Role of Culture, Diet, Genetics in Gout Management: History
Please note this is an old version of this entry, which may differ significantly from the current revision.

Gout is a metabolic disorder, and one of the most common inflammatory arthritic conditions, caused by elevated serum urate (SU). Gout prevalence is globally rising, partly due to global dietary changes and the growing older adult population. Gout was known to affect people of high socioeconomic status. Currently, gout disproportionately affects specific population subgroups that share distinct racial and ethnic backgrounds. While genetics may predict SU levels, nongenetic factors, including diet, cultural traditions, and social determinants of health (SDOH), need to be evaluated to optimize patient treatment outcomes. A cultural assessment may inform the development of culturally tailored dietary recommendations for patients with gout. Causal and association studies investigating the interaction between diet, genetics, and gout, should be cautiously interpreted due to the lack of reproducibility in different racial groups. Optimal gout management could benefit from a multidisciplinary approach, involving pharmacists and nurses.

  • acculturation
  • gout management
  • hyperuricemia
  • culture
  • diet
  • genetics

1. Introduction

Gout is a metabolic disorder, and one of the most common inflammatory arthritic conditions worldwide, caused by persistent hyperuricemia. Developing gout is multifactorial, ushering in different methodological approaches to ascertain the risk factors associated with developing hyperuricemia and gout. Despite substantial advancement in understanding the biological basis of gout, it remains one of the most poorly managed chronic conditions in healthcare. Uncontrolled gout is associated with a poor quality of life, joint damage, an increase in missed days of work, and a higher utilization of the healthcare system resources [1][2][3]

Gout is a chronic inflammatory condition caused by persistent hyperuricemia, leading to the formation and deposition of monosodium urate crystals into and around the distal joints. The development of hyperuricemia and gout is heterogenous, and, therefore, different research approaches are needed to identify and quantify the distinct risk factors in the pathogenesis of both conditions. For example, the Mendelian Randomization (MR) approach provides a pathway to ascertain causality, exploiting the natural randomization of allele causal disease. However, this approach is not without limitations, possibly due to the pleiotropic effect of the selected instrumental variables [4]. As gout continues to disproportionately affect non-EUR populations, there is a growing need to increase the representation of minorities in genetic research and cross-validation of genetic findings in multiple populations. To that end, it recognized that developing hyperuricemia and gout is a multifactorial process founded in genetics and modulated by epigenetic factors, including medications, lifestyle factors, diet, and the potential interactions between all of them. While genetic polymorphisms in ABCG2 and SLC2A9 remain two of the most significant signals in developing hyperuricemia and gout across different populations, evaluating nongenetic factors across selected populations through a cultural lens is an adjunct approach to further stratify hyperuricemia and gout risk and optimize gout management. This encompassing approach could be a valuable tool for gout patients with strong cultural identities and distinct racial or ethnic backgrounds. A summary of the major genes associated with regulating uric acid in humans is listed in Table 1.

Table 1. Summary of major urate regulation genes.
Gene Protein Possible Functions
ABCG2 ATP binding cassette subfamily G member 2: ABCG2 Regulating renal and gut excretion of urate. Gene polymorphisms are strongly linked to urate underexcretion and the risk of early-onset gout in men. Genetic polymorphisms may also influence the therapeutic response to allopurinol and other statin medications.
GCKR Glucokinase regulator Regulatory protein that inhibits glucokinase in the liver and pancreatic islet cells by forming an inactive complex with the enzyme. Gene polymorphisms are associated with fasting glucose, maturity-onset type-2 diabetes, hyperuricemia, and gout.
LRRC16A Capping protein regulator and myosin 1 linker 1: CARMIL1 Cytoskeleton-associated protein. Gene polymorphisms are associated with urate concentrations and gout subtypes.
PDZK1 PDZK domain-containing scaffolding protein Mediates the localization of cell surface proteins and plays a critical role in cholesterol metabolism. Gene polymorphisms are linked to dyslipidemia, hyperuricemia, and gout.
SLC2A9 Solute carrier family 2 member 9: GLUT9 Regulating renal uric acid reabsorption. Gene polymorphisms are linked to the risk of gout in women.
SLC16A9 Solute carrier family 16 member 9: MCT9 Regulating monocarboxylic acid transporter. Gene polymorphisms are linked to uric acid concentrations.
SLC17A1 Solute carrier family 17 member 1: NPT1 Sodium phosphate cotransporter. Gene polymorphisms are linked with hyperuricemia and gout.
SLC22A11 Solute carrier family 22 member 11: OAT4 Urate reabsorption transporter. A target for some uricosuric drugs. Gene polymorphisms are associated with hyperuricemia.
SLC22A12 Solute carrier family 22 member 12: URAT1 Uric acid reabsorption transporter. A major target for uricosuric drugs. Gene polymorphisms are associated with hyperuricemia and gout. Loss of function in the gene can also lead to hypouricemia.

