Researchers have a new theory on why some kids get unexplained tummy aches.
In some people, the small intestine is unable to efficiently break down fructose (and sometimes other forms of sugar). This problem is sometimes referred to as fructose intolerance. The undigested fructose passes into the large intestine, where it is broken down by bacteria. A by-product of this process is the creation of carbon dioxide and hydrogen. These two gases build up in the intestine, causing bloating, gas, pain and diarrhea. In some cases, the problem can affect absorption of important nutrients, like calcium and iron.
Researchers estimate about 33 percent of Americans have some level of sensitivity to sugar, most commonly to fructose, but the symptoms are often vague. Some people with fructose intolerance can eat small amounts of the sugar and not have any problems, making diagnosis even trickier.
Daniel Lustig, M.D., Pediatric Gastroenterologist at Mary Bridge Children’s Health Center in Tacoma, WA, says patients with chronic digestive problems should have a physician’s evaluation to rule out other possible causes of the symptoms, like Celiac disease or Crohn’s disease. Once those conditions have been ruled out, he recommends a diagnostic tool called the breath hydrogen test.
A patient is given a dose of fructose. Then, periodically, he/she breathes into an air collection bag. The gases from the bag are retrieved and analyzed for the presence of hydrogen (one of the gases given off when fructose is broken down in the large intestine). Patients whose hydrogen levels exceed 20 points beyond a baseline reading are likely to be fructose intolerant.
Lustig explains the main treatment of fructose intolerance is avoidance of foods containing fructose. That includes fruits, fruit juices, sodas and processed foods and drinks with high fructose corn syrup. Since fructose is in so many foods, it can be tricky to find and hard to avoid.
Lustig recently performed a study to look at possible fructose intolerance in 245 children and adolescents (ages 2 to 18) with unexplained chronic abdominal pain, gas or bloating. The breath hydrogen test found that nearly 54 percent of the participants tested positive for fructose intolerance. Lustig says the problem appeared to be especially high among teen girls.
Those who were judged to be fructose intolerant were given advice on using a low-fructose diet. The investigators found that nearly 68 percent of those who followed the recommended diet had an improvement or resolution in their symptoms.
A new study finds that drinking orange juice, soda and other beverages high in the sugar fructose could increase the small risk that middle-age and elderly women have of developing gout. Gout is a painful form of arthritis caused by too much uric acid in the blood. For women in the study who drank two or more servings of these beverages per day, the risk of gout was more than double that for women who drank sugary sodas and juices less than once per month. Because gout is relatively rare among women, the drinks probably contribute only moderately to a woman's chances of developing it. Still, this is the first study linking sodas and sweetened fruit juices to women's gout risk. Previous research found such a link for men.
The study will be published in the Nov. 24 issue of the Journal of the American Medical Association, and is being presented today (Nov. 10) at the American College of Rheumatology annual scientific meeting.
Gout occurs when levels of uric acid in the blood become too high, and uric acid crystallizes around the joints, leading to inflammation, swelling and pain. Foods than can increase the levels of uric acid in the blood include organ meats (such as kidneys and livers), asparagus and mushrooms, according to the Mayo Clinic. Fructose is also known to increase blood uric acid levels, the researchers said. While gout is not common in the United States, the rate of incidences has more than doubled over a 20-year period, from 16 cases per 100,000 Americans in 1977 to 42 per 100,000 in 1996. Over this period, the researchers noted, the population also consumed increasing amounts of soda and other drinks sweetened with fructose.
The new study followed 78,906 women for 22 years, from 1984 to 2006, as part of the Nurses' Health Study. At the beginning of the study, none of the women had gout. By the end, 778 had developed it. Women who drank one serving of soda per day were 1.74 times more likely to develop gout than those who drank less than one serving per month. Those who drank two or more servings per day were 2.4 times more likely to develop gout. Drinking two or more servings of soda per day caused an additional 68 cases of gout per 100,000 women per year, compared with drinking less than one serving of soda per month, the researchers said. Drinking orange juice also increased the risk. Women who drank one serving of orange juice per day were 1.41 times more likely to develop gout, and those who drank two or more servings were 2.4 times more likely to report gout.
