Who is
Majid Ali, M.D.
► Dr. Ali's CV

Majid Ali is a pioneer who is changing the face of medicine with his innovative and spirited approach.

His credentials are impeccable Complementary Medicine Journal

"I stand in awe of Ali's superb scientific knowledge, his insights into the nature of the the healing process and his ability to explain hard science."

Aubrey Worrell, MD
Past President, the American Academy of
Environmental Medicine

Majid Ali, M.D.
Editor, The Journal of Integrative Medicine

Formerly, Associate Professor of Pathology (adj.), College of Physicians and Surgeons of Columbia University, NY

Formerly, President of Staff and
Chief Pathologist, Holy Name Hospital, Teaneck, NJ

Fellow, Royal College of Surgeons of England - Diplomate,

American Board of Anatomic and Clinical Pathology

Diplomate, American Boards of Environmental Medicine

Past President Capital University of Integrative Medicine

Aging Healthfully Supplements
Now You Can Order Online

Oral Chelation

Aging Healthfully proudly offers the
Oral EDTA Chelation Protocol
developed and used by
Majid Ali, M.D.
in his practice for
over twenty years.

Sugar Shortens Life
Majid Ali, M.D.

Excess Sugar Shortens Life
Excess sugar is inflaming, fattening, and oxygen-depleting—and, as a consequence, life- shortening. I delineated these relationships in Oxygen and Aging (2000).¹ Briefly, excess sugar builds grease on cells membranes, and suffocates them when the grease is not expediently removed by the body's detergent system. Suffocated cells cannot breathe and rapidly bloat with acids and internal grease on mitochondria and other crucial cell innards. The end result of all this is a decrease in the supply of oxygen and impairment of its functions. Of course, rancid fats, mangled proteins, cellular waste and metabolic debris add to the cellular grease. This is the basic nature of the "oxygen-sugar-shortened-life connection." These phenomena are described and illustrated at length in my forthcoming book Darwin’s Drones, Oxygen, and Diabetes (2010).²

Direct evidence for my view has been established in experimental studies. For example, in one series of experiments, the life span of a common form of yeast increased by 25% when the glucose level in the culture is reduced from 2% to 0.5%.³ More important, recently Professor Cynthia Kenyon and colleagues at the University of California showed that glucose shortens the lifespan of C. elegans round worm.⁴

Insulin Toxicity
Next to oxygen, insulin is the most metabolic Dr. Jekyll/Mr. Hyde in the body. In its narrow healthful range, the Dr. Jekyll is pro-health, anti-diabetes, anti-immune, anti-degenerative, anti- hypertensive, anti-stroke, anti-heart attack, and anti-premature aging. When in excess, the Mr. Hyde is anti-health, pro-diabetes, pro-immune, pro-degenerative, pro-hypertensive, pro-stroke, pro-heart attack, and pro-premature aging. A clear comprehension of these Dr. Jekyll/Mr. Hyde roles of insulin is essential for understanding the Oxygen-sugar-shortened-life-connection which I present here. I present this subject at length in several companion articles on this website and on www.majidali.com.

Theories of Oxygen and the Oxygen-sugar-shortened-life Connection
Below is text adapted from my earlier writings to shed light on the oxygen-sugar-shortened- life connection and its clinical significance.

During 1930s, Clive McKay established that caloric restriction extends life span in many species.⁵ He implied that is the only way of increasing the lifespan of mammals. Since that classic work, an enormous body of literature has accumulated validating the direct relationship between caloric restriction and longevity.^6-11 This linkage has been documented in yeast, mosquitoes, flies, and rats. Since glucose is the primary energetic currency of human metabolism and fats and proteins in the body are converted to glucose when needed, it would be expected that less food intake means less glucose. In a larger sense, McKay's work established the basic tenets of the oxygen-sugar- shortened-life connection.

In 1983, I put forth my Spontaneity of Oxidation Model of Aging.¹² This model holds that aging involves loss of energy triggered, perpetuated, and completed by the ongoing and spontaneous loss of electrons in the body. Even a cursory look at the cross-linkage, free radical, and immune theories makes it clear that the Spontaneity of Oxidation Model is fully consistent with all three. Indeed, my model then represented an extension of those theories in the sense that it provided a clear underlying mechanism for all three.

In 1996, Professor Cynthia Kenyon and colleagues at the University of California showed that the lifespan of C. elegans round worm can be extended by removing one copy of a "stop the clock" (daf-2) gene.^13-15 They concluded that the program, which controls longevity in the worm, can be uncoupled from other physiological processes. In that year, Guy Ruvkun demonstrated that daf-2 and age-1 genes were part of the same genetic pathway, and that daf-2 encodes an insulin receptor, thus linking aging to insulin signaling.^16-17

During the late 1990s, Leonard Guarente and David Sinclair showed that the lifespan of yeast can be extended when its DNA is stabilized (rearrangements are prevented).^18-20 Specifically, the yeast live about one-third longer when an extra copy of Sir2 gene is inserted in it to stabilize its DNA. The Sir2 gene is considered to be the founding member of the family of genes that encode sirtuins, proteins that evolved about a billion years ago to preserve the life span of various species during periods of stress.

