Gouty arthritis is an inflammatory disorder involving joint or joints, tendon, and their surrounding tissues, in which uric acid deposits, becomes crystallized, and causes inflammation, swelling, and pain. Uric acid can also be present in the kidney as tophi, kidney stones, or urate nephropathy. Most frequent location for gouty attack is the metatarsophalangeal joint (MPJ) of the great toe. Gouty arthritis can also involve other joints such as knees, heels, wrists, and fingers. The prevalence of gout and hyperuricemia in the US general population had increased sharply, based on The National Health and Nutritional Examination Survey 2007-2008. [1]
Although the level of serum uric acid is not always correlated to the prevalence of gouty arthritis, higher levels of serum uric acid increase the risk. 
High level of uric acid or hyperuricemia is defined as serum urate level greater than 7 mg/dL in men and 5 mg/dL in women. Hyperuricemia is also a risk factor for many disorders including hypertension and atherosclerosis, which can cause coronary artery disease and stroke.
Either excessive production or reduced excretion of uric acid, or both lead to hyperuricemia. Humans and higher primates, as well as guinea pig, do not produce urate oxidase, which is an enzyme required for metabolizing uric acid further into allantoin and carbon dioxide. Allantoin does not result in gouty arthritis. Unfortunately, uric acid is the end-metabolite of purine, an amino acid, in their bodies.
Consuming purine-rich foods can increase serum uric acid level and trigger gouty attack. Purine-rich foods include red meat, dark green vegetables such as spinach and asparagus, seafood such as sardines and mussels. Other foods can also cause high levels of uric acid such as roasted nuts, sugar and white flour products, dried fruits, caffeine, eggs, lentils, and many more. Medications such as aspirin, acetaminophen, and those medications containing caffeine can increase the uric acid level too. Some medical conditions such as hypothyroidism, leukemia, obesity, and others can also increase the level of uric acid. [2, 3, 4, 5, 6]
On the other hand, reducing renal excretion of uric acid is an equally important cause of hyperuricemia, Poor urinary output as a result of kidney disease or dehydration, and using certain diuretics can reduce the amount of uric acid excreted in urine. Another important situation, which is often overlooked and causes hyperuricemia as well as gouty arthritis, is changes in the pH of the blood and the urine. The higher the pH of the blood is, the lower the uric acid level in the blood. And, the higher the pH of the urine is, the larger the amount of uric acid in the urine. The normal pH range of the blood is between 7.35 and 7.45. Thus, it is healthier to maintain the blood pH closer to 7.45, although too much alkalosis is equally harmful to the health. [7]
Some people advocate “alkalinizing the body and blood” by eating alkalinizing foods. Unfortunately, most of today’s foods are acidifying, which include most carbohydrates and animal foods.
Restricting carbohydrates does help avoid some of the most acidifying foods and stabilize blood glucose levels within normal range. Normal blood glucose level prevents initiating and fueling inflammation. Thus, carbohydrate restriction is able to minimize the magnitude of gouty attack, should an individual develop hyperuricemia. However, carbohydrate restriction alone cannot prevent hyperuricemia and/or a gouty attack, until the individual’s blood pH is leaning toward alkaline, in which condition, his serum uric acid level would be lower, and the uric acid excreted in his urine would be higher.
Modern medicine offers few remedies for preventing and treating gouty attack. Those medications including, for prevention: Allopurinal and Probenecid, and for treatment: Nonsteroid anti-inflammatory drugs (NSAIDs), Colchicine, Corticosteroids. Needless to say, those medications also cause side effects. [2]
Those who are conscious about keeping good health, without medication because of their side effects, prefer natural remedy to chemical compounds. The natural remedies include lemon juice and Vitamin C, which along with lime, apple cider vinegar, baking soda, and tart (sour) cherry, are useful in maintaining good health and preventing gouty attack.
The mechanism, that how these natural remedies are able to prevent and treat hyperuricemia and gouty attack, remains unclear. Some claimed that these remedies are able to alkalinize the body and blood and make their pH closer to 7.4 or even 7.45. Based on the findings on how the levels of uric acid of the blood and the urine related to the alkalinity of the blood and the urine, respectively, the claims seem sensible.
In conclusion, carbohydrate-restricted dieters should mindfully include boiled green leafy vegetables in their daily menu for supplying minerals such as potassium, sodium, and magnesium, at the same time, for preventing constipation. They should also include daily consumption of lemon juice, apple cider vinegar or tart cherries, and/or 2-4 grams of Vitamin C, which dosage is depending on their body weight, for preventing and treating hyperuricemia and gouty attack.
(Write your comment here too.)
Robert Su, Pharm.B., M.D.
Order my book: Carbohydrates Can Kill.
Want to support my campaign? Please click the “Donate” button in the right-hand column of this page.
References:
1. Zhu, Y., Pandya, B. J. and Choi, H. K. (2011), Prevalence of gout and hyperuricemia in the US general population: The National Health and Nutrition Examination Survey 2007–2008. Arthritis & Rheumatism, 63: 3136–3141. doi: 10.1002/art.30520 http://onlinelibrary.wiley.com/doi/10.1002/art.30520/full
2. Mayo Clinic Staff, Gout. http://www.mayoclinic.com/health/gout/DS00090/METHOD=print&DSECTION=all
3. Dawson,D & Walters M, Uric acid and xanthine oxidase: future therapeutic targets in the prevention of cardiovascular disease? British Journal of Clinical Pharmacology DOI:10.1111/j.1365-2125.2006.02785.x Br J Clin Pharmacol. 2006 December; 62(6): 633–644. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1885190/
4. Johnson RJ, et al, Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease? Hypertension. 2003;41:1183-1190; originally published online April 21, 2003; http://hyper.ahajournals.org/content/41/6/1183
5. RODRIGUES, TC et al, Serum Uric Acid Predicts Progression of Subclinical Coronary Atherosclerosis in Individuals Without Renal Disease. Diabetes Care 33:2471–2473, 2010. http://www.ncbi.nlm.nih.gov/pubmed/20798338
6. Wen S, et al, Serum uric acid levels and the clinical characteristics of depression , Clin Biochem. 2012 Jan;45(1-2):49-53. doi: 10.1016/j.clinbiochem.2011.10.010. Epub 2011 Oct 20. http://www.ncbi.nlm.nih.gov/pubmed/22040815
7. Kanbara A, et al, Effect of urine pH changed by dietary intervention on uric acid clearance mechanism of pH-dependent excretion of urinary uric acid. Nutrition Journal 2012, 11:39 http://www.nutritionj.com/content/11/1/39
