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The Oxygen-Bone-Metabolism  Connections

_ An Evolutionary Perspective

Majid Ali, M.D.

 

Nature chose oxygen to drive all aspects of human evolution. Connectivity in all structural and functional diversities was - and continues to be - the central preoccupation of evolution. This simple evolutionary intelligent would be expected to assign the bone tissue important roles in the energy economy of the body. This would have been dismissed as frivolous conjecture in 1983, when I published a monograph entitled "Spontaneity of Oxidation in Nature and Aging. In 2011, the scientific evidence for this view is clear and conclusive. In this article, I summarize the main lines of evidence supporting my evolutionary view "oxygen-bone-metabolism connections." Below are brief comments to provide a frame of reference for this.

Diseases Begin with Derangement of Oxygen Signaling

My core point in this evolutionary view is that all diseases begin with derangement of oxygen signaling. In the following decades I elaborated and expanded that model by proposing oxygen models of various diseases (listed under in the section on Molecular Biology of Oxygen, Advanced). These models not only had strong explanatory powers for the pathogenesis (causes and processes) but also provided scientifically sound integrative managemnt plans for reversing these disease.

The Oxygen Model of Osteoporosis

In 2005, I proposed the Oxygen Model of Osteoporosis with the following words: "The human anatomy and physiology evolved under the organizing influence of oxygen.1-4 Accordingly, oxygen not only provides signaling for all developmental, differentiative, and dying processes, it also serves as the principal nutrient for the body. Viewed in that light, bone homeostasis is but one face of oxygen homeostasis. Based on those considerations, I recently put forth the Oxygen Model of osteoporosis that recognizes disturbances of oxygen homeostasis in the bone tissue as the fundamental energetic-molecular events that lead to bone loss clinically designated as osteopenia and osteoporosis.5"

In the prevailing model of rheumatology, discussions of the treatment of osteoporosis begin with trivial statements about calcium, vitamin D, and phosphate. Then there is usually a perfunctory reference to the need for physical exercise. Then quickly the focus shifts to the use of pharmacologic agents, largely of drugs that block osteoclastic activity. I have never heard a rheumatologist emphasize issues of oxidosis, acidosis, and dysoxygenosis the energetic-molecular lesions that disrupt bone homeostasis and set the stage for osteoporosis. Rheumatologists, of course, are not interested in disruptions of the bowel, blood, and liver ecosystems that cause oxidosis, acidosis, and dysoxygenosis in bone. Indeed, had doctors prescribing drugs for osteoporosis taken an enlightened view of the bone homeostasis and of energetic-molecular dynamics that cause bone loss there would have been no need for anyone to propose the Oxygen Model of osteoporosis.

* People with eating disorders anorexia, bulemia, and others lose bone mass, while obese individuals have thicker bones. Obese women are likely to develop osteopenia.

* Leptin is a "fat-loss" protein found only in animals with bony skeletons- a clear clue to the bone-metabolism connections. Leptin is secreted by fat cells and suppresses appetite. Mice with deleted leptin gene (leptin knockout mice) have denser bones.- a 4050% increase in bone mass compared with wild-type mice.

* Leptin also serves a braking function on bone growth by inhibiting serotonin production. This, in turn, slows bone building by mechanisms, including the regulation of the sympathetic nervous system.

* All aspects of homeostasis are regulated by oxygen and insulin, its minister of energy and metabolism.

* All aspects of the endocrine system involve feedback loops. If leptin released from fat cells affects bone metabolism, it would be highly probable that bone must also regulate energy economy of the body. Indeed, osteocalcin knockout mice are prediabetic - being glucose intolerant, insulin resistant, and have a diminished insulin production.

My Crank-Crank-Shaft Model of Diabetes recognizes the insulin receptor dysfunction as the central lesion caused by "plasticization of membranes" which jams the receptor protein embedded in it, immobilizing the crank-shaft, so to speak. This model predicts that mice with deleted gene for the insulin-receptor protien (receptor knockout mice) would be fat and insulin-resistant. That, indeed, is the case as revealed with knockout studies.

Osteocalcin As An Energy-regulating hormone

(Taken from Nature 1020;466:914-915.