The Oxygen Model of Aging
In Oxygen and Aging (2000), I proposed my unifying Oxygen Model of Aging.²¹ This model integrates all known aspects of the the aging process. Models in medicine are proposed for two primary reasons: (1) for their power to bring together seemingly disparate findings to make a meaningful whole; and (2) to provide scientific rationale and/or basis for designing strategies for meaningful interventions. The dysox model of aging has enormous explanatory power for nearly all, if not all, clinical, epidemiologic, and experimental observations concerning the aging processes in humans as well animal aging models.

As for designing intelligent interventional strategies, the Oxygen Model of Aging shifts the focus from the dynamics of individual genes to a holistic view of the three primary regulatory mechanisms of the body: oxygen homeostasis, redox equilibrium, and acid-base balance. For addressing those issues, I employ the Sun-Soil Model of the health/dis-ease/disease continuum. The Sun in that model symbolizes a person's spiritual belief in the healing dynamics, whereas the soil is represented by ecologic dynamics and inter-relationships among the bowel, blood, and liver ecosystems. The Sun-Soil Model of health and healing has been described at length in Darwin and Dysox Triology, the tenth, eleventh, and twelfth volumes of The Principles and Practice of Integrative Medicine (2009).

In closing, I offer comments on another aspect of the sugar problem. The dangers of sugar are not duly recognized by influential medical journals. In some cases, there is outright deception. To cite one example, below is text from a review article on ADHD published in The New England Journal of Medicine on January 13, 2005²¹:

 

The writer of the article never practiced nutritional medicine. Nor did the authors of the three articles he cites to support his assertion. They limit their work with children with ADHD to prescriptions of various drugs, as well as to suppressing the field of clinical nutrition.

For further discussion, see my article entitled “The Oxygen-ADHD-Sugar Connection”

References
1. Lin SJ, Defossez PA, Guarente L. Requirement of NAD and SIR2 for life-span extension by calorie restriction in Saccharomyces cerevisiae. Science 2000;289; 2126-2128.
2. Ali M. Oxygen and Aging,. L 2000. Life Span Press, Denville, New Jersey.
3. Ali M. Darwin’s Drones, Oxygen, and Diabetes. 2010. New York. Institute of Integrative Medicine Press.
4. Lee S-J, Murphy CT, Kenyon C. Glucose Shortens the Life Span of C. elegans by Downregulating DAF-16/FOXO Activity and Aquaporin Gene Expression. Cell Metabolism, 2009; 5, 379-391.
5. McKay CM. Chemical Aspects of Aging and the Effect of Diet upon Aging. In: Cowdry's Problems of Ageing. 3rd ed. 1952. Eds. AI Lansing. New York. Williams and Williams. p139.
6. Carlston AH.Hoelzel F. Apparent prolongation of the life span of rats by intermittent fasting. J Nutrition 1946;31:363-7.
7. Weindruch W. Walford RL. The Retardation of Aging and Diseases by Dietary Restriction. Thomas, Springfield, Illinois, 1998.
8. Roth GS, Ingram D K, Lane MA. Calorie restriction in primates: will it work and how will we know? J. Am. Geriatr. Soc. 1999;47:896-903
9. Yu BP. Modulation of Aging Processes by Dietary Restriction. CRC Press, Boca Raton, Florida, 1994.
10. Ross M. Length of life and nutrition in the rat. J Nutrition, 1961;75:197-201.
11. Sohal RS. Weindruch R. Oxidative stress, caloric restriction, and aging. Science 1996;273: 59-63.
12. Ali M. Spontaneity of Oxidation in Nature and Aging. Monograph. 1983. Teaneck, New Jersey.
13. Kenyon C. Ponce d'elegans: genetic quest for the fountain of youth. Cell. 1996;84:501-504.
14.. Kenyon C. The nematode Caenorhabditis elegans. Science. 1988;240:1448-1453.
15. McCarroll, S. A., Murphy, C. T., Zou, S., Pletcher, S. D., Jan, Y. N., Kenyon, C., Bargmann, C. I., and Li, H. "Comparative functional genomics: Shared transcriptional program of adult maturation and aging in C. elegans and Drosophila." Nature Genetics. 2004;36: 197-204.
16. Kimura KD, Tissenbaum HA, Liuv Y, Ruvkun G. (1997) daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans. Science. 1997; 15:942-946.
17. Morris JZ, Tissenbaum HA, Ruvkun G. (1996) A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans. Nature (London) 382,536-539.
18. Guarente L. Sir2 links chromatin silencing, metabolism, and aging. Genes Dev. 2000;14:1021-1026.
19. Lamming DW, Wood JG, Sinclair DA. Small molecules that regulate lifespan: evidence for xenohormesis. Mol Microbiol. 2004;53:1003-9
20. Tissenbaum HA, Guarente L. Increased dosage of a sir-2 gene extends lifespan in Caenorhabditis elegans. Nature. 2001;410:227-230.
21. Rappley MD. Attention Deficit-Hyperactivity Disorder. N Eng J Med. 2005;352:165.