Insulin resistance measure may be ‘simple and cost-effective’ gout prediction tool
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Key takeaways:
- Gout risk rises with each unit increase in triglyceride glycemic index score.
- The association was not impacted by age, race, BMI, hypertension and other covariates.
U.S. adults with higher triglyceride glycemic index scores demonstrate a greater likelihood of developing gout, according to data published in the Journal of Health, Population and Nutrition.
“The [triglyceride glycemic (TyG)] index was considered a good and novel index that could reflect insulin resistance (IR),” Tao Li, of Jiaying University, in China, and colleagues wrote. “It integrates triglycerides and fasting glucose, and was calculated by fasting triglycerides(mg/dl)*fasting glucose (mg/dl)/2, which was developed by Mendía et al. in 2008 and has been investigated widely.
“As it is more convenient and easily accessible in clinical settings compared to the complex technique of the plasma insulin in the homeostasis model assessment of IR, the TyG index may be a useful tool or reliable biomarker for assessing IR and its implication in metabolic diseases,” they added. “Accumulating evidence has shown that IR plays a role in the pathological process of gout.”
To analyze the link between triglyceride glycemic index score and gout in the United States, Li and colleagues conducted a cross-sectional study using National Health and Nutrition Examination Survey data from 2007 to 2017. Their analysis included 11,768 adults (73.26% aged younger than 60 years; 50.32% women), 5.12% of whom had gout.
Gout status was assessed using self-reported questionnaires. The researchers examined connections between triglyceride glycemic index and gout using weighted multivariable logistic regression analysis, subgroup analysis and interaction tests.
According to the researchers, each unit increase in the triglyceride glycemic index was linked to a 40% greater chance of developing gout (OR = 1.4; 95% CI, 1.82-2.66), after adjustment for all covariates. Individuals in the highest tertile of the triglyceride glycemic index demonstrated greater gout risk (OR = 1.64; 95% CI, 1.06-2.54) than those in the lowest tertile.
The association between triglyceride glycemic index and gout was not impacted by age, race, marital status, poverty-income ratio, education, BMI, smoking or drinking status, hypertension or diabetes mellitus in interaction tests, according to the researchers.
“Our findings highlight that the TyG index is a reliable biomarker of IR; management of IR among adults may prevent or alleviate the development of gout; meanwhile, the TyG index may be a simple and cost-effective method to detect gout,” Li and colleagues wrote.
“Further longitudinal studies are needed to examine the causal association between the TyG index and gout in the broader population to elucidate the potential mechanism of IR on gout,” they added.
Perspective
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Clinical gout is something that rheumatologists are very familiar with and in general are very good at treating. The understanding of the science, meanwhile, continues to be elucidated.
Recognizably, it is a complex inflammatory metabolic disorder that continues to puzzle us with certain paradoxes and unclarity. For example, uric acid can have both a proinflammatory role and an anti-oxidative function. Another is the relationship of serum uric acid level and the development of clinical gout. The process is not straightforward.
In their large cross-sectional analysis, Li and colleagues used data from 11,768 eligible patients from NHANES to demonstrate a relationship between triglyceride glycemic index (TGI) and the prevalence of gout. The TGI is calculated as triglycerides (mg/dl) x fasting glucose (mg/dl)/2. The researchers found 40% increase odds of gout at each defined increase increment of TGI.
This large of a study, adjusted for covariates, has not been conducted previously. The researchers acknowledge the previous demonstration of TGI as a marker of insulin resistance, thus perhaps further validating a relationship of insulin resistance (IR) and gout.
As discussed in their study, we again see a confusing relationship as hyperuricemia may contribute to IR while hyperinsulinemia may affect uric acid secretion at the kidney. However, as the researchers point out, studies with IR are more complex and time consuming. They acknowledge certain limitations in their analysis and the need for additional prospective studies.
From a clinical perspective, I don’t envision practicing rheumatologists to start calculating TGIs any time soon. However, with further research and validation, biomarkers such as this may expand our understanding of this disorder. Ultimately, it could perhaps be used to identify at risk populations.
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