 

Related Tutorials

* The Musculoskeletal System: An Evolutionary Perspective

* The Oxygen-Bone-Metabolism  Connections -  An Evolutionary Perspective

* Arthritis: Pathogenesis and Types

* URIC ACID: A DEMONIZED ANGEL

* Diseases of Bones and Joints

* Introduction to Diseases of Bone and Joints

 

 

References


1. Ali M. Spontaneity of Oxidation in Nature and Aging (monograph), Teaneck, NJ, 1983.
2. Ali M. Darwin, fatigue, and fibromyalgia. J Integrative Med 1999;3:5-10.
3. Ali M. Darwin, oxidosis, dysoxygenosis, and integration. J Integrative Med 1999;3:11-16.
4. Ali M. Dysoxygenosis. J Integrative Med 2002;5:47-82.
5. Ali M. The oxygen model of osteoporosis. J Integrative Med 2004;8:19-37.
6. Whiting SJ, Lemke B. Nutr Rev 1999;6:192-5 and 2000;8:249-50.
7. Rapuri PB, et al. Smoking and bone metabolism in elderly women. Bone 2000;27: 429-36.
8. Cornuz J., et al. Smoking, smoking cessation, and risk of hip rracture in women. Am J Med 1999; 106:311-4.
9. Steinbrech DS, Mehrara BJ, Saadeh PB, et al. Hypoxia regulates VEGF expression and cellular proliferation by osteoblasts in vitro. Plast Reconstr Surg 1999 Sep;104(3):738-47.
10. Fini M, Giavaresi G, Torricelli P, Giardino R. Pericellular partial oxygen pressure (pO2) measurement in osteopenic bone-derived osteoblast cultures. Artif Cells Blood Substit Immobil Biotechnol 2001 May;29(3):213-23.
11. Rajpurohit R, Koch CJ, Tao Z, Teixeira CM, Shapiro IM. Adaptation of chondrocytes to low oxygen tension: relationship between hypoxia and cellular metabolism. J Cell Physiol 1996 Aug;168(2):424-3.
12. Brighton CT, Schaffer JL, Shapiro DB, Tang JJ, Clark CC. Proliferation and macromolecular synthesis by rat calvarial bone cells grown in various oxygen tensions. J Orthop Res 1991 Nov;9(6):847-54.
13. Semb H. Experimental disuse osteoporosis. II. Oxygen saturation and oxygen tension in intramedullary blood from immobilized rabbit tibial bones. Acta Soc Med Ups 1966;71:96-107.
14. Semb H. Experimental disuse osteoporosis. I. Acid-base status in intramedullary blood from immobilized rabbit tibial bones. Acta Soc Med Ups 1966;71(1):83-95.
15. Minchenko A, Bauer T, Salceda S, and Caro J. Hypoxic stimulation of vascular endothelial growth factor expression in vivo and in vitro. Lab Invest 1994;71: 374-379.
16. Thomas, K. Vascular endothelial growth factor, a potent and selective angiogenic agent. J Biol Chem 1996;271: 603-606.
17. Tuncay OC, Ho D, Barker MK. Oxygen tension regulates osteoblast function. Am J Orthod Dentofacial Orthop 1994;105:457-63.
18. Rowley JA, Timmins M, Galbraith W, et al. Oxygen consumption as a predictor of growth and Differentiation of MC3T3 E1 osteoblasts on 3D biodegradable scaffolds. http://www.bdbiosciences.com/discovery_labware/Products/
drug_discovery/polystyrene_microplates/oxygen_biosensor_system/pdf/S02B097R1.pdf ACCESSED January 19, 2005
19. Ramamurthy NS, Vernillo AT, Greenwald RA, Lee HM, Sorsa T, Golub LM, Rifkin BR. Reactive oxygen species activate and tetracyclines inhibit rat osteoblast collagenase. J Bone Miner Res 1993 Oct;8(10):1247-53.

 

 

 

 

Related Articles

* The Musculoskeletal System: An Evolutionary Perspective

*The dysox model of aging. Townsend Letter for Doctors and Patients.2005;269:130-134.

* Bone homeostasis is but one face of oxygen homeostasis. Townsend Letter for Doctors and Patients. 2005;261:86-93.

 

 

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