The Negative And Detrimental Effects Of High Fructose On The Liver, Wi

Content

• Recent Blog Articles
• Fructose
• Gout: Forget The Purines; Skip The Sugar?
• A Role For Uric Acid In Fructose
• Health Solutions

Several in vitro and in vivo studies have shown that high fructose consumption increases blood UA levels . In addition, consuming fructose over several days and intravenous fructose administration are both associated with an increase in fasting serum UA levels. It is not yet clear whether circulating UA levels increase when fructose is taken in small doses over several days or when it is taken as a single large dose. It is also unclear whether a high-fructose diet alters the renal clearance of UA or the fractional excretion of UA . Moreover, a growing body of evidence suggests that high levels of serum UA are also biomarkers for cardiovascular disease morbidity and mortality . African Americans have been observed to have higher serum uric acid levels than Caucasian Americans .

And, it turns out, serious health risks are not limited to liquid sources of sugar; the sugars found in processed solid foods, including many that do not even taste sweet, can be hazards, too, if overconsumed. Usually, salt gets the blame for this condition, also called hypertension. But some researchers say another white crystal -- sugar -- may be a more worrisome culprit. One way they believe sugar raises blood pressure is by making your insulin levels spike too high.

Recent Blog Articles

If diet soda is your vice, you may not have to worry as much about developing gout. We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. However, if the load of uric acid becomes too great, then it builds up in the bloodstream before being deposited in a joint. Gout is more common in men, with a prevalence of 5 per cent in men over 65, and is associated with obesity and a high alcohol intake. A disease that finds it hard to shake off its 18th century image and association with the excesses of the ruling classes, gout was believed to be brought on by high living and gluttony. THE LAST time I wrote about gout I signed off with a statement that gout was no longer a disease of the affluent.

Fructose

Blood lipid distribution of hyperinsulinemic men consuming three levels of fructose. We thank Gary Taubes for his personal discussions and for his book, “Good Calories, Bad Calories,” which provided some excellent historical references on sugar and its relationship to diabetes. To better understand how fructose acts, we will first review certain unique characteristics of its metabolism. There have been some studies, including in 2011 and 2012, that suggest cherries might potentially help treat or even cure gout.

Insulin resistance contributes to hyperuricemia, and hyperuricemia induces insulin resistance. The most common source of fructose was sugar-sweetened beverages, which usually use HFCS as the sweetener. Men have a higher incidence of gout, which may lead to a falsely low effect size in many studies which include only women, despite a matched intake of fructose in both genders.

Extracellular UA can also enter endothelial cells and vascular smooth muscle cells through URAT1, GLUT9, and potentially other transporters activating the NF-κB axis, which leads to an increase in MCP-1, IL-8, VCAM-1, and ICAM-1 . As a result, it has been hypothesized that intracellular XO activity and increased ROS production might be factors in endothelial dysfunction, which leads to the development of essential hypertension . In this regard, ROS generation and vascular endothelial dysfunction can be reduced by drugs such as allopurinol and febuxostat, which inhibit XO activity and consequently reduce UA production . This is because vitamin C competes with UA for renal resorption in the proximal tubule , producing a uricosuric effect. UA causes endoplasmic reticulum stress; this, in turn, activates SREBP-1c, which stimulates fat accumulation in the liver . Indeed, Cheung et al. recently reported that XOR-knockout mice have a central defect in adipogenesis and fail to gain fat .

There is mounting evidence from studies looking at the association between fructose and obesity and metabolic syndrome that primary fructose malabsorption in children was negatively associated with obesity . In obese African-Americans, high rates of fructose malabsorption were associated with reduced liver fat thought to be protective against fatty liver disease . The SLC2A9 allele protects its possessors against gout by increasing the renal uric acid excretion. However, high levels of sugar intake lead to negation of its protective effects and the onset of hyperuricemia, with each serving of sugar-sweetened beverage increasing gout risk by 15% in allele-positive subjects. 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. This rise was even higher in people who already had hyperuricemia or gout.

Uric Acid, Fructose And Hypertension

Thus, there is a positive correlation between circulating UA and obesity, especially visceral obesity . Accordingly, although hyperuricemia is often considered to be a secondary phenomenon in metabolic syndrome, it is also an independent predictive factor for obesity and hyperinsulinemia . In themselves, UA accumulation and lack of vitamin C do not cause obesity.

