Fact vs. Fallacy, Part 1
So that you don't have any lingering questions or doubts about the safety of the Atkins Nutritional Approach™, we dispel one of the most common misconceptions: that ketosis is dangerous.
One reason the Atkins Nutritional Approach has not been part of mainstream thinking (although the tide is beginning to change) has been misinformation. If you've heard that Atkins is dangerous, not to mention ineffective, you may have mixed feelings about starting a lifetime of controlled carbohydrate eating. Once doctors have adequate experience with Atkins, most of them agree that this program should be the treatment of choice not only for obesity but for diabetes and several other diet-related disorders. But sadly, the misinformation has prevented so many people in need from using and benefiting from the best treatment available, ultimately propagating epidemic, life-threatening conditions.
Modern medical history contains few examples of such vast discrepancies between what is said in print and the truth. You may find the following explanations a bit scientific, but this was done on purpose. You should have the full complement of information at your disposal to counter any challenge you get. Armed with information supported by a host of scientific studies, you will be able to hold your own—and likely to sway opinion—in any debate that comes your way.
Fallacy: Ketosis is dangerous and causes a variety of medical problems.
Fact: Our bodies have only two fuel delivery systems to provide us with energy. Our primary fuel is based on carbohydrate and is delivered as glucose. People who eat three so-called balanced meals every day get virtually all their energy from glucose. But the alternate backup fuel is stored fat, and this fuel system delivers energy by way of ketones whenever our small supply of glucose is used up (in a maximum of two days).
When a person doing Atkins releases ketones, he or she is in ketosis. Ketosis occurs when you are taking in a very low level of carbohydrate from the food you eat, as you will during much of the weight-loss phases of Atkins. Ketones are secreted in the urine (and at times in one's breath), a perfectly normal and natural function of the body. The more ketones you release, the more fat you have dissolved.
Part of this fallacy is the claim that ketones can build up to dangerous levels in the body. Studies show that ketone bodies are very tightly regulated in the body and will not increase beyond the normal range in healthy individuals. (Uncontrolled diabetics, alcoholics and people who have been on prolonged fasts might see an increase in ketones beyond the normal range.) The body regulates ketone levels the same way it regulates blood-glucose or pH levels1-4. And Dr. Atkins' medical practice repeatedly observed that overweight patients produce just enough ketones to meet their immediate needs for fuel—and no more. A person will have no more ketones after three months of controlling carbohydrates than they do after three days. It is highly unlikely that people, other than insulin-dependent diabetics, will build up ketones.
Confusion about ketosis often comes from people mistaking it for ketoacidosis, a condition found in Type I diabetics; this occurs when a person's blood sugar is out of control and he or she cannot produce insulin. No doctor should have trouble differentiating physiologic ketosis, which you will experience while doing Atkins, from ketoacidosis. Further, since people are often overweight specifically because of an overabundance of insulin, it is essentially impossible for them to be in ketoacidosis.
Some individuals at the ketogenic level of controlled carbohydrate eating may experience mild symptoms such as unusual breath odor and constipation. However, the vast majority of individuals do not develop problems. One study of a severely ketogenic diet showed that ketosis was benign, with no complications or side effects when studied in metabolic ward conditions. The month-long study documented heart, kidney, liver and blood-cell functions in the patients and found no adverse effects5.
In other studies, it has been shown that bone health was not compromised6-12 and that renal (kidney) function was found to be stable1, 14-16 on controlled carbohydrate diets. There is even scientific literature on hyperlipidemia (elevated blood fats, such as cholesterol and triglycerides), showing improved values on controlled carbohydrate diets17-28.
So the next time you read that the ketosis produced by the Atkins Nutritional Approach is dangerous, challenge the speaker or writer (in a letter to the editor, if necessary) and ask, "What is so dangerous about using up your stored fat?"
For more, see Fact vs. Fallacy, Part 2
Phinney, S.D., Bistrian, B.R., Wolfe, R.R., et al., "The Human Metabolic Response to Chronic Ketosis Without Caloric Restriction: Physical and Biochemical Adaptation," Metabolism, 32(8), 1983, pages 757-768.
Yancy, W. S., Bakst, R., Bryson, W., et al., "Effects of a Very-Low-Carbohydrate Diet Program Compared With a Low-Fat, Low-Cholesterol, Reduced Calorie Diet ," October 7, 2001, North American Association for the Study of Obesity Annual Meeting, Quebec City, Canada.
Hoffer, L.J., "Metabolic Consequences of Starvation," 1999, Modern Nutrition in Health and Disease, Shils, M.E. et al. (editors), Lippincott Williams & Wilkens, 9th ed, pages 645-665.
Sharman, M.J., Volek, J.S., Gómez, A.L., et al., "Fasting and Postprandial Lipoprotein Responses to a Ketogenic Diet," May 31-June 2, 2001, Abstract of the 48th Annual American College of Sports Medicine Conference, Abstract #3295, Baltimore, MD.
Spencer, H., Kramer, L., Osis, D., "Do Protein and Phosphorus Cause Calcium Loss?," Journal of Nutrition, 118(6), 1998, pages 657-660.
