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Review
.2022 Aug 26;14(17):3525.
doi: 10.3390/nu14173525.

Gout and Diet: A Comprehensive Review of Mechanisms and Management

Affiliations
Review

Gout and Diet: A Comprehensive Review of Mechanisms and Management

Yingling Zhang et al. Nutrients..

Abstract

Gout is well known as an inflammatory rheumatic disease presenting with arthritis and abnormal metabolism of uric acid. The recognition of diet-induced systemic metabolic pathways have provided new mechanistic insights and potential interventions on gout progression. However, the dietary recommendations for gouty patients generally focus on food categories, with few simultaneous considerations of nutritional factors and systemic metabolism. It is worthwhile to comprehensively review the mechanistic findings and potential interventions of diet-related nutrients against the development of gout, including purine metabolism, urate deposition, and gouty inflammation. Although piecemeal modifications of various nutrients often provide incomplete dietary recommendations, understanding the role of nutritional factors in gouty development can help patients choose their healthy diet based on personal preference and disease course. The combination of dietary management and medication may potentially achieve enhanced treatment effects, especially for severe patients. Therefore, the role of dietary and nutritional factors in the development of gout is systematically reviewed to propose dietary modification strategies for gout management by: (1) reducing nutritional risk factors against metabolic syndrome; (2) supplementing with beneficial nutrients to affect uric acid metabolism and gouty inflammation; and (3) considering nutritional modification combined with medication supplementation to decrease the frequency of gout flares.

Keywords: dietary intervention; gout; nutritional factors; purine; systemic pathways; uric acid.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Potential mechanisms of diet-induced gout progression in humans. Diets provide abundant raw materials of purine, which is mainly metabolized in the liver, promoting uric acid production. Meanwhile, it can interfere with the intestinal environment, homeostasis, and urate transport to induce high levels of uric acid, leading to hyperuricemia and ultimately to gout. Additionally, gouty inflammation is caused by IL-1β production after the activation of NLRP3 by macrophages that ingest MSU crystals, and a second signal is required in humans by stimulating the activation of TLR signaling pathways that can be induced by diets. Moreover, neutrophil infiltration and diet-induced low-grade inflammatory states will exacerbate gouty inflammation. AMP, adenosine monophosphate. ASC, apoptosis-associated speck-like protein containing a caspase recruitment domain. GMP, guanine monophosphate. IL, interleukin. IMP, inosine monophosphate. LPS, lipopolysaccharide. MSU, monosodium urate. MyD88, myeloid differentiation factor88. NF-κB, nuclear factor kappa B. NLRP3, pyrin domain-containing protein 3. TLR, toll-like receptor. TNF, tumor necrosis factor. XO, xanthine oxidase.
Figure 2
Figure 2
Nutrition-induced systemic metabolism involved in gouty disease. Metabolites of fat, carbohydrate and protein and the resulting metabolic diseases promote the development of gout, including changing intestinal flora, accelerating purine metabolism, promoting MSU deposition, activating macrophages, and inhibiting uric acid excretion. ADP, adenosine diphosphate. AMP, adenosine monophosphate. ATP, adenosine triphosphate. FFAs, free fatty acids. F6P, fructose 6 phosphate. KHK, ketohexokinase. LPS, lipopolysaccharide. MSU, monosodium urate. NAFLD, nonalcoholic fatty liver disease. NAFPD, nonalcoholic fatty pancreas disease. TG, triglyceride. TLR, toll-like receptor. UA, uric acid. XO, xanthine oxidase.
Figure 3
Figure 3
Recommended food-derived nutritional interventions with anti-gouty mechanisms. Dietary management recommendations for gout patients include appropriate intake of fiber, minerals, and vitamins, as well as the selection of high-quality sugars, fats, and proteins, which are usually of plant origin. In addition, the consumption of products containing probiotics helps regulate intestinal homeostasis in patients with gout. ↑—increase; ↓—decrease; →—maintain; UA—uric acid; HQ—high-quality.
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