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Uric Acid: A Demonized Angel

Majid Ali, M.D.

(Three segments on the subject posted on YOU TUBE)

Uric acid has been demonized by people who sell uric acid drugs. It is a powerful antioxidant, nearly fifty-fold stronger than vitamin C. Like all bodily antioxidants that act as anti-inflammatory substances, uric acid is an anti-inflammatory agent within the physiologic range. Other crucial physiologic roles of uric acid involve healing immune responses and autoimmune responses. Notably, the acid provides a molecular link between cell injury and immunity. Most fascinating, uric acid facilitates cellular cross-talk between dead and living cells. When the body is insulted and inflamed, it uses uric acid as one of its messengers. Just taking a drug to lower uric acid level is simply killing the messenger.

Uric acid is entrenched in the medical thinking, as well as in the minds of the general public, as a demon (usual laboratory blood level range : 3.6 to 8.5 mg/dL (~214 µmol/L). It is considered as the:

* Cause of gouty arthritis,

*Cause of uric acid stones,

* Risk factor for hypertension, and

* Risk factor for cardiovascular disorders.

The disturbing aspect of this sad story is that people who speak ill of uric acid do not think about its place in evolution’s intelligent design of the human body nor do they study its molecular biology to understand the true significance of changes in its blood levels.

Gout, A Disease of Celebrities

It seems to me that the public infatuation with the 'disease-of-the-celebrities' is not a new malady. The mystique of gout has been inculcated and perpetuated throughout history by many celebrities. Alexander the Great, Charlemagne, Benjamin Franklin, Leonardo da Vinci, Newton, and Darwin were among the luminaries who suffered from gout. Their accounts seemed to have fired the imagination of the public about swollen big toes.

Mammals generally have lower serum uric acid levels (0.5 to 1.0 mg/dL) than humans, owing to the existence in them of the enzyme uricase that converts uric acid into allantoin. Our homonoid ancestors lost that enzyme during the Miocene Epoch. Interestingly, it appears that resulted from several parallel mutations which initially involved the promoter region but eventually silenced the whole gene.

Uric Acid Facilitates Dead-Cell-Living-Cell Cross-talk

That uric acid is a principal endogenous danger signal released from dead and dying cells calls for a major shift in the way we look at this molecule. Uric acid stimulates dendritic cells to their maturation. When such cells are co-injected with antigen in vivo, CD8+ T cell responses are significantly enhanced by the generation of responses from CD8+ T cells. Furthermore, in vivo elimination of uric acid inhibits the immune response to antigens associated with dead and dying cells, but that is not the case when antigens are presented by activated dendritic cells.

Was Lead the Cause of the Roman and English Epidemics of Gout?

Gout was generally associated with intemperance and gluttony. There have been two celebrated epidemics of gout: one in ancient Rome during the years of the decline of the Roman empire and the second in England during the 17th to 19th centuries. As for the Roman epidemic, Seneca (4 B.C.) recognized the increasing frequency of gout among women and observed that was so because women "rival men in every kind of lasciviousness." Both Roman and English epidemics were — and continue to be — attributed to lead toxicity in the belief that lead is toxic to the kidneys and such toxicity leads to uric acid calculus formation. But was lead the only culprit? If so, what do we make of many other roles of the acid? For example, premenopausal women have lower uric acid levels. More significantly, how do we reconcile the prevailing, and very limited, view of uric acid in human illness with the acid being a crucially important signaling molecule?

Dead and dying cells, when co-injected with antigen into animals, provide an adjuvant effect for priming T-cell responses. Such endogenous adjuvant activity occurs in the cytosol of cells and is markedly enhanced during the process of cell injury, such as that inflicted by exposure to ultraviolet irradiation. This was shown by experiments in which HIV gp120 antigen was co-injected with the irradiated cells which resulted in effective priming of CD8+ T-cell responses. Similarly, in infectious processes microbial components provide signals that alert the immune system and activate innate and acquired immune responses. Such danger signaling has been considered to stimulate dendritic cells to maturation so they can present alien antigens to T lymphocytes. Furthermore, other as yet undefined types of signaling has also been found to emanate from injured and dying mammalian cells. Such signaling is critical to the integrity of some immune responses since their absence is associated with weakened or absent immune responses or the development of tolerance. That led to the important concept that the immune system responds only to antigens that are associated with cell injury or infections.

Uric Acid Reveals Stresses on Cellular Oxygen Functions

Looking through the prism of oxygen homeostasis, I take a different view of the roles of uric acid in the health/dis-ease/disease continuum. I suggest a different mechanism by which the well-documented epidemics of gouty arthritis in history occurred. I propose that uric acid production increased as a compensatory response to cellular oxidosis and dysoxygenosis resulting from a host of food-related and environomenatal factors. The precipitation of uric acid crystals in the joints and the development of gouty arthritis developed as consequences of that response. Lead toxicity may have played a role in the pathogenesis of arthritis in that setting to the degree that lead, like mercury, inflicts oxidative damage and disrupts oxygen homeostasis in many ways (see Heavy Metal Load and Toxicity, the seventh volume of this series for details).

The Oxygen Model of Pathophysiology of Uric Acid

The Oxygen-Uric Acid Model has three principal strengths:

1. It compels us to look at the toxicities of foods, environment, and thought that raise blood uric acid levels and precipitate the acid into tissues in and around the joints to cause "gouty arthritis." The prevention of gout then becomes then becomes a matter of addressing the relevant issues of foods, environment, and thought, and not merely using allopurinol to suppress uric acid production.

2. It provides a highly plausible explanation of the well-established association of hyperurecemia with the spreading epidemic of the cardiovascular disease that is gripping the United States, and to a lesser degree most other countries in the world.

3. It offers the opportunity to use uric acid as a marker of dysoxygenosis as well as for monitoring the benefits of integrative management plans to control the dietary and nutritional factors that cause dysoxygenosis and raise serum levels of the acid.

References

All citations are included in Integrative Nutritional Medicine, volume 5 of The Principles and Practice of Integrative Medicine.

* Arthritis Course

* Arthritis: Pathogenesis and Types

* URIC ACID: A DEMONIZED ANGEL

* Healing After Spinal Surgery

 

* The Musculoskeletal System: An Evolutionary Perspective

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

* Diseases of Bones and Joints

* Introduction to Diseases of Bone and Joints

 

*

 

 

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