Gout (podagra)

Life extension and
disease treatment through
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caloric restriction -
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Overweight = 25-29.9
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Gout (podagra)
can be treated and prevented by caloric restriction and physical activity. Clinical evidence:

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.
Dessein PH1, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J.
Insulin resistance (IR) has been increasingly implicated in the pathogenesis of gout. The lipoprotein abnormalities described in hyperuricaemic subjects are similar to those associated with IR, and insulin influences renal urate excretion. In this study it was investigated whether dietary measures, reported to be beneficial in IR, have serum uric acid (SU) and lipid lowering effects in gout.
Thirteen non-diabetic men (median age 50, range 38-62) were enrolled. Each patient had had at least two gouty attacks during the four months before enrollment. Dietary recommendations consisted of calorie restriction to 6690 kJ (1600 kcal) a day with 40% derived from carbohydrate, 30% from protein, and 30% from fat; replacement of refined carbohydrates with complex ones and saturated fats with mono- and polyunsaturated ones. At onset and after 16 weeks, fasting blood samples were taken for determination of SU, serum cholesterol (C), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), and triglycerides (TGs). Results were expressed as median (SD).
At onset, the body mass index (BMI) was 30.5 (8.1) kg/m(2). Dietary measures resulted in weight loss of 7.7 (5.4) kg (p=0.002) and a decrease in the frequency of monthly attacks from 2.1 (0.8) to 0.6 (0.7) (p=0.002). The SU decreased from 0.57 (0.10) to 0.47 (0.09) mmol/l (p=0.001) and normalised in 7 (58%) of the 12 patients with an initially raised level. Serum cholesterol decreased from 6.0 (1.7) to 4.7 (0. 9) mmol/l (p=0.002), LDL-C from 3.5 (1.2) to 2.7 (0.8) mmol/l (p=0. 004), TGs from 4.7 (4.2) to 1.9 (1.0) mmol/l (p=0.001), and C:HDL-C ratios from 6.7 (1.7) to 5.2 (1.0) (p=0.002). HDL-C levels increased insignificantly. High baseline SU, frequency of attacks, total cholesterol, LDL-C and TG levels, and total C:HDL-C ratios correlated with higher decreases in the respective variables upon dietary intervention (p<0.05).
The results suggest that weight reduction associated with a change in proportional macronutrient intake, as recently recommended in IR, is beneficial, reducing the SU levels and dyslipidaemia in gout. Current dietary recommendations for gout may need re-evaluation.

Avoid purine-rich foods, drink a lot, reduce weight. The most important recipes against hyperuricemia.
MMW Fortschr Med. 2003 Aug 7;145(31-32):36-8.
In 99% of the cases, the underlying cause of gout is an inborn disorder of uric acid excretion. In addition to acute arthritis, clinical consequences include tophi, chronic destruction of joints, and ulcers. The patient is endangered by the frequent renal involvement, with hypertension and renal insufficiency. Furthered by such exogenous factors as overweight, high-calorie, purine-rich foods and immoderate consumption of alcohol, hyperuricemia may develop. Basic treatment comprises dietary measures and, up to a serum uric acid concentration of 8.5 mg/dl, should be the sole measure required. The aim is to achieve a permanent lowering of uric acid concentrations in the blood to < 6.5 mg/dl. This may be achieved by reduction of overweight (including regular exercise), an energy-adapted diet with only moderate amounts of fat, restriction--or, better, banishment--of alcohol, an ovolactovegetarian diet low in purine (care must be taken with high-purine vegetablesl), moderate intake of readily assimilated carbohydrates, and adequate amounts of calorie-free liquids.

Attenuating the mortality risk of high serum uric acid: the role of physical activity underused.
Ann Rheum Dis. 2014 Jul 22. pii: annrheumdis-2014-205312. doi: 10.1136/annrheumdis-2014-205312.
Chen JH1, Wen CP2, Wu SB3, Lan JL1, Tsai MK3, Tai YP3, Lee JH3, Hsu CC3, Tsao CK4, Wai JP5, Chiang PH6, Pan WH3, Hsiung CA3.
High serum uric acid (sUA) has been associated with increased mortality risks, but its clinical treatment varied with potential side effects. The role of physical activity has received limited attention.
A cohort, consisting of 467 976 adults, who went through a standard health screening programme, with questionnaire and fasting blood samples, was successively recruited between 1996 and 2008. High sUA is defined as uric acid above 7.0 mg/dL. Leisure time physical activity level was self-reported, with fully active defined as those with 30 min per day for at least 5 days a week. National death file identified 12 228 deaths with a median follow-up of 8.5 years. Cox proportional model was used to analyse HRs, and 12 variables were controlled, including medical history, life style and risk factors.
High sUA constituted one quarter of the cohort (25.6%). Their all-cause mortality was significantly increased [HR: 1.22 (1.15-1.29)], with much of the increase contributed to by the inactive (HR: 1.27 (1.17-1.37)), relative to the reference group with sUA level of 5-6 mg/dL. When they were fully active, mortality risks did not increase, but decreased by 11% (HR: 0.89 (0.82-0.97)), reflecting the benefits of being active was able to overcome the adverse effects of high sUA. Given the same high sUA, a 4-6 years difference in life expectancy was found between the active and the inactive.
Physical activity is a valuable alternative to pharmacotherapy in its ability to reduce the increases in mortality risks from high sUA. By being fully active, exercise can extend life span by 4-6 years, a level greater than the 1-4 years of life-shortening effect from high sUA.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Significance of serum uric acid levels on the risk of all-cause and cardiovascular mortality.
Kuo CF1, See LC, Yu KH, Chou IJ, Chiou MJ, Luo SF.
To assess the associations between serum uric acid (SUA) level and mortality.
The study included 354 110 subjects without a history of gout and whose SUA levels were tested at Chang Gung Memorial Hospital in Taiwan. Cox regression models were used to estimate hazard ratios and 95% CIs for mortality in six predefined SUA strata (≤0.17, 0.18-0.29, 0.30-0.41, 0.42-0.53, 0.54-0.65 and ≥0.66 mmol/l), after adjusting for age, sex, SUA stratum, estimated glomerular filtration rate, fasting glucose, total cholesterol and history of hypertension, diabetes mellitus, coronary heart disease, stroke, heart failure or chronic kidney disease.
There were 33 562 all-cause deaths during the study period. Crude all-cause mortality rates across the SUA strata were 52.5, 19.7, 17.4, 20.0, 28.0 and 41.1 deaths per 1000 person-years. Using the stratum 3 of SUA as a reference, the age- and sex-adjusted hazard ratios (95% CIs) across SUA strata were 2.79 (2.62, 2.96), 1.32 (1.28, 1.36), 1.00, 1.10 (1.07, 1.14), 1.42 (1.37, 1.48) and 2.12 (2.01, 2.23) for all-cause mortality; 2.24 (1.93, 2.59), 1.18 (1.10, 1.27), 1.00, 1.21 (1.14, 1.29), 1.74 (1.60, 1.88) and 2.53 (2.28, 2.81) for cardiovascular mortality and 3.41 (3.11, 3.73), 1.48 (1.42, 1.55), 1.00, 0.88 (0.84, 0.92), 0.91 (0.85, 0.98) and 1.23 (1.11, 1.36) for cancer-related mortality.
Individuals with SUA levels at either extremes are at higher risk for all-cause and cardiovascular mortality. SUA levels of 0.30-0.41 mmol/l were associated with the lowest mortality rate and should be regarded as optimal.
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