Does Soda Cause Gout?

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• Gout And Sugar From Soft Drinks
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• Vascular Effects
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The difference in serum uric acid levels between genders is likely due to the increased renal urate clearance by estrogen in women, particularly before menopause . A Japanese study showed a combination of estrogen and progesterone resulting in a significant drop in serum uric acid among hyperuricemic women, whereas there was no drop among controls . Similarly, the Heart and Estrogen-Progestin Replacement Study reported that one year of estrogen plus progesterone therapy resulted in a slight drop in serum uric acid levels, as compared with placebo (0.2 mg/dL at one year of follow-up) . Lipids are likely required as an energy source and for membrane formation, and as signaling molecules in cancer .

Infusion of Ang II decreased adiponectin and potentiated fructose-mediated insulin resistance in fructose-fed rats . The presence of renin-angiotensin aldosterone in adipose tissue has been described [110–112] in which Ang II increased NADPH oxidase activity and WAT mediated inflammation and blocked RAAS thereby preventing the onset of diabetes. Blocking ROS via the inhibition of Ang II converting enzyme reduced obesity in rats and dysregulation of inflammatory cytokines released by adipocytes . Plasma Ang II is associated with markers of insulin resistance and obesity .

Gout And Sugar From Soft Drinks

Here, we unpack what we know about how fructose impacts the body and why it’s best avoided in your diet, especially as an added sweetener of any kind . Fructose is a simple sugar that occurs naturally in ripe fruits, sweeteners like honey, palm sugar, maple sugar, and agave syrup, and in small quantities in some vegetables like asparagus, onions, and peppers. But today, it’s primarily known in the context of high-fructose corn syrup , a sweetener added to many processed foods, such as sodas, candies, and frozen meals.

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A) Effects of dnMLX in the mRNA response of PKL (Pyruvate kinase-liver specific) to high glucose levels. B) Sequencing of both putative proximal and distal ChoRES identified in the KHK promoter in multiple species incuding humans and primates. Another issue with all three metanalyses is that they included control groups that ingested sucrose, which can be questioned because sucrose is a disaccharide that contains fructose (81–83). Gout is a type of painful arthritis that can affect one or more joints. There have been some studies, including in 2011 and 2012, that suggest cherries might potentially help treat or even cure gout.

According to the paper, previous animal studies had shown a potential link between dragon fruit consumption and better control of diabetes. This is because dragon fruit encourages the growth of pancreatic cells that produce insulin. A meta-analysis that appeared in the journal PLOS ONE looks at the effects of consuming dragon fruit on blood glucose control in those with prediabetes and those with type 2 diabetes. You get over to the evidence-based crowd and they say it’s all calories in calories out, and there does seem to be a little wrinkle of nuance here.

Vascular Effects

Recent research suggests that hyperuricemia may be caused by elevated activity of the enzyme xanthine oxidase . Xanthine oxidase inhibitors have thus been proposed as a strategy for reducing UA and oxidative stress. Both are risk factors for gout, chronic kidney disease , CVD, obesity, insulin resistance, and metabolic syndrome. Humans and great apes produce UA via XO-catalyzed oxidation of purines. Unlike other mammals, humans and great apes cannot synthesize the uricase enzyme and so cannot metabolize UA to allantoin. As a result, UA blood concentrations in humans and great apes are at least 10 times higher than in other mammals, with the consequent risk of developing hyperuricemia .

So what’s going on in the body that leads to such different effects from glucose and fructose intake? First, the body metabolizes the two types of sugars very differently. Glucose is absorbed in the small intestine into the bloodstream, delivered to cells throughout the body.

Research indicates tart Montmorency cherries reduce inflammation , lower cholesterol and triglycerides , even speed up muscle recovery after a workout, and aid sleep. That tart taste is an indication a high amount of antioxidants and anthocyanins, which contribute to the first few benefits. Other studies indicate that cherries could even help prevent Alzheimer’s disease. A paper entitled "Cytokines in Rheumatoid Arthritis " published in Intech Open showed that the release of cytokines could cause synovial inflammation.

Since the prevalence of risk factors for gout and its incidence tend to be higher in the general population and among African Americans, the magnitude of the absolute risk increase associated with these beverages might be greater than the increase we observed. Fructose is taken up by the liver following absorption and converted to fructose-1-phosphate, which causes a reduction in ATP levels. The resulting increase in AMP means it is converted to IMP instead, in the absence of phosphate for phosphorylation. Increasing fructose intake and lowered ATP levels may lead to an increase in purine nucleotide production with increased uric acid being a side effect. A 2016 meta-analysis suggested that fructose consumption may contribute to higher incidences of gout. Other studies have reported that fructose intake was not associated with increased hyperuricemia risk.

