Gout Holistic Treatments

Gout Eraser

The Gout Eraser is a guide written to give the readers tips on how to treat their gout naturally and effectively. The guide was put together to be something that can be done at home without a need to visit an expert as regards its use. This program is a proven home method useful in eliminating gout rapidly and permanently.The book is a quick fix that has been designed to help the user get a cure for their gout in 7 days. The system requires their full attention, persistence, and discipline. The methods employed in this book are natural ones that have been proven by many specialists. The system comes with bonus E-books- 'Sleeping Solace'(The Key To Using Sleep To Cure Gout) and 'Stress Soothers (How To Overcome Stress, which is a top cause of gout), How To Lose 10 Pounds Naturally (The Key To Losing Pounds to Fight Gout).The book is in a digital format (PDF) and has been created at a very affordable price.One big knowledge that would linger on the mind of the users is that fighting gout is hard. However, with Gout Eraser, you will be freed from the pain that comes with gout Read more...

Gout Eraser Summary


4.7 stars out of 13 votes

Contents: Ebook
Author: Robert Miller
Official Website: gouteraser.com
Price: $37.00

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Highly Recommended

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All the testing and user reviews show that Gout Eraser is definitely legit and highly recommended.

Gout Remedy Manual

The Gout Remedy Report is an easy to follow step-by-step gout remedy system written by Joe Barton, with the most comprehensive gout information available, including alternative remedies, treatments, and rock-solid prevention strategies. You will learn the 7 Best Alternative Treatments available, as well as doctor-approved ways you can improve the effectiveness of traditional medical treatments. It is a little-known, proven cure related to how you sleep. Actually, this shocking discovery can help to cure your gout once and for all. Since arthritis is a complex problem, results from treatment methods given in this report is going to be different for different individuals and nothing can be guaranteed for sure. Those people who read the report and implement the natural remedies do have a chance of getting rid of gout permanently. Read more...

Gout Remedy Report Summary

Contents: Ebook
Author: Joe Barton
Official Website: outwithgout.com
Price: $39.97

The Ultimate Gout Diet

Gout and You: The Ultimate Gout Diet & Cookbook is an eBook written by Spiro Koulouris. Spiro Koulouris first found out he had gout in 2002. He was able to reduce his medications to a minimum and achieve a healthier and happier lifestyle just using the dieting and exercise plan he reveals in this book. The book contains a lot of nutrition advice on gout and recipes that can be used in the management of gout. It gives examples of diets to avoid like too much fat and sugar which have mostly empty calories and those that are healthy. It contains an optimized gout diet called the 80-10-10 diet which helps improve conditions of people with gout and helps reduce uric acid levels. This diet is discussed in more detail inside the book. The recipes are easy to follow and are written in a way that newbies can understand. In addition to this, the recipes also help in preventing diseases like diabetes and hypertension. This product is good for people suffering from gout, who want to prevent chronic diseases like hypertension and diabetes. Read more...

Gout and You Summary

Contents: Ebook
Author: Spiro Koulouris
Official Website: goutandyou.com
Price: $22.00

Cure Gout Now

You'll learn: How to cure gout quickly and naturally in seven easy steps these tips will put you on the fast track to better health. 6 high-risk factors for gout if you read nothing else, you absolutely must know this . this information will have a dramatic positive effect on how you live your life. The primary causes of gout and what this means for you and your future. The painful symptoms of gout and how to quickly and easily eliminate them. The secondary causes of gout and how to quickly assess your risks. Who's at the greatest risk of developing gout and how to dramatically lessen your chances of getting it. And so much more including over 20 delicious recipes that won't set off a gout attack. How to change the underlying cause of your gout. How to stop painful gout symptoms in their tracks. How to lose weight quickly and easily. How to lower your levels of uric acid naturally and effectively. Gout friendly foods as well as how to avoid unhealthy options that will set of another attack. Read more...

Cure Gout Now Summary

Contents: Ebook
Author: Lisa McDowell
Official Website: www.cure-gout-now.com
Price: $29.95


Gout is a metabolic disorder that results from high levels of uric acid (a waste product of cell metabolism) in the blood. The condition can lead to joint inflammation, deposits of uric acid in and around the joints, reduced kidney function, and sometimes the development of kidney stones (see page 289). Gout is nine times more common in men than in women. Risk factors for gout include obesity, moderate to heavy alcohol consumption, high blood pressure, and kidney disorders. Certain drugs (such as aspirin) can worsen gout, and certain diseases that affect kidney function (such as diabetes and sickle-cell disease) can be a factor. Acute attacks of gout can be brought on by dehydration, joint injury, fever, large meals, high alcohol intake, stress, or recent surgery. Certain foods, such as shellfish, sardines, and organ meats, also may trigger attacks. The small joint at the base of the big toe is the most common location for an acute gout attack. Other joints affected may include the...

