Why Does Added Sugar Influence Gout?

Content

• Foods That Increase Uric Acid
• The Risk Of Hyperuricemia
• Science In Renal Medicine
• How To Add To The Diet
• Sleep Apnea Increases The Risk For Gout, Study Suggests
• Processed Sugar

The administration of fructose to animals and humans increases BP and the development of metabolic syndrome. These changes occur independently of caloric intake because of the effect of fructose on ATP depletion and uric acid generation. Fructose ingestion may also be a risk factor for kidney disease that includes glomerular hypertension, renal inflammation, and tubulointerstitial injury in animals.

A more recent study done by the same group confirmed these results by using two differently acting urate lowering drugs, allopurinol, and probenecid . This study clearly implicated uric acid as the biochemical mediator of increased blood pressure. Animal data suggested that uric acid induced hypertension has two phases. The first is salt insensitive which is likely to be managed by urate lowering drugs, while the second phase is salt sensitive. Due to a paucity of outcome data, recommendations on how to treat uric acid associate hypertension cannot be made at this time although the mechanism appears clear, especially in the early stages before the development of salt sensitivity.

Foods That Increase Uric Acid

Recent relevant clinical research has sought to verify if XO inhibition could benefit patients with high circulating UA levels, focusing on the XO inhibitor allopurinol and its active metabolite oxypurinol. Allopurinol has displayed beneficial effects on blood pressure in adolescents with newly diagnosed essential hypertension , and in patients with heart failure, coronary artery disease, and stroke . Allopurinol may thus improve endothelial function and endothelium-dependent vasodilation in chronic heart failure patients .

Woodward O.M., Kottgen A., Coresh J., Boerwinkle E., Guggino W.B., Kottgen M. Identification of a urate transporter, ABCG2, with a common functional polymorphism causing gout. Friedl H.P., Till G.O., Ryan U.S., Ward P.A. Mediator-induced activation of xanthine oxidase in endothelial cells. Stack A.G., Hanley A., Casserly L.F., Cronin C.J., Abdalla A.A., Kiernan T.J., Murthy B.V., Hegarty A., Hannigan A., Nguyen H.T. Independent and conjoint associations of gout and hyperuricaemia with total and cardiovascular mortality. As noted above, most mammals can degrade UA to allantoin in a reaction catalyzed by uricase, an enzyme present in peroxisomes. Most mammals thus have relatively low UA circulation levels (0.5 to 2.0 mg/dL). However, humans and great apes cannot synthesize functional uricase and therefore have much higher blood UA levels.

The Risk Of Hyperuricemia

Furthermore, it is fructose’s unfortunate ability to induce increasing sensitivity with increasing exposure that makes it increasingly relevant in a society that is rapidly increasing its total fructose intake. Many epidemiologists have pointed out the temporal association between the increase in the use of HCFS and total percentage of fructose in the diet, with the increased prevalence of gout and hyperuricemia. A major meta-analysis found that most observational studies support the role of high fructose consumption as a risk marker for the occurrence of gout. In contrast, we did not find previously published literature examining the relationship specifically between dietary fiber intake and hyperuricemia risk in the general adult population. A possible mechanism of higher fiber intake associated with lower serum uric acid concentration and reduced hyperuricemia risk could be that dietary fiber inhibits purine or adenine absorption in the digestive system . Also, higher fiber intakes are usually associated with healthier diets and lifestyle.

Science In Renal Medicine

Fructose, either alone or as a part of sucrose, is commonly added to foods for taste enhancement. However, like other sugars, excessive consumption of fructose contributes to insulin resistance, obesity, and metabolic syndrome. Of interest, the blockade of intracellular uric acid with allopurinol could inhibit the effect of fructose to increase fat accumulation.

Does tea increase uric acid?

Orange Juice and Gout Risk
Many sugar-sweetened juices can increase your risk for gout, but naturally-sweetened juices like orange juice may also be a gout risk trigger.