2. Heritability of Urate Levels and Urate-Modifying Factors

Twin studies have demonstrated that serum urate (SU) levels and hyperuricemia are genetically linked with heritable estimates of 40 and 60%, respectively [5][6]. While high SU levels are strongly predictive for developing gout, not all hyperuricemia cases will result in gout, suggesting that gout is a trait influenced more by the environmental factors than the inherited factors [5]. This knowledge supports that many cases of gout could be preventable. Furthermore, specific dietary and other social and behavioral factors could significantly influence SU levels [7]. For example, social lifestyle factors such as smoking and alcohol intake could decrease and increase SU levels, respectively [8]. Health and nutritional supplements (e.g., niacin, vitamin C, cherries, and fish oil) and physical activity levels can further modulate SU concentrations and the prognostications of chronic hyperuricemia [9][10][11]. Certain medications may also affect SU levels, which warrants using or avoiding certain prescription drugs in patients with gout when compelling indications persist [12]. A summary of the effect of major dietary patterns and lifestyle factors on uric acid levels and gout risk is listed in Table 2.
Table 2. Effect of dietary patterns and lifestyle factors on serum urate and gout risk management.
Diet/Food/Lifestyle Factor Serum Urate Level Incident Gout Gout Flare Risk ACR 2020 Recommendations [13] References
DASH diet Nutrients 14 03590 i001 Nutrients 14 03590 i002 Nutrients 14 03590 i003 No recommendation [14][15][16]
Mediterranean diet Nutrients 14 03590 i004 Nutrients 14 03590 i005 Nutrients 14 03590 i006 No recommendation [17]
Ketogenic diet Nutrients 14 03590 i007 No data No data No recommendation [18]
Low-fat dairy
Nutrients 14 03590 i008 Nutrients 14 03590 i009 Nutrients 14 03590 i010 No recommendation [19][20]
Cherries Nutrients 14 03590 i011 Nutrients 14 03590 i012 Nutrients 14 03590 i013 No recommendation [21][22]
Coffee Nutrients 14 03590 i014 Nutrients 14 03590 i015 Nutrients 14 03590 i016 Nutrients 14 03590 i017 No recommendation [23][24][25][26]
Tea Nutrients 14 03590 i018 Nutrients 14 03590 i019 No data No data No recommendation [25][26][27]
High-fructose corn syrup (HFCS) Nutrients 14 03590 i020 Nutrients 14 03590 i021 Nutrients 14 03590 i022 Conditionally recommends limiting the intake of HFCS [28][29]
Weight loss Nutrients 14 03590 i023 Nutrients 14 03590 i024 Nutrients 14 03590 i025 Conditionally recommends a weight loss program [30][31]
Physical exercise Nutrients 14 03590 i026 No data No data No recommendation [9][30]
Smoking Nutrients 14 03590 i027 Nutrients 14 03590 i028 Nutrients 14 03590 i029 No data No recommendation [32][33][34]
Alcohol Nutrients 14 03590 i030 Nutrients 14 03590 i031 Nutrients 14 03590 i032 Conditionally recommends limiting alcohol intake [35][36][37]
Vitamin B complex (B6-B12-Folic acid) Nutrients 14 03590 i033 No data No data No recommendation [38]
Vitamin C Nutrients 14 03590 i034 Nutrients 14 03590 i035 No data Nutrients 14 03590 i036 Conditionally recommends against use [10][39][40]
Fish Oil/Omega-3-fatty acids Nutrients 14 03590 i037 No data Nutrients 14 03590 i038 No recommendation [11][41][42]

