Uric Acid and Metabolic Disease
Uric Acid and Metabolic Disease
Metabolic Syndrome, Prevention, Uric Acid
Metabolic disease is characterized as the presence of a jumbo of risk factors that increase the risk of diabetes, heart disease, and/or stroke. Fortunately metabolic syndrome can be prevented with your lifestyle choices. The basic one you can control is reducing your sugar intake due to the fact that during metabolizing carbohydrates, fructose is the main one that produces uric acid.
Uric Acid is a component of urine, and he production and breakdown of uric acid is a product of metabolic breakdown which in turn is influenced by many different factors including the regulation of how much uric acid is produced by the liver, as well as how much is excreted by the kidneys and gut. Uric acid is produced from 2 parts:
1. Purines in the diet
2. Purines produced by the body
Liver, intestines, muscles, kidneys, and vascular endothelium are the main sources of endogenous uric acid production.
Hyperuricaemia refers to an abnormally high concentration of uric acid in serum:
>7 mg/dL (416 μmol/L) in men and >6 mg/dL in women (look it up on google what it looks like. Can be mistaken for edema).
Hyperuricaemia and Metabolic disease
Those with obesity, metabolic syndrome, and type 2 diabetes often have hyperuricemia due to the idea that is may be caused by insulin resistance reducing the urinary excretion of uric acid thus lowering serum uric acid may improve insulin resistance.
There seems to be a trend that as uric acid levels increase, there is a corresponding increase in the incidence of individual metabolic syndrome components, such as high blood sugar, high triglycerides, low HDL cholesterol, and hypertension (high blood pressure) (Choi 2007) (Borghi 2015). In adolescents there was a study of 5,748 individuals between 10 to 15 years of age and were followed for a median of 7.2 years that their elevated uric acid was predictive of developing metabolic syndrome in males but not in females (Sun 2015).
Gout
Gout is a form of arthritis characterized by severe pain and inflammation at the joints. This occurs when there is too much uric acid that crystallizes and deposits itself into the joint. Fortunately you can reduce uric acid levels by lowering your sugar intake, and using a extract used in Chinese medicine: Biota orientalis (BO).
Both clinical trials and clinical practice shoot to lower serum uric acid (SUA) levels in gout treatment, such as < 6.0 mg/dl or < 5.0 mg/dl (Zhang 2006, Wortmann 2005). Monosodium urate crystals tend to form when urate levels exceed 6.8 mg/dl.
The key take away from this article is to reduce or at least control your sugar intake. Avoid processed canned foods as they usually put fillers, and sugar. i.e canned corn, canned vegetables and fruit. Always choose frozen or fresh veggies and fruit – never canned, and always read the ingredients in packaged food. The more ingredients in the product, the more you should stay away! If you do choose sugar, choose the bitter fruits: berries, grapefruit, pomegranate.
Be well.
Yelena
References
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Choi HK, Ford ES (2007). Prevalence of the metabolic syndrome in individuals with hyperuricemia. Am J Med,120(5): 442-7.
D'Silva KM, Yokose C, Lu N, McCormick N, Lee H, Zhang Y, Choi HK (2021). Hypouricemia and Mortality Risk in the US General Population. Arthritis Care Res (Hoboken). 73(8): 1171-1179.
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Russo E, Leoncini G, Esposito P, Garibotto G, Pontremoli R, Viazzi F (2020). Fructose and Uric Acid: Major Mediators of Cardiovascular Disease Risk Starting at Pediatric Age. Int J Mol Sci, 24;21(12):4479.
Sun HL, Pei D, Lue KH, Chen YL (2015). Uric Acid Levels Can Predict Metabolic Syndrome and Hypertension in Adolescents: A 10-Year Longitudinal Study. PLoS One, 10(11): e0143786.
Wortmann RL (2005). Recent advances in the management of gout and hyperuricemia. Curr Opin Rheumatol,17(3): 319-24.
Xue L, Liu Y, Xue H, Xue J, Sun K, Wu L, Hou P (2017). Low uric acid is a risk factor in mild cognitive impairment. Neuropsychiatr Dis Treat, 11; 13: 2363-2367.
Zhang W, Doherty M, Bardin T, Pascual E, Barskova V, Conaghan P, Gerster J, Jacobs J, Leeb B, Lioté F, McCarthy G, Netter P, Nuki G, Perez-Ruiz F, Pignone A, Pimentão J, Punzi L, Roddy E, Uhlig T, Zimmermann-Gòrska I (2006); EULAR Standing Committee for International Clinical Studies Including Therapeutics. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis; 65(10): 1312-24.