Reply To: 62 yo M with Gout

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Welcome! Forums 62 yo M with Gout Reply To: 62 yo M with Gout

Carrie Decker, ND

Hello Debbie,

Thank you for posing this question here. It always is good to review some biochemistry and other factors that contribute to a common condition such as gout which many individuals who suffer from tend to experience repeatedly. However, this is often because many lifestyle (alcohol use, diet) and other factors such as obesity, diabetes, hyperlipidemia, and hypertension are contributing factors and for many these things are not changed or improved upon, hence the ongoing higher risk for gout.

Gout is caused by the deposition of monosodium urate crystals. In the absence of urate saturation of the serum (serum urate levels >6.8 mg/dL [405 micromol/L]) gout is unlikely to occur. A variety of things may contribute to high uric acid levels in the blood. This includes alcohol use, diet, hypertension, obesity, diabetes, and hyperlipidemia as previously mentioned, as well as certain medications such as thiazide diuretics, beta-blockers, and aspirin. The clinical consequences of hyperuricemia include tophi, chronic destruction of joints, and ulcers.

The major site of uric acid production is the liver, from the degradation of dietary and endogenously synthesized purine compounds. The urate production process (purine degradation) involves the breakdown of the purine mononucleotides, guanylic acid (GMP), inosinic acid (IMP), and adenylic acid (AMP), ultimately into the purine bases, guanine and hypoxanthine. These latter two compounds are then metabolized to xanthine. In the final step of the xanthine oxidase reaction, xanthine is irreversibly oxidized to produce uric acid. Renal under-excretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. This is often due to genetic polymorphisms of renal transporters of urate.

Richette P, et al. Gout. Lancet. 2010 Jan 23;375(9711):318-28.

Torralba KD, et al. The interplay between diet, urate transporters and the risk for gout and hyperuricemia: current and future directions. Int J Rheum Dis. 2012 Dec;15(6):499-506.

Nutritional and lifestyle strategies such as achievement of ideal body weight, limitation of ethanol consumption, management of hyperlipidemia and hypertension, and dietary changes to reduce consumption of high purine foods may be beneficial. That said, purine-rich plant foods like legumes and vegetables do not increase the risk of gout. Although the dietary strategy of severe-purine restriction has often been employed, studies have shown that this only results in the urinary reduction of purine excretion by 200 to 400 mg/day, and an associated reduction of serum urate levels by 1 mg/dL (59 micromol/L). Thus for someone who has serum uric acid levels close to the level of saturation, this may pull them below the threshold.

Nickolai B, et al. [Nutritional therapy of gout]. Ther Umsch. 2016;73(3):153-8.

Other dietary strategies have also been shown to be effective. A diet which includes caloric restriction, the replacement of refined with complex carbohydrates, a decrease in saturated fat, but allows an increased proportion of protein has been shown to reduce serum uric acid by 1.7 mg/dL (100 micromol/L) and gouty attacks from 2.1 to 0.6 per month, however this was associated with an average weight loss of 7.7 kg. Dietary shifts to increased protein intake from low-fat dairy products and plant sources with decreases in the intake of red meat and fish have also have been shown effective. Coffee consumption also may be associated with a lower risk of gout. Meta-analysis has shown that coffee intake of 1 cup/day or more is significantly associated with reduction of the risk of gout.

Dessein PH, et al. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000 Jul;59(7):539-43.

Teng GG, et al. Food Sources of Protein and Risk of Incident Gout in the Singapore Chinese Health Study. Arthritis Rheumatol. 2015 Jul;67(7):1933-42.

Dalbeth N, et al. Effects of dairy intake on hyperuricemia and gout. Curr Rheumatol Rep. 2011 Apr;13(2):132-7.

Zhang Y, et al. Is coffee consumption associated with a lower risk of hyperuricaemia or gout? A systematic review and meta-analysis. BMJ Open. 2016 Jul 8;6(7):e009809.

Park KY, et al. Effects of coffee consumption on serum uric acid: systematic review and meta-analysis. Semin Arthritis Rheum. 2016 Apr;45(5):580-6.

Fatty meals have been implicated in precipitating acute flares of gout. In part, the effect of diet in contributing to flares may not be due to the immediate increase in uric acid or intraarticular crystals, but rather may be due to the effect of foods on inflammation. Free saturated fatty acids have been shown to increase IL-1β release from peripheral blood mononuclear cells in the presence of uric acid tophi, which may better explain the acute attacks of gout. Other things which may contribute to occurrence of acute gout either by altering the uric acid levels or the pro-inflammatory response include trauma, surgery, starvation, other dietary overindulgence, and dehydration. Although I am unaware of studies looking at the effects of other food sensitivities on the occurrence of acute gouty attacks, it is possible that food sensitivities and allergies also may contribute by leading to an increase in inflammation and IL-1β.

Joosten LA, et al. Engagement of fatty acids with Toll-like receptor 2 drives interleukin-1β production via the ASC/caspase 1 pathway in monosodium urate monohydrate crystal-induced gouty arthritis. Arthritis Rheum. 2010 Nov;62(11):3237-48.

Dietary supplementation of cherries has been shown to reduce the risk of recurrent gout, although the mechanism by which this occurs is unknown. Supplemental vitamin C has a mild but persistent urate-lowering effect. Vitamin C at a dosage of 500mg/day was observed to reduce serum urate levels by 0.5 mg/dL (30 micromol/L). Supplementation with folic acid also may be supportive as it inhibits xanthine oxidase, the enzyme which converts convert purines into uric acid. Folic acid and tetrahydrofolic acid were shown in animal studies to be many times more potent than allopurinol as inhibitors of xanthine oxidase.

Zhang Y, et al. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum. 2012 Dec;64(12):4004-11.

Jacob RA, et al. Consumption of Cherries Lowers Plasma Urate in Healthy Women. J Nutr. 2003 Jun;133(6):1826-9.

Huang HY, et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005 Jun;52(6):1843-7.

Lewis AS, et al. Inhibition of mammalian xanthine oxidase by folate compounds and amethopterin. J Biol Chem. 1984 Jan 10;259(1):12-5.

Other discussions on the topic of gout can be found at the Clinical Education group here – and You may find other pearls of treatment from other providers with the review of this information.


The following supplements are suggested for you to consider in light of your relevant expertise and understanding of the needs of your client or patient. They may be used in isolation or as part of a multi supplement strategy, but at all times the consideration of their use should be tied into the specific needs of the individual you are responsible for.

Foods to reduce – High Purine Foods: Liver, Kidney, Heart, Brains, Sweetbreads, Game, Goose, Anchovies, Mackerel, Scallops, Sardines, Herring, Muscles. Bouillon, Broth, Consommé, Meat Extracts. Meat gravy. Alcohol (esp. Beer). Fructose-containing beverages. Yeast. Food sensitivities and allergies.

Include daily:

Buffered Vitamin C (ARG): 2 caps, twice daily, until uric acid levels come down, then 1-2 caps daily.

5-MTHF Plus Forte (BRC): ½ tablet daily. Supplies (6S)-5-Methyltetrahydrofolic acid and methylcobalamin.

4-8 oz of unsweetened cherry juice

Please consider these suggestions in light of the other clinical information pertaining to this individual. If you have any more information about the specific problems this individual is experiencing, further refinement of these suggestions may be considered. I hope this information is helpful, and if you have any further questions or information specific to the problems this individual is experiencing, please do provide feedback.

In health,
Dr. Decker