Linda Stern, MD; Nayyar Iqbal, MD; Prakash Seshadri, MD; Kathryn L. Chicano, CRNP; Denise A. Daily, RD; Joyce McGrory, CRNP; Monica Williams, BS; Edward J. Gracely, PhD; Frederick F. Samaha, MD
Acknowledgment: The authors thank Dr. Stephen E. Kimmel and Dr. David Asch for their detailed review and comments on this manuscript, as well as Dr. Justine Shults for her valuable consultation on the statistical analyses.
Grant Support: By the Veterans Affairs Healthcare Network Competitive Pilot Project Grant.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Frederick F. Samaha, MD, Cardiology, 8th Floor, MC 111C, Philadelphia Veterans Affairs Medical Center, University and Woodland Avenue, Philadelphia, PA 19104; e-mail, email@example.com.
Current Author Addresses: Drs. Stern, Iqbal, Seshadri, and Samaha, Ms. Chicano, Ms. Daily, Ms. McGrory, and Ms. Williams: Philadelphia Veterans Affairs Medical Center, Cardiology, 8th Floor MC 111C, University and Woodland Avenues, Philadelphia, PA 19104.
Dr. Gracely: Family, Community, and Preventive Medicine, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA 19129.
Author Contributions: Conception and design: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, E.J. Gracely, F.F. Samaha.
Analysis and interpretation of the data: P. Seshadri, E.J. Gracely, F.F. Samaha.
Drafting of the article: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, F.F. Samaha.
Critical revision of the article for important intellectual content: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, E.J. Gracely, F.F. Samaha.
Final approval of the article: L. Stern, N. Iqbal, P. Seshadri, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, E.J. Gracely, F.F. Samaha.
Provision of study materials or patients: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, F.F. Samaha.
Statistical expertise: E.J. Gracely, F.F. Samaha.
Obtaining of funding: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, F.F. Samaha.
Administrative, technical, or logistic support: F.F. Samaha.
Collection and assembly of data: L. Stern, N. Iqbal, P. Seshadri, K.L. Chicano, D.A. Daily, J. McGrory, M. Williams, F.F. Samaha.
A previous paper reported the 6-month comparison of weight loss and metabolic changes in obese adults randomly assigned to either a low-carbohydrate diet or a conventional weight loss diet.
To review the 1-year outcomes between these diets.
Philadelphia Veterans Affairs Medical Center.
132 obese adults with a body mass index of 35 kg/m2 or greater; 83% had diabetes or the metabolic syndrome.
Participants received counseling to either restrict carbohydrate intake to <30 g per day (low-carbohydrate diet) or to restrict caloric intake by 500 calories per day with <30% of calories from fat (conventional diet).
Changes in weight, lipid levels, glycemic control, and insulin sensitivity.
By 1 year, mean (±SD) weight change for persons on the low-carbohydrate diet was −5.1 ± 8.7 kg compared with −3.1 ± 8.4 kg for persons on the conventional diet. Differences between groups were not significant (−1.9 kg [95% CI, −4.9 to 1.0 kg]; P = 0.20). For persons on the low-carbohydrate diet, triglyceride levels decreased more (P = 0.044) and high-density lipoprotein cholesterol levels decreased less (P = 0.025). As seen in the small group of persons with diabetes (n = 54) and after adjustment for covariates, hemoglobin A1c levels improved more for persons on the low-carbohydrate diet. These more favorable metabolic responses to a low-carbohydrate diet remained significant after adjustment for weight loss differences. Changes in other lipids or insulin sensitivity did not differ between groups.
These findings are limited by a high dropout rate (34%) and by suboptimal dietary adherence of the enrolled persons.
Participants on a low-carbohydrate diet had more favorable overall outcomes at 1 year than did those on a conventional diet. Weight loss was similar between groups, but effects on atherogenic dyslipidemia and glycemic control were still more favorable with a low-carbohydrate diet after adjustment for differences in weight loss.
In 2003, the authors reported that severely obese adults lost more weight and had better serum lipid patterns after 6 months of a low-carbohydrate diet rather than a conventional low-fat diet.
After 1 year, these same patients still had more favorable triglyceride and high-density lipoprotein cholesterol levels on the low-carbohydrate diet than on the conventional diet. However, weight loss and the other metabolic parameters were similar in the 2 diet groups.
The effect of the modest improvements in high-density lipoprotein cholesterol and triglyceride levels on the development of diabetes and cardiovascular disease is unknown.
