Gout is a painful inflammatory condition arising from the formation of needle-like monosodium urate crystals in joints, tendons and other tissues. It is popularly associated with over-eating and excessive drinking, the indulgences being punished with a very painful big toe (podagra). There is, however, considerable variation in sensitivity to diet among sufferers.

Crystals are formed from uric acid which is the normal product of purine breakdown (DNA, RNA). Crystallisation results from elevated blood levels of uric acid, measurable in the urine (hyperuricemia), leading to acute gouty arthritis. This can be caused by a diet rich in purines, the under-excretion of uric acid by the kidneys and gut, or a genetic predisposition (enzyme abnormalities affecting purine metabolism, or mutations in kidney proteins affecting excretion).

Men are more than twice as likely to suffer gout than women, and the prevalence increases with age. Women catch up with men in the postmenopausal years. While gout was once considered a disease of the wealthy, it is now associated with the general urban lifestyle featuring a poor diet, lack of exercise and metabolic syndrome (obesity, hypertension, insulin resistance, dyslipidaemia). It is also associated with osteoarthritis and poor vascularity in the extremities, hence the big toe being most commonly affected. Pharmaceutical medications may also cause gout (aspirin, blood pressure drugs).

In chronic cases the joints are damaged and painless nodules called tophi may form on fingers, ears, elbows and the Achilles tendons. Diagnosis may be made by measuring blood levels of uric acid; however, elevated levels are not always conclusive because only 0.5% of cases with elevated levels develop gout (asymptomatic hyperuricemia). Gout may also be present with normal levels. Nodules should be differentiated from lipomas, rheumatoid nodules, osteoarthritic Heberden’s and Bouchard’s nodules.¹

Gout is diagnosed by the presence of monosodium urate crystals in synovial fluid. The condition is commonly treated with  drugs that work by several different mechanisms: those which block uric acid production by inhibiting the enzyme xanthine oxidase (allopurinol, febuxostat); drugs which encourage secretion of uric acid (probenecid); and those which reduce acute joint inflammation (colchicine, NSAIDS, steroids).

Treatment:

General

Uric acid is a normal byproduct of purine metabolism, the external sources being diet, and the internal being cellular turnover. Increased cellular turnover occurs in cancer, blood disease and inflammatory diseases. Obesity enhances production of uric acid via elevated levels of the hormone leptin.

Dietary sources and over-production account for about 10% of cases, while under-excretion due to kidney insufficiency or genetics account for the rest. An effort should be made to lose weight, avoid ultra-processed foods, increase water consumption, and do regular exercise.

Diet

Vegetables, meats (beef, pork, lamb) and seafood contain purines. Reducing the intake of certain meats (organ meats, anchovies, oily fish) will certainly help lower uric acid levels; however, vegetables high in purines are not considered a problem (beans, lentils, mushroom, peas, legumes). Foods rich in vitamin C, low-fat dairy, and olive oil reduce the risk of hyperuricemia or gout. High-fructose corn syrup, especially contained in sugar-sweetened beverages, is also a major risk factor so avoid sweetened factory foods and bottled juices. Fresh fruit is not a problem.²

Alcohol increases synthesis and inhibits break down. Some patients are more sensitive to alcohol, with the least problematic being wine, and the worst being beer. Yeast also contains purines and may need to be avoided. Apple cider vinegar can help alkalise the body.

For those suffering acute attacks an anti-inflammatory diet is best. This may be the traditional Mediterranean diet (low red meat, wholegrains and legumes, plenty of salads and vegetables). Fish oil supplements are anti-inflammatory. Drink plenty of vegetable juices which alkalise the body. Quercetin and bromelain are anti-inflammatory.

Herbs

Kidneys herbs such as celery seed,³ nettle, burdock, dandelion, and wild carrot will help remove uric acid. Turmeric, Boswelia, guaiacum, and white willow reduce inflammation. Meadowsweet is used to alkalise the body. Comfrey ointment can be applied externally.

Tissue Salts

Ferrum Phos is ani-inflammatory. Sodium phos helps remove acidity.

Homeopathy

Apis—hot, swollen joints. Burning, stinging pain.

Benzoic-ac—swollen, red, painful, cracking joints esp. knee < night

Berberis-v—stinging and burning in kidney. Uric acid with pain in kidneys. Kidney stones

Bryonia—red, swollen, painful joint. Pain is worse from movement, but better heat

Causticum—elbow pain especially, sore tendons, contracted, deformed joints

Colchicum—gout typically of the big toe, very sensitive. Dark, inky urine. Weak, irritable, restless. Worse movement, slight touch, night.

Ledum—knee, ankle, heel swollen and painful, pain travels upwards. Better cold applications

Lycopodium—heel pain, cold sweaty feet. Sandy in urine.

Rhus-t—stiff, joints sensitive to weather change and damp. Improves with movement

Urtica—high uric acid.

Disclaimer: this article is intended for the purpose of general education only, and is not a substitute for diagnosis, treatment advice, or a prescription that is given in a consultation with a qualified physician.

References:

1.         Ragab G, Elshahaly M, Bardin T. Gout: An old disease in new perspective – A review. J Adv Res 2017;8:495.

2.         Zgaga L, Theodoratou E, Kyle J, et al. The Association of Dietary Intake of Purine-Rich Vegetables, Sugar-Sweetened Beverages and Dairy with Plasma Urate, in a Cross-Sectional Study. PLoS ONE 2012;7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368949/

3.         Dolati K, Rakhshandeh H, Golestani M, Forouzanfar F, Sadeghnia R, Sadeghnia HR. Inhibitory Effects of Apium graveolens on Xanthine Oxidase Activity and Serum Uric Acid Levels in Hyperuricemic Mice. Prev Nutr Food Sci 2018;23:127.