OXYGEN, GOUT, URIC ACID, AND DARWIN

Majid Ali, M.D.

OXYGEN, GOUT, URIC ACID, AND DARWIN A prism splits white light into a luminous rainbow—then emboldens the colors. For me, the “oxygen prism” splits the energetic domains of the body—then sparkles them. This is the core of oxygen thinking. It de-fogs issues. Doctors look at uric acid as a molecular villain. In this essay, I look at it through the oxygen prism to seek clarity, not only for understanding uric acid but also for rational, safe, and effective measures for the prevention and treatment of gout. Recently, a colleague, Dr. Sabitha Dasoju, M.B.,B.S, told me that her mother in India saw an orthopedic surgeon for chronic arthritis pain in her knees and hips. The doctor noted an elevated blood uric acid value and promptly prescribed five drugs, including a high-dose steroid level. When my colleague protested that her mother did not have gout but osteoarthritis, the orthopod shrugged her off by saying, “This is our standard treatment for treating high uric acid levels.”
I asked fifteen practitioners (five physicians, one nurse, one physician assistant, two nutrition advisors, four laboratory technologists, and two administrative staff members) to answer the following two questions:
► What is your general sense about vitamin C, is it a good player or a bad player? ► What is your general sense about uric acid, is it a good player or a bad player?
Thirteen called vitamin C a good player and considered uric acid to be a bad player. The remaining two said uric acid could go either way. That did not surprise me since uric acid is embedded deep in drug medicine thinking as a villain. A raised blood uric acid level is used to diagnose gout arthritis, as well as to detect an increased risk of heart attacks and strokes. This is what medical textbooks teach medical students and doctors. Next, I wondered what the oxygen prism and Darwin might have to say about uric acid.
Killing the Messenger Uric acid is a marker of tissue injury. Rising blood levels herald pathologic inflammation that causes cell death. When I see elevated blood uric acid level in my patients’ lab reports, I see it as injured cells’ call for relief. To me this the lab abnormality requires diligent efforts to detect and eliminate all relevant insults to the body. I do not see uric acid as an evil player that must be snuffed with drugs.
Uric Acid Is a Potent Antioxidant Over half the antioxidant capacity of human blood plasma is derived from uric acid. It is is fifty-fold stronger antioxidant than vitamin C. So, if we consider vitamin C to be a good player, we must consider uric acid as fifty times as good. Why is this fact not generally known? The answer: no drug company or medical journal profits from disseminating this information.
Uric acid has been successfully employed in the prevention and treatment of an animal model of multiple sclerosis. A 2006 study found that oral use of inosine raised serum uric acid values in patients with this disease, without causing any adverse effects. It does not surprise me that this nutritional possibility for multiple sclerosis was not explored further since no one can make obscene profits from it.
Uric Acid Is An Immune Booster This is likely to surprise nearly all readers. I myself never considered uric acid biology in a broader context during the first twenty-five years of my work as a surgeon and pathologist. This is gift of understanding from my patients. They forced me to think differently when I recognized how they responded to overhydration and nondrug therapies (listed below) that normalize the inflammatory response by focusing on ecologic disruptions of the bowel, blood, and liver ecosystems.
Uric Acid Facilitates Cross-talk Between Dead and Living cells Uric acid is a principal endogenous danger signal released from dead and dying cells. This basic but generally unrecognized fact of uric acid biology calls for a major shift in the way we look at it. Uric acid stimulates a type of immune cell (dendritic cell) to its maturation. When such cells are injected along with certain substances in experimental animals, another type of immune cell (CD8+ T cell) becomes stronger in its responses to microbes and noxious chemicals. In other experiments, removal of uric acid weakens certain types of immune responses, indicating immune- boosting effects of uric acid.
What Might Darwin Teach us About Uric Acid? Why do blood uric acid levels rise? What might be the basis of observed association between raised uric acid levels and increased risks of insulin resistance, diabetes, heart attacks, and strokes?
History informs us about two great epidemics of gout, one in Roman times and the other in England in 17th to 19th centuries. What might have triggered those epidemics? We do not find answers to these questions in medical textbooks written by doctors paid by drug companies to promotes the use of drugs. We need the oxygen prism and Charles Darwin to enlighten us.
Uric acid is produced by the enzyme, xanthine oxidase, from xanthine and hypoxanthine, which in turn are produced from purine. Evolutionary design for the redox systems in living organisms is simple: if you increase oxidative stress, the antioxidant systems are upregulated. When the body is insulted by the trio of toxicities of foods, environments, and thoughts—the trio that sets the stage for insulin toxicity, the so-called metabolic syndrome, heart attacks, strokes, and gouty arthritis—the body gears up its antioxidant defenses. Uric acid, a potent weapon in the body’s antioxidant armamentarium, is produced in excess to cope with incremental oxidative stress. So, the blood uric acid levels go up. It is not the body’s cries for drugs, only for relief from the trio of toxicities.