Adiponectin is synthesized and released only by the adipocyte and has an essential role in vascular and renal function. To keep uric acid low, getting rid of fructose and beer is probably a better bet than going crazy over purine levels in meat. It is wise for people with a history of gout to replace sugary drinks with water or at least with diet drinks to reduce gout attack frequency, while those at risk of gout would also do well to avoid consuming such drinks more than once or twice a month. Non-drinkers have been shown to have lower uric acid levels than those who drink beer or spirits.

The research suggests that uric acid stimulates an enzyme called aldose reductase that’s involved in the conversion of glucose to fructose. Fructose is metabolized in the liver, but excess consumption can cause fat buildup, leading to insulin resistance in the liver and non-alcoholic fatty liver disease. Some of these medications are used as indicated, others are used off-label. In people receiving hemodialysis, sevelamer can significantly reduce serum uric acid, apparently by adsorbing urate in the gut.

Are eggs bad for gout?

Eggs are a good protein source for people with gout, because eggs are naturally low in purines.

The non-steroidal anti-inflammatory drugs diclofenac, naproxen, piroxicam, but not ibuprofen, may also be used for the pain during an acute attack . HFCS, a sweetener used extensively used in USA , is derived from corn starch . Corn starch, a chain of glucose molecules, is broken down to individual molecules to produce corn syrup . Enzymes, added to corn syrup, convert approximately half of the glucose molecules to fructose molecules. HFCS 42 contains 42% fructose while HFCS 55 contains 55% fructose, the remainder is water and glucose. HFCS 42 is used in the production of processed foods while HFCS 55 is used in the production SSBs.

A Role For Uric Acid In Fructose

They found the HFCS diet decreased levels of healthy bacteria, whereas eating the same amount of fructose through fruit led to more positive changes, likely because of the fiber content in fruits and vegetables. fructose metabolism reduces the proteins that maintain the gut barrier, a mucus-covered layer of cells that keeps toxins from leaking out of our intestines. This weakened gut barrier leads to the leaking of endotoxins, which causes inflammation, including in the liver. This triggers a process that contributes to the accumulation of fat in the liver that drives NAFLD.

Why does fructose increase uric acid?

As the body breaks down fructose, chemical compounds called purines are released. The breakdown of purines produces uric acid—the substance that forms painful crystals in the joints and causes gout. Within minutes after you drink high fructose corn syrup-sweetened soda, your uric acid levels rise.

Another study reported that lowering uric acid improves HbA1c levels in normotensive diabetic subjects . Clearly, more studies are indicated before any definitive conclusions can be made with regards to the benefit of lowering uric acid for the treatment of insulin resistance. A number of conditions associated with hyperuricemia are also associated with increased risk for insulin resistance or diabetes, including chronic lead intoxication and gestational diabetes mellitus. Many drugs associated with insulin resistance are also associated with hyperuricemia, such as calcineurin inhibitors and thiazide diuretics.

192) that reported that both caloric- and diet soft drinks predict obesity and metabolic syndrome may be deceiving unless total fructose intake is considered. Wang D.D., Sievenpiper J.L., de Souza R.J., Chiavaroli L., Ha V., Cozma A.I., Mirrahimi A., Yu M.E., Carleton A.J., Di Buono M., et al. The effects of fructose intake on serum uric acid vary among controlled dietary trials. In general, epidemiologists and other scientists have attempted to prove a causal link between dietary fructose intake and metabolic disorders, such as obesity, diabetes, and metabolic syndrome. Some folks are really in the camp that LDL cholesterol and LDL lipoproteins are the driver of cardiovascular disease, other people are more nuanced that they are a piece of the puzzle.

Health Solutions

(A–B) ChREBP protein expression in liver extracts from control, fructose-fed and fructose with allopurinol-fed rats. (C–D) ChREBP and KHK expression in nuclear and cytoplasmic extracts of liver extracts from control, fructose-fed and fructose with allopurinol-fed rats. A) KHK mRNA expression in cells exposed to fructose (5 mmol/L) for different time points.