Posted on 07/15/2013 12:21:38 PM PDT by neverdem
A Wake Forest Baptist Medical Center study on dietary fructose has provided more evidence of the potential for controversy when researchers target products affecting consumer spending and corporate profits. This time, researchers are on the receiving end of sharp criticism from the Corn Refiners Association after reporting that fructose rapidly caused liver damage even without weight gain with primates.
The researchers acknowledged when they released the study results that the role of dietary fructose in the development of obesity and fatty liver diseases “remains controversial.”
Researchers determined that over a six-week study period, liver damage more than doubled in the monkeys fed a high-fructose diet as compared to those in a control group. The study was published online by the American Journal of Clinical Nutrition and was funded through three National Institutes of Health grants.
“Is a calorie a calorie? Are they all created equal? Based on this study, we would say not,” said Kylie Kavanagh, an assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.
There are non-Wake Forest Baptist studies, including at Duke University, that have shown increased dietary fructose can alter the body’s metabolism and energy balance.
However, other studies say eating fructose in whole fruit “is not associated with adverse effects up to the limits of human consumption.”
Dr. David Ludwig, a pediatrician and endocrinologist at Children’s Hospital in Boston, said at the conclusion of a 2013 study that any “recommendation to replace fructose with glucose lacks an evidence basis.”
“Few modern studies have compared the long-term effects of glucose, fructose and starch under physiologically relevant condition, and such research should assume high priority,” Ludwig said.
The Corn Refiners Association said Wake Forest Baptist researchers “have failed to prove anything about human consumption of high fructose corn syrup. The study fails to reproduce anything close to resembling real world conditions for consuming fructose.”
Ruth Kava, a researcher for the American Council on Science and Health, concluded her January study by saying “scientific evidence does not support the notion that high-fructose corn syrup is uniquely responsible for the American obesity epidemic.”
“Experimental evidence, as well as analyses of epidemiologic data, indicate that sucrose and high-fructose corn syrup have equivalent effects on food intake, and therefore on body weight.”
Chad Campbell, a spokesman for Wake Forest Baptist, said the center “stands behind our researchers and the science published in a peer-review journal regarding fructose in an animal model.”
Monkeys and weight gain
The latest Wake Forest Baptist study followed up on research conducted by Kavanagh’s group that allowed monkeys to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period.
The researchers found the monkeys that were allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They developed diabetes at three times the rate of the control group and also developed non-alcoholic fatty liver disease.
The goal of the latest study was determining whether weight gain caused the liver damage. Researchers studied 10 middle-aged, normal weight monkeys who had never eaten fructose.
The monkeys were divided into two groups based on comparable body shapes and waist circumference. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with 0.5 percent fructose.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group’s diet was made from flour, butter, pork fat, eggs and fructose -- the main ingredient in corn syrup – similar to what many people eat.
By comparison, the control group’s diet was made from healthy complex carbohydrates and soy protein.
Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain.
At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.
“What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor,” Kavanagh said. “Six weeks in monkeys is roughly equivalent to three months in humans.”
Researchers found that the type of intestinal bacteria hadn’t changed in the high fructose group, but they were migrating to the liver more rapidly and causing damage there.
The Corn Refiners Association called the study flawed in part because the primate subjects were fed pure fructose amounting to close to a quarter of the total calories consumed.
“This is over three times the average amount of fructose consumed from all sources in the human diet and twice the 95th percentile level in humans,’ the lobbying group said.
“Additionally, primates have different body functions than humans. This is why the 2010 Dietary Guidelines Committee only considered studies conducted with humans to be viable for developing policy.”
The lobbying group said the problems of obesity and obesity-related diseases, such as nonalcoholic fatty liver disease, “are a serious health issue that continues to plague our nation.”
“However, attempts to demonize one food or ingredient without appropriate scientific research only lead to confusion among consumers and inhibit the development of real solutions.”
Limits of research
One study limitations for the Wake Forest researchers was that it only tested for fructose, and not dextrose. Fructose and dextrose are simple sugars found naturally in plants.
“We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can’t say conclusively that fructose caused the liver damage,” Kavanagh said. “What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.
“The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems.”
The next step is studying monkeys using the same controls, but testing both fructose and dextrose over a longer time frame.
The Wake Forest Baptist study drew similar conclusions to a separate study released in September by Duke University researchers that found potential liver damage in obese patients with type 2 diabetes who consume higher amounts of fructose.
Energy depletion in the liver may be associated with liver injury in patients with non-alcoholic fatty liver disease and in those at risk for developing this metabolic condition.
“There is an alarming trend of increased rates of obesity, type 2 diabetes and non-alcoholic fatty liver disease in the U.S.,” said lead author Dr. Manal Abdelmalek of Duke. “Given the concurrent rise in fructose consumption and metabolic diseases, we need to fully understand the impact of a high-fructose diet on liver function and liver disease.”
A study released in May by Emory University researchers found nonalcoholic fatty liver disease is the most common chronic liver disease in adults and children.
A number of genetic and environmental factors are known to predispose individuals to the disease, while certain dietary sugars, particularly fructose, are suspected to contribute to its development and progression.
“The increasing quantity of fructose in the diet comes from sugar additives, most commonly sucrose and high fructose corn syrup, in beverages and processed foods,” according to the Emory researches.
“Substantial links have been demonstrated between increased fructose consumption and obesity, dyslipidemia, and insulin resistance. Growing evidence suggests that fructose contributes to the development and severity of the disease. In human studies, fructose is associated with increasing hepatic fat, inflammation, and possibly fibrosis.
“Whether fructose alone can cause the disease, or if it serves only as a contributor when consumed excessively in the setting of insulin resistance, positive energy balance, and sedentary lifestyle, is unknown. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added – fructose-containing – sugars.”
HFCS is Frankenfood. The junk is pure poison. We spend millions in sugar tariffs and subsides for the HFCS lobby. Better living doesn’t always come from chemistry.
Try to find food without it. Good luck it is everywhere.
Like ethanol, another stupid unnatural use of corn. The truth will keep coming out on this crap and none of it will be good.
Cell phones, high power lines, over cooked meat, baked goods, wheat, coffee, chromium in the water, chromium on your bumper, plastic bottles, all cause cancer, fallen arches and inflation.
And I’m expected to worry about fructose?
LOL! Still easier to just admit...
I got an orange one with sugar and it wasn’t half bad. I also dug out the 100mm macro and played with it some in hopes in it maybe paying for itself if a clip ever sells.
This is one of a few.
http://footage.shutterstock.com/video.html?id=4199971
Won't happen till we get rid of the tariffs and import quotas on the stuff. That's the reason we're all being fed this high-fructose crap. Too bad Moochelle doesn't know enough about nutrition to criticize that.
You're right, but the protection-nazis on FR won't like that.
Good point on Moochelle. On the use of “real” sugar, maybe lost sales will have some bearing eventually, as more and more people avoid HFCS.
Good advice when applicable. Why don’t you try following it?
That's a good point. I would have done it with identical diets except the test group got fructose and the control group got an equal amount of glucose. Both are sugars with six carbon atoms.
Non-alcoholic fatty liver disease, aka hepatic steatosis, was unknown before the advent of using high fructose corn syrup in soft drinks.
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