Was Lead the Cause of the Roman and English Epidemics of Gout? Gout was generally associated with intemperance and gluttony. Of the two gout epidemics mentioned above, gout in ancient Rome was linked to excessive eating. 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?
Uric Acid and Oxygen Homeostasis 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 it resulted from several parallel mutations which initially involved the promoter region but eventually silenced the whole gene.
In the prevailing medical thought, there is little, if any, appreciation that uric acid is a very potent antioxidant, by some estimation as much as fifty-fold stronger than ascorbic acid. That makes this normal metabolite to be potentially of great clinical significance in the present context of oxygen homeostasis. There are yet other crucial roles of uric acid in inflammation and autoimmunity. Notably, the acid provides a molecular link between cell injury and immunity . Here, I use this normal metabolite to illustrate some aspects of the larger view of oxygen homeostasis.
Elevated Serum Uric Acid Level As A Marker of Cellular Oxidosis and Dysoxygenosis In the context of looking at uric acid through the prism of oxygen homeostasis, I take a different view of its roles in the health/dis-ease/disease continuum. I suggest a different mechanism by which the two well-noted epidemics of gouty arthritis mentioned earlier 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 environomental 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 arthitis 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). My oxygen view of uric acid has two principal strengths: (1) It provides a highly plausible explanation of the well-established association of hyperurecemia with the spreading epidemics of insulin toxicity, obesity, diabetes, and cardiovascular disorders that are gripping the United States, and to a lesser degree most other countries in the world; and (2) 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.
Why Are the Gout Genes Angry—and Getting Agrier By the Decade?  The incidence of gout is rising worldwide. Gene enthusiasts are diligently working to identify gout genes. I wish them best of luck. For others, I suggest they look for answers in incremental global chemicalization and poisoning of societies—with anger, depleted foods, contaminated water, and polluted air.
Prevention and Treatment of Gout Inflammation in acute gout arthritis is caused by the trio of toxicities of foods, environments, and thoughts. The rational and scientific approach to the prevention and treatment of gout is to systematically identify and address all relevant elements of toxicity. In decades of clinical work, I have not found any natural remedy that by itself gives good long-term results. My preferred therapies are: (1) castor-pres; (2) hydrogen peroxide foot soaks; (3) optimal hydration; (4) control of gut fermentation and leaky gut state; (5) and liver detox. (See http://www.ethics7.org for full details). Some dietary measures are very helpful. Uric acid is derived from compounds called purines, which are found in large amounts in animal food products, such as liver, kidneys, and sardines. Lesser amounts are in pork, beef, poultry, seafood, and certain vegetables (asparagus, cauliflower, spinach, mushrooms, and green peas), and certain grains (oatmeal, wheat bran and wheat germ). So, it is advisable to eliminate these items during acute attacks, and reduce their intake in general.
In drug medicine, symptoms are managed with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and colchicine. These approaches can be justified only in unusual circumstances for short periods of time to relieve acute symptoms that cannot be rapidly controlled with nondrug therapies.
Uric Acid Stones Uric acid stones form when there is deficiency of functioning oxygen in the kidney tissues and the urine becomes highly acidic. This explains the increased risk of uric acid stone formation in chronic dehydration, chronic inflammatory conditions, insulin toxicity, diabetes, excessive gut fermentation, leaky gut state, and impaired liver detox systems. Regrettably, these fundamental facts of uric acid biology are not known to most doctors. I offer detailed information on these subjects on this web site. About 70% of uric acid is cleared through the kidneys. Reduced clearance of uric acid via the kidneys can also raise blood levels and, in excess, increase the risk of the formation of calcium oxalate stones.
Wikipedia’s Contribution to Disinformation The crucial oxygen issues—excess acidity (acidosis), incremental free radical activity (oxidosis), and clotting-unclotting dysequilibrium (CUD)—continue to be ignored. Why does uric acid continue to be cast as a bad player? Reason: An unremitting campaign of misinformation by the monsters of the American Disease Maintenance System. Consider the following quotes from Wikipedia (as shown on April 20, 2010) written by some drug doctor:
The association of high serum uric acid with insulin resistance has been known since the early part of the 20th century, nevertheless, recognition of high serum uric acid as a risk factor for diabetes has been a matter of debate.
