What Is Fructose & Is Fructose Bad For You?

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• Uric Acid
• The Role Of Fructose And Uric Acid In The Development Of Obesity And Metabolic Syndrome
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• Fructose And Hypertension
• Uric Acid Metabolism

This approach allows clinicians to make simple recommendations, such as to restrict intake to food scores 1 and 2, as well as, presenting patients a simple regime. Additionally, the score system may give hope to the patient that with improvements, a wider range of foods will become available. Furthermore, it allows patients to choose which foods to consume and gives a reason for avoiding some foods. Importantly, the amount of a food is also significant as 200 g of a food contains twice as much fructose/purines as 100 g. Uric acid is a weak acid, with a pKa of 5.75, and almost all (98%) of the uric acid circulates in the serum as monosodium urate. Monosodium urate has a low solubility limit (6 mg/dl) and at higher concentrations (7 mg/dl) urate crystals precipitate in the synovial fluid .

Uric Acid

In starchy foods, glucose is found primarily in polymer forms, such as amylose and amylopectin. These two starches provide over half of the food energy in the USA . Digestive enzymes from saliva and the pancreas cleave glucose-glucose bonds.

The Role Of Fructose And Uric Acid In The Development Of Obesity And Metabolic Syndrome

Uric acid is the by-product of purine metabolism made by the enzyme xanthine oxidase and is excreted in the kidneys. Diets high in purine, HFCS, and sucrose can all cause an elevation in uric acid levels within the body (Johnson et al., 2013). Fructose is a major component of the American diet, and is primarily in table sugar and in high fructose corn syrup. Intake of these sugars is associated with increased risk for high blood pressure, and for obesity, diabetes and fatty liver. And those sugars also are associated with higher uric acid levels and the problems that causes.

What is the fastest way to lower uric acid?

The following foods are low in purine.Eggs, nuts, and peanut butter.
Low-fat and fat free cheese and ice cream.
Skim or 1% milk.
Soup made without meat extract or broth.
Vegetables that are not on the medium-purine list below.
All fruit and fruit juices.
Bread, pasta, rice, cake, cornbread, and popcorn.

Inefficient renal excretion of UA is the main cause of both primary and secondary hyperuricemia . Renal UA reabsorption is mediated by urate transporter 1 and glucose transporter 9 . 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 .

There’s literally nobody in free living societies that have a cholesterol level that high. Does that implicitly mean that it is negative for your cardiovascular disease potential, maybe not, but it’s fucking high like that. It’s funny when I wrote The Paleo Solution, I didn’t even include like a cardiovascular disease chapter because I was of the opinion, if you eat paleo you can’t get cardiovascular disease. I think that as time goes on and one of the hottest topics in The Healthy Rebellion is cardiovascular disease. Not to say that everybody does well with fruit, but just metabolically, they’re not the same thing.

But gout is still very much with us, and the number of Americans affected seems to be increasing, at least partly because of the obesity epidemic. Gout remains a disease that mainly affects middle-aged and older men, although postmenopausal women are vulnerable too, perhaps because they lack the protective effect of estrogen. The diuretics ("water pills") that many people take to control high blood pressure are another contributing factor. There are several reasons for this but medications, such as cyclosporine, taken to reduce the chances of organ rejection and reduced kidney function are major contributors.

Blame Sweet Soda For Gout?

I’ve never been a heavy drinker, always drink plenty of water, don’t drink a lot of soft drinks and generally skip desserts. My doctor pegged genetics and severe sleep deprivation (with a toddler who hasn’t slept well his entire young life) as being two other causes. It seems that besides possible genetic predispositions, the main culprit is once again resistance to insulin.

The list of foods for people who have kidney disease to avoid is also similar to the list for gout and fructose is not on that list but probably should be. But once gout became easily treatable, in the early 1960s, with the discovery of the drug allopuranol, clinical investigators and researchers began to lose interest. The researchers add that their findings have practical implications for the prevention of gout in women, and that physicians should be aware of the potential effect of these beverages on the risk of gout. "Our data provide prospective evidence that fructose poses an increased risk of gout among women, thus supporting the importance of reducing fructose intake." Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood.

Although the RRs of gout associated with fructose-rich beverages among women were substantial, the corresponding absolute risk differences were modest given the low incidence rate of gout among women. Although the RR data suggest a substantial biologic link, the risk difference data suggest that their contribution to the risk of gout in the population is likely modest given the low incidence rate among women. Because the urate-increasing effect of fructose is greatest in patients with gout and hyperuricemia,8-10,28 our findings may be even more relevant in those patients. The mechanisms by which consuming fructose-sweetened beverages may lead to elevated hyperuricemia is not clear. Researchers suspect that fructose can produce uric acid by increasing the degradation of adenosine triphosphate hydrolysis, which is involved in the production of uric acid. And, consuming high doses of fructose, can induce insulin resistance, impair glucose tolerance and hyperuricemia.

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). Before we analyze these studies, it is important to understand the complexity related to their interpretation. First, many clinical studies use fructose alone—and often at relatively high doses—in order to evaluate the effects of fructose per se. This allows one to directly address the effects of fructose, and the use of high doses is a common experimental approach to allow one to identify metabolic effects that could otherwise take much longer periods to show.

Men are also more likely to develop gout earlier — usually between the ages of 30 and 50 — whereas women generally develop signs and symptoms after menopause. Traditionally, gout prevention strategies have focused on limiting protein-rich foods and alcohol, which can encourage uric acid accumulation in the body. This new research, however, suggests that cutting back on soda consumption may be just as important in preventing future gout attacks. Choi and his colleagues did find a slight increase in gout risk with consuming high-fructose fruits, such as apples and oranges. However, Choi emphasizes, artificially added fructose found in soda is linked to a higher risk of gout than naturally occurring sources of fructose like fruit.

However, while uric acid is an antioxidant in the extracellular environment, it has prooxidative effects inside the cell . For example, high-dose allopurinol improves endothelial dysfunction in subjects with heart failure whereas the lowering of uric acid with probenecid was ineffective . However, this could simply relate to the relative superiority of allopurinol to lower intracellular uric acid as it blocks synthesis.

Despite the similarity in their chemical structures, fructose and glucose are metabolized in completely different ways and utilize different GLUT transporters . In the liver, fructose bypasses the two highly regulated steps of glycolysis, catalyzed by glucokinase/hexokinase and phosphofructokinase both of which are inhibited by increasing concentrations of their byproducts. Instead, fructose enters the pathway at a level that is not regulated and is metabolized to fructose-1-phosphate primarily by fructokinase or ketohexokinase . Fructose may also be metabolized by hexokinase; however, the Km for fructose is much higher than glucose, and hence minimal amounts of fructose are metabolized via this pathway . Fructokinase has no negative feedback system, and ATP is used for the phosphorylation process. As a result, continued fructose metabolism results in intracellular phosphate depletion, activation of AMP deaminase, and uric acid generation which is harmful at the cellular level .