3. Gout Risk and Acculturation

Dietary habits are mirrors of cultural customs and traditions. Certain population subgroups tend to follow a specific diet for personal, social, and religious norms [43][44]. Nonetheless, immigration or acculturation could significantly impact the lifestyle and dietary habits of the same population groups [44][45][46]. These changes could have significant effects on the individuals’ overall health, ranging from energy expenditure-related activities to their gut microbiome. Collectively, these changes could have a consequential impact on developing cardiometabolic risk factors, including hyperuricemia and gout. Similarly, Filipinos living in the US were reported to have higher gout rates and elevated means SU levels than those residing in the Philippines, suggesting significant gene–environment interactions [47][48]. Conversely, developing hyperuricemia or gout among US immigrant groups could be owing to a more permissive environment, increasing the penetrance of risk alleles by equivalent effects [44][49]. For example, the joint effect of alcohol consumption and carrying the risk allele of ABCG2 rs2231142 G > T was associated with a greater risk for developing hyperuricemia than the risk allele alone, especially among women [50]. Therefore, ascertaining the dietary and social lifestyle habits among distinct racial and ethnic groups could shed additional light on the hypothesis of gene–diet/gene–social habits interactions and population-specific risk for developing hyperuricemia or gout [35][51]. Additionally, this ascertainment may provide more evidence on the role of preserving a cultural identity in disease prevention and the generational effect on disease onset among immigrant groups.

4. Gout Risk and Health Beliefs

Developing gout was deeply rooted in the lifestyle of excessive alcohol consumption, seafood, and red meat [52]. The framework of dietary excess for developing gout significantly contributed to the misconception of gout being a self-inflicted disease; this ingrained perception of gout rendered specific dietary restrictions to be a widely accepted gout management approach among gout patients and some healthcare professionals. This dietary framework could be contributing to poor adherence to urate-lowering therapy and fewer gout patients being prescribed urate-lowering treatments [53][54]. While there is data supporting the role of dietary-based interventions in lowering SU, dietary changes are often viewed as either a preventative or adjunct treatment approach for gout [14]. Nonetheless, the interplay between gout and developing cardiometabolic diseases may provide a window of opportunity that could be leveraged to manage gout and other existing comorbidities [55]. Collectively, this opportunity could also benefit the patient to form a healthy lifestyle extending beyond gout [55]. However, it should be recognized that access to healthy foods is not equally distributed across the population, which may hinder the effectiveness and sustainability of diet-based interventions. Therefore, patients diagnosed with gout should ideally be evaluated for other comorbidities to garner the added benefits from dietary changes. This approach will allow for patient-centered recommendations and increase the likelihood of patients adopting the provided dietary-based recommendations. Moreover, implementing novel gout management approaches embedded in real-time self-monitoring, such as home SU monitoring, may help reconstruct the dietary framework for disease management among patients with gout.
Root cause analysis of frequent hospital admissions for acute gout flares could provide additional insights to identify the barriers associated with poor disease outcomes. A qualitative semi-structured study demonstrated that treatment avoidance behaviors and recurrent gout flares could be the result of viewing gout as an insignificant disease primarily occurring in older adults [56]. Additionally, gaps in the providers’ knowledge of gout diagnosis and management, coupled with limited patient education by healthcare professionals, were also reported to impede the optimal management of gout, especially among multimorbid gout patients [56]. Among gout patients not viewing gout as a chronic disease that requires long-term treatment was identified as a barrier to adherence to ULT [57]. This perceived psychosocial burden associated with considering gout a chronic condition renders many patients reliant on hospital admissions to receive gout care.

