Fructose And Gout

Content

• Hepatic Effects
• Sugar
• Overnutrition And Neurodegenerative Diseases
• Teasing Relationships Between Uric Acid, Fructose, And Hypertension
• Got Gout? Eat Like This
• Aside From Alcohol And Purine

What the researchers found was that as one drank more sweetened soft drinks the more risk increased for a gout attack. Compared to men who only drank one soft drink a month, those that drank 5-6 soft drinks a week had a 29% higher chance of developing gout and those that drank 2 or more soft drinks a day had a 85% chance of developing the disease. Too much of the sweet stuff contributes to obesity, and with it, diseases like diabetes and heart disease.

All of the sugars and starches in our diet, whether natural or artificial, ultimately break down into glucose, fructose, or a combination of the two. A decent amount of the fructose, as much as 54%, actually turned into glucose! Fructose doesn’t trigger insulin spikes, and you need insulin to turn on fat-building pathways. Insulin is a growth hormone that tells the liver to grow and store; when insulin levels are low, fat-building pathways are turned off. Glucose and fructose travel separate roads for just the first few steps of processing.

Hepatic Effects

Obese patients with type 2 diabetes who consume higher amounts of fructose display reduced levels of liver adenosine triphosphate -- a compound involved in the energy transfer between cells. Nevertheless, large-scale epidemiologic quantification of potential impact from these conditions has been limited to several relatively common conditions, such as hypertension and renal insufficiency . Similarly, there are many substances and medications that can elevate serum uric acid levels and the risk of gout; however, large-scale epidemiologic data have been limited to several agents such as diuretics and postmenopausal hormone therapy . While much work has focused on fructose as driving obesity, insulin resistance, and cardiorenal disease, not all fructose sources may be the same.

Overdoing it on one type of sugar in particular—the high fructose corn syrup found in sodas and processed foods—can also set off painful gout. Considering that the average American eats 22 to 30 teaspoons of sugar daily, gout is yet another health risk worth noting. Recently, a number of investigators have presented meta-analyses that suggest fructose does not have a causal relationship with obesity or metabolic syndrome (81–83).

Sugar

The validity of gout ascertainment in this cohort and our companion male cohort4,18,19 has been documented by the high degree of concordance with medical record review. According to the Third US National Health and Nutritional Examination Survey (NHANES III, 1988–1994) study , the estimated mean serum uric acid concentration of the US population was 5.33 mg/dL (95% CI (5.29–5.37 mg/dL)). Overall, men had higher serum concentrations (6.06 mg/dL) than women (4.66 mg/dL) by approximately 1.4mg/dL. The mean serum uric acid concentrations did not appear to differ significantly across race/ethnicity in this nationally representative study . Heme oxygenase 1 , a potent antioxidant, decreases UA levels and adipocyte dysfunction by decreasing levels of ROS and XO .

As many as two-thirds of children and one-third of adults malabsorb fructose . This is likely because of variable expression of the fructose transporter GLUT5 in the gut. Expression of GLUT5 and the enzyme KHK, however, are enhanced with repeated exposure to fructose.

Finally, the HPFS Study reported that men who had lost weight had a significantly lower risk of incident gout . These data collectively indicate that adiposity is a prominent determinant for hyperuricaemia and gout. Hyperuricemia is the precursor of gout, which is the most common inflammatory arthritis among men . Hyperuricemia is also associated with several metabolic and cardiorenovascular conditions, including diabetes and coronary artery disease (3–8). Furthermore, hyperuricemia and gout have been linked to premature mortality in some studies . Serum uric acid levels and the frequency of gout have been rising during the last decades (10–23), coinciding with a worsening trend of risk factor profiles, such as obesity, metabolic syndrome, and life-style factors.

Medical Conditions And Medications

News-Medical spoke to Professor Peter M Nilsson about cardiovascular disease risk and whether this is affected by the number of siblings you have. Fructose is a simple monosaccharide sugar and is usually found in fruits, by itself or as part of sucrose. It is also currently found to varying amounts in high-fructose corn syrup , which is a modified form of corn sucrose syrup. Being a liquid sugar and inexpensive to produce, it is widely used in developed countries. Choi HK. A prescription for lifestyle change in patients with hyperuricemia and gout. Forman JP, Choi H, Curhan GC. Fructose and vitamin C intake do not influence risk for developing hypertension.

Why does fructose cause hyperuricemia?

Briefly, fructose metabolism effectively boosts the production of uric acid. It weakens the excretion of uric acid, and the overproduction and underexcretion of uric acid are significant contributors to gout and hyperuricemia [49].

Be sure to consume only one serving of fruit at a time, such as a small apple or orange, 4 ounces (1/2 cup) of juice, 1 ounce (a palm-full) of dried fruit, or a half-cup of fresh fruit. Gout triggers can be individual, so pay attention to the fruits you eat and if they seem to set off a gout attack. Gout is one of the oldest recognized forms of arthritis, with a medical history dating back to the Middle Ages. It was originally known as a “rich man’s disease” because it was associated with rich foods and alcohol, which were generally unavailable to the lower classes.

The relation of coffee consumption to serum uric Acid in Japanese men and women aged 49–76 years. Wu T, Willett WC, Hankinson SE, Giovannucci E. Caffeinated coffee, decaffeinated coffee, and caffeine in relation to plasma C-peptide levels, a marker of insulin secretion, in U.S. women. Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population.

Recently, fructose consumption has fallen under scrutiny due to its harmful effects on the body. Fructose metabolism in the liver leads to the production of uric acid, a metabolic waste-product which is normally filtered out of the bloodstream by the kidneys. However, too much uric acid in the blood can lead to hyperuricemia, a condition that causes gout and can lead to kidney disease. This is a concerning issue due to the recent increase in added sugars to food items, including high-fructose corn syrup.

The intake of fructose is not effective in stimulating insulin and leptin secretion in humans, and hence may not induce a satiety response . For example, a high intake of fructose induces leptin resistance in rats . Fructose also encourages food intake due to stimulation of dopamine in the mesolimbic system and effects on the hypothalamus . Food intake is also stimulated by hepatic ATP depletion , which occurs in animals and humans administered fructose . A recent study in humans documented a reduction in resting energy expenditure in overweight and obese subjects fed fructose but not glucose . These associations were found to be constant irrespective of alcohol use, body mass index, age, blood pressure or the presence of kidney disease.

Got Gout? Eat Like This

Choi HK, De Vera MA, Krishnan E. Gout and the risk of type 2 diabetes among men with a high cardiovascular risk profile. The HFCS consumption estimates are based on data from reference , whereas gout prevalences are based on data from references (32, 133–135) (National Health Interview Survey ). The results are based on the data reported in Zeng et al.’s review article, not original studies. Wu A.H., Ghali J.K., Neuberg G.W., O’Connor C.M., Carson P.E., Levy W.C. Uric acid level and allopurinol use as risk markers of mortality and morbidity in systolic heart failure. Suzuki T. Nitrosation of uric acid induced by nitric oxide under aerobic conditions.