Ketosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]

Overview

Ketosis (IPA pronunciation: [ki'tosɪs]) is a stage in metabolism occurring when the liver converts fat into fatty acids and ketone bodies which can be used by the body for energy.

Historical Perspective

It was identified by Dr. Stephen Moody in 1969.

Pathophysiology

Adipose tissue consists of highly specialized cells which store energy in the form of a triglyceride and release it upon hydrolysis in a process known as lipolysis, yielding three fatty acids and one glycerol molecule.[1] Ketosis is the accumulation of excessive keto acids in the blood stream (specifically acetoacetate and beta-hydroxy butyrate), these ketone bodies are a by-product of the lipid metabolic pathway after the fat is converted to energy.[2] [3] [4] [5] [6]

Most medical resources regard ketosis as a physiological state associated with chronic starvation. Glucose is regarded as the preferred energy source for all cells in the body with ketosis being regarded as a crisis reaction of the body to a lack of carbohydrates in the diet. In recent years this viewpoint, both the body's preference for glucose and the dangers associated with ketosis, has been challenged by some doctors.[7][8][9]

Ketone bodies, from the breakdown of fatty acids to acetyl groups, are also produced during this state, and are burned throughout the body. Excess ketone bodies will slowly decarboxylate into acetone. That molecule is excreted in the breath and urine. When glycogen stores are not available in the cells (glycogen is primarily created when carbohydrates such as starch and sugar are consumed in the diet), fat (triacylglycerol) is cleaved to give 3 fatty acid chains and 1 glycerol molecule in a process called lipolysis. Most of the body is able to utilize fatty acids as an alternative source of energy in a process where fatty acid chains are cleaved to form acetyl-CoA, which can then be fed into the Krebs Cycle. During this process a high concentration of glucagon is present in the serum and this inactivates hexokinase and phosphofructokinase-1 (regulators of glycolysis) indirectly, causing most cells in the body to use fatty acids as their primary energy source. At the same time, glucose is synthesized in the liver from lactic acid, glucogenic amino acids, and glycerol, in a process called gluconeogenesis. This glucose is used exclusively for energy by cells such as neurons and red blood cells.

Differentiation of Ketosis from other Disorders

Ketosis should not be confused with ketoacidosis (diabetic ketoacidosis or the less common alcoholic ketoacidosis), which is severe ketosis causing the pH of the blood to drop below 7.2. Ketoacidosis is a medical condition usually caused by diabetes and accompanied by dehydration, hyperglycemia, ketonuria and increased levels of glucagon. The high glucagon, low insulin serum levels signals the body to produce more glucose via gluconeogenesis, glycogenolysis and ketogenesis. High levels of glucose causes the failure of tubular reabsorption in the kidneys, causing water to leak into the tubules in a process called osmotic diuresis, causing dehydration and further exacerbating the acidosis.

Since non-medically trained people often confuse ketosis with ketoacidosis, Dr Robert Atkins proposed that ketosis that occurs through deliberate carbohydrate restriction be referred to as "benign dietary ketosis."

Diet

If the diet is changed from a highly glycemic diet to a diet that does not substantially contribute to blood glucose, the body goes through a set of stages to enter ketosis. During the initial stages of this process the adult brain does not burn ketones, however the newborn brain makes immediate use of this important substrate for lipid synthesis in the brain. After about 48 hours of this process, the adult brain starts burning ketones in order to more directly utilize the energy from the fat stores that are being depended upon, and to reserve the glucose only for its absolute needs, thus avoiding the depletion of the body's protein store in the muscles.

Whether ketosis takes place can be checked by using special urine test strips such as Ketostix.

Deliberately induced ketosis through a low-carbohydrate diet has been used to treat medical conditions although most such treatments remain controversial.[10] [11] The ketogenic diet is an approach to treating epilepsy, and the Atkins Nutritional Approach (and many similar diets) is marketed for treating obesity. The very low calorie, medically supervised Bernstein, Lighter Life, Cambridge Diet, Lindora diets and Medifast also use ketosis for weight loss. [5][6] [7]

It must be noted that the Lighter Life and the Cambridge diet are the same.

See Also

References

  1. "DEVELOPING A MORE SENSITIVE ASSAY TO ANALYZE FATTY ACID RELEASE FROM HUMAN FAT CELLS: PRELIMINARY STUDIES." (PDF), University of Maryland School of Medicine, p. 18, August 5 2005 Check date values in: |date= (help)
  2. "http://www.jhu.edu/~jhumag/495web/fat.html", John Hopkins University External link in |title= (help)
  3. "http://www.med.upenn.edu/nutrimed/MedNutandDisSampleCase.shtml", University of Pennsylvania School of Medicine External link in |title= (help)
  4. "http://www.med.umich.edu/diabetes/patients/dictionary.htm", University of Michigan Medical School External link in |title= (help)
  5. "http://www.orcbs.msu.edu/occupational/programs_guidelines/right_to_know/gloss/ketosis.htm", Michigan State University External link in |title= (help)
  6. "http://depts.washington.edu/chdd/outlook/outlook00_13.1.pdf" (PDF), University of Washington School of Medicine External link in |title= (help)
  7. Eaton, S. Boyd (1985). "Paleolithic nutrition: a consideration of its nature and current implications". New England Journal of Medicine. 312: 283–89. Unknown parameter |coauthors= ignored (help)
  8. Eades, M. et al. Protein Power Lifeplan[1]
  9. William S Yancy, Jr, Marjorie Foy, Allison M Chalecki, Mary C Vernon, and Eric C Westman (2005). "A low-carbohydrate, ketogenic diet to treat type 2 diabetes". Journal of Nutrition and Metabolism. 2.
  10. G.D Foster et al, NEJM2003;348:2082-90[2]
  11. Bravata et al., Journal of the American Medical Association, Apr, 2003; 289(14):1837-50[3]



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