The role of diet in gout

Gout is caused by an excess of uric acid (urate) in the system, which can then form crystals in various places, including the joint of the big toe. Crystals in the joint cause inflammation and pain.

Excess uric acid can be due to excessive dietary intake of purines, insufficient urinary excretion of uric acid, or both.

Purines include a number of substances found in the diet, but two important purines are adenine and guanine; thus, two out of the five nucleic acids which are the building blocks of DNA and RNA are purines. Since every cell (except for red blood cells) has a full complement of DNA and RNA, the implication is that foods which have high concentrations of cells are also high in purines. Meats have a high concentration of cells, and organ meats (liver, kidney, pancreas, thymus, heart, brain) have the highest concentration. This may have led to the traditional association of rich diets with gout.

Insufficient urinary excretion of uric acid is probably the more important cause of gout, however. Studies have shown that a less acid urine (higher pH) permits more urinary excretion of uric acid, compared to more acid urine. Since the acidity of urine is dependent on what foods we eat, choosing a diet for its effect on urine acidity may be more important that a diet low in purines.

A particular food’s effect on urine acidity is not necessarily through the acidity of the food itself. Rather, the concentration of sulfur-containing amino acids (methionine and cysteine) in the food is a major determinant of the how much acid is generated through metabolism of that food, and therefore of how much acid is excreted in the urine. On the other hand, cations such as magnesium, calcium, and potassium also found in foods, buffer acids and make the urine less acidic (raise the pH). Phosphorus and chlorine are anions which lower pH. Finally, many foods contain significant quantities of phenols, which after metabolism are ultimately excreted in the urine as hippuric acid.

There are charts on the internet and elsewhere of acid foods vs alkaline foods. Most of the time, this refers to the capacity of the food in question to raise or lower the acidity of urine, and not to the inherent acidity of the food itself. For example, lemons are rich in citric acid, yet are considered an alkaline food. Unfortunately, much of the information on the internet about acid and alkaline food is misleading, and sometimes just plain wrong. Many web articles talk about the acid content of the food, or the effect of food on acidifying the blood. The important issue is neither of these: we need to focus on the effect that food composition has on how much acid is generated by its metabolism, and therefore on how much acid has to be eliminated in the urine.

In terms of gout, other elements of food composition besides acid or alkaline can affect uric acid levels. For example, high levels of dietary fructose contribute to raising uric acid levels (1). Traditional foods considered part of rich diets, such as honey, dates, and raisins, are high in fructose. In modern times, various soft drinks and other processed foods are sweetened with high-fructose corn syrup.

Another factor related to diet is how much insulin is secreted. It appears that insulin stimulates the kidney to reduce uric acid excretion. Thus, the high insulin levels found in metabolic syndrome, in most individuals with type 2 diabetes, and in people with type 2 diabetes who are being treated with insulin, may contribute to higher uric acid levels in the blood. High carbohydrate content in food, together with rapid carbohydrate absorption, stimulate insulin secretion. Protein also stimulates insulin secretion. Thus, reducing dietary protein and choosing foods with a low glycemic index may help control uric acid levels. Again, these measures mean avoiding so-called rich foods.

Certain foods have a long history of use in folk medicine as treatments for obesity and type 2 diabetes. What they appear to have in common is that they decrease insulin levels, in some cases by decreasing the absorption of carbohydrate from the small intestine. Bitter melon is one such food (2, 3). Coffee, because of its high chlorogenic acid content, also reduces insulin levels (4), although caffeine may undo this effect. Yerba maté tea, widely consumed in South America as a stimulant and to counter obesity, lowers insulin (5).

Finally, certain dietary approaches appear to reduce inflammation. Even if one already has uric acid crystals in one’s joints, less inflammation means less pain and less limitation of activity. Methionine restriction is a diet strategy that has been shown to reduce inflammation (6, 7), and also reduce levels of insulin (6).

References

1. Lecoultre V, Egli L, Theytaz F, Despland C, Schneiter P, Tappy L. Fructose-induced hyperuricemia is associated with a decreased renal uric acid excretion in humans.[letter]. Diabetes Care 2013;36(9):e149-50.

2. Wang ZQ, Zhang XH, Yu Y et al. Bioactives from bitter melon enhance insulin signaling and modulate acyl carnitine content in skeletal muscle in high-fat diet-fed mice. J Nutr Biochem. 2011;22:1064-1073.

3. Zhu Y, Dong Y, Qian X et al. Effect of superfine grinding on antidiabetic activity of bitter melon powder. Int J Mol Sci. 2012;13:14203-14218.

4. Johnston KL, Clifford MN, Morgan LM. Coffee acutely modifies gastrointestinal hormone secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and caffeine. Am J Clin Nutr. 2003;78:728-733.

5. Gambero A, Ribeiro ML. The positive effects of yerba maté (Ilex paraguariensis) in obesity. Nutrients. 2015;7:730-750.

6. Perrone CE, Malloy VL, Orentreich DS, Orentreich N. Metabolic adaptations to methionine restriction that benefit health and lifespan in rodents. Exp Gerontol. 2012

7. Orgeron ML, Stone KP, Wanders D, Cortez CC, van NT, Gettys TW. The impact of dietary methionine restriction on biomarkers of metabolic health. Prog Mol Biol Transl Sci. 2014;121:351-376.

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