Sugar substitutes may cut calories, but no health benefits for individuals with obesity: York U

Public Release: 24-May-2016

 

The study suggests that the bacteria in the gut may be able to break down artificial sweeteners, resulting in negative health effects

York University

TORONTO, May 24, 2016 — Artificial sweeteners help individuals with obesity to cut calories and lose weight but may have negative health effects, according to researchers at York University’s Faculty of Health.

“Our study shows that individuals with obesity who consume artificial sweeteners, particularly aspartame, may have worse glucose management than those who don’t take sugar substitutes,” says Professor Jennifer Kuk, obesity researcher in the School of Kinesiology and Health Science.

Normally, weight loss is associated with several improvements in health. Artificial sweeteners are often used to help individuals cut calories and manage their weight as they are not digested by the body. However, the recent study suggests that the bacteria in the gut may be able to break down artificial sweeteners, resulting in negative health effects.

“We didn’t find this adverse effect in those consuming saccharin or natural sugars,” says Kuk. “We will need to do future studies to determine whether any potentially negative health effects of artificial sweeteners outweigh the benefits for obesity reduction.”

Currently, there are many new sugar substitutes that are used in foods. The researchers note that further investigation is needed to determine if there are any health effects of using these sweeteners.

For the study, data from 2856 U.S. adults from the Third National Health and Nutrition Survey (NHANES III) was used. Individuals reported their diet over the past 24 hours and were categorized as consumers of artificial sweeteners (aspartame or saccharin), or high or low consumers of natural sugars (sugar or fructose). Diabetes risk was measured as the ability to manage blood sugars using an oral glucose tolerance test.

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The Canadian Institutes of Health Research funded study, “Aspartame intake is associated with greater glucose intolerance in individuals with obesity,” was published today in Applied Physiology, Nutrition and Metabolism.

York University is helping to shape the global thinkers and thinking that will define tomorrow. York’s unwavering commitment to excellence reflects a rich diversity of perspectives and a strong sense of social responsibility that sets us apart. A York U degree empowers graduates to thrive in the world and achieve their life goals through a rigorous academic foundation balanced by real-world experiential education. As a globally recognized research centre, York is fully engaged in the critical discussions that lead to innovative solutions to the most pressing local and global social challenges. York’s 11 faculties and 27 research centres are thinking bigger, broader and more globally, partnering with 288 leading universities worldwide. York’s community is strong – 55,000 students, 7,000 faculty and staff, and more than 250,000 alumni.

Media Contact:

Gloria Suhasini, York University Media Relations, 416 736 2100 ext. 22094, suhasini@yorku.ca

NOTE: York U media studio is available for double-ended broadcast interviews.

Artificially sweetened beverages consumed in pregnancy linked to increased infant BMI

Public Release: 9-May-2016

 

The JAMA Network Journals

Daily consumption of artificially sweetened beverages by women during pregnancy may be associated with increased infant body mass index (BMI) and may be associated with an increased risk of being overweight in early childhood, according to an article published online by JAMA Pediatrics.

Obesity may be rooted in early life with more than 20 percent of preschool children classified as overweight or obese. Added sugar is associated with obesity and as a result sugar replacements or nonnutritive sweeteners (NNSs) are popular. Literature suggests that chronic NNS consumption may paradoxically increase the risk of obesity and metabolic disease. Little is known about the effect of NNS exposure during pregnancy.

Meghan B. Azad, Ph.D., of the University of Manitoba, Winnipeg, Canada, and coauthors studied 3,033 mother-infant pairs to examine the association of consuming artificially sweetened beverages during pregnancy and its effect on infant BMI in the first year of life. A food questionnaire was used for dietary assessments during pregnancy and infant BMI was measured when they were 1 year old.

The authors report the average age of the pregnant women was 32.4 years. For infants, their average BMI z score (which measures deviations in BMI) was 0.19 at 1 year old and 5.1 percent of the infants were overweight. More than a quarter of the women (29.5 percent) reported drinking artificially sweetened beverages during pregnancy, including 5.1 percent of women who reported drinking them daily.

Study results indicate that daily consumption of artificially sweetened beverages, compared with no consumption of such beverages, was associated with an increase in infant BMI z score and a two-fold increased risk of an infant being overweight at 1 year of age. Consumption of sugar-sweetened beverages was not associated with infant BMI z scores.

The authors acknowledge study limitations that include the potential for error in self-reported dietary outcomes. The study also cannot prove a causal association.

“To our knowledge, our results provide the first human evidence that artificial sweetener consumption during pregnancy may increase the risk of early childhood overweight. Given the current epidemic of childhood obesity and the widespread consumption of artificial sweeteners, further research is warranted to replicate our findings in other cohorts, evaluate specific NNS and longer-term outcomes, and study the underlying biological mechanisms,” the authors conclude.

(JAMA Pediatr. Published online May 9, 2016. doi:10.1001/jamapediatrics.2016.0301. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor’s Note: The study includes funding/support disclosures. Please see article for additional information, including other authors, author contributions and affiliations, etc.

Maternal Consumption of Artificially Sweetened Beverages and Infant Weight Gain: Causal or Casual?

“Despite these caveats, the findings by Azad et al warrant attention and further research. Experimental studies in animals and small intervention trials among pregnant women can explore mechanisms. Observational cohort studies should incorporate substitution as well as addition models and pay close attention to confounding. Randomized clinical trials substituting ASBs for SSBs [sugar-sweetened beverages] or, equally valuable, water for ASBs would be particularly helpful,” write Mark A. Pereira, Ph.D., of the University of Minnesota, Minneapolis, and Matthew W. Gillman, M.D., S.M., of Harvard Medical School, Boston, in a related editorial.

(JAMA Pediatr. Published online May 9, 2016. doi:10.1001/jamapediatrics.2016.0555. Available pre-embargo to the media at http://media.jamanetwork.com.)

Editor’s Note: The study includes conflict of interest disclosures. Please see article for additional information, including other authors, author contributions and affiliations, etc.

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Media Advisory: To contact corresponding author Meghan B. Azad, Ph.D., call Ilana Simon at 204-789-3427 or email Ilana.simon@umanitoba.ca. To contact corresponding editorial author Mark A. Pereira, Ph.D., call Caroline Marin at 612-624-5680 or email crmarin@umn.edu.

To place an electronic embedded link to this study in your story Links will be live at the embargo time: http://archpedi.jamanetwork.com/article.aspx?doi=10.1001/jamapediatrics.2016.0301; http://archpedi.jamanetwork.com/article.aspx?doi=10.1001/jamapediatrics.2016.0555

High-fructose diet during pregnancy may harm placenta, restrict fetal growth

Public Release: 4-May-2016

 

Drug prescribed to treat gout, kidney stones may negate the sugar’s ill effects

Washington University in St. Louis

Consuming a high-fructose diet during pregnancy may cause defects in the placenta and restrict fetal growth, potentially increasing a baby’s risk for metabolic health problems later in life, according to research in mice and people by a team at Washington University School of Medicine in St. Louis.