Although uric acid can act as an antioxidant, excess serum accumulation is often associated with cardiovascular disease. It is not known whether this is causative (e.g., by acting as a prooxidant) or a protective reaction taking advantage of urate’s antioxidant properties.
… It is unclear whether elevated levels of uric acid in diseases associated with oxidative stress such as stroke and atherosclerosis are a protective response or a primary cause.


Rather than clarify crucial scientific issues, Wikipedia only adds to the prevailing doubt and confusion about the molecular biology of uric acid.
Darwin’s Message Darwin’s message for us is: No part can be understood without understanding its relationships with the whole. So for understanding uric acid biology and for rational measures for the prevention and treatment of gout, first and foremost, we must understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.
Charles Robert Darwin himself suffered from gout. I wonder how he might react if he were to read this essay. I think he would have smiled at this disciple of him. He might also want me to include here a brief evolutionary perspective.
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.
In higher primates, the loss of uricase appears to parallel the loss of the species’ ability to synthesize vitamin C, creating a double antioxidant jeopardy. In reptiles and birds, uric acid also is the end product of purine metabolism, but it is excreted in feces as a dry mass. This is energetically expensive compared to the generation of nitrogenous waste products, such as urea and ammonia, for these species. The evolutionary advantage of this costly and complex metabolic pathway is that it reduces water loss

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Healing  Seminars Dr. Ali’s Course on Healing  Seminar 1 – Introduction Dr. Ali’s Course on Healing Seminar 2 – Cellular Fermentation Forms    Dr. Ali’s Course on Healing Seminar 3 The Oxygen Model of Inflammation Dr. Ali’s Course on Healing Seminar  4  Dr. Ali’s Breakfast   Dr. Ali’s Course on Healing Seminar  5 Top Seven Natural Remedies    Dr. Ali’s Course On Healing  Seminar 6  Natural Anti-inflammatory  Remedies Dr. Ali’s Course on Healing Seminar  7 BOWEL Detox Dr. Ali’s Course on Healing Seminar  8 Liver Detox Dr. Ali’s Course On Healing Seminar 9 –  Oxygen Model of Health and Disease  Dr. Ali’s Course On Healing Seminar 10 –  Acid-Alkali Balance Dr. Ali’s Course on Healing Seminar  11 Oxidant –  Antioxidant Regulation  Oxygen’s 3 M Model of Health and Disease –  Dr. Ali’s Course on Healing Intermediate Part 1  

Reversing Diabetes Say NO to  Dialysis Part 1   Say NO to  Dialysis Part 2 Diabetes Reversing  Diabetes Reversing By Regenerating  Pancreas Seminar   Insulin Reduction Protocol    NEW Insulin Toxicity and  Reversal of Diabetes
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Nutrition Dr. Ali’s Course on Nutrition – Seminar 1 * Principles and Philosophy of Nutrition   Dr. Ali’s Course on Nutrition Seminar 2 – Nutrition –  Scientific and Simplified   Dr. Ali’s Course on Nutrition Seminar 3 – Food Individuality and Responses    Dr. Ali’s Nutrition Course Seminar 4 – Nutrient Supplementation  Breakfast Shake Seminar Gout Arthritis Seminar H. pylori Misunderstood and Mismanaged   
Oral Hygiene and  Bad Breath Bad Breath   Mouth Fermentation  and Sores   Gingivitis and Jaw Bone Loss Seminar   Oral Hygene  
OXYGEN, GOUT, URIC ACID, AND DARWIN A prism splits white light into a luminous rainbow—then emboldens the colors. For me, the “oxygen prism” splits the energetic domains of the body—then sparkles them. This is the core of oxygen thinking. It de-fogs issues. Doctors look at uric acid as a molecular villain. In this essay, I look at it through the oxygen prism to seek clarity, not only for understanding uric acid but also for rational, safe, and effective measures for the prevention and treatment of gout. Recently, a colleague, Dr. Sabitha Dasoju, M.B.,B.S, told me that her mother in India saw an orthopedic surgeon for chronic arthritis pain in her knees and hips. The doctor noted an elevated blood uric acid value and promptly prescribed five drugs, including a high-dose steroid level. When my colleague protested that her mother did not have gout but osteoarthritis, the orthopod shrugged her off by saying, “This is our standard treatment for treating high uric acid levels.”
I asked fifteen practitioners (five physicians, one nurse, one physician assistant, two nutrition advisors, four laboratory technologists, and two administrative staff members) to answer the following two questions:
► What is your general sense about vitamin C, is it a good player or a bad player? ► What is your general sense about uric acid, is it a good player or a bad player?
