Does Soda Cause Gout?

Content

• Get Fresh Food News Delivered To Your Inbox
• Win Your Health
• Gout
• Evidence That Fructose Mediates Fatty Liver And Insulin Resistance In Humans
• Epidemiology Of Uric Acid

As part of this metabolism, ATP depletion may occur, generating uric acid with systemic effects that block insulin-dependent NO-mediated vascular dilation as well as direct cellular effects on the adipocyte. Fructose also causes de novo lipogenesis that can lead to intracellular triglycerides that can also induce insulin resistance. DAG, Diacylglycerol; PKC, protein kinase C; VLDL, very low-density lipoprotein. Fructose is a simple sugar that is present in fruits and honey and is responsible for their sweet taste. However, the major source of fructose worldwide is sucrose, or table sugar, which is derived from sugar cane and sugar beets. Sucrose is a disaccharide that consists of 50% fructose and 50% glucose.

In addition, the study demonstrates that changes in the plasma are different for fructose and glucose, fructose increases plasma fructose and lactate levels but not glucose, whereas glucose increases plasma glucose but not fructose or lactate. As noted above, lactate reduces renal uric acid excretion, so fructose ingestion increases SUA and decreases renal urate excretion. In contrast, the uric acid derived from purine rich food increases SUA but does not change the renal urate excretion.

Get Fresh Food News Delivered To Your Inbox

These drugs mostly work by URAT1 inhibition, which explains their uricosuric effect . UA excretion is also regulated by breast cancer resistance protein , which belongs to the superfamily of ATP-binding cassette transporters . Unlike ABC transporters, however, BCRP has only one N-terminal ATP-binding domain . Reduced intestinal excretion of UA is often associated with polymorphisms of the BCRP gene or with a lack of BCRP dimerization, which is due to oxidative stress .

The significant reduction in fat accumulation raises the possibility that uric acid may have additional mechanisms whereby it may control fat accumulation. The mechanism whereby fructose induces fat accumulation is thought to be induced by activating de novo lipogenesis. This activation is mediated by the ability of fructose to be metabolized to Acetyl-CoA and glyceraldehyde, the substrates for fatty acid synthase .

Win Your Health

However, we could not observe decreased ChREBP expression in the cytoplasm possibly because ChREBP may be activating its own transcription . Exposure to fructose is known to increase KHK expression in hepatocytes of animals , and humans thus sensitizing the cells to its metabolic/lipogenic effects. In this manuscript, we studied the mechanisms whereby fructose up-regulates KHK expression in human hepatocytes. Here, we demonstrate that uric acid stimulates the up-regulation of KHK in response to fructose and that blockade of its production by inhibition of xanthine oxidase results in lower KHK levels and amelioration of the lipogenic effects of fructose. Conversely, fructose-induced lipogenesis was significantly increased in hepatocytes pre-exposed to uric acid in a dose-dependent manner. Therefore, the observed differences in responsiveness to fructose in humans could be accounted in part to the role that uric acid plays on the expression of KHK in hepatocytes.

Effect of febuxostat on the progression of renal disease in 5/6 nephrectomy rats with and without hyperuricemia. Relationship between resistance to insulin-mediated glucose uptake, urinary uric acid clearance, and plasma uric acid concentration. Small amounts of fructose markedly augment net hepatic glucose uptake in the conscious dog. Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men.

The increase in HFCS has also paralleled the increase in obesity, metabolic syndrome, and chronic kidney disease (Johnson et al., 2013). Fructose varies from other sugars because of its ability to cause intracellular adenosine triphosphate depletion and nucleotide turnover and promote the generation of uric acid. Uric acid is the by-product of purine metabolism made by the enzyme xanthine oxidase and is excreted in the kidneys.

Harm: Liver Disease

A study in California showed that the banning of soft drinks in schools resulted in a reduction in overall soft drink intake with a decrease in obesity in children 6 to 11 years of age . Less effect was observed in older children, possibly because the overall reduction in soft drink intake in this latter group was less effective . Soft drink intake in the U.S. has decreased since peaking in 1999, and this is also associated with a leveling of the rates of obesity. Recent studies suggest that this “side event” in fructose metabolism may be critical for how fructose induces metabolic syndrome. In contrast, KHK-A phosphorylates fructose slowly and consumes minimal ATP .