However, giving the mice allopurinol, a generic drug frequently prescribed to treat gout and kidney stones, appears to mitigate the negative maternal and fetal effects. The findings suggest it may be possible to devise a prenatal screening test and treatment plan for pregnant women with high fructose levels.

The study is available online in Scientific Reports, a journal affiliated with Nature Publishing Group.

Fructose, a sugar occurring naturally in fruits and honey, has been popular for decades among food manufacturers who process it into high-fructose corn syrup used to sweeten food and beverages. In fact, researchers have reported that the refined sugar accounts for more than half of all sweeteners used in the U.S. food-supply chain. And in recent years, there’s growing concern that fructose in processed foods and sugary drinks may be linked to diabetes and obesity.

“Since the early 1970s, we’ve been eating more fructose than we should,” said Kelle H. Moley, MD, the School of Medicine’s James P. Crane Professor of Obstetrics and Gynecology and the study’s senior author. “It is becoming increasingly critical to understand how fructose consumption is impacting human health. This study shows potentially negative effects of a high-fructose diet during pregnancy.”

Fructose is processed differently than other sugars such as glucose, which the body converts into energy. Instead, fructose is broken down by liver cells that turn the sugar into a form of fat known as triglycerides while also driving high levels of uric acid, a normal waste product found in urine and stool. Too much uric acid can create metabolic mayhem resulting in obesity, type 2 diabetes and other health conditions.

Studying mice, the researchers found elevated uric acid and triglycerides in otherwise healthy mice who were fed a high-fructose diet during pregnancy. Additionally, the mice developed smaller fetuses and larger placentas than those fed standard rodent chow.

Genetically, Moley said, a small fetus may become wired to grow more after birth than a normal-sized fetus. “The body tries to compensate for the small growth in utero,” Moley said. “These babies can become kids and then adults struggling with obesity and other health problems.”

Maternal health also may suffer. Metabolic problems caused by high levels of uric acid and fat increase a woman’s risk of developing pregnancy complications such as preeclampsia — a potentially serious condition in pregnancy often marked by high blood pressure, swelling and high protein levels in the urine — and gestational diabetes, Moley said.

To assess the relevance of the mouse data in pregnant women, the researchers examined the association between fructose and placental uric acid levels in a small controlled group of 18 women who underwent scheduled cesarean sections. The women had no disorders that would have caused elevated uric acid. “We found a correlation suggesting similar maternal and fetal effects occur in humans,” Moley said.

In the mouse model, researchers found that giving mice with high-fructose levels the common drug allopurinol – a prescription medication that reduces uric acid — reversed the refined sugar’s negative maternal and fetal effects by reducing the levels of uric acid in the placenta.

“The negative effect of excess fructose in humans is likely to lead to an exacerbation of the problems seen in the mice,” said Moley, who believes additional research may lead to a prenatal screening test for measuring fructose levels. This can be determined by simple blood work.

Besides advising pregnant women to limit fructose in their diets, treatment for those with high-fructose levels may include administering allopurinol, which crosses the placenta and generally is considered safe to take late in the second trimester or third trimester during pregnancy, Moley said.

“One of the best ways to ensure healthy maternal and fetal outcomes is by eating natural foods,” she said. Future studies will test the effectiveness of giving allopurinol to pregnant women when there is concern about fetal growth, Moley added.

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The study’s lead author was Zeenat Asghar, a graduate student in molecular cell biology in the university’s Division of Biology and Biomedical Sciences.

High Fructose Diet in Pregnancy Leads to Fetal Programming of Hypertension, Insulin Resistance and Obesity in Adult Offspring

Public Release: 4-Feb-2016

Impact of high fructose on health of offspring

Society for Maternal-Fetal Medicine

ATLANTA (Feb. 4, 2016)–In a study to be presented on Feb. 5 in the oral session at 1:15 p.m. EST, at the Society for Maternal-Fetal Medicine’s annual meeting, The Pregnancy Meeting™, in Atlanta, researchers will present findings on the effects of antenatal exposure to a high fructose diet on the offspring’s development of metabolic syndrome-like phenotype and cardiovascular disease later in life.

The study, titled High fructose diet in pregnancy leads to fetal programming of hypertension, insulin resistance and obesity in adult offspring, randomly allocated either a fructose solution or water as the only drinking fluid for pregnant mice from first day of pregnancy through delivery. Offspring were then started on regular chow and evaluated after one year of life. Percent of visceral adipose tissue was measured along with liver fat infiltrates using computed tomography, and blood pressure using a non-invasive monitor. Glucose tolerance testing was also performed and serum concentrations of glucose, insulin, triglycerides, total cholesterol, leptin and adiponectin were measured.

Maternal weight, pup number and average weight at birth were similar between the two groups. Male and female offspring born to mothers who received the fructose solution group had higher peak glucose compared with controls. Female offspring from the fructose group were heavier and had a higher percent of visceral adipose tissue, liver fat infiltrates, fasting homeostatic model assessment scores, higher serum concentrations of leptin and lower concentrations of adiponectin.

No significant differences in these parameters were noted in male offspring. Serum concentrations of triglycerides and total cholesterol were not different between the two groups or either gender.

“While this study was done in a mouse model, it is an important indicator of the effect of the mothers’ diet during pregnancy on the health of their children later in life,” explained Antonio Saad, M.D. with UTMB Galveston and the lead researcher of the study. “Through this study, we know that consuming high fructose during pregnancy putts the child at future risk for a variety of health conditions including obesity and the many complications it causes.”

The study concluded that, while maternal intake of high fructose leads to fetal programming of adult obesity, hypertension, and metabolic dysfunction–all of which risk factors for cardiovascular disease; limiting high fructose enriched diets in pregnancy may have a significant impact on long term health.

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A copy of the abstract is available at http://www.smfmnewsroom.org and below. For interviews please contact Vicki Bendure at Vicki@bendurepr.com 202-374-9259 (cell).

The Society for Maternal-Fetal Medicine (est. 1977) is the premiere membership organization for obstetricians/gynecologists who have additional formal education and training in maternal-fetal medicine. The society is devoted to reducing high-risk pregnancy complications by sharing expertise through continuing education to its 2,000 members on the latest pregnancy assessment and treatment methods. It also serves as an advocate for improving public policy, and expanding research funding and opportunities for maternal-fetal medicine. The group hosts an annual meeting in which groundbreaking new ideas and research in the area of maternal-fetal medicine are shared and discussed. For more information visit http://www.smfm.org.

