High Fructose Corn Syrup Increases Liver Disease and Makes Us Fat

Tags: High Fructose Corn Syrup Causes Obesity Kills Our Liver May Lead to Dementia

Medical doctors are now accepting the fact that obesity in the world is caused mainly from High Fructose Corn Syrup in soft drinks and almost all prepared foods. It makes up about 16 percent of our diet. Fructose metabolism in the liver results in metabolic products of about 30 percent very low density lipoproteins which leads to increased heart disease and likely dementia. Early onset of Alzheimer's Disease results from a gene defect that cannot metabolize this very low density lipoprotein which some scientists already that early and late onset Alzheimer's Disease depend on how much of this is in our diet.

I stopped eating large sweet apples and drinking lots of orange juice and started drinking 2 glasses a day of 1% organic skim milk from Costco. Fructose made me hungry all the time. Now I never need to eat before I go to sleep or during the day between meals. I am just not hungry!

When I went on a complete fructose ban for two weeks to reduce fructose metabolism enzymes in all my cells, my weight was 155 lbs. By greatly reducing fructose consumption after my fast, I now weigh 143 lbs.

I reduced my known fructose consumption to one orange and blueberries every other day. Also I stopped eating sardines fairly frequently to reduce purines in my blood which convert to uric acid which causes inflammation of my arteries which increases plaque formation. I went from 5.8 (too high according to Dr Johnson, Nephrologist, MD, who has a great and easy to read book The Sugar Fix: The high-Fructose Fallout That Is Making You Fat and Sick,) to less than 5.4 mg/dl.

As my cells accumulated fructose enzymes, it started destroying my ATP, the energy element of cells, to produce purines which convert to uric acid.

I will say again that regular cane or beet sugar does help suppress appetite and fructose does not. Even though many smart reporters and doctors say they are equivalent chemically, they are really not because our body handles them differently. Both the free glucose and fructose go immediately to our liver. The glucose is immediately converted to glycogen. That is why the old Gatorade was very popular with athletes who needed energy fast. The new Gatorade uses regular sugar now because half of Americans now believe fructose is not good for them. Regular sugar prices will go up because there is a shortage now because we refuse to stop the tariffs on it.

Dr. Oz www.doctoroz.com has finally said that obesity is primarily the result of excess High Fructose Corn Syrup or about 16% of American diets. The only explanation why after Reagan made corn extremely cheap in 1985 and the increase in obesity correlated with the doubling of obesity in the 1990s.

Jim Kawakami, Nov 2, 2010, http://jimboguy.blogspot.com

Question

William F. Balistreri, MD Oct 27, 2010 http://www.medscape.com/viewarticle/730873?src=mp&spon=17&uac=26057PR

I read that high-fructose corn syrup can induce or exacerbate fatty liver disease. What is the evidence?

Response from William F. Balistreri, MD Dorothy M. M. Kersten Professor of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio; Medical Director, Liver Transplantation Program, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio

Although the pathogenesis of nonalcoholic fatty liver disease (NAFLD) is complex, increasing evidence suggests that fructose is a contributing factor. In the search for dietary triggers for NAFLD, fructose has been consistently identified as a candidate; this makes sense, given the metabolic events attendant to fructose ingestion. The digestion, absorption, and metabolism of fructose differ from those of glucose.[1] Unlike glucose, fructose does not stimulate insulin secretion, enhance leptin production, or suppress hunger. Insulin and leptin are key afferent signals in the regulation of food intake and body weight; thus, dietary fructose may contribute to increased energy intake and weight gain. Hepatic metabolism of fructose has been shown to elicit potentially deleterious metabolic perturbations -- risk factors for NAFLD. Consumption of fructose-sweetened but not glucose-sweetened beverages increases fat mass, visceral adiposity, de novo lipogenesis, and inflammation, and it induces insulin resistance and postprandial hypertriglyceridemia, particularly in overweight individuals.[2-8]

The dietary goals to prevent the development of NAFLD or to forestall transition to nonalcoholic steatohepatitis (NASH) are to reduce adipose tissue mass and the associated inflammation, restore insulin sensitivity, and reduce de novo lipogenesis.[9,10] However, scientific evidence supporting specific diets or dietary restrictions is lacking. That said, a spate of recent investigations has identified overconsumption of high-fructose corn syrup, primarily in the form of soft drinks, as a modifiable risk factor/environmental exposure that increases the risk for NAFLD and the likelihood of progressing to NASH.[1,11]