Table 1. Baseline Characteristics of Study Participants
Table 2. Changes in Dietary Composition between Baseline and 1 Year for the 2 Diets
Comparison of mean weight loss in kg between participants on the conventional diet and participants on the low-carbohydrate diet at 6 months (n= 118) and at 1 year (n= 126).PPP
Table 3. Change in Serum Lipids, Glycemic Indices, Creatinine Levels, and Uric Acid Levels at 1 Year
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Frederick F. Samaha
Philadelphia VA Medical Center
June 30, 2004
Low Carbohydrate Diets and Cardiovascular Risk
We share Dr. Ornish's concerns from our study that neither the conventional low fat diet nor the low carbohydrate diet reduced total or LDL cholesterol (LDL-C)(1). The scientific evidence that aggressive LDL-C lowering reduces atherosclerosis and ischemic coronary events is strong, although complicated by concomitant beneficial effects in these studies on inflammatory markers such as C-reactive protein. The evolving data regarding the long-term benefits of HDL-cholesterol (HDL-C)-raising and triglyceride lowering, at least by pharmacologic means, are also promising with regard to impact on coronary heart disease (2). Moreover, abnormal levels of HDL-C and triglycerides are core features of the metabolic syndrome, which has been strongly associated with atherosclerosis (3). Nevertheless, we agree that extrapolation of these findings to dietary effects on HDL-C may be complicated by unknown effects on reverse cholesterol transport.
The referenced study of subjects following an extremely low fat diet(4) provided important preliminary findings regarding favorable effects of this diet on LDL-C and coronary artery disease. However, this study was also limited by its small size (n=40), and by uncontrolled confounding variables such as restricting the counseling of exercise, smoking cessation, and stress management to the experimental group. There was also greater weight loss in the experimental group. In contrast, a much larger study (n=423) of patients following a Mediterranean diet, which did not include severe fat restriction, decreased long-term cardiovascular event rates (5). In truth, we still do not know the ideal dietary composition to prevent cardiovascular disease and increase weight loss. A focus on fat restriction that results in excessive refined carbohydrate intake would be expected to exacerbate features of the metabolic syndrome, and thus may increase cardiovascular risk. Hopefully there is common ground from the available studies that the ideal goals of dietary modification should be both to reduce LDL cholesterol and improve features of the metabolic syndrome. A diet that helps attain either of these goals merits further investigation of its impact on long-term cardiovascular outcomes.
We also wish to clarify that the patient in our study with an ischemic cardiomyopathy already had this condition prior to enrollment, as stated in the manuscript.
1. Stern L, Iqbal N, Seshadri P, et al. The Effects of Low- Carbohyrate versus Conventional Weight Loss Diets in Severely Obese Adults: One Year Follow-Up of a Randomized Trial. Ann Intern Med. 2004;140:778-785.
2. Rubins HB, Robins SJ, Collins D, et al. Gemfibrozil for the Secondary Prevention of Coronary Heart Disease in Men with Low Levels of High-Density Lipoprotein Cholesterol. N Engl J Med. 1999;341(6):410-418.
3. Solymoss BC, Bourassa MG, Campeau L, et al. Effect of increasing metabolic syndrome score on atherosclerotic risk profile and coronary artery disease angiographic severity. Am J Cardiol. 2004;93:159-164.
4. Ornish D, Scherwitz LW, Billings JH, et al. Intensive Lifestyle Changes for Reversal of Coronary Heart Disease. JAMA. 1998;280(23):2001- 2007.
5. de Lorgeril M, Salen P, Martin J-L, Monjaud I, Delaye J, Mamelle N. Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction : Final Report of the Lyon Diet Heart Study. Circulation. 1999;99(6):779-785.
University of California at San Francisco
August 3, 2004
Low Carbohydrate Diet
Although purporting to show that a low-carbohydrate "˜Atkins' diet is more beneficial than a conventional "low-fat" AHA/NCEP diet, these two studies really documented that neither diet is very effective in lowering weight or LDL-cholesterol (LDL-C). In both studies, LDL-C did not change significantly and there were no significant differences in weight after one year (only about 3% weight loss), which was also seen in an earlier study.
The conventional AHA/NCEP "˜low-fat' diet is not very low in fat or cholesterol and reduces LDL-C by only 5% in most patients, if at all. Since this diet is often high in refined carbohydrates (which increase triglycerides), an Atkins diet often shows greater reductions in triglycerides, especially when taking fish oil.
In contrast, a diet containing 10% of calories from fat with little saturated fat and dietary cholesterol decreased LDL C by an average of 40% after one year in patients not taking lipid-lowering drugs. Also, they lost 24 pounds during the first year and kept off more than one-half of that weight five years later, whereas randomized control group patients on an AHA/NCEP diet did not lose weight. Exercise levels were not significantly different.