Are Bananas high in fructose?

A high-salt diet has been found to lower blood levels of uric acid, a recognised trigger of gout, according to a study by US researchers.

In both adults and children, WHO recommends reducing the intake of free sugars to less than 10% of total energy intake . 2) On the one hand, dietary intervention can change SUA by 1-2 mg/dl while on the other hand SUA is tightly controlled by XO levels and kidney activity . Nutritional supplements to reduce SUA may focus on inhibiting XO, enhancing intestine excretion or enhancing renal excretion. However, little is known about intestinal uric acid elimination and renal elimination involves many genes, so what works for one individual many have no effect on another individual. Table 8 Fructose, glucose and sucrose levels in prepared beverages g per 100 g 1, 2, 3. This group will be assigned to a 2 week period of low fructose diet (less than 10 grams/day ) followed by a 4 week period of less than 20 grams/day fructose diet levels.

Potential Outcomes And Associated Conditions Of Hyperuricemia

I’m tempted to up my sodium further two LMNT packets and 500 milligrams of salt capsules per day. So all this leads to the question, how do you tell if you need to increase your electrolytes and sodium, or to decrease your intake, the symptoms on Google seem to overlap. So clearly, there’s something more to it than that, clearly LDL is a player in it. Some people like Malcolm Kendrick make the case that it’s actually playing a role in the repair and recovery process of the damaged endothelium. And if you address the damage, whatever the vector of damages, then the LDL doesn’t really matter, or it doesn’t really matter so much. Again, you have some folks like Peter Attia that I think are very, very smart and much more conservative on this.

Wannamethee S.G., Shaper A.G., Whincup P.H. Serum urate and the risk of major coronary heart disease events. Le M.T., Frye R.F., Rivard C.J., Cheng J., McFann K.K., Segal M.S., Johnson R.J., Johnson J.A. Effects of high-fructose corn syrup and sucrose on the pharmacokinetics of fructose and acute metabolic and hemodynamic responses in healthy subjects. Cox C.L., Stanhope K.L., Schwarz J.M., Graham J.L., Hatcher B., Griffen S.C., Bremer A.A., Berglund L., McGahan J.P., Keim N.L., et al. Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans. Berger L., Gerson C.D., Yu T.F. The effect of ascorbic acid on uric acid excretion with a commentary on the renal handling of ascorbic acid. Sui X., Church T.S., Meriwether R.A., Lobelo F., Blair S.N. Uric acid and the development of metabolic syndrome in women and men.

How A Cgm Can Help You Find Your Optimal Diet And Lower Blood Sugar

When the New England Journal of Medicine published Willett’s gout study, it ran an editorial to accompany it written by the University of Florida nephrologist Richard Johnson. Compared with women who consumed less than a glass (6 oz.) of orange juice per month, women who consumed 1 serving per day had a 41 percent higher risk of gout, and there was a 2.4 times higher risk with 2 or more servings per day. Also, compared with women in the lowest quintile of free fructose intake, women in the highest quintile had a 62 percent higher risk of gout. During 22 years of follow-up, the researchers documented 778 newly diagnosed cases meeting American College of Rheumatology survey criteria for gout. They found that increasing intake of sugar-sweetened soda was associated with increasing risk of gout.

Fructose: The Worst Sugar

With increasing sugar-sweetened soda consumption, intake of fructose, sucrose, meat, high-fat dairy foods, and coffee tended to increase, but mean age, prevalence of menopause, and intake of low-fat dairy, fruit, and vitamin C tended to decrease . Alcohol intake was lower in the middle categories of sugar-sweetened soda consumption. With increasing free fructose consumption, body mass index and intake of alcohol, coffee, meat, and high-fat dairy foods tended to decrease but prevalence of menopause and intake of fruit and vitamin C tended to increase . Experiments involving the administration of fructose orally or intravenously have shown that it is followed by a quick rise in uric acid levels in the blood as purines are broken down and more purines are synthesized.

However, if uric acid is part of the “switch”, how do we explain people that eat healthy and show no signs of metabolic symptoms but have high uric acid? Vice versa; those that have low uric acid but show metabolic symptoms. For many of us, no matter how much we exercise or eat healthy, uric acid number does not change significantly. There are several papers that suggest food has minimal effect on uric acid number. Purines are a group of chemicals present in all body tissues and in many foods. Our bodies are continually processing purines, breaking them down and recycling or removing the byproducts.