William S. Yancy Jr., MD, MHS; Maren K. Olsen, PhD; John R. Guyton, MD; Ronna P. Bakst, RD; Eric C. Westman, MD, MHS
Acknowledgments: The authors thank Keith Tomlin, Bill Bryson, Juanita Hepburn, Christine Perkins, and Angela Braswell for assistance with the interventions and data collection; David Simel and John Williams for manuscript review; and John J.B. Anderson, Howard Eisenson, Jarol Boan, Jim Lane, Truls Ostbye, and Robert Rosati, members of the Oversight Committee.
Grant Support: By the Robert C. Atkins Foundation, New York, New York. Dr. Yancy is supported by a Veterans Administration Health Services Research Career Development Award.
Potential Financial Conflicts of Interests:Grants received: E.C. Westman (Robert C. Atkins Foundation); Grants pending: E.C. Westman and W.S. Yancy Jr. (Robert C. Atkins Foundation).
Requests for Single Reprints: Eric C. Westman, MD, MHS, Duke University Medical Center, Box 50, Suite 200-B Wing, 2200 West Main Street, Durham, NC 27705; e-mail, email@example.com.
Current Author Addresses: Drs. Yancy and Olsen: Health Services Research and Development (152), Veterans Affairs Medical Center, 508 Fulton Street, Durham, NC 27705.
Dr. Guyton: Duke Lipid Clinic, Duke University Medical Center, Box 3510, Durham, NC 27710.
Ms. Bakst: Duke University Medical Center, Box 3921, Durham, NC 27710.
Dr. Westman: Duke University Medical Center, Box 50, Suite 200-B Wing, 2200 West Main Street, Durham, NC 27705.
Author Contributions: Conception and design: W.S. Yancy Jr., E.C. Westman.
Analysis and interpretation of the data: W.S. Yancy Jr., M.K. Olsen, J.R. Guyton, E.C. Westman.
Drafting of the article: W.S. Yancy Jr., J.R. Guyton, E.C. Westman.
Critical revision of the article for important intellectual content: W.S. Yancy Jr., M.K. Olsen. J.R. Guyton, R.P. Bakst, E.C. Westman.
Final approval of the article: W.S. Yancy Jr., M.K. Olsen, J.R. Guyton, R.P. Bakst, E.C. Westman.
Provision of study materials or patients: W.S. Yancy Jr., E.C. Westman.
Statistical expertise: W.S. Yancy Jr., M.K. Olsen, E.C. Westman.
Obtaining of funding: E.C. Westman.
Administrative, technical, or logistic support: R.P. Bakst, E.C. Westman.
Collection and assembly of data: W.S. Yancy Jr., R.P. Bakst, E.C. Westman.
Low-carbohydrate diets remain popular despite a paucity of scientific evidence on their effectiveness.
To compare the effects of a low-carbohydrate, ketogenic diet program with those of a low-fat, low-cholesterol, reduced-calorie diet.
Randomized, controlled trial.
Outpatient research clinic.
120 overweight, hyperlipidemic volunteers from the community.
Low-carbohydrate diet (initially, <20 g of carbohydrate daily) plus nutritional supplementation, exercise recommendation, and group meetings, or low-fat diet (<30% energy from fat, <300 mg of cholesterol daily, and deficit of 500 to 1000 kcal/d) plus exercise recommendation and group meetings.
Body weight, body composition, fasting serum lipid levels, and tolerability.
A greater proportion of the low-carbohydrate diet group than the low-fat diet group completed the study (76% vs. 57%; P = 0.02). At 24 weeks, weight loss was greater in the low-carbohydrate diet group than in the low-fat diet group (mean change, −12.9% vs. −6.7%; P < 0.001). Patients in both groups lost substantially more fat mass (change, −9.4 kg with the low-carbohydrate diet vs. −4.8 kg with the low-fat diet) than fat-free mass (change, −3.3 kg vs. −2.4 kg, respectively). Compared with recipients of the low-fat diet, recipients of the low-carbohydrate diet had greater decreases in serum triglyceride levels (change, −0.84 mmol/L vs. −0.31 mmol/L [−74.2 mg/dL vs. −27.9 mg/dL]; P = 0.004) and greater increases in high-density lipoprotein cholesterol levels (0.14 mmol/L vs. −0.04 mmol/L [5.5 mg/dL vs. −1.6 mg/dL]; P < 0.001). Changes in low-density lipoprotein cholesterol level did not differ statistically (0.04 mmol/L [1.6 mg/dL] with the low-carbohydrate diet and −0.19 mmol/L [−7.4 mg/dL] with the low-fat diet; P = 0.2). Minor adverse effects were more frequent in the low-carbohydrate diet group.
We could not definitively distinguish effects of the low-carbohydrate diet and those of the nutritional supplements provided only to that group. In addition, participants were healthy and were followed for only 24 weeks. These factors limit the generalizability of the study results.
Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level increased more with the low-carbohydrate diet than with the low-fat diet.
Low-carbohydrate weight reduction diets are popular despite a dearth of data on long-term efficacy and adverse effects.
Community-dwelling hyperlipidemic persons were randomly assigned to either a low-carbohydrate, ketogenic diet or a low-fat, low-cholesterol, reduced-calorie diet for 24 weeks. Compared to the low-fat group, patients in the low-carbohydrate group lost more weight, had a greater decrease in triglyceride levels, and had higher high-density lipoprotein cholesterol levels. Levels of low-density lipoprotein cholesterol remained stable in both groups. Side effects were more common in the low-cholesterol group but were generally mild.
While the study suggests the efficacy and relative safety of the low-cholesterol diet, the high dropout rate, self-directed adherence to the diet, and relatively short observation period challenge the generalizability of the findings.
Flow of participants into the study.
Table 1. Baseline Characteristics
Expected mean body weight over time, by diet group.P
Individual body weight trajectories, by diet group.LCDleftLCKDright
Reasons for discontinuation and individual weight trajectories for participants who dropped out, by diet group.Top.LFDBottom.LCKD
Table 2. Effect of Diet Programs on Fasting Lipid Profiles
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May 21, 2004
Calorie intake with Low Carb group
Having lost 90 lbs using a low carbohydrate diet while counting calories as well, I noticed that my calorie count went down substantially while on a low carb diet. In fact without realizing it my calorie intake dropped significanly more than 500 to 1000 cals. Could the weight loss effect simply be from this effect combined with a satiety level obtained by eating more fat. PS It would be helpful if you qualified for the scientific community if the 20 gram carb restriction included fiber or if fiber was subtracted. I ask this because two cups of salad vegetables and one cup of acceptable vegetable is well under 20 grams if you subtract fiber.
Michele E McAlister, M.S.,R.D.L.D.
May 24, 2004
Re: Calorie intake with Low Carb group
I just have to wonder if the improvement in the triglycerides and HDL were as a result of the nutritional supplementation and less by the actual diet. We currently treat our patients with high triglycerides with omega 3 fish oil supplements. To really assess whether the effects were from the low carb diet or the nutritional supplementation, the low fat diet should be supplemented with the same supplements.
I also would like to know how the patients were monitored as far as if they were truly following the low fat diet. In working with patients for over 14 years I find that many people do not know how to translate the recommendations for 30% fat in to real people terms. They often mistakenly think they are to limit fat grams to 30 grams. Were they instructed to use more MUFA? I also would like to know if the patients were instructed to limit white flour products because that would also affect the triglyceride levels.
My last question is regarding to the method of analyzing fat loss versus muscle loss. How was this determined? My biggest concern is when people lose weight too fast they seem to lose more muscle mass which in turn slows the metabolism dowm.
Your consideration in this regard is certainly appreciated.
Medisys Health Group
June 14, 2004
low carb low down
The low carb diet may be more effective in rapid weight loss, however the improved triglycerides levels and the weight loss may be temporarily.
In this study, subjects in low carb group were given chromium picolinate which is compound that interacts with insulin and helps maintain regular blood sugar levels and it is commonly used for diabetic patients. Chromium which serves as an appetite suppressant was used only in the low carb group. Would the result have been as significant without such supplements?
Also as seen in my own practice as a dietitian, the low carb diets can not be maintained for extended periods of time. Generally the cravings for sweets and simple carbs are increased once the chromium is stoped and the allowed carbohydrate intake level is increased. Therefore the weight loss is temporarily and the triglycerides are also increased again depending on the level simple carbohydrate intake.
And finally, the increased HDL level, could it simply be due to higher cholesterol intake? Could the HDL be simply used to circulate the extra load of dietary cholesterol?
To determine the fate of low carb diets, all these and many other factors, some mentioned here some elsewhere, need to be evaluated in a different study and preferably one that is not funded by the Atkins foundation.
University of California at San Francisco
August 13, 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.
Hospital Monte Naranco
November 12, 2004
Is there a parasympathetic response to caloric restriction
Knowing that this response is a late response, I should like to pose a question to the authors. In both regimes the blood pressure and the heart rate diminishes. Can it be a parasympathetic effect?. If so, can it explain why the caloric restriction has no effect in the long term as it is compensated by a decreased energy expenditure?.
William S. Yancy, Maren K. Olsen, John R. Guyton, Ronna P. Bakst, Eric C. Westman. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: A Randomized, Controlled Trial. Ann Intern Med. 2004;140:769–777. doi: 10.7326/0003-4819-140-10-200405180-00006
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Published: Ann Intern Med. 2004;140(10):769-777.
Cardiology, Coronary Risk Factors, Dyslipidemia.
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