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The Oxygen Model of Obesity

Majid Ali, M.D. 

Obesity is cellular oxygen deficiency. This is the core of my Oxygen Model of Obesity. In Integrative Nutritional Medicine, the fifth volume of my textbook, the Principles and Practice of Integrative Medicine, I explained my model in the following simple words: 

Chemicalized foods, chronic anger, fatigue that prevents exercise, and bad science of nutrition put them together and you have a prescription for an obesity epidemic. The commonality in the trio of toxicities of foods, environment, and thought is dysfunctional oxygen metabolism.

Two thirds of American are overweight at present. For that tragedy, I hold responsible the gurus of weight control industry who engage in frivolous debates about low-carb, low-fat, and other dieting plans, and ignore the real causes of obesity given above. And the high priests of 'nutrition science' at the American Medical Association, the National Institutes of Health, The New England Journal of Medicine, and Food and Nutrition Board? None of them has the courage to speak out against those chemicalize our foods, pollute our environment, or victimize overweight individuals with toxic information.

Obesity Is Adipomyocytic Dysox

In 2004, in an article entitled "Hypothesis: Obesity Is Adipomyocytic Dysoxygenosis," I introduced the concept that excess body weight that cannot be lost by ordinary efforts of reduced caloric intake and increased physical activity is a cellular oxygen deficiency state caused by impaired mitochondrial function (the dys-ox state) in adipocytes and myocytes.1 In that "adipomyocytic dysoxygenosis (AD) model," the fundamental electron transport enzymatic pathways that initiate metabolic events and sustain a robust metabolism and an optimal weight are injured by toxic foods, toxic environment, toxic emotions, and toxic thinking. In persistent obesity, adipocytes are increased in number and distended with fat. More importantly, the mitochondria are dysfunctional and the cells have impaired oxygen utilization. That, simply stated, is the root cause of the spreading epidemic of obesity in the United States and elsewhere in the world. For the general readership, I also published a second article entitled "Oxygen Is Cellular Oxygen Deficiency State," to provide a rational and scientifically sound approach to achieving and maintaining an individual's optimal weight.2

Three Furies of Obesity

Excess fat in the adipocyte is oxidizing. Excess oxidation in the adipocyte impairs cellular oxygen utilization. Adipocyte dysoxygenosis so produced evokes"molecular inflammation" in the cell. Molecular inflammation in adipose tissue activates macrophages and vascular endothelial cells, and so sets the stage for cellular inflammation. Adipose inflammation so produced further stokes the oxidative fires in adipocytes. More fat, more oxidation, more oxygen dysfunction, more inflammation the cycle perpetuates itself, increasing the degrees of oxidosis, acidosis, and dysoxygenosis (the three furies of obesity). That, simply stated, is the inflammatory theory of obesity.

Note

This article has some highly technical technical language. For the general reader, I suggest my video seminar on a DVD entitled "Obesity and Weight Loss" available at http://www.majidali.com

Related Articles

The Oxyegn Model of Diabetes

* The Oxygen Model of Obesity

*Insulin's Evolutionary Design

* Less Insulin, More Life

* Evidence for Insulin Toxicity

k  The Oxyegn Model of Diabetes

k The Oxygen Model of Obesity

k The Insulin-Obesity-Diabetes Continuum

k Diabetes Pandemic

k Diabetes - Now You See It, Now You Don't

*Insulin Evolutionary

* Seven Stages of Insulin Toxicity

 

 

Adipomyocytic Dysoxygenosis

The adipomyocytic dysoxygenosis model of obesity is distinct from the views of obesity held by purists in the fields of clinical bariatrics, energy homeostasis, and genomics on the one side and the authors of weight control books, who with uncommon exceptions are mere ghost writers for the enormously rich weight control industry. The adipomyocytic dysoxygenosis model of obesity in my view is superior to other prevailing notions for the following six principal reasons:

1. It holds the cellular energetics and energy homeostasis in the muscle and fat cells as its two centerpieces, which simply cannot be optimally maintained without daily physical exercise.3

2. t focuses on the issue of altered cellular metabolism as the primary phenomenon in the causation of obesity, rather than on gene mutations currently in fashion among academics.4-8

3. It makes a sharp distinction between foods and ecologic factors that preserve cellular oxygen homeostasis and those elements that put it in jeopardy, rather than engage in meaningless low-carb/low-fat debates.9-17

4. It addresses the critically important factors of food allergy and related adverse food effects, as well as large variations among individuals in their requirements for nutrients. Those factors are taken into account neither by promoters of various weight loss diets nor by the academics.18-22

5. It has a strong explanatory power for molecular pathways that link obesity to coronary heart disease, cancer, and other disorders discussed in a later section.

6. It provides sound scientific basis of integrative plans to effectively address the problem of obesity, rather than the use of drugs like leptin, dexfenfluramine (taken off the market) and sibutramine (modulators of serotonin), and others, none of which have proven safe and effective in the long run

References

1. Ali M. Hypothesis: obesity is adipomyocytic dysoxygenosis. J Integrative Medicine. 2004;9:19-38.

2. Ali M. Oxygen is cellular oxygen deficiency state. Aging Healthfully 2004;7:2-5.

3. Barsh GS, Farooqi S, O'Rahilly S. Genetics of body-weight regulation. Nature.2000;404:644-651.

4. Comuzzie, A. G. & Allison, D. B. The search for human obesity genes. Science. 1998;280: 1374-1377.

5. Lander, E. & Kruglyak, L. Genetic dissection of complex traits: guidelines for interpreting and reporting linkage results. Nature Genet. 1995;11:241-247.