Abstract 67 High Fructose Diet in Pregnancy Leads to Fetal Programming of Hypertension, Insulin Resistance and Obesity in Adult Offspring

Authors: Antonio Saad1, Joshua Disckerson1, Phyllis Gamble1, Huaizhi Yin1, Talar Kechichian1, Ashley Salazar1, Igor Patrikeev2, Massoud Motamedi2, George Saade1, Maged Costantine1
1UTMB Galveston, Galveston, TX, 2UTMB Center of Biomedical Engineering, Galveston, TX

Objective: Consumption of fructose rich diets in the U.S is on the rise and thought to be associated with obesity and cardio-metabolic diseases. Our objective was to determine the effects of antenatal exposure to high fructose diet on offspring’s development of metabolic syndrome-like phenotype and other cardiovascular disease (CVD) risk factors later in life.

Study Design: Pregnant C57BL/6J dams were randomly allocated to fructose solution (FRC, 10% W/V, n=10) as only drinking fluid or water (CTR, n=10) from day 1 of pregnancy until delivery. Pups were then started on regular chow, and evaluated at 1 year of life. We measured % visceral adipose tissue (VAT) and liver fat infiltrates using computed tomography (CT), and blood pressure using CODA/ non-invasive monitor. Intraperitoneal glucose tolerance testing (IPGTT), with corresponding insulin concentrations were obtained. Serum concentrations of glucose, insulin, triglycerides (TG), total cholesterol (TC), leptin, and adiponectin were measured in duplicate using standardized assays. Fasting homeostatic model assessment (HOMA- IR) was also calculated to assess insulin resistance.

Results: Maternal weight, pup number and average weight at birth were similar between the two groups. Male and female FRC offspring had higher peak glucose and area under the IPGTT curve, compared with CTR (Figures 1A&B), and higher mean arterial pressure compared to CTR (Figure 1C). Female FRC offspring were heavier and had higher % VAT (Figure 1D), liver fat infiltrates, HOMA-IR scores, insulin area under the IPGTT curve, serum concentrations of leptin, and lower concentrations of adiponectin compared to female CTR offspring (Table). No significant differences in these parameters were noted in male offspring. Serum concentrations of TG or TC were not different between the 2 groups for either gender.

Conclusion: Maternal intake of high fructose leads to fetal programming of adult obesity, hypertension and metabolic dysfunction, all risk factors for CVD. This fetal programming is more pronounced in female offspring. Limiting intake of high fructose enriched diets in pregnancy may have significant impact on long term health.

Processed Fructose bad for the Brain TBI


Processed Fructose from corn ( as in HFCS) – The sweetener interfered with the ability of neurons to communicate with each other, rewire connections after injury, record memories and produce enough energy to fuel basic functions.

We review the study the UCLA study, published in the Journal of Cerebral Blood Flow and Metabolism.

New research exposes the health risks of fructose and sugary drinks

Public Release: 28-Sep-2015

  • as high as a 26 percent greater risk of developing type 2 diabetes,
  • a 35 percent greater risk of heart attack or fatal heart disease, and
  • a 16 percent increased risk of stroke

Researchers call for more aggressive efforts to reduce consumption of products containing added sugar

American College of Cardiology

Washington, DC (Sept. 28, 2015) – There is compelling evidence that drinking too many sugar-sweetened beverages, which contain added sugars in the form of high fructose corn syrup or table sugar (sucrose), can lead to excess weight gain and a greater risk of developing type 2 diabetes and cardiovascular disease, according to a new review paper published today in the Journal of the American College of Cardiology.

The review–the most comprehensive review of the evidence on the health effects of sugar-sweetened beverages to date–also takes a closer look at the unique role fructose may play in the development of these conditions.

“Since we rarely consume fructose in isolation, the major source of fructose in the diet comes from fructose-containing sugars, sucrose and high fructose corn syrup, in sugar-sweetened beverages,” according to Frank Hu, MD, PhD, Professor of Nutrition and Epidemiology at Harvard T.H. Chan School of Public Health and lead investigator of the paper. “Our findings underscore the urgent need for public health strategies that reduce the consumption of these drinks.”

Sweeteners such as high fructose corn syrup, produced from corn starch, have been widely used in the U.S. as a low-cost alternative to sucrose in foods and beverages. While the consumption of sugar-sweetened beverages has decreased moderately in the past decade, they are still the single greatest source of added sugar intake in the U.S. diet. In fact, half of the U.S. population consumes these types of drinks every day, with one in four getting at least 200 calories per day from them and 5 percent consuming more than 500 calories per day, which is the equivalent of four cans of soda.

“This is particularly concerning as the research shows that consuming one or more sugar-sweetened beverages a day has been linked to greater weight gain and obesity in numerous published studies,” said Hu. “Regular consumption of sugar-sweetened beverages can lead to weight gain because the liquid calories are not filling, and so people don’t reduce their food intake at subsequent meals.”

The paper, which reviewed data from recent epidemiological studies and meta-analyses of these studies, reveals that consuming one or two servings a day has been linked to:

  • as high as a 26 percent greater risk of developing type 2 diabetes,
  • a 35 percent greater risk of heart attack or fatal heart disease, and
  • a 16 percent increased risk of stroke

The research team also explored how fructose is metabolized in the body and its link to weight gain and the development of metabolic and cardiovascular conditions.

“Part of the problem is how fructose behaves in the body,” said Hu. Glucose, another component of sugar, is readily absorbed from the gastrointestinal tract into the bloodstream where it is transported through the action of insulin into the body’s cells to be used as fuel. Fructose, on the other hand, is metabolized in the liver where it can be converted to fatty compounds called triglycerides, which may lead to fatty liver disease and insulin resistance, a key risk factor for developing diabetes and cardiovascular disease. Overconsumption of fructose can also lead to too much uric acid in the blood, which is associated with a greater risk of gout, a painful inflammatory arthritis.

The researchers point out that since fructose and glucose typically travel together in sugar-sweetened beverages and foods, it is important to reduce total amounts of added sugars, especially in the form of sugar-sweetened beverages. They outline a number of alternatives to sugar-sweetened beverages that include water, coffee, and tea.

Hu says that while artificially sweetened drinks may be preferable to sugary drinks in the short-term, but further studies are needed to evaluate their long-term health effects.

Hu says additional research is needed to explore the health effects of different types of sugars and how liquid vs. solid forms of sugar affect the body. However, he says there is sufficient evidence to support the need for more aggressive public policy interventions to help reduce consumption of sugar-sweetened beverages. The World Health Organization and the 2015 U.S. Dietary Guidelines Advisory Committee recommend that added sugars comprise no more than 10 percent of total calories consumed.

“Although reducing the consumption of sugar-sweetened beverages or added sugar alone is unlikely to solve the obesity epidemic entirely, limiting intake is one simple change that will have a measurable impact on weight control and prevention of cardio-metabolic diseases,” Hu and his team conclude.

Hu adds that he is hopeful that changes to nutritional labeling, which are expected to clearly define the amount of added sugar in a product and the percent daily value for added sugar, will also help to educate consumers and ultimately reduce the daily intake of these and other products packed with sugar.

The review paper is part of a comprehensive Population Health Promotion issue of the Journal of the American College of Cardiology focusing on issues that broadly impact public health and the prevention of cardiovascular disease and related conditions. Population health is a strategic priority of the American College of Cardiology, which recently brought together experts from around the world to address issues such as smoking and nutrition in the context of developing public health strategies for improving population health.