It is worth mentioning that one thing that continues to perplex me in this whole story is that the claim is that this is a directly gradient-driven process, the higher the LDL particles, the greater the disease potential. But then when people are put on things like PCSK9 inhibitors, which absolutely crush LDL levels, we’ll cut them in half, it does not cut disease potential in half. To a layperson unfamiliar with subtle nutritional influences, these and similar findings may appear convincing, but they rarely survive independent scientific scrutiny. You may have encountered contrary findings — reports that seemed to exonerate sugar consumption as a health hazard. Companies that produce sugar-laden foods and drinks would like you to believe that ailments linked to sugars result from excess calories, not sugars themselves. Don’t believe them; most reports holding sugar blameless are from sources tied directly or indirectly to financial support from the industries that depend on caloric sweeteners.

Evidence That Fructose Mediates Fatty Liver And Insulin Resistance In Humans

If other members of your family have had gout, you're more likely to develop the disease. An attack of gout can occur suddenly, often waking you up in the middle of the night with the sensation that your big toe is on fire. The affected joint is hot, swollen and so tender that even the weight of the bedsheet on it may seem intolerable.

Is pineapple good for gout?

Carbohydrates such as bread, pizza, and pasta do not increase uric acid levels. Alcohol (but beer in particular more so than other types of alcohol), organ meets (liver, kidney, etc), and seafood (notably shellfish) can increase uric acid levels.

In a meta-analysis of 17 studies involving 42,000 adults, the relative risk of gout for those with the highest alcohol intakes was almost double compared to non-drinkers or occasional drinkers. While one study found a higher risk of gout with higher fruit intakes, another found a lower risk. The opposing results are partly confounded by the variation in fructose content of different fruits. In our method, the Food Commodity Intake Databases , released by the U.S. Environmental Protection Agency in and the USDA National Nutrient Database for Standard Reference , published on the website of USDA Agricultural Research Service were used to document the fructose contents for fructose-containing food commodities. In total, fructose content data of 119 from 548 commodities were obtained.

Previous studies have found that high doses of vitamin C supplementation lower serum uric acid via a uricosuric effect (77–81). A double-blinded placebo-controlled randomized trial among 184 non-smoking participants showed that supplementation with 500 mg/day of vitamin C for 2 months reduced serum urate levels by 0.5 mg/dL (95% CI 0.3 to 0.6) . Several observational studies from Taiwan and from the US extended the evidence for the inverse link between Vitamin C intake and the lower risk of hyperuricemia or gout. In this review, we sought to summarize available epidemiologic data related to serum uric acid levels and their trends. We also discuss determinants of uric acid levels from an epidemiologic perspective, with a special focus on the data on fructose and soft drink consumption and their link to serum uric acid and associated conditions. Finally, we provide an update on comorbidities and potential outcomes of hyperuricemia, particularly metabolic-cardiovascular-renal conditions.

Recently, it was found that adiposity and metabolic syndrome were prevented in mice lacking both KHK isoforms but exacerbated in mice lacking KHK-A . It was also demonstrated that neither KHK isoform is required for normal growth and development in rats . Serum leptin, triglycerides, and fasting blood glucose levels are higher in humans placed on a high fructose diet for four weeks compared with those on a starch-based diet . Alcohol is a known factor to raise uric acid levels, and fruits and vegetables are associated with decreasing uric acid levels . Therefore, alcohol and fiber intakes were examined as indicators of model appropriateness. It is expected that this work, utilizing a large population-based approach and data obtained under real-life setting, can provide more understanding of the potential association between dietary fructose and uric acid concentration under typical living conditions.

Glucose 6-phosphate, a fructose metabolite, is metabolized by three sequential reactions to produce NADPH for reducing oxidative stress with GSH production in the oxidative pathway. In turn, two forms of fructose carbon backbones, fructose 6-phosphate and glyceraldehyde-3-phosphate, are catalyzed by transketolase to enter the non-oxidative pathway. The activation of the transketolase drives nucleotide formation through ribose 5- phosphate while erythrose 4-phosphate are metabolized into amino acid. Liu et al. found that using pancreatic cancer cells, fructose and glucose exhibited the same effect on cell proliferation, but their intracellular metabolism was different . The productions of lactate, CO2, and fatty acid were significantly higher in cells with glucose compared to those with fructose. However, fructose was more potent to activate the non-oxidative pentose phosphate pathway in association with intracellular transketolase activation, and accelerate ribose synthesis and uric acid production .