Sugar, Uric Acid, And The Etiology Of Diabetes And Obesity

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High fructose corn syrup -- a mixture of glucose and fructose -- is used as a sweetener in consumer food products such as bread, cereal, and soda. Prior research reports that fructose consumption in the U.S. has more than doubled in the past 30 years. In fact, studies have shown that Americans' fructose intake climbed from 15 grams per day in the early 1900s to 55 grams per day in 1994, which experts believe stems from an increase in soft drink consumption. It is a scientific fact that the administration of clinically relevant doses of fructose acutely raises blood pressure in humans , and similar increases in blood pressure have been observed following ingestion of 24 ounces of HFCS or sucrose-containing beverages .

I know that one tophi came from drinking a few dark lagers, and I am not much of a drinker, and another tophi, almost within a week, of eating a nutritional yeast supplement. Now I am having trouble walking, can’t wear any shoes except flipflops. I use black cherry juice every day and I thought I had the gout under control because some of the tophi were shrinking. I have started eating according to the Perfect Health Diet by the Jaminets which makes more sense that any diet I have read which means limiting protein. I do not eat out, I do not buy any food containing more than 3 ingredients, cook from scratch. I started having tophi after eating according to the blood type 0 diet, then WestonAPrice guidelines with organ meats and nutritional yeast.

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Nevertheless, lowering uric acid has also been found to block the development of hepatic steatosis in fructose-fed rats . These studies supported the tight association of hyperuricemia with fatty liver; prospective studies have also reported that an elevated uric acid independently predicts the development of NAFLD . Hyperuricemia is even associated with NAFLD in hemodialysis subjects who have a BMI below 20 . The metabolism of fructose to fructose-1-phosphate by KHK occurs primarily in the liver, is rapid and without any negative feedback, and results in a fall in intracellular phosphate and ATP levels (14–16). This has been shown to occur in the liver in humans with relatively small doses of oral fructose .

Adiposity is one of the strongest risk factors for hyperuricemia and gout (2, 12, 38, 61–64). Adiposity likely increases uric acid levels both by decreasing renal excretion of urate and in part by increasing urate production . Prospective cohort studies have found a strong relation between higher adiposity and both hyperuricemia and an increased risk of incident gout (2, 12, 22, 61–64). A recent study also documented that weight reduction leads to a considerable reduction of serum urate . Similarly, in the Swedish Bariatric Surgery Outcome study, gastric surgery-induced weight reduction was associated with a substantially lower odds of hyperuricemia . Finally, the HPFS Study reported that men who had lost weight had a significantly lower risk of incident gout .

Fructose And Hypertension

The fructose-mediated increase in ROS via activation of the adipocyte renin-Ang II system may lead to adipocyte dysfunction and insulin resistance. Adipose tissue is a key endocrine organ, the function of which, via interaction with the vascular endothelium system, regulates lipid uptake, storage, synthesis, and secretion of paracrine and autocrine factors that regulate insulin sensitivity. However, fructose-mediated vascular dysfunction may have a negative effect on adipocyte function and the secretion of anti-inflammatory molecules such as adiponectin, IL-1, and IL-10. 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 . We also conducted stratified analyses to evaluate whether the association between sweetened soda and fructose consumption and risk of gout varied according to body mass index, alcohol use, and dairy intake. Relative risks from these stratified analyses consistently suggested associations similar to those from main analyses, and there was no significant interaction with these variables (all P ≥.14 for interaction) .

KHK-C is primarily expressed in the liver, kidney, pancreas, and duodenum, while KHK-A is expressed more widely including adipose tissue, heart, and the adrenal gland . KHK-A has a higher Km for fructose (7 mmol/L) than does KHK-C (0.8 mmol/L) suggesting that it phosphorylates fructose poorly at physiological concentrations . 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 .

While some genetic polymorphisms in various enzymes involved in fructose metabolism and urate transport have been linked with metabolic syndrome and hypertension (98–100), several genome-wide association studies could not show such associations . An elevated serum uric acid is also one of the best independent predictors of diabetes and commonly precedes the development of both insulin resistance and diabetes . An elevated uric acid also independently predicts the development of fatty liver , obesity , hypertension (rev. in 71), and elevations in C-reactive protein . Furthermore, metabolic syndrome is associated with a high frequency of hyperuricemia, and similarly, hyperuricemia is associated with metabolic syndrome .

Overall, there is a lot of research about the impact of excess fructose on our biology, and the impact is not good. The Kitavans eat a lot of it without any ill effect but they do so seasonally, not all year around and certainly not any refined fructose, both practices which are characteristics of the standard American/Western diet . Their overall fat intake is less than what we consume in the west but their saturated fat intake (which makes up 80% of their fat consumption) is about 10% higher than what we consume in the west.

Even though most vegetables are low in purines, a few have a significant amount. But in the NEJM study linked above and in this one , purine-rich vegetables weren’t associated with gout at all. Gout is more common in men than in women, but rates in both sexes have been steadily increasing for the last couple of decades. 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.

What fruits can reduce uric acid?

If you have been diagnosed with high uric acid, increase the consumption of dietary soluble fibres such as oats, apples, oranges, broccoli, pears, strawberries, blueberries, cucumbers, celery, carrots and barley. Have bananas as including them in your diet is beneficial in lowering excess uric acid levels.

Clinical studies have documented the metabolic effects of fructose. Studies from the 1960s through the 1980s showed that sucrose, or fructose, can worsen hypertriglyceridemia and insulin resistance, especially if subjects were hyperinsulinemic . More recently Stanhope et al. fed 25% of diet as fructose or glucose to overweight individuals for 10 weeks.