Heaney, R.P., "Excess Dietary Dietary Protein May not Adversely Affect Bone," Journal of Nutrition, 128(6), 1998, pages 1054-1057.
Heaney, R.P., "Protein and Phosphorous Do not Affect Calcium Absorption," The American Journal of Clinical Nutrition, 72(3), 2000, pages 758-761.
Moriguti, J.C., Ferriolli, E., Marchini, J.S., "Urinary Calcium Loss in Elderly Men on a Vegetable:Animal (1:1) High-Protein Diet," Gerontology, 45(5), 1999, pages 274-278.
Spencer, H., Kramer, L., "Osteoporosis, Calcium Requirement, and Factors Causing Calcium Loss," Clinical Geriatric Medicine, 3(2), 1987, pages 389-402.
Spencer, H., Kramer, L., Osis, D., et al., "Effect of a High Protein (Meat) Intake on Calcium Metabolism in Man," The American Journal of Clinical Nutrition, 31, 1978, pages 2167-2180.
Lausen, B., "No Evidence for Dietary Protein and Dietary Salt as Main Factors of Calcium Excretion in Healthy Children and Adolescents," The American Journal of Clinical Nutrition, 69(4), 1999, pages 742-743.
Skov, A.R., Toubro, S., Bülow, J., et al., "Changes in Renal Function During Weight Loss Induced by High vs Low-Protein Low-Fat Diets in Overweight Subjects," International Journal of Obesity, 23, 1999, pages 1170-1177.
Bellomo, R., Seacombe, J., Daskalakis, M., et al., "A Prospective Comparative Study of Moderate Versus High Protein Intake for Critically Ill Patients With Acute Renal Failure," Renal Failure, 19(1), 1997, pages 111-120.
Blum, M., Averbuch, M., Wolman, Y., et al., "Protein Intake and Kidney Function in Humans: Its Effect on 'Normal Aging' ," Archives of Internal Medicine, 149(1), 1989, pages 211-212.
Newbold, H.L., "Reducing the Serum Cholesterol Level With a Diet High in Animal Fat," Southern Medical Journal, 81(1), 1988, pages 61-63.
Wolfe, B.M., "Potential Role of Raising Dietary Protein Intake for Reducing Risk of Atherosclerosis," Canadian Journal of Cardiology, 11, (Supplement G), 1995, pages 127G-131G.
Gillman, M.W., Cupples, L.A., Millen, B.E., et al., "Inverse Association of Dietary Fat With Development of Ischemic Stroke in Men," Journal of the American Medical Association, 278(24), 1997, pages 2145-2150.
Cerami, A., Vlassara, H., Brownlee, M., et al., "Protein Glycosylation and the Pathogenesis of Atherosclerosis," Metabolism, 34(12 Supple), 1985, pages 37-42.
Cerami, A., Vlassara, H., Brownlee, M., et al., "Role of Nonenzymatic Glycosylation in Atherogenesis," Journal of Cellular Biochemistry, 30(2), 1986, pages 111-120.
Nelson, G.J., Schmidt, P.C., Kelley, D.S., "Low-Fat Diets Do not Lower Plasma Cholesterol Levels in Healthy Men Compared to High-Fat Diets With Similar Fatty Acid Composition at Constant Caloric Intake," Lipids, 30(11), 1995, pages 969-976.
Reaven, G.M., Hoffman, B.B., "Hypertension as a Disease of Carbohydrate and Lipoprotein Metabolism ," The American Journal of Medicine, 87(Suppl 6A), 1989, pages 2S-6S.
Gaziano, J.M., Hennekens, C.H., O'Donnell, C.J., et al., "Fasting Triglycerides, High-Density Lipoprotein, and Risk of Myocardial Infarction," Circulation, 96(8), 1997, pages 2520-2525.
Austin, M.A., Hokanson, J.E., Edwards, K.L., "Hypertriglyceridemia as a Cardiovascular Risk Factor," The American Journal of Cardiology, 81(4A), 1998, pages 7B-12B.
Pieke, B., von Eckardstein, A., Gülbahce, E., et al., "Treatment of Hypertriglyceridemia by Two Diets Rich Either in Unsaturated Fatty Acids or in Carbohydrates: Effects on Lipoprotein Subclasses, Lipolytic Enzymes, Lipid Transfer Proteins, Insulin and Leptin," International Journal of Obesity and Related Metabolic Disorders, 24(10), 2000, pages 1286-1296.
Abbasi, F., McLaughlin, T., Lamendola, C., et al., "High Carbohydrate Diets, Triglyceride-Rich Lipoproteins, and Coronary Heart Disease Risk," The American Journal of Cardiology, 85, 2000, pages 45-48.
Stavenow, L., Kjellström, T., "Influence of Serum Triglyceride Levels on the Risk for Myocardial Infarction in 12,510 Middle Aged Males: Interaction With Serum Cholesterol ," Atherosclerosis, 147, 1999, pages 243-247.
Our thanks to the Atkins Center for this article. This article will give you some basic information about the Atkins Diet Approach for Weight Loss and Good Health, but is not a substitute for reading the books for the details of this plan (or the book for whatever low carb plan you choose to follow.)