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Dr. Hu is also the author of “Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study,” a study appearing in this issue.

The American College of Cardiology is a 49,000-member medical society that is the professional home for the entire cardiovascular care team. The mission of the College is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications. For more information, visit acc.org.

The Journal of the American College of Cardiology, which publishes peer-reviewed research on all aspects of cardiovascular disease, is the most widely read cardiovascular journal worldwide. JACC is ranked No. 1 among cardiovascular journals worldwide for its scientific impact.

Fructose produces less rewarding sensations in the brain

Public Release: 25-Jun-2015

University of Basel

 

IMAGE

Caption

The MRI image clearly shows how the brain’s reward, or limbic, system behaves differently when administered a placebo (top) or one of two types of sugar, glucose (center) and fructose (bottom).

Credit: (Image: University of Basel, Department of Biomedicine)

Fructose not only results in a lower level of satiety, it also stimulates the reward system in the brain to a lesser degree than glucose. This may cause excessive consumption accompanied by effects that are a risk to health, report researchers from the University of Basel in a study published in the scientific journal PLOS ONE. Various diseases have been attributed to industrial fructose in sugary drinks and ready meals.

Fruit sugar, or fructose, is a carbohydrate that occurs naturally in fruits and vegetables and is generally harmless in this form. Despite their similar structures, fructose and glucose – that is, pure grape sugar – affect the body very differently: an intake of glucose causes a sharp increase in blood insulin within minutes, whereas fructose stimulates insulin secretion to a limited degree only.

Continue reading “Fructose produces less rewarding sensations in the brain”

High Fructose Sweetener can lead to fatal heart failure

Fructose powers a vicious circle

ETH Zurich

‘Walk through any supermarket and take a look at the labels on food products, and you’ll see that many of them contain fructose, often in the form of sucrose (table sugar)’ — that’s how Wilhelm Krek, professor for cell biology at ETH Zurich’s Institute for Molecular Health Sciences, summarises the problem with today’s nutrition. Prepared foods and soft drinks in particular, but even purportedly healthy fruit juices contain fructose as an artificial additive — often in high quantities. In recent decades fructose spread throughout the food market, due to a reputation as being less harmful than glucose. In contrast to glucose, fructose barely increases blood glucose levels and insulin secretion. This avoids frequently recurring insulin spikes after any glucose consumption, which are judged harmful. In addition, fructose is sweeter to the taste.

But there’s a downside: the liver converts fructose very efficiently into fat. People who consume too much high-fructose food can in time become overweight and develop high blood pressure, dyslipidaemia with fatty liver and insulin resistance — symptoms that doctors group together under the name metabolic syndrome.

Continue reading “High Fructose Sweetener can lead to fatal heart failure”

High Fructose decreases physical activity and increases body fat signifigantly over glucose

Public Release: 1-Jun-2015

“Fructose decreases physical activity and increases body fat without affecting hippocampal neurogenesis and learning relative to an isocaloric glucose diet,”

Beckman Institute for Advanced Science and Technology

In the last 40 years, fructose, a simple carbohydrate derived from fruit and vegetables, has been on the increase in American diets. Because of the addition of high-fructose corn syrup to many soft drinks and processed baked goods, fructose currently accounts for 10 percent of caloric intake for U.S. citizens. Male adolescents are the top fructose consumers, deriving between 15 to 23 percent of their calories from fructose–three to four times more than the maximum levels recommended by the American Heart Association.

A recent study at the Beckman Institute for Advanced Science and Technology at the University of Illinois found that, matched calorie for calorie with the simple sugar glucose, fructose causes significant weight gain, physical inactivity, and body fat deposition.

Continue reading “High Fructose decreases physical activity and increases body fat signifigantly over glucose”

New report links frequency of diet soda use to waist increases

Public Release: 6-Apr-2015

University of Texas Health Science Center at San Antonio

SAN ANTONIO, Texas, U.S.A. (April 6, 2015) — Those who drink diet soda thinking it will help them shed unwanted belly fat may see their waistlines expand instead. New analyses from an observational study of San Antonio men and women age 65 and older seem to indicate this.

The San Antonio Longitudinal Study of Aging (SALSA), led by Helen P. Hazuda, Ph.D., professor of medicine in the School of Medicine at The University of Texas Health Science Center at San Antonio, gathered data on health status and lifestyles of 749 Mexican-American and European-American elders, then tracked the health outcomes in 466 survivors for more than nine years. The number of sodas they consumed – and whether they were diet or regular – was recorded by interviews at the beginning of the study and at each of three follow-up visits, where SALSA personnel measured participants’ waist circumferences and other parameters.

Continue reading “New report links frequency of diet soda use to waist increases”

Diet soda linked to increases in belly fat in older adults

Public Release: 17-Mar-2015

Wiley

A new study published in the Journal of the American Geriatrics Society shows that increasing diet soda intake is directly linked to greater abdominal obesity in adults 65 years of age and older. Findings raise concerns about the safety of chronic diet soda consumption, which may increase belly fat and contribute to greater risk of metabolic syndrome and cardiovascular diseases.

Metabolic syndrome–a combination of risk factors that may lead to high blood pressure, diabetes, heart disease, and stroke–is one of the results of the obesity epidemic. In fact, the World Health Organization (WHO) estimates that 1.9 billion adults were overweight (body mass index [BMI] of 25 or more) in 2014. Of this group, 600 million people fell into the obese range (BMI of 30 or more)–a figure that has more than doubled since 1980.

In an effort to combat obesity, many adults try to reduce sugar intake by turning to nonnutritive or artificial sweeteners, such as aspartame, saccharin, or sucralose. Previous research shows that in the past 30 years, artificial sweeteners and diet soda intake have increased, yet the prevalence of obesity has also seen a dramatic increase in the same time period. Many of the studies exploring diet soda consumption and cardiometabolic diseases have focused on middle-aged and younger adults.

Continue reading “Diet soda linked to increases in belly fat in older adults”

High Fructose Corn Syrup found to kill animals almost twice as fast as table sugar

High Fructose Corn Syrup found to kill animals almost twice as fast as table sugar
– SALT LAKE CITY, Jan. 5, 2015 – When University of Utah biologists fed mice sugar in doses proportional to what many people eat, the fructose-glucose mixture found in high-fructose corn syrup was more toxic than sucrose or table sugar, reducing both the reproduction and lifespan of female rodents.“This is the most robust study showing there is a difference between high-fructose corn syrup and table sugar at human-relevant doses,” says biology professor Wayne Potts, senior author of a new study scheduled for publication in the March 2015 issue of The Journal of Nutrition.

