Gout information

Introduction

There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't. The diseases caused by our incorrect and unnatural diets are those featured on these pages.

Dietary causes:

Introduction

The prosperous, usually aristocratic, man with the hugely bandaged and gouty foot is a caricature beloved of comedy programmes. But gout is a painful and far from a laughable form of arthritis.

Gout is one of the most common of the inflammatory forms of arthritiis. It is "a metabolic disorder manifested by an inflammatory arthritis associated with monosodium urate (MSU) crystal deposition within joints, tophus formation, uric acid urolithiasis". All sufferers have high levels of uric acid in their bloodstream.

Although the term "gout" was not used until the 12th century, the condition has been recorded since antiquity, with the ancient Egyptians first describing it in 2500 BC, and Hippocrates calling it "the unwalkable disease" around 600 BC.[1] There have been many further reports of gout through the ages, possibly due to its occurrence in many well-known historical figures, including Charles Darwin, Theodore Roosevelt, Martin Luther King, Benjamin Franklin, Thomas Jefferson, Karl Marx, and Sir Isaac Newton.

Today, data suggest that in the United States gout is the most common inflammatory arthritis in men over 40 years of age, and its prevalence and incidence continue to increase. A descriptive study from a US managed-care database suggested the prevalence of gout increased from 2.9 cases per 1000 population in 1990 to 5.2 cases per 1000 population in 1999.[2]

The incidence of gout shows a similar increase over the past decades. The Rochester Epidemiology Project showed the age- and sex-adjusted annual incidence of gout increased from 45.0 new cases per 100,000 population in 1977 to 1978 to 62.3 new cases per 100,000 population in 1995 to 1996.[3]

Metabolic Syndrome and gout

The metabolic syndrome is a group of interrelated atherosclerotic risk factors (including obesity, insulin resistance, and hypertension) that affects more than 50 million Americans.[4] There is a close association between the presence of the metabolic syndrome and gout; a total of 63% of gout patients fulfill the criteria for metabolic syndrome, compared with only 25% of people without gout.[5] This pattern increases with aging.

Mean serum urate levels in patients with the metabolic syndrome are approximately 0.5-1.0 mg/dL higher than in controls,[6] and levels increase with the number of components of the metabolic syndrome present, even when adjusted for age, gender, creatinine clearance, alcohol intake, and diuretic use.[7]

Patients with the metabolic syndrome are known to have a reduced ability to excrete uric acid,[6] through hyperinsulinemia-enhanced proximal tubular sodium reabsorption.[8] Reduced uric acid excretion due to enhanced sodium reabsorption has also been reported in two of the most common metabolic syndrome-related conditions: obesity and hypertension.[9]

As well as reduced excretion, some evidence suggests an increase in uric acid production in metabolic syndrome through increased fructose intake. Fructose-based products have been widely used over the past decades as a cheap alternative to sucrose in food, which may account for the increased prevalence of the metabolic syndrome (and hence gout) in recent years.[10]

One of the main contributing factors to the metabolic syndrome is obesity. Many patients with gout are overweight or obese, and there is a strong association between the risk of gout and increasing BMI scores.[11] Obesity is also linked with increases in serum urate through increased uric acid production and a decrease in renal excretion.[12] Given that approximately 60% of Americans are overweight and one-third are obese (as measured by BMI), it is important for physicians and patients to understand this increased risk. Fortunately the increased risk of gout due to obesity is reversible, with men who lose 10lb of weight showing a risk ratio of 0.61.

Higher insulin levels in the circulation (a consequence of insulin resistance) reduce the renal excretion of uric acid[13] and may enhance renal urate reabsorption.

Dietary misadvice

For decades, gout sufferers have been advised to avoid high purine-containing foods. Purines are the chemicals that form uric acid in the body, which in turn causes painful deposition of urate crystals in the joints. Examples of these are: kidneys, sweetbreads, liver, bacon, beef, pork, duck, shellfish and venison.

However, a study published in 2000 presented a challenge to the ‘low-purine, high-carbohydrate’ diet usually advised for gout patients. As insulin resistance has been increasingly implicated in the development of gout, and changes in blood cholesterol levels seen in persons with gout are similar to those associated with insulin resistance, an investigation was conducted at the University of Witwatersrand, Johannesburg, South Africa, of non-diabetic men, each of whom had had at least two gout attacks during the four months immediately prior to the study. In the study, each man ate a diet which restricted carb intake and increased fats and protein. They were also encouraged to increase their intakes of fish and poultry, which are relatively high in the purines which are classically avoided in managing gout. After 16 weeks on this diet, not only had the men lost an average 17 lb (7.7 kg) in weight, gout attacks were reduced from an average of 2.1 per month to 0.6 per month. Not surprisingly, the researchers stated that ‘current dietary recommendations for gout might need re-evaluation.’[12]

Another cause is the fruit sugar, fructose, both in high-fructose corn syrup and too much fruit.[14,15] So be careful with those ‘five portions’.

References

1. Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthritis Res Ther 2006; 8(suppl 1): S1.
2. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol 2004; 31: 1582-1587.
3. Arromdee E, Michet CJ, Crowson CS, et al. Epidemiology of gout: is the incidence rising? J Rheumatol 2002; 29: 2403-2406.
4. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA. 2002;287(3):356-359.
5. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-115.
6. Lopez-Suarez A, Elvira-Gonzalez J, Bascunana-Quirell A, et al. Serum urate levels and urinary uric acid excretion in subjects with metabolic syndrome. Med Clin (Barc). 2006;126(9):321-324.
7. Hjortnaes J, Algra A, Olijhoek J, et al. Serum uric acid levels and risk for vascular diseases in patients with metabolic syndrome. J Rheumatol. 2007;34(9):1882-1887.
8. Strazzullo P, Barbato A, Galletti F, et al. Abnormalities of renal sodium handling in the metabolic syndrome. Results of the Olivetti Heart Study. J Hypertens. 2006;24(8):1633-1639.
9. Strazzullo P, Puig JG. Uric acid and oxidative stress: relative impact on cardiovascular risk? Nutr Metab Cardiovasc Dis. 2007;17(6):409-414.
10. Nakagawa T, Tuttle KR, Short RA, Johnson RJ. Hypothesis: fructose-induced hyperuricemia as a causal mechanism for the epidemic of the metabolic syndrome. Nat Clin Pract Nephrol. 2005;1(2):80-86.
11. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the Health Professionals Follow-Up Study. Arch Intern Med. 2005;165(7):742-748.
12. Dessein PH, Shipton EA, Stanwix AE, 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;59(7):539-543.
13. Ter Maaten JC, Voorburg A, Heine RJ, et al. Renal handling of urate and sodium during acute physiological hyperinsulinaemia in healthy subjects. Clin Sci (Lond). 1997;92(1):51-58.
14. Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005;143(7):499-516.
15. Johnson RJ, et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardio-vascular disease. Am J Clin Nutr 2007; 86: 899-906.
16. Choi HK, et al. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ 2008; 336: 309-312.