Thirteen called vitamin C a good player and considered uric acid to be a bad player. The remaining two said uric acid could go either way. That did not surprise me since uric acid is embedded deep in drug medicine thinking as a villain. A raised blood uric acid level is used to diagnose gout arthritis, as well as to detect an increased risk of heart attacks and strokes. This is what medical textbooks teach medical students and doctors. Next, I wondered what the oxygen prism and Darwin might have to say about uric acid.
Killing the Messenger Uric acid is a marker of tissue injury. Rising blood levels herald pathologic inflammation that causes cell death. When I see elevated blood uric acid level in my patients’ lab reports, I see it as injured cells’ call for relief. To me this the lab abnormality requires diligent efforts to detect and eliminate all relevant insults to the body. I do not see uric acid as an evil player that must be snuffed with drugs.
Uric Acid Is a Potent Antioxidant Over half the antioxidant capacity of human blood plasma is derived from uric acid. It is is fifty-fold stronger antioxidant than vitamin C. So, if we consider vitamin C to be a good player, we must consider uric acid as fifty times as good. Why is this fact not generally known? The answer: no drug company or medical journal profits from disseminating this information.
Uric acid has been successfully employed in the prevention and treatment of an animal model of multiple sclerosis. A 2006 study found that oral use of inosine raised serum uric acid values in patients with this disease, without causing any adverse effects. It does not surprise me that this nutritional possibility for multiple sclerosis was not explored further since no one can make obscene profits from it.
Uric Acid Is An Immune Booster This is likely to surprise nearly all readers. I myself never considered uric acid biology in a broader context during the first twenty-five years of my work as a surgeon and pathologist. This is gift of understanding from my patients. They forced me to think differently when I recognized how they responded to overhydration and nondrug therapies (listed below) that normalize the inflammatory response by focusing on ecologic disruptions of the bowel, blood, and liver ecosystems.
Uric Acid Facilitates Cross-talk Between Dead and Living cells Uric acid is a principal endogenous danger signal released from dead and dying cells. This basic but generally unrecognized fact of uric acid biology calls for a major shift in the way we look at it. Uric acid stimulates a type of immune cell (dendritic cell) to its maturation. When such cells are injected along with certain substances in experimental animals, another type of immune cell (CD8+ T cell) becomes stronger in its responses to microbes and noxious chemicals. In other experiments, removal of uric acid weakens certain types of immune responses, indicating immune- boosting effects of uric acid.
What Might Darwin Teach us About Uric Acid? Why do blood uric acid levels rise? What might be the basis of observed association between raised uric acid levels and increased risks of insulin resistance, diabetes, heart attacks, and strokes?
History informs us about two great epidemics of gout, one in Roman times and the other in England in 17th to 19th centuries. What might have triggered those epidemics? We do not find answers to these questions in medical textbooks written by doctors paid by drug companies to promotes the use of drugs. We need the oxygen prism and Charles Darwin to enlighten us.
Uric acid is produced by the enzyme, xanthine oxidase, from xanthine and hypoxanthine, which in turn are produced from purine. Evolutionary design for the redox systems in living organisms is simple: if you increase oxidative stress, the antioxidant systems are upregulated. When the body is insulted by the trio of toxicities of foods, environments, and thoughts—the trio that sets the stage for insulin toxicity, the so-called metabolic syndrome, heart attacks, strokes, and gouty arthritis—the body gears up its antioxidant defenses. Uric acid, a potent weapon in the body’s antioxidant armamentarium, is produced in excess to cope with incremental oxidative stress. So, the blood uric acid levels go up. It is not the body’s cries for drugs, only for relief from the trio of toxicities.
Was Lead the Cause of the Roman and English Epidemics of Gout? Gout was generally associated with intemperance and gluttony. Of the two gout epidemics mentioned above, gout in ancient Rome was linked to excessive eating. 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?
Uric Acid and Oxygen Homeostasis 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 it resulted from several parallel mutations which initially involved the promoter region but eventually silenced the whole gene.
In the prevailing medical thought, there is little, if any, appreciation that uric acid is a very potent antioxidant, by some estimation as much as fifty-fold stronger than ascorbic acid. That makes this normal metabolite to be potentially of great clinical significance in the present context of oxygen homeostasis. There are yet other crucial roles of uric acid in inflammation and autoimmunity. Notably, the acid provides a molecular link between cell injury and immunity . Here, I use this normal metabolite to illustrate some aspects of the larger view of oxygen homeostasis.