* First published December 10, 2014, doi: 10.3945/jn.114.202531
http://healthresearchreport.me/2015/01/08/high-fructose-corn-syrup-more-toxic-than-table-sugar-in-mice/

Continue reading “High Fructose Corn Syrup found to kill animals almost twice as fast as table sugar”

Woman who drink 2 or more Diet sodas/fruit juice a day were 30 percent more likely to suffer a cardiovascular event and 50 percent more likely to die from related disease ( by association )

EEV: Reposted from our HRR site
PUBLIC RELEASE DATE:
29-Mar-2014

tumblr_lhxnsqYrbh1qh4vdzo1_500

Too many diet drinks may spell heart trouble for older women

 

Largest study of its kind looks at diet drinks and cardiovascular outcomes, mortality

It appears healthy postmenopausal women who drink two or more diet drinks a day may be more likely to have a heart attack, stroke or other cardiovascular problems, according to research to be presented at the American College of Cardiology’s 63rd Annual Scientific Session.

In fact, compared to women who never or only rarely consume diet drinks, those who consumed two or more a day were 30 percent more likely to suffer a cardiovascular event and 50 percent more likely to die from related disease. Researchers analyzed diet drink intake and cardiovascular risk factors from 59,614 participants in the Women’s Health Initiative Observational Study, making this the largest study to look at the relationship between diet drink consumption, cardiac events and death. Continue reading “Woman who drink 2 or more Diet sodas/fruit juice a day were 30 percent more likely to suffer a cardiovascular event and 50 percent more likely to die from related disease ( by association )”

Pancreatic cancers use ( HFCS ) fructose, common in the Western diet, to fuel their growth ( Smoking Gun )

Public release date: 2-Aug-2010

HRR: Research was mostly ignored and covered up in 2010 – To date there has been no update on this study

– this is the first time a link has been shown between fructose and cancer proliferation

Between 1970 and 1990, the consumption of HFCS in the U.S. has increased over 1,000 percent

– found that the pancreatic cancer cells could easily distinguish between glucose and fructose even though they are very similar structurally, and contrary to conventional wisdom, the cancer cells metabolized the sugars in very different ways

In the case of fructose, the pancreatic cancer cells used the sugar in the transketolase-driven non-oxidative pentose phosphate pathway to generate nucleic acids, the building blocks of RNA and DNA, which the cancer cells need to divide and proliferate.

They have major significance for cancer patients, given dietary refined fructose consumption.”

Animation of the structure of a section of DNA...
Animation of the structure of a section of DNA. The bases lie horizontally between the two spiraling strands. (Photo credit: Wikipedia)

Pancreatic cancers use the sugar fructose, very common in the Western diet, to activate a key cellular pathway that drives cell division, helping the cancer to grow more quickly, a study by researchers at UCLA’s Jonsson Comprehensive Cancer Center has found.

Although it’s widely known that cancers use glucose, a simple sugar, to fuel their growth, this is the first time a link has been shown between fructose and cancer proliferation, said Dr. Anthony Heaney, an associate professor of medicine and neurosurgery, a Jonsson Cancer Center researcher and senior author of the study. Continue reading “Pancreatic cancers use ( HFCS ) fructose, common in the Western diet, to fuel their growth ( Smoking Gun )”

Researchers say fructose does not impact emerging indicator for cardiovascular disease / Funded by the Calorie Control Council – MASSIVE CONFLICT OF INTEREST

HRR: Before you read the article it may be a half truth. Using data from naturally occurring fruit sugars, and not modified fructose products. This is a meta-analysis so confirmation is difficult. However in the face of conventional data, and extreme COI’s this manipulation of the subject mater is about as bad as it can get.

calorie control council

Companies and Products ( Calories Control Council)

ABBOTT NUTRITION  Brands: Ensure®, Glucerna®, Zone Perfect®, EAS®, Similac®, Isomil®, PediaSure,® PediaLyte®ABIC INTERNATIONAL INC.

AJINOMOTO U.S.A., INC. Products: Aspartame

ALCAN SPECIALTY CHEMICALS Products: Suppliers of sodium saccharin and calcium saccharin, calcium and sodium cyclamates, potassium sorbate, food additives and vitamins, xylitol, aspartame

ARCHER DANIELS MIDLAND Products: CornSweet® Crystalline Fructose, Liquid Sorbitol, Crystalline Sorbitol, NovaXan™ Xanthan Gums, Fibersol®-2 Digestion Resistant Maltodextrin, Clintose® Maltodextrin

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High Fructose Corn Syrup and interesting ways to create pandemics. Part 1

corn-field

This is to open up an honest debate into the scientific rationale to why High Fructose Corn Syrup may have been a mistake. This is only part 1 of my collection of publically available unedited studies on the subject. Please feel free to re-post, as long as you link me as the original source. This will allow the reader to be aware of future releases as they become available.

Ralph Turchiano

High Fructose Corn Syrup and interesting ways to create pandemics. Part 1

Fructose: the poison index

A ruling on fructose boosts the powerful sugar industry, either by incompetence or collusion, but is based on pseudoscience

    • Robert Lustig
    • The Guardian,              Monday 21 October 2013 16.00 EDT
Fructose Lustig

Fizzy drinks can have a ‘serum fructose concentration of six micromolar, enough to do major arterial and pancreatic damage’. Photograph: Nathalie Louvel/Getty Images

The battle over the compound fructose now reaches new levels of obfuscation. The food industry is a strong – and loud, and rich – proponent, hard to ignore. The European Food and Safety Agency has just weighed in, in favour of the substitution of sucrose (table sugar: a disaccharide composed of the monosaccharides glucose and fructose) with fructose alone, the sweeter of the two – even to the point of allowing health claims for fructose on the packaging of processed foods.

And yet the scientific data on fructose says it is one of the most egregious components of the western diet, directly contributing to heart disease and diabetes, and associated with cancer and dementia. Nature magazine has just published a scathing indictment of fructose by Dr Lewis Cantley, one of the US’s leading cancer researchers. But the EFSA says it sees no harm, justifying its stance on the basis that fructose has a lower glycaemic index than glucose.

The concept of glycaemic index is simple. This is how high your blood glucose rises after ingesting 50 grams of carbohydrate in any specific food, which is a measure of a food’s generation of an insulin response, and is used as a way of showing a food’s potential for weight gain. Glycaemic index is a proxy for how high your insulin level will rise, which determines whether that blood glucose will get shunted to fat cells for storage. Low-glycaemic-index diets promote blood sugar stability and are associated with weight loss. But the EFSA has missed the point. Glycaemic index is not the issue.

Glycaemic load is where it’s at. This takes into account how much of a given food one must eat to obtain 50 grams of carbohydrate. The perfect example is carrots. Carrots have a high glycaemic index – if you consume 50 grams of carbohydrate in carrots, your blood sugar will rise pretty high. But you would have to eat 1.3lbs – 600 grams – of carrots to get 50 grams of carbohydrate. Highly unlikely. Any high-glycaemic-index food can become a low-glycaemic-load food if it’s eaten with its inherent fibre. That means “real food”. But fructose is made in a lab. It’s anything but “real”.