It is important to distinguish between risk factors such as lipoproteins from direct measures of disease. Studies using serial coronary arteriography to assess patients consuming an AHA/NCEP diet revealed that the majority showed worsening of coronary atherosclerosis.4 In contrast, patients who followed a 10% fat unrefined foods diet demonstrated significant regression of coronary atherosclerosis after one year as measured by quantitative coronary arteriography and even more regression after five years.5 In addition, they had 2.5 times fewer cardiac events than randomized control group patients following an AHA/NCEP diet, who showed more progression of atherosclerosis after five years than after one year. There was a direct correlation between the intake of dietary cholesterol and total fat and changes in coronary atherosclerosis. Similar results were found by others. Also, 99% of experimental group patients stopped or reversed the progression of CHD as measured by cardiac PET scans.
Only one peer-reviewed study examined the effects of an Atkins diet on cardiovascular disease rather than only risk factors. Myocardial perfusion improved on a very low-fat whole foods diet but worsened on an Atkins diet. The burden of proof is on advocates of low carbohydrate diets to show otherwise in randomized controlled trials using direct measures of cardiovascular disease, not just risk factors or epidemiological studies, especially given data linking diets high in saturated fat and red meat with the incidence of heart disease, cancer, osteoporosis, and renal disease.
The harmful effects of a high fat diet may be mediated through other mechanisms than traditional risk factors. For example, dietary fat intake increases plasma levels of factor VII coagulant activity (VIIc).4 Indeed, one man in the low-carbohydrate group developed angina and CAD near the end of the study even though his risk factors had improved,1 and another died of ischemic cardiomyopathy.2
We need to move beyond simplistic notions that anything which raises HDL-C is beneficial and anything that lowers HDL-C is harmful. Reducing dietary fat and cholesterol may cause a decrease in HDL-C because there is less need for it. There are no data showing that the physiologic reduction of HDL-C levels with a low fat diet is detrimental.
The debate should not be "˜low carbohydrate' versus "˜low fat.' Patients have a spectrum of dietary choices. To the degree they reduce their intake of refined carbohydrates and excessive fats and increase their intake of unrefined carbohydrates (fruits, vegetables, whole grains, legumes) and sufficient omega 3 fatty acids, they may feel better, lose weight, and gain health.
Dean Ornish, M.D. Preventive Medicine Research Institute Clinical Professor of Medicine, University of California, San Francisco
Yancy WS, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low- carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia. Ann Intern Med. 2004; 140:769-777.
Stern L, Nayyar I, Seshadri P, Chicano KL, Daily DA, McGrory JM, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 2004; 140:778-785.
Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003; 348:2082-90.
Ornish D. Concise Review: Intensive lifestyle changes in the management of coronary heart disease. In: Harrison s Principles of Internal Medicine (online), edited by Eugene Braunwald et al., 1999, and In: Braunwald E. Harrison s Advances in Cardiology. New York: McGraw Hill, 2002.
Ornish D, Scherwitz L, Billings J, et al. Intensive lifestyle changes for reversal of coronary heart disease Five-year follow-up of the Lifestyle Heart Trial. JAMA. 1998;280:2001-2007.
Ornish D. Was Dr. Atkins right? Journal of the American Dietetic Association. 2004;104(4):537-542.
Esselstyn CB Jr. Updating a 12-year experience with arrest and reversal therapy for coronary heart disease. Am J Cardiol. 1999 Aug 1;84(3):339-41, A8.
Gould KL, Ornish D, Scherwitz L, et al. Changes in myocardial perfusion abnormalities by positron emission tomography after long-term, intense risk factor modification. JAMA. 1995;274:894-901.
Fleming R, Boyd LB. The effect of high-protein diets on coronary blood flow. Angiology. 2000;51: 817-826.
Connor WE, Connor SL. The case for a low-fat, high-carbohydrate diet. N Engl J Med. 1997;337(8):562-563.
Stern L, Iqbal N, Seshadri P, et al. The Effects of Low-Carbohydrate versus Conventional Weight Loss Diets in Severely Obese Adults: One-Year Follow-up of a Randomized Trial. Ann Intern Med. 2004;140:778–785. doi: https://doi.org/10.7326/0003-4819-140-10-200405180-00007
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Published: Ann Intern Med. 2004;140(10):778-785.
Cardiology, Coronary Risk Factors, Dyslipidemia, Obesity.
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