Maintaining a Healthy Weight

Slow and steady weight loss of no more than 2 pounds per week is the safest way to lose weight. Too rapid a weight loss can cause you to lose muscle mass rather than fat tissue and also can increase your chances of developing other health problems, such as gallstones, gout, and nutrient deficiencies. Making long-term improvements in your diet combined with exercising more is the best way to lose weight and keep it off.

Oral Xanthine Oxidase Artificial Cells in a Patient with Lesch Nyhan Disease

This leads to overproduction of purine and accumulation of oxypurine intermediates and uric acid. It has been suggested that damage to the brain in Lesch-Nyhan disease may be secondary to the accumulation of oxypurines such as hypoxanthine (Lloyd et al., 1981). The enzyme HPRT is very complex and difficult to extract on a large scale. However, there is an enzyme, xanthine oxidase, produced by fermentation and can be easily purchased. We, therefore, look into giving xanthine oxidase (XOD) artificial cells orally (Chang, 1989a Palmour, Chang et al., 1989). As they move through the intestine, the XOD artificial cells act as a microscopic combined dialyser-enzyme reactor (Fig. 6.1). The enclosed XOD is protected from tryptic enzymes, but the ultrathin selectively permeable membranes allow passive entry of small substrate molecules like hypoxanthine. Hypoxanthine is highly lipid soluble, and can therefore equilibrate rapidly between the body fluid and the intestine. In this way,...

Patient with Lesch Nyhan disease

Purines were measured by high-performance liquid chromatography and uric acid and creatinine were measured enzymatically and colorimetrically, respectively. After withdrawal of the allopurinol, uric acid excretion rose rapidly baseline uric acid creatinine ratios at 0900h ranged between 3.5 UA uric acid HX hypoxanthine INO inosine XAN Xanthine Fig. 6.7. Effect of oral XOD artificial cells on cerebral spinal fluid concentrations of uric acid, hypoxanthine, inosine and xanthine (modified from Palmour et a ., 1989). and 4.1. With the introduction of XOD artificial cells, the morning and afternoon ratios fell to normal within 3 days. During a febrile episode of otitis media the ratios rose transiently. Urinary hypoxanthine excretion also responded promptly to the XOD treatment, the pattern of transient escape during the febrile illness being repeated. The CSF hypoxanthine levels fell by 25 after 10 days of XOD artificial cell administration (Fig. 6.7) and the CSF inosine levels fell by 32...

Disorders of the Soft Tissues

A bursa is a fluid-filled sac between a bone and a tendon or muscle that allows the tendon to slide smoothly over the bone. Bursitis occurs when repeated stress and overuse cause the bursa to become inflamed and swollen with excess fluid. Bursitis also can result from injury, rheumatoid arthritis, gout, or infection. Bursitis most often occurs in the shoulder but also can affect the hip, knee, elbow, Achilles tendon, or ankle. Often the nearby tendon also becomes swollen. Bursitis usually can be treated with rest, ice, and nonsteroidal anti-inflammatory medication. Occasionally it is necessary for a doctor to withdraw excess fluid from the bursa using a needle and syringe. If an infection is present, the doctor will prescribe antibiotics. If there is no infection, the doctor may inject a

Biochemical Basis for Neutrophil Function

Briefly, the function of neutrophils is to phagocytose invading pathogens such as bacteria or other foreign material (e.g., a uric acid crystal found in a gouty knee joint). Once pathogenic material has been phagocytosed, it is degraded in lyso-somal granules within the neutrophil via lysosomal enzymes such as lysozyme and myeloperoxidase. Energy derived from glycolysis and the pentose monophosphate pathway within the neutrophils is required for phagocytosis and lysosomal fusion. NADP (nicotinamide adenine dinucleotide phosphate) formed in the pentose pathway is regenerated by NADPH oxidase enzyme, producing NAD, the oxidized form of the coenzyme and hydrogen peroxide (H2O2). Thus, the energy burst in neutrophils, derived significantly from the pentose monophosphate pathway, results in the production of H2O2, which reacts with myeloperoxidase released from the lysosome and, in the presence of halides such as chloride or iodide, effects the killing of bacteria.