Yes, fructose has a low glycaemic index of 19, because it doesn’t increase blood glucose. It’s fructose, for goodness sake. It increases blood fructose, which is way worse. Fructose causes seven times as much cell damage as does glucose, because it binds to cellular proteins seven times faster; and it releases 100 times the number of oxygen radicals (such as hydrogen peroxide, which kills everything in sight). Indeed, a 20oz soda results in a serum fructose concentration of six micromolar, enough to do major arterial and pancreatic damage. Glycaemic index is a canard; and fructose makes it so. Because fructose’s poisonous effects have nothing to do with glycaemic index; they are beyond glycaemic index.

The food industry is fond of referring to a 1999 study showing that liver fat generation from oral fructose occurs at a very low rate (less than 5%). And that’s true, if you’re thin, insulin sensitive, fasting (and therefore glycogen-depleted), and given just fructose alone (which is poorly absorbed). Conversely, if you’re obese, insulin resistant, well fed, and getting both fructose and glucose together (like a sizable percentage of the population), then fructose gets converted to fat at a much higher rate, approximating 30%. In other words, the toxicity of fructose depends on context.

The industry points to meta-analyses of controlled isocaloric “fructose for glucose” exchange studies that demonstrate no effect from fructose on weight gain or other morbidities. Perhaps one reason for this is because crystalline fructose is incompletely absorbed. When that happens, residual fructose in the gastrointestinal system causes pain, bloating, and diarrhoea: ask any child the morning after Halloween in between trips to the bathroom relieving his diarrhoea. Furthermore, those meta-analyses where fructose was supplied in excess do show weight gain, high levels of lipids in the blood, and insulin resistance. The dose determines the poison.

The EFSA has boosted the position of the sugar industry, either through incompetence or collusion. But it is clear that this recommendation is scientifically bogus. Nutritional policy should be based on science – not pseudoscience, as we have seen over the past 30 years.

http://www.theguardian.com/commentisfree/2013/oct/21/fructose-poison-sugar-industry-pseudoscience

 

Obesity experts appalled by EU move to approve health claim for fructose / high-fructose corn syrup is a healthy alternative

Food firms using fructose will be able to boast of health benefits despite fruit sugar being implicated in soaring US obesity levels

    • Sarah Boseley, health editor
    • The Guardian,  Thursday 17 October 2013 16.27 EDT
Fizzy drink can

Fructose, the sugar found in fruit, is used in Coca-Cola, Pepsi and other sweetened drinks. Photograph: Alamy

Obesity experts say they are appalled by an EU decision to allow a “health claim” for fructose, the sweetener implicated in the disastrous upsurge in weight in the US.

Fructose, the sugar found in fruit, is used in Coca-Cola, Pepsi and other sweetened US drinks. Many believe the use of high-fructose corn syrup caused obesity to rise faster in the US than elsewhere in the world. Europe has largely used cane and beet sugar instead.

But the EU has now ruled that food and drink manufacturers can claim their sweetened products are healthier if they replace more than 30% of the glucose and sucrose they contain with fructose.

The decision was taken on the advice of the European Food Safety Authority (Efsa), on the grounds that fructose has a lower glycaemic index (GI) – it does not cause as high and rapid a blood sugar spike as sucrose or glucose.

But, say obesity experts, fructose is metabolised differently from other sugars – it goes straight to the liver and unprocessed excess is stored there as fat, building up deposits that can cause life-threatening disease.

There is potential for products high in sugar including soft drinks, cereal bars and low-fat yoghurts to make health claims by using fructose. Lucozade Original contains 33g of sugar in a 380ml bottle, Sprite has 21.8g of sugar in 330ml cans and Dr  Pepper 34.1g per 330ml.

Kellogg’s Nutri-Grain Elevenses bars have 18g of sugar in a 45g bar – so are more than a third sugar.

Barry Popkin – distinguished professor in the department of public health at the University of North Carolina at Chapel Hill, in the US, who co-authored the groundbreaking paper linking high-fructose corn syrup to obesity in 2003 – said the ruling would lead to claims from food and drink firms that would mislead consumers.

“This claim is so narrow and it will confuse a whole lot of people,” he said. “That’s what the industry does an awful lot of. People see it and think, ‘ah maybe it’s healthy.’

“It brings into question the whole area of health claims. They are made on such short-term effects.”

Drinking pomegranate juice might give you all the vitamin C and antioxidants you need that day, but six months of regular drinking could raise the risk of diabetes, he said.

A health claim relating to a lower glycaemic index ignored the wider and more important public health issue, he said: that we should all consume less fructose and other sugars.

George Bray, head of the division of clinical obesity and metabolism at the Pennington biomedical research centre in Louisiana and co-author of the fructose paper, said he could see no rational reason for adding pure fructose to the diet.

“Assuming that it is correct that manufacturers can substitute up to 30% fructose for glucose or sucrose, it would be a very sad commentary on their review of the literature,” he said.

“The quantity of fructose appearing in the diet is already excessive in my view. [Focusing on the fact that] fructose does not raise glucose as much ignores all of the detrimental effects of fructose from whatever source.”

Michael Goran, director of childhood obesity research at the University of Southern California, said that although it had a lower GI, “in the long term, excess fructose is more damaging metabolically for the body than other sugars”.

He added: “This opens the door for the beverage and food industry to start replacing sucrose with fructose, which is presumably cheaper.”

More people in Europe will be consuming more fructose as a result, he said. “This is a dangerous and problematic issue. There is going to be a big increase in fructose exposure.  There is going to be a big increase in fructose exposure.”

The European Heart Network raised concerns with DG Sanco, the European commission’s health department, and asked it to share its views with member states. Its director, Susanne Logstrup, warned that replacing glucose and sucrose with “healthier” fructose might make people think a drink or food was less fattening.

“If the replacement of glucose/sucrose is not isocaloric, replacement could lead to a higher caloric content. In the EU, the intake of sugar-sweetened beverages is generally too high and it would not be in the interest of public health if intake were to increase,” she said.

Professor Mike Rayner, director of the British Heart Foundation health promotion research group at Oxford University and an adviser to the European Heart Network, said it was important the EU looked at nutritional health claims – and that it had in recent years taken a tougher stance.

“But here is an example in fructose of a claim that is technically probably true but has no public health benefit,” he said.

Industry is delighted by the EU ruling. Galam Group, an Israeli fructose manufacturer, called the move “a game-changing step” in comments to the trade journal Nutra Ingredients. It said it expected a surge in sales from 2 January, when the ruling takes effect.

http://www.theguardian.com/society/2013/oct/17/obesity-experts-appalled-eu-fructose-health-claim-approval

Sugar is toxic to mice in ‘safe’ doses

Contact: Annalisa Purser annalisa.purser@utah.edu 801-581-7295 University of Utah

New test hints 3 sodas daily hurt lifespan, reproduction

SALT LAKE CITY, Aug. 13, 2013 – When mice ate a diet of 25 percent extra sugar – the mouse equivalent of a healthy human diet plus three cans of soda daily – females died at twice the normal rate and males were a quarter less likely to hold territory and reproduce, according to a toxicity test developed at the University of Utah.

