. Knowler: Unfortunately I don't know the answer to that question.

Dr. Hill: The studies that have been published on the Atkins diet have not looked at that. They have looked at total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein and triglycerides. We are doing a study right now collecting those data but we won't have any results for a while.

Dr. Mingdao Chen: From your first several slides you put the carbohydrate plus monounsaturated fatty acids together, two substances which are not falling into the same category. What is the ratio between carbohydrate and monounsaturated fatty acids?

Dr. Knowler: Ms. Franz or Dr. Bantle might want to respond to that question, because I took this from their paper. There has been a lot of agreement that saturated and trans-saturated fat are unhealthy and should be limited. The question is if you are going to limit them, what do you replace them with? The two obvious choices are carbohydrate or polyunsaturated and monounsaturated fats. The monounsaturated fat tend to be neutral in terms of their effects on dyslipidemia. There is some evidence that in some people very high carbohydrate diets may contribute to hypertriglyc-eridemia. So I think the view is that if you are going to reduce saturated fats, the monounsaturated fats are may be a good thing to replace them with. A particular recommendation was one that the sum of carbohydrate and monounsaturated fats should be 60 or 70%. Might I just ask Ms. Franz to comment more specifically what she recommends?

Ms. Franz: The American Diabetes Association is in the process of updating their nutrition recommendations. In regard to percentages for macronutrient distribution we could find no evidence to support ideal percentages from macronutrients. Support is given to the Dietary Reference Intakes report that recommends meeting the body's nutritional needs while minimizing the risk of chronic diseases. Adults should consume 45-65% of total energy from carbohydrate, 20-35% from fat, and 10-35% from protein [3]. Saturated fat intake should be <7% of total calories and intake of trans fat should be minimized. Either mono- or polyunsaturated fats can be used to replace saturated fats in the diet.

Dr. L. Wilkin: No one as mentioned dietary salt. I am wondering if there is not a relationship between salty snacks and the consumption of sweetened drinks, especially among young people? So if we could cut the salt, would we not reduce the amount of soda that they drink?

Dr. Knowler: That is a good question. Specifically I didn't address dietary salt because I am not aware of data of it having direct effects on glycemia or lipids, which was my charge. But you are right, salt in the diet is very often correlated to fat in these salty snacks so it is an example of changing one aspect of diet, it is hard to isolate dietary components because they are also correlated.

References

1 Herman WH, Hoerger TJ, Brandie M, et al, Diabetes Prevention Program Research Group: The cost-effectiveness of lifestyle modification or metformin in preventing type 2 diabetes in adults with impaired glucose tolerance. Ann Intern Med 2005;142:323-332.

2 Eddy DM, Schlessinger L, Kahn R: Clinical outcomes and cost-effectiveness of strategies for managing people at high risk for diabetes. Ann Intern Med 2005;143:251-264.

3 Institute of Medicine: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, National Academies Press, 2002.

Bantle JP, Slama G (eds): Nutritional Management of Diabetes Mellitus and Dysmetabolic Syndrome. Nestlé Nutr Workshop Ser Clin Perform Program, vol 11, pp 107-125, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2006.

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