Hyperuricemia and gout

Elevated uric acid levels (hyperuricemia) are in many cases hereditary. However, whether this develops into painful gout is usually determined by lifestyle. In addition to purine-rich animal foods and alcohol, high-glycemic carbohydrate sources and fructose in particular also play a role.

Uric acid is formed in the body during the disposal of purines, which either come from our food or are produced during the breakdown of purine nucleotides. The most important purines in the body are adenine and guanine, which, as components of purine nucleotides, are important for the formation of the genetic material DNA as well as for energy carriers such as ATP (adenosine triphosphate) and GTP (guanosine triphosphate). Consequently, purines accumulate in the body primarily when cells die and DNA is broken down (as happens to a greater extent in cancer therapies, for example) and when there is a high energy turnover with the consumption of ATP.

What role do sugars play in hyperuricemia and gout?

In addition to purine-rich meat and fish, alcohol and obesity, a diet high in fructose also contributes to increased uric acid levels and thus to an increased risk of gout. Originally, the only relevant sources of fructose in the human diet were fruit, vegetables and honey, which provided the body with a manageable amount of fructose. With modern foods such as fruit juice, smoothies, household sugar, sweetened products such as drinks, sweets, fruit yoghurt, ready-made sauces or products with glucose-fructose syrup such as ice cream and dessert cream, fructose intake is now significantly higher. The problem here is that unlike glucose, which reaches the liver from the intestine and is passed on to other body tissues for further utilization, the breakdown of fructose mainly takes place in the liver tissue. The more fructose reaches the liver, the more it has to break down. In doing so, it consumes energy in the form of the energy carrier ATP, producing purines, which are further broken down into uric acid. This uric acid-increasing metabolic pathway is already triggered at quantities below 0.5 g fructose per kg body weight ¹. For an average person, this would be around 35 g, the amount of fructose contained in 3 large glasses of orange juice alone, for example. Especially in children, with their lower weight, the preference for products rich in sugar can contribute to a problematically high sugar and therefore also fructose intake.

Another factor could be the fact that insulin apparently inhibits uric acid excretion via the kidneys ². High-glycemic carbohydrate sources promote a high release of insulin and could also contribute to increased uric acid levels.

What contribution can Dr. Coy's sugars make to hyperuricemia and gout?

With the exception of isomaltulose, Dr. Coy's sugars do not contain fructose and therefore do not contribute to increased fructose intake. At the same time, the consumption of intelligent sugars only leads to a moderate release of insulin, if at all.

Galactose is slowly absorbed, converted into glucose in the liver or used to build up sugar stores (glycogen). In addition, insulin-independent absorption, e.g. in brain and muscle cells, ensures an even distribution in the body. To date, there is no evidence that increased galactose intake increases uric acid levels.

Tagatose is utilized in the body in a similar way to fructose, but much smaller quantities reach the liver due to the moderate absorption rate. Diabetics who took 25 g of tagatose (about 5 teaspoons) with meals over a period of several weeks did experience a brief slight increase in uric acid after eating. However, this did not reach a clinically relevant level. Over the test weeks as a whole, however, the uric acid level did not change, making tagatose with its high sweetening power an interesting sweetening alternative to household sugar ³.

Trehalose is a pure source of glucose whose two glucose building blocks are distributed by the liver to other body tissues via the bloodstream. They therefore do not contribute to increased uric acid formation in the liver. Compared to pure glucose, however, the release of insulin after consuming trehalose is significantly lower ⁴.

Erythritol is excreted by the body unchanged and therefore does not contribute to the formation of uric acid or the release of insulin. Especially in combination with stevia, e.g. in Erythritol-Stevia, Erythritol is therefore an ideal sweetening alternative to household sugar.