“Our results provide evidence that added sugar consumed at concentrations currently considered safe exerts dramatic adverse impacts on mammalian health,” the researchers say in a study set for online publication Tuesday, Aug. 13 in the journal Nature Communications.

“This demonstrates the adverse effects of added sugars at human-relevant levels,” says University of Utah biology professor Wayne Potts, the study’s senior author. He says previous studies using other tests fed mice large doses of sugar disproportionate to the amount people consume in sweetened beverages, baked goods and candy.

“I have reduced refined sugar intake and encouraged my family to do the same,” he adds, noting that the new test showed that the 25 percent “added-sugar” diet – 12.5 percent dextrose (the industrial name for glucose) and 12.5 percent fructose – was just as harmful to the health of mice as being the inbred offspring of first cousins.

Even though the mice didn’t become obese and showed few metabolic symptoms, the sensitive test showed “they died more often and tended to have fewer babies,” says the study’s first author, James Ruff, who recently earned his Ph.D. at the University of Utah. “We have shown that levels of sugar that people typically consume – and that are considered safe by regulatory agencies – impair the health of mice.”

The new toxicity test placed groups of mice in room-sized pens nicknamed “mouse barns” with multiple nest boxes – a much more realistic environment than small cages, allowing the mice to compete more naturally for mates and desirable territories, and thereby revealing subtle toxic effects on their performance, Potts says.

“This is a sensitive test for health and vigor declines,” he says, noting that in a previous study, he used the same test to show how inbreeding hurt the health of mice.

“One advantage of this assay is we get the same readout no matter if we are testing inbreeding or added sugar,” Potts says. “The mice tell us the level of health degradation is almost identical” from added-sugar and from cousin-level inbreeding.

The study says the need for a sensitive toxicity test exists not only for components of our diet, but “is particularly strong for both pharmaceutical science, where 73 percent of drugs that pass preclinical trials fail due to safety concerns, and for toxicology, where shockingly few compounds receive critical or long-term toxicity testing.”

The study was funded by the National Institutes of Health and the National Science Foundation.

A Mouse Diet Equal to What a Quarter of Americans Eat

The experimental diet in the study provided 25 percent of calories from added sugar – half fructose and half glucose – no matter how many calories the mice ate. Both high-fructose corn syrup and table sugar (sucrose) are half fructose and half glucose.

Potts says the National Research Council recommends that for people, no more than 25 percent of calories should be from “added sugar,” which means “they don’t count what’s naturally in an apple, banana, potato or other nonprocessed food. … The dose we selected is consumed by 13 percent to 25 percent of Americans.”

The diet fed to the mice with the 25 percent sugar-added diet is equivalent to the diet of a person who drinks three cans daily of sweetened soda pop “plus a perfectly healthy, no-sugar-added diet,” Potts says.

Ruff notes that sugar consumption in the American diet has increased 50 percent since the 1970s, accompanied by a dramatic increase in metabolic diseases such as diabetes, obesity, fatty liver and cardiovascular disease.

The researchers used a mouse supply company that makes specialized diets for research. Chow for the mice was a highly nutritious wheat-corn-soybean mix with vitamins and minerals. For experimental mice, glucose and fructose amounting to 25 percent of calories was included in the chow. For control mice, corn starch was used as a carbohydrate in place of the added sugars.

House Mice Behaving Naturally

Mice often live in homes with people, so “mice happen to be an excellent mammal to model human dietary issues because they’ve been living on the same diet as we have ever since the agricultural revolution 10,000 years ago,” Potts says.

Mice typically used in labs come from strains bred in captivity for decades. They lack the territoriality shown by wild mice. So the study used mice descended from wild house mice that were “outbred” to prevent inbreeding typical of lab mice.

“They are highly competitive over food, nesting sites and territories,” he says. “This competition demands high performance from their bodies, so if there is a defect in any physiological systems, they tend to do more poorly during high competition.”

So Potts’ new test – named the Organismal Performance Assay, or OPA – uses mice “in a more natural ecological context” more likely to reveal toxic effects of whatever is being tested, he says.

“When you look at a mouse in a cage, it’s like trying to evaluate the performance of a car by turning it on in a garage,” Ruff says. “If it doesn’t turn on, you’ve got a problem. But just because it does turn on, doesn’t mean you don’t have a problem. To really test it, you take it out on the road.”

A big room was divided into 11 “mouse barns” used for the new test. Six were used in the study. Each “barn” was a 377-square-foot enclosure ringed by 3-foot walls.

Each mouse barn was divided by wire mesh fencing into six sections or “territories,” but the mice could climb easily over the mesh. Within each of the six sections was a nest box, a feeding station and drinking water.

Four of the six sections in each barn were “optimal,” more desirable territories because the nest boxes were opaque plastic storage bins, which mice entered via 2-inch holes at the bottom. Each bin had four nesting cages in it, and an enclosed feeder.

The two other sections were “suboptimal” territories with open planter trays instead of enclosed bins. Female mice had to nest communally in the trays.

Running the Experiment

The mice in the experiment began with 156 “founders” that were bred in Potts’ colony, weaned at four weeks, and then assigned either to the added-sugar diet or the control diet, with half the males and half the females on each diet.

The mice stayed in cages with siblings of the same sex (to prevent reproduction) for 26 weeks while they were fed these diets. Then the mice were placed in the mouse barns to live, compete with each other and breed for 32 more weeks. They all received the same added-sugar diet while in the mouse barns, so the study only tested for differences caused by the mice eating different diets for the previous 26 weeks.

The founder mice had implanted microchips, like those put in pets. Microchip readers were placed near the feeding stations to record which mice fed where and for how long. A male was considered dominant if he made more than 75 percent of the visits by males to a given feeding station. In reality, the dominant males made almost 100 percent of male visits to the feeder in the desirable territory they dominated.

With the 156 founder mice (58 male, 98 female), the researchers ran the experiment six times, with an average of 26 mice per experiment: eight to 10 males (competing for six territories, four desirable and two suboptimal) and 14 to 18 females.

The Findings: Added Sugar Impairs Mouse Lifespan and Reproduction

  • After 32 weeks in mouse barns, 35 percent of the females fed extra sugar died, twice the 17 percent death rate for female control mice. There was no difference in the 55 percent death among males who did and did not get added sugar. Ruff says males have much higher death rates than females in natural settings because they compete for territory, “but there’s no relation to sugar.” 

     

  • Males on the added-sugar diet acquired and held 26 percent fewer territories than males on the control diet: control males occupied 47 percent of the territories while sugar-added mice controlled less than 36 percent. Male mice shared the remaining 17 percent of territories. 

     

  • Males on the added-sugar diet produced 25 percent fewer offspring than control males, as determined by genetic analysis of the offspring. The sugar-added females had higher reproduction rates than controls initially – likely because the sugar gave them extra energy to handle the burden of pregnancy – but then had lower reproductive rates as the study progressed, partly because they had higher death rates linked to sugar. 