Studies in Humans

The intake of simple carbohydrates is higher in patients with NAFLD compared with the general population, suggesting that this dietary imbalance plays a role in the development and progression of NAFLD.[6,11,12] A dietary history and paired serum and liver tissue samples were obtained from patients with biopsy-proven NAFLD without cirrhosis and control patients matched for sex, age, and body mass index.[6] Consumption of fructose among patients with NAFLD was 3-fold higher than in controls. Abdelmalek and colleagues investigated the relationship between fructose consumption and disease severity in adults with NAFLD enrolled in the NASH Clinical Research Network.[12] Increased fructose consumption was associated with younger age, male sex, hypertriglyceridemia, low high-density lipoprotein cholesterol levels, increased calorie intake, and hyperuricemia. Daily fructose consumption was associated with increased hepatic inflammation and hepatocyte ballooning. Patients who drank the most fructose were more likely to have hepatic scarring and to progress to cirrhosis. These studies identify fructose as a readily modifiable environmental risk factor that can ameliorate disease progression in patients with NAFLD.

Studies in Animals

In animal models, ingestion of fructose (in contrast to glucose) causes fatty liver, along with development of leptin resistance and vascular inflammation.[13,14] A high-fructose diet induces changes similar to those seen in models of long-term alcohol intake and high-fat diets, including increased gut permeability, endotoxemia, increased hepatic tissue necrosis factor production, and hepatic steatosis.[15] We hypothesized that mice exposed to a high-fructose diet would develop NASH with fibrosis associated with increased hepatic oxidative stress.[16] Adult mice were randomly assigned to receive standard chow or high-fat, high-carbohydrate (HFHC) diets for 16 weeks; the HFHC group received water with 55% fructose and 45% sucrose. The HFHC group developed increased body weight and fat mass, became insulin-resistant, had elevated hepatic triglyceride and plasma alanine aminotransferase levels, and had a NASH-like phenotype with significant fibrosis. Hepatic oxidative stress was highest in HFHC-fed mice.

The mechanism of fibrosis might involve fructose inducing increased reactive oxygen species resulting in collagen deposition and histologically visible hepatic fibrosis. Spruss and colleagues have postulated another possible mechanism for fructose-induced hepatic steatosis in mice: the interaction between Toll-like receptor 4 and gut-derived endotoxins, such as lipopolysaccharide.[17]

Fructose: A Marker or a Mediator?

Whether increased fructose consumption merely correlates with factors responsible for the development of NAFLD or directly promotes the transition from NAFLD to NASH and more advanced stages of liver damage remains unclear. Further research is needed, including well-designed prospective controlled dietary intervention studies to evaluate whether a low-fructose diet improves the metabolic disturbances associated with NAFLD and alters the natural history of NAFLD in those at risk for disease progression. These studies should also determine whether a threshold amount of fructose triggers the postulated adverse effects or if genetic susceptibility is responsible for these outcomes. In the interim, it seems prudent to reduce intake of fructose.

Subtract Added Sugars

Although long-term trials to study the effects of reducing the intake of fructose are needed, current data support dietary guidelines that target a reduction in consumption of all added sugar (caloric sweeteners used as ingredients in processed or prepared foods). Welch and colleagues tested the association between consumption of added sugars and adverse outcomes.[18] A statistically significant correlation exists between excessive consumption of added sugars and several important measures of dyslipidemia, an important risk factor for NAFLD and cardiovascular disease. This, in turn, has been linked with several metabolic abnormalities and adverse health conditions, as well as shortfalls of essential nutrients. Although trial data are limited, evidence from observational studies indicates that a higher intake of added-sugar soft drinks is associated with greater energy intake, higher body weight, and lower intake of essential nutrients. On the basis of the 2005 US dietary guidelines, intake of added sugars greatly exceeds discretionary calorie allowances, regardless of energy needs; a mean of 16% of consumed calories was from added sugars. In view of these data, the American Heart Association has recommended reductions in the intake of added sugars.[19] A prudent upper limit of intake is half of the discretionary calorie allowance, which for most women is no more than 100 calories per day and for most men is no more than 150 calories per day from added sugars.

Bottom Line

We should consume less of all added sugars -- including fructose -- which are an increasing and potentially modifiable component of our diets. However, the makers of high-fructose corn syrup applied last month to the US Food and Drug Administration to change the name to "corn sugar" for use on food labels. "A rose by any other name will taste as sweet" -- thus, consumption will probably continue.

References