Lifestyle and diet
The rise in gout cases is most likely due to changes in lifestyle and diet and an increase in conditions associated with gout, such as metabolic syndrome, said study researcher Dr. Hyon K. Choi of the Boston University School of Medicine. The results held even after the researchers took into account factors that could have influenced the findings, such as age, body mass index and whether the women had gone through menopause, Choi said.
The findings suggest diets to prevent gout should reduce fructose intake, the researchers said.
The study was funded by the National Institutes of Health.
Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.
They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types. “These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA's Jonsson Cancer Center and colleagues wrote. “They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”
Americans take in large amounts of fructose, mainly in high fructose corn syrup, a mix of fructose and glucose that is used in soft drinks, bread and a range of other foods. Politicians, regulators, health experts and the industry have debated whether high fructose corn syrup and other ingredients have been helping make Americans fatter and less healthy.
Too much sugar of any kind not only adds pounds, but is also a key culprit in diabetes, heart disease and stroke, according to the American Heart Association. Several states, including New York and California, have weighed a tax on sweetened soft drinks to defray the cost of treating obesity-related diseases such as heart disease, diabetes and cancer. The American Beverage Association, whose members include Coca-Cola (KO.N) and Kraft Foods (KFT.N) have strongly, and successfully, opposed efforts to tax soda. The industry has also argued that sugar is sugar.
Heaney said his team found otherwise. They grew pancreatic cancer cells in lab dishes and fed them both glucose and fructose. Tumor cells thrive on sugar but they used the fructose to proliferate. “Importantly, fructose and glucose metabolism are quite different,” Heaney's team wrote. “I think this paper has a lot of public health implications. Hopefully, at the federal level there will be some effort to step back on the amount of high fructose corn syrup in our diets,” Heaney said in a statement.
Now the team hopes to develop a drug that might stop tumor cells from making use of fructose.
U.S. consumption of high fructose corn syrup went up 1,000 percent between 1970 and 1990, researchers reported in 2004 in the American Journal of Clinical Nutrition.
The researchers analyzed data from the National Health and Nutrition Examination Survey (2003-2006) which consisted of 4,528 US adults 18 years of age or older that had no previous hypertension diagnosis. The survey asked about dietary habits and what foods and beverages that they consumed. The researchers said that those who ate 74 grams (about 2.5 cans of sugared soda) or more each day of fructose sugar, had shown an increased risk for developing hypertension. There was a 26 percent chance for these individuals to have high blood pressure reading at 135/85mmHg , a 30 percent higher risk to have high blood pressure measured at 140/90, and a 77 percent higher risk for having blood pressure measured at 160/100 mmHg. A normal blood pressure reading is under 120/80 mmHg.
The researchers point out that even though this shows a potential trigger for high blood pressure, a randomized clinical study would need to be conducted in order to prove that a low fructose diet would prevent hypertension.
The study was conducted in mice, some of which were fed a normal diet of rodent chow and some a 16-week diet of fructose and sucrose-enriched drinking water and trans-fat solids. Their liver tissue was then analyzed for fat content, scar tissue formation (fibrosis), and the biological mechanism of damage. This was done by measuring reactive oxygen stress, inflammatory cell type and plasma levels of oxidative stress markers, which are known to play important roles in the development of obesity-related liver disease and its progression to end-stage liver disease.
The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans-fat alone or a combination of trans-fat and high fructose) became obese and had fatty liver disease.
“Interestingly, it was only the group fed the combination of trans-fat and high fructose which developed the advanced fatty liver disease which had fibrosis,” says Dr. Kohli. “This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.”
Dr. Kohli hopes to further investigate the mechanism of liver injury caused by high fructose and sucrose enriched drinking water and study a therapeutic intervention of antioxidant supplementation. Antioxidants are natural defenses against oxidative stress and may reverse or protect against advanced liver damage, according to Dr. Kohli.