Elevated Serum Uric Acid Level As A Marker of Cellular Oxidosis and Dysoxygenosis In the context of looking at uric acid through the prism of oxygen homeostasis, I take a different view of its roles in the health/dis-ease/disease continuum. I suggest a different mechanism by which the two well-noted epidemics of gouty arthritis mentioned earlier 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 environomental 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 arthitis 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). My oxygen view of uric acid has two principal strengths: (1) It provides a highly plausible explanation of the well-established association of hyperurecemia with the spreading epidemics of insulin toxicity, obesity, diabetes, and cardiovascular disorders that are gripping the United States, and to a lesser degree most other countries in the world; and (2) 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.
Why Are the Gout Genes Angry—and Getting Agrier By the Decade?  The incidence of gout is rising worldwide. Gene enthusiasts are diligently working to identify gout genes. I wish them best of luck. For others, I suggest they look for answers in incremental global chemicalization and poisoning of societies—with anger, depleted foods, contaminated water, and polluted air.
Prevention and Treatment of Gout Inflammation in acute gout arthritis is caused by the trio of toxicities of foods, environments, and thoughts. The rational and scientific approach to the prevention and treatment of gout is to systematically identify and address all relevant elements of toxicity. In decades of clinical work, I have not found any natural remedy that by itself gives good long-term results. My preferred therapies are: (1) castor-pres; (2) hydrogen peroxide foot soaks; (3) optimal hydration; (4) control of gut fermentation and leaky gut state; (5) and liver detox. (See http://www.ethics7.org for full details). Some dietary measures are very helpful. Uric acid is derived from compounds called purines, which are found in large amounts in animal food products, such as liver, kidneys, and sardines. Lesser amounts are in pork, beef, poultry, seafood, and certain vegetables (asparagus, cauliflower, spinach, mushrooms, and green peas), and certain grains (oatmeal, wheat bran and wheat germ). So, it is advisable to eliminate these items during acute attacks, and reduce their intake in general.
In drug medicine, symptoms are managed with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, and colchicine. These approaches can be justified only in unusual circumstances for short periods of time to relieve acute symptoms that cannot be rapidly controlled with nondrug therapies.
Uric Acid Stones Uric acid stones form when there is deficiency of functioning oxygen in the kidney tissues and the urine becomes highly acidic. This explains the increased risk of uric acid stone formation in chronic dehydration, chronic inflammatory conditions, insulin toxicity, diabetes, excessive gut fermentation, leaky gut state, and impaired liver detox systems. Regrettably, these fundamental facts of uric acid biology are not known to most doctors. I offer detailed information on these subjects on this web site. About 70% of uric acid is cleared through the kidneys. Reduced clearance of uric acid via the kidneys can also raise blood levels and, in excess, increase the risk of the formation of calcium oxalate stones.
Wikipedia’s Contribution to Disinformation The crucial oxygen issues—excess acidity (acidosis), incremental free radical activity (oxidosis), and clotting-unclotting dysequilibrium (CUD)—continue to be ignored. Why does uric acid continue to be cast as a bad player? Reason: An unremitting campaign of misinformation by the monsters of the American Disease Maintenance System. Consider the following quotes from Wikipedia (as shown on April 20, 2010) written by some drug doctor:
The association of high serum uric acid with insulin resistance has been known since the early part of the 20th century, nevertheless, recognition of high serum uric acid as a risk factor for diabetes has been a matter of debate.
Although uric acid can act as an antioxidant, excess serum accumulation is often associated with cardiovascular disease. It is not known whether this is causative (e.g., by acting as a prooxidant) or a protective reaction taking advantage of urate’s antioxidant properties.
… It is unclear whether elevated levels of uric acid in diseases associated with oxidative stress such as stroke and atherosclerosis are a protective response or a primary cause.
Rather than clarify crucial scientific issues, Wikipedia only adds to the prevailing doubt and confusion about the molecular biology of uric acid.
Darwin’s Message Darwin’s message for us is: No part can be understood without understanding its relationships with the whole. So for understanding uric acid biology and for rational measures for the prevention and treatment of gout, first and foremost, we must understand how oxygen governs human biology. Next, it requires ecologic thinking and holism.
Charles Robert Darwin himself suffered from gout. I wonder how he might react if he were to read this essay. I think he would have smiled at this disciple of him. He might also want me to include here a brief evolutionary perspective.
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.
In higher primates, the loss of uricase appears to parallel the loss of the species’ ability to synthesize vitamin C, creating a double antioxidant jeopardy. In reptiles and birds, uric acid also is the end product of purine metabolism, but it is excreted in feces as a dry mass. This is energetically expensive compared to the generation of nitrogenous waste products, such as urea and ammonia, for these species. The evolutionary advantage of this costly and complex metabolic pathway is that it reduces water loss

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