Metabolic Mechanism for OA

Generally, both cross-sectional and longitudinal studies have not revealed factors that that may help explain the association between obesity and OA. Adjusting for blood pressure, body fat distribution, serum lipids, serum uric acid, and blood glucose has generally failed to reduce the association between obesity and OA, implying that these metabolic factors are not significant mediators of the obesity-OA relationship (28,29,42,59-61).

The Interactions Between Stress Lipid Profiles Cortisone HPA Axis and Inflammation Immunity

In an earlier study, Francis investigated the correlations between serum uric acid, cortisol, HDL cholesterol, LDL cholesterol, and psychometric indices of stress, including anxiety, hostility, and depression, in 20 students over a 2.5-month academic quarter. The students' serum cholesterol and the LDL cholesterol levels were significantly elevated above control levels. The ratio of HDL cholesterol total cholesterol was significantly lower 102 . Agarwal et al. also estimated the serum cholesterol, triglycerides, and total lipids in 12 students exposed to a varying degree of examination stress. Serum cholesterol and triglycerides exhibited a rise proportional to the degree of examination stress, whereas other lipids exhibited an initial rise followed by a fall. The rise in serum cholesterol and triglycerides seems to be caused by stress-induced changes in hormonal levels and peripheral lipolysis, respectively 103 .

Chemical Defense Based On Alkaloids

The evolution of complex metabolic pathways for the synthesis of alkaloids is simply not consonant with the conclusion that this biosynthetic elegance has been evolved in order to synthesize nitrogenous waste products for elimination. Plant ecologists emphasize that nitrogen is the most limiting nutrient for plants, being required for key processes such as reproduction, growth, and development. Consequently, it would hardly be adaptive to jettison the element that has been incorporated into novel ring structures and which possesses great biological activities, if for no other reason than the plant is also eliminating an essential component of the peptides, proteins, and other nitrogen-containing compounds that are of such great metabolic significance for all organisms. It may well be that the excretion of uric acid or urea by carnivorous animals, which ingest an excess of proteins and nucleic acids, is responsible for the belief that organisms eliminate large amounts of nitrogenous...

Effect on Mature MiRNA Function

One of the targets specific to the miR-376a edited at the +4 site by ADAR2 was phosphoribosyl pyrophosphate synthetase 1 (PRPS1), an essential housekeeping enzyme involved in purine metabolism and the uric acid synthesis pathway. The importance of tight control of PRPS1 expression is demonstrated by an X-chromosome-linked human disorder characterized by gout and neurodevelop-mental impairment with hyperuricemia due to a 2-4-fold increase in PRPS1 levels. ADAR2 knockout mice had PRPS1 levels and uric acid levels both upregulated * 2-fold in the cortex. By contrast, the levels of TTK, a target of unedited miR-376a-5p, in the cortex were not affected. Nor were PRPS1 levels or uric acid levels in the liver. The latter is consistent with the observation that half of pri-miR-376a +4 site adenosines were edited in wild-type mouse cortex, while pri-miR-376a +4 editing was barely detected in wild-type mouse liver. This shows that ADAR2 influences uric acid levels in a tissue-specific manner by...

Disorders of the Kidney

Why kidney stones form in some people and not in others remains unknown. Men, especially white men, develop kidney stones more frequently than women. Kidney stones usually develop between ages 20 and 40, and once one stone has been diagnosed, more are likely to develop. A family history of kidney stones increases the risk, as do certain disorders of the kidney and recurrent kidney infections. Other diseases (such as gout and chronic inflammatory disorders) and certain medications (such as diuretics and calcium-based antacids) also can cause kidney stones.

Infectious bovine rhinotracheitis virus

Infectious bronchitis virus (IBV) The type species of the genus Coronavirus. The cause of a common, contagious, acute respiratory disease of chicks. Neutralization tests using chick embryos indicate multiple variant antigenic types. All strains show some antigenic relationships but are unrelated to other coronaviruses. Beaudette strain (IBV-42) is serologically similar to Massachusetts strain, although on egg passage it has become lethal for chick embryos but has lost infectivity for older birds. Chicks up to 4 weeks old are most susceptible. They show depression and gasping rales are heard. The disease lasts 6-18 days and the mortality is up to 90 . In laying birds there is a drop in egg production and eggs are defective. Pheasants may be infected. Mild endemic infection may result in poor egg production and predispose to bacterial respiratory disease. Avian nephrosis and visceral gout may be caused by the virus, possibly by certain strains (see Australian infectious bronchitis...