The investigators also would like to use this model to better understand human fatty liver disease and perform clinical trials using novel therapeutic and monitoring tools.
“Our data suggest that supplementation with pharmaceuticals agents should be tested on our new model to establish whether one is able to reverse or protect against progressive liver scarring and damage,” says Dr. Kohli.
The study was supported by grants from the National Institutes of Health and the Children's Digestive Health and Nutrition Foundation.
NAFLD is the most common cause of liver disease worldwide and research suggests the number of cases will climb given an increasing trend toward higher fat diets, obesity, decreased physical activity, and a rise in diabetes. Past studies indicate that more than 30 million Americans have NAFLD and approximately 8 million may have nonalcoholic steatohepatitis (NASH).
In the first study, Ramón Bataller, M.D., and colleagues from the Hospital Clínic in Barcelona, Spain investigated the effects of cigarette smoking (CS) in obese rats. Rats were divided into 4 groups (n=12 per group): obese smokers, obese non-smokers, control smokers and control non-smokers. Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. Researchers found that obese rats exposed to CS showed a significant increase in ALT serum levels (indicating liver disease), while this effect was not observed in control rats.
“Our results show that CS causes oxidative stress and worsens the severity of NAFLD in obese rats,” said Dr. Bataller. “Further studies should investigate longer exposures to CS, and assess whether this finding also occurs in patients with obesity and NAFLD.”
In her editorial, also published in Hepatology this month, Claudia Zein, M.D., from the Cleveland Clinic, noted that “the importance of these results is that taken together with other experimental and clinical data, they support that cigarette smoking appears to aggravate liver injury in patients with liver disease.” Dr. Zein added, “Studies characterizing the effects of cigarette smoking in human NAFLD will be crucial because of the vast number of patients that may benefit from modification of this risk factor.”
Additionally, prior studies suggest an over consumption of high fructose corn syrup (HFCS), primarily in the form of soft-drinks, have contributed to weight gain and the rise in obesity, particularly in children and adolescents. Table sugar (sucrose) and HFCS are the two major dietary sources of fructose. Over the past 40 years, consumption of dietary fructose has increased 1,000% according to Bray et al, and doctors believe it to be a major cause of NAFLD.
Researchers from Duke University studied 341 adults enrolled in the NASH Clinical Research Network who responded to a Block food questionnaire within 3 months of a liver biopsy. Fructose consumption was estimated conservatively by including that found in beverages, which accounts for 50% of dietary fructose intake. Results showed that 27.9% of participants consumed at least 1 fructose-containing beverage per day, 52.5% had 1 to 6 beverages with fructose per week, and 19.7% drank no beverages with fructose.
“In patients with NAFLD, daily fructose ingestion was associated with reduced fatty liver (steatosis), but we found increased fibrosis,” noted Manal Abdelmalek, M.D., M.P.H, and lead author of the study. “Further dietary intervention studies are needed to evaluate whether a low-fructose diet improves metabolic disturbances associated with NAFLD and improves patient outcomes for those at risk of disease progression,” concluded Dr. Abdelmalek.
A second fructose study led by Ling-Dong Kong, M.D., from Nanjing University in China investigated the effects of curcumin on fructose-induced hypertriglyceridemia and fatty liver in rats. Curcumin, a compound derived from turmeric (curcuma root), is sold as an herbal supplement and is believed to have anti-inflammatory, anti-tumor, and anti-viral properties. Researchers observed a hyperactivity of hepatic protein tyrosine phosphatase 1B (PTP1B), which is associated with defective insulin and leptin signaling, in fructose-fed rats.
For the first time this study demonstrated that curcumin inhibited hepatic PTP1B expression and activity in fructose-fed rats. “Our results provide novel insights into the potential therapeutic mechanisms of curcumin on fructose-induced hepatic steatosis associated with insulin and leptin resistance,” said Dr. Kong.
These studies indicate modifying risks such as smoking and fructose consumption offer potential benefits for those with liver diseases. Further studies are needed to explore these benefits in preventing the progression of liver disease.