6. Comuzzie, A. G. et al. A major quantitative trait locus determining serum leptin levels and fat mass is located on human chromosome 2. Nature Genet. 1997;15:273-276.

7. Hager, J. et al. A genome-wide scan for human obesity genes reveals a major susceptibility locus on chromosome 10. Nature Genet. 1998;20:304-308.

8. Perusse, L., Chagnon, Y. C., Weisnagel, J. & Bouchard, C. The human obesity gene map: the 1998 update. Obes. Res. 1999;7:111-129.

9. Ware JH. Interpreting Incomplete Data in Studies of Diet and Weight Loss. Volume 2003;348:2136-2137.

10. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082-2090.

11. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med 2003;348:2074-2081.

12. Larosa JC, Fry AG, Muesing R, Rosing DR. Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. J Am Diet Assoc 1980;77:264-270.

13. Serdula MK, Mokdad AH, Williamson DF, Galuska DA, Mendlein JM, Heath GW. Prevalence of attempting weight loss and strategies for controlling weight. JAMA 1999;282:1353-1358.

14. St Jeor ST, Howard BV, Prewitt TE, Bovee V, Bazzarre T, Eckel RH. Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation 2001;104:1869-1874.

15. Kennedy ET, Bowman SA, Spence JT, Freedman M, King J. Popular diets: correlation to health, nutrition, and obesity. J Am Diet Assoc 2001;101:411-420.

16. Westman EC. A review of very low carbohydrate diets for weight loss. J Clin Outcomes Manage 1999;6(7):36-40.

17. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE. Effect of 6-month adherence to a very low carbohydrate diet program. Am J -Med 2002;113:30-36.

18. Eades MR, Eades MD. Protein power lifeplan. New York: Warner Books, 2000:434.

19. Atkins RC. Dr. Atkins' new diet revolution. New York: Avon Books, 1992.

20. Eades MR, Eades MD. Protein power. New York: Bantam Books, 1999.

21. The truth about dieting. Consumer Reports. June 2002:26-32.

22. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obes Res 2001;9:Suppl 1:1S-40S.[ISI][Medline]

23. Blackburn GL, Phillips JCC, Morreale S. Physician's guide to popular low-carbohydrate weight-loss diets. Cleve Clin J Med 2001;68:761, 765-6, 768.

24. Bray, G. A. Current and Contemporary Management of Obesity. 1998. Newtown, PA. Handbooks in Health Care.

25. Bray, G. A. & Greenway, F. L. A review of current and potential drugs for treatment of obesity. Endocr. Rev. 1999;20:805-875.

26. Rolls, B. J., Shide, D. J., Thorwart, M. L. & Ulbrecht, J. S. Sibutramine reduces food intake in non-dieting women with obesity. Obes. Res. 1998;6:1-11.

27. Astrup, A., Breum, L., Toubro, S., Hein, P. & Quaade, F.The effect and safety of an ephedrine/caffeine compound compared to ephedrine, caffeine and placebo in obese subjects on an energy-restricted diet. A double-blind trial. Int. J. Obes. Relat. Metab. Disord.1992;16:269-277.

28. Bray GA, Tartaglia LA. Medicinal strategies in the treatment of obesity. Nature.2002;404:672-677

29. Kopelman PG. Obessity as a medical problem. Nature.2000;404:635-43. p635.

30. Chicural M. What happened to leptin? Nature. 2000;404:538-40.

31. Friedman, J. M. & Halaas, J. L. Leptin and the regulation of body weight in mammals. Nature. 1998;395:763-770.

32. Ahima, R. S. et al. Role of leptin in the neuroendocrine response to fasting. Nature. 1996; 382:250-252.

33. Friedman JM. Obesity in the new millennium. 2000;404:632-4.p633.

34. Ali M: Fibromyalgia: an oxidative-dysoxygenative disorder (ODD). J Integrative Medicine 1999; 3:17-37.

35. Ali M. Dysoxygenosis. J Integrative Medicine. 2002;6:1-34

36. Ali M. The oxidative-dysoxygenative perspective of allergic disorders. J Integrative Med. 2000; 4:1-17

37. Ali M. Beyond insulin resistance and syndrome X: The oxidative-dysoxygenative insulin dysfunction (ODID) model. J Capital University of Integrative Medicine

Related Articles

Tutorial GG.16 The Dysox Model of Diabetes and De-Diabetization Potential. Townsend Letter-The examiner of Alternative Medicine. 2007; 286:137-145.

*Insulin Evolutionary

* Less Insulin, More Life

* Evidence for Insulin Toxicity

* If Mice Can Reverse Diabetes, Why Can't People?

* Dysox Explains the Exercise-Weight-Loss Disconnect

 

 

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