Ischemia Reperfusion

Ischemia stimulates the production of hypoxanthine. Under normal conditions, xanthine dehydrogenase reduces purines to uric acid. During ischemia, this enzyme is converted into the xanthine oxidase form at a rate proportional to the duration of ischemia. When the tissue is again perfused with oxygen, reperfusion, xanthine oxidase converts hypoxanthine into superoxide. Via several mechanisms, superoxide results in the formation of oxygen radicals that can cause tissue injury. The enzymes in red blood cells help to prevent this to a limited extent. Thus, SOD converts superoxide into hydrogen peroxide that is in turn converted by CAT into water and oxygen. However, in severe and prolonged ischemia the normal amounts of these enzymes in the red blood cells are not enough to prevent ischemia-reperfusion injury. We have, therefore, prepared a PolyHb-CAT-SOD complex (PolyHb-CAT-SOD) with more CAT and SOD than are normally present in red blood cells. The idea is to have an oxygen carrier with...

Letter To The Editor

I read with great interest an article by Dr. Bartosz published in the recent issue of the Journal (B2). This review article covers in detailed and comprehensive manner the contribution of exo- as well as endogenous substances to the total antioxidant capacity (TAC). Although excellent in many respects, this article doubts and misinterprets the role of increased TAC caused by elevated serum bilirubin levels in subjects with Gilbert syndrome (GS) characterized with mild benign hyperbilirubinemia. First, as a consequence of decreased bilirubin conjugation in the liver tissue, unconjugated bilirubin is the only different primary biochemical parameter in GS. For a long time bilirubin was believed to be only a waste product, however, this bile pigment exhibits potent antioxidant capacity. Indeed, bilirubin was demonstrated in in vitro study by Wu and colleagues to be almost 30 times more efficient in preventing LDL oxidation than Trolox, a water-soluble analogue of alpha-tocopherol (W1)....


Although it was long thought bilirubin to be a nonfunctional waste product of metabolism and hyperbilirubinemia to be even neurotoxic, there is now increasing experimental evidence that moderately increased serum bilirubin concentration (especially unconjugated bilirubin) might act as a powerful chain-breaking antioxidant in biological systems, contributing to plasma, cellular, tissue protection, and thereby contributing to prevent the development and progression of cardiovascular disease and other diseases associated with enhanced oxidative stress. The apparent paradox between toxic and protective effects is supported by biological and clinical evidences that bilirubin, like other metabolic compounds such as uric acid 53 , may become antioxidant in certain situations, particularly when they are present in blood at moderately increased concentrations. The distinct inverse correlation between serum bilirubin concentration and CHD risk may have important clinical and diagnostic...

Biological Evidences

Have been suggested to play a potential role in the antiatherogenic and cardioprotective effects of bilirubin (as schematically summarized in Table 1). Bilirubin has been considered a toxic by-product associated with the potentially fatal conditions of neonatal hyperbilirubinemias, acute hepatitis, and cirrhosis until the 1980s, when its antioxidant activity was first identified 29 . Afterward, several experimental studies, both in vitro and in vivo, confirmed that bilirubin acts as an effective antioxidant compound that efficiently scavenges peroxyl radicals and suppresses the oxidation of lipids and lipoproteins, especially low-density lipoprotein lipid (LDL-C) peroxidation, and might thereby counteract atherosclerotic plaque formation and its subsequent clinical complications. This antioxidant process involves an electron donation pathway, where bilirubin is reconverted to biliverdin, but biliverdin reductase quickly regenerates bilirubin, thereby greatly boosting its antioxidant...

The Kidneys

The wall of the descending limb is impermeable to solutes but permeable to water, which is removed by osmosis into the tissue fluid surrounding this section of the loop. The thick region of the ascending limb of the loop of Henle is highly permeable to Na + and Cl_ but impermeable to water and contains chloride pumps, which remove sodium and chloride ions from the fluid in the lumen by active transport. The fluid in the two limbs of the loop of Henle flows in opposite directions, and the active removal of ions from the ascending limb and their constant inflow in the descending limb create an osmotic gradient along the length of the loop of Henle, which is known as a counter current multiplier system. The peritubular capillaries that surround the loop of Henle passively absorb the water and the ions that have been removed. The filtrate enters the distal tubule where electrolytes and water are reabsorbed under hormonal control (aldosterone and arginine vasopressin (AVP),...

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