Effect of insulin on renal sodium and uric acid handling in essential hypertension. Serum concentrations of uric acid and the metabolic syndrome among US children and adolescents. Polynesian women are also at risk for hyperuricaemia and gout because of a genetic defect in renal urate handling. A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men.

Interestingly, recent studies have shown that microbiota in the gastrointestinal tract plays a substantial role in fructose metabolism . Fru1P is subsequently metabolized by aldolase B and triokinase to dihydroxyacetone phosphate and glyceraldehyde-3-phosphate to enter the glycolytic pathway distal to phosphofructokinase. Recently, a key role of aldolase B in cancer growth was shown that aldolase B mediates colon cancer liver metastasis and that reducing dietary fructose diminishes liver metastatic growth in mice .

Rather, intestinal or “extra-renal” elimination involves the absorption of uric acid, from the circulation, by the intestinal epithelial cells . The excretion of uric acid occurs in the digestive juices secreted in the upper small intestine, primarily the duodenum, with uric acid concentrations of 0.2 mg/ml having been reported in mice . Limited uric acid excretion may also occur via the jejunum, the ileum and the colon . As humans produce between one and two litres intestinal digestive secretions per day , the efficiency of these intestinal secretions in removing uric acid is clinically relevant. The uric acid secreted into the intestines appears to be completely degraded by uricolytic bacteria to waste substances, except in cases of dysbiosis where uric acid is excreted in faeces . Exogeneous urate, resulting from the digestion of purines, may be either absorbed by the intestine or degraded in the intestine but normally, it is not found in the faeces .

Fructose consumption as a risk factor for non-alcoholic fatty liver disease. Although we suggest that these mutations likely provided a survival advantage at that time, in today’s setting in which dietary purines, fructose, and salt are ingested at high levels, these mutations may predispose us to hypertension, obesity, and diabetes. Hence, we suggest that genes involving vitamin C, fructose, and uric acid metabolism represent the thrifty genes postulated by Neel. 307), we also need additional studies to determine how the SLC2A9 modulates intracellular uric acid levels in response to fructose. Potential mechanisms by which fructose and uric acid may induce insulin resistance. Fructose enters cell via a transporter where it is acted on by fructokinase .

The glucose or fructose-mediated decrease in vascular function increases adipocyte size resulting in decreased levels of adiponectin, but increased levels of MCP-1, IL-6, and TNF-α that have systemic effects on β cells . One of the major risk factors for gout is hyperuricemia or high blood uric acid levels. Uric acid is the end product of purine breakdown, and purines are obtained primarily from red meat. Figure 2 indicates hyperuricemia rates by quartiles of dietary fructose intake.

Alcoholic beverages, especially beer, and drinks sweetened with fruit sugar promote higher levels of uric acid. Dr. Choi also points out that fructose is used to make high-fructose corn syrup, a substance commonly used to sweeten many foods and beverages besides soda. Managing uric acid levels is an important topic for individuals who have risk factors for gout because high uric acid levels increase the likelihood of developing gout.

Processed Sugar

It can also happen because of other health conditions, like skin infections and blood vessel issues. Psoriatic arthritis is a chronic, inflammatory autoimmune disease of the joints, tendons, and ligaments that connect your bones. When you’re exposed to a really hot environment and your blood vessels expand, they might leak some fluid into your soft tissues.

Why Does Added Sugar Influence Gout?

Small amounts of sucrose occur naturally in the roots and fruits of plants, but commercial sources of sucrose are derived from sugar cane and sugar beets . The bonding between fructose and glucose is relatively strong, so sucrose does not readily hydrolyse in water. During digestion the intestinal digestive enzyme, sucrase, splits the sucrose molecule into fructose and glucose . When deriving total fructose intake measures in foods, it is important to combine free fructose values and add 50% of the sucrose value to account for the fructose segment of the sucrose. In the classical pathway, triglycerides are a direct product of fructose metabolism by the action of multiple enzymes including aldolase B and fatty acid synthase . As a consequence, the ACO2 substrate, citrate, accumulates and is released to the cytosol where it acts as substrate for TG synthesis through the activation of ATP citrate lyase and fatty acid synthase.