5. Gout and Social Determinants of Health

Many factors could lead to ethnic and racial disparities in the prevalence and management of chronic diseases, including gout [43][44][58][59][60]. While the biomedical framework for inequality remains the operational framework to provide insights into addressing gout health disparities, little is known about the role of SDOH and gout. This role is compounded by the association between gout and multiple cardiometabolic diseases [61]. It is presumed that optimal management of gout-related comorbidities may confer added benefits for gout management itself. Therefore, optimal management of gout is believed to be within the context of the optimal chronic disease management framework. However, the management of gout remains poor, despite the availability of effective and affordable treatments. Many factors, ranging from individual to organizational causes, can lead to suboptimal management of gout. On an individual level, financial barriers, health insurance, health literacy, and access to healthy food choices are significant predictors for optimal gout management. On an organizational level, the knowledge base of gout management among healthcare professionals, adequate teaching of gout in health profession programs, patient-physician relationships, and conflicting guidelines for gout management are crucial elements for delivering optimal care for patients with gout. Assessing the role of SDOH in patients with gout may provide a window of opportunity to address treatment goals and eliminate barriers to receiving care. Furthermore, future gout studies are also needed to quantify the impact of SDOH on disease onset and treatment outcomes to inform the value of a comprehensive assessment for optimal gout management.

6. Multidisciplinary Approach to Gout Management

A multidisciplinary approach to chronic disease management improves treatment outcomes across many disease states. Similarly, gout management could be optimized by engaging multiple healthcare professionals in addition to physicians, including nurses, pharmacists, and dietitians. According to the 2020 American College of Rheumatology guidelines, an augmented treat-to-target protocol by nonphysician providers is conditionally recommended over the usual care [13]. Recognizing that patients with gout are more than likely to have other comorbidities, which also require close monitoring and complex treatment regimens, the pharmacist is well-positioned to optimize gout management outcomes. Indeed, pharmacist-led interventions to improve adherence to allopurinol and gout treatment had better treatment outcomes than the usual care. Specifically, a one-year pharmacist-led intervention, incorporating automated telephone technology, led to a 70% improvement in adherence rates to allopurinol and more than a two-fold increase in the number of patients achieving SU levels less than 6 mg/dL, compared with the usual care. Moreover, participants in the intervention arm were twice as likely to have their allopurinol dose escalated compared with the standard of care [62]. These results support the role of a pharmacist-staffed gout management clinic to improve gout treatment outcomes compared with the standard of care. Regardless of the clinical setting, including virtual gout clinics, pharmacist involvement in gout management significantly improves the number of individuals achieving SU levels of less than 6 mg/dL, with these patients having fewer gout flares than those receiving the standard of care [63][64]. As new patient care models continue to emerge, community-based pharmacy practice may also play a role in health equity and increasing access to healthcare among patients with chronic diseases [65].

7. Pharmacogenomics and Gout Management

Pharmacogenetics (PGx) is a growing field within the precision medicine era, focusing on how gene variations affect the patient’s response to treatment. Pharmacogenetics is a promising tool to optimize the selection and dosing of medications, including ULTs among patients with gout [66]. Genetic and experimental findings have demonstrated that genetic polymorphisms associated with SU pathology are also of pharmacogenetic interest [66]. Patients with gout often present with several comorbidities, warranting the use of several acute and long-term medications that increase their pill burden and the risk of adverse drug events. Implementing PGx testing can identify individuals who are more or less likely to benefit from a given treatment, thereby potentially improving medication adherence and reducing pill burden. The strongest evidence today suggests that individuals carrying the HLA-B*58:01 allele are at a higher risk of serious and life-threatening skin reactions when taking allopurinol [13][67]
Emerging evidence of clinically significant drug–gene pairs among various gout therapies is growing. Allopurinol remains the most widely prescribed ULT; therefore, identifying sources of variability in response to allopurinol is an active area of research. Genes that were found to modulate the response to allopurinol include AOXABCG2, and SLC22A12 [68][69][70][71]. Meanwhile, UGT1A1 appears to modulate the response to febuxostat. While CYP2C9 may modulate the toxicity of benzbromarone, SLC22A12 and ABCB1 were found to modulate the response to both benzbromarone and probenecid. The genes CYP2D6ABCB1, gene cluster (rs6916345 G > A), and SEPHS1 were recently reported to modulate the safety and efficacy of colchicine [66][72]. Finally, HCG22 and IL1RN could be linked with the response to corticosteroids and anakinra, respectively [66].

This entry is adapted from the peer-reviewed paper 10.3390/nu14173590


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