The researchers studied another group of mice for metabolic changes. The only differences were minor: cholesterol was elevated in sugar-fed mice, and the ability to clear glucose from the blood was impaired in female sugar-fed mice. The study found no difference between mice on a regular diet and mice with the 25 percent sugar-added diet when it came to obesity, fasting insulin levels, fasting glucose or fasting triglycerides.

“Our test shows an adverse outcome from the added-sugar diet that couldn’t be detected by conventional tests,” Potts says.

Human-made toxic substances in the environment potentially affect all of us, and more are continually discovered, Potts says.

“You have to ask why we didn’t discover them 20 years ago,” he adds. “The answer is that until now, we haven’t had a functional, broad and sensitive test to screen the potential toxic substances that are being released into the environment or in our drugs or our food supply.”

###

 

Potts and Ruff conducted the study with University of Utah biology lab manager Linda Morrison and undergraduates Amanda Suchy, Sara Hugentobler, Mirtha Sosa and Bradley Schwartz, and with researchers Sin Gieng and Mark Shigenaga of Children’s Hospital Oakland Research Institute in California.

University of Utah Communications  75 Fort Douglas Boulevard  Salt Lake City, UT 84113  801-581-6773 fax: 801-585-3350  http://www.unews.utah.edu

 

 

The dark side of artificial sweeteners

Contact: Mary Beth O’Leary moleary@cell.com 617-397-2802 Cell Press

More and more Americans are consuming artificial sweeteners as an alternative to sugar, but whether this translates into better health has been heavily debated. An opinion article published by Cell Press on July 10th in the journal Trends in Endocrinology & Metabolism reviews surprising evidence on the negative impact of artificial sweeteners on health, raising red flags about all sweeteners—even those that don’t have any calories.

“It is not uncommon for people to be given messages that artificially-sweetened products are healthy, will help them lose weight or will help prevent weight gain,” says author Susan E. Swithers of Purdue University. “The data to support those claims are not very strong, and although it seems like common sense that diet sodas would not be as problematic as regular sodas, common sense is not always right.”

Consumption of sugar-sweetened drinks has been linked to obesity, type 2 diabetes, and metabolic syndrome—a group of risk factors that raises the risk for heart disease and stroke. As a result, many Americans have turned to artificial sweeteners, which are hundreds of times sweeter than sugar but contain few, if any, calories. However, studies in humans have shown that consumption of artificially sweetened beverages is also associated with obesity, type 2 diabetes, and metabolic syndrome as well as cardiovascular disease. As few as one of these drinks per day is enough to significantly increase the risk for health problems.

Moreover, people who regularly consume artificial sweeteners show altered activation patterns in the brain’s pleasure centers in response to sweet taste, suggesting that these products may not satisfy the desire for sweets. Similarly, studies in mice and rats have shown that consumption of noncaloric sweeteners dampens physiological responses to sweet taste, causing the animals to overindulge in calorie-rich, sweet-tasting food and pack on extra pounds.

Taken together, the findings suggest that artificial sweeteners increase the risk for health problems to an extent similar to that of sugar and may also exacerbate the negative effects of sugar. “These studies suggest that telling people to drink diet sodas could backfire as a public health message,” Swithers says. “So the current public health message to limit the intake of sugars needs to be expanded to limit intake of all sweeteners, not just sugars.”

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Trends in Endocrinology & Metabolism, Swithers et al.: “Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements.”

Dietary fructose causes liver damage in animal model, study finds

Contact: Marguerite Beck marbeck@wakehealth.edu 336-716-2415 Wake Forest Baptist Medical Center

WINSTON-SALEM, N.C. – June 19, 2013 – The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.

However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain. The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.

The study is published in the June 19 online edition of the American Journal of Clinical Nutrition.

“Is a calorie a calorie? Are they all created equal? Based on this study, we would say not,” said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.

In a previous trial which is referenced in the current journal article, Kavanagh’s team studied monkeys who were allowed 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. Not surprisingly, the animals 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 hepatic steatosis, or non-alcoholic fatty liver disease.

The big question for the researchers was what caused the liver damage. Was it because the animals got fat from eating too much, or was it something else?

To answer that question, this study was designed to prevent weight gain. Ten middle-aged, normal weight monkeys who had never eaten fructose 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 only a negligible amount of fructose, approximately 0.5 percent.

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, while 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.”

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn’t changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.

One of the limitations of the study 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 Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.

###

 

The study was supported by Wake Forest School of Medicine and grants RR019963, OD010965 and AG033641 from the National Institutes of Health.

Co-authors are Ashley Wylie and Kelly Tucker, B.S., of Wake Forest Baptist; John Culler, D.V.M., Ph.D., of North Carolina State University; Timothy Hamp, B.S., Anthony Fodor, Ph.D., and Raad Gharaibeh, Ph.D., of the University of North Carolina at Charlotte.

Soda and illegal drugs cause similar damage to teeth

CHICAGO (May 28, 2013)—Addicted to soda? You may be shocked to learn that drinking large quantities of your favorite carbonated soda could be as damaging to your teeth as methamphetamine and crack cocaine use. The consumption of illegal drugs and abusive intake of soda can cause similar damage to your mouth through the process of tooth erosion, according to a case study published in the March/April 2013 issue of General Dentistry, the peer-reviewed clinical journal of the Academy of General Dentistry (AGD).

Tooth erosion occurs when acid wears away tooth enamel, which is the glossy, protective outside layer of the tooth. Without the protection of enamel, teeth are more susceptible to developing cavities, as well as becoming sensitive, cracked, and discolored.

The General Dentistry case study compared the damage in three individuals’ mouths—an admitted user of methamphetamine, a previous longtime user of cocaine, and an excessive diet soda drinker. Each participant admitted to having poor oral hygiene and not visiting a dentist on a regular basis. Researchers found the same type and severity of damage from tooth erosion in each participant’s mouth.

“Each person experienced severe tooth erosion caused by the high acid levels present in their ‘drug’ of choice—meth, crack, or soda,” says Mohamed A. Bassiouny, DMD, MSc, PhD, lead author of the study.

“The citric acid present in both regular and diet soda is known to have a high potential for causing tooth erosion,” says Dr. Bassiouny.

Similar to citric acid, the ingredients used in preparing methamphetamine can include extremely corrosive materials, such as battery acid, lantern fuel, and drain cleaner. Crack cocaine is highly acidic in nature, as well.

The individual who abused soda consumed 2 liters of diet soda daily for three to five years. Says Dr. Bassiouny, “The striking similarities found in this study should be a wake-up call to consumers who think that soda—even diet soda—is not harmful to their oral health.”

AGD Spokesperson Eugene Antenucci, DDS, FAGD, recommends that his patients minimize their intake of soda and drink more water. Additionally, he advises them to either chew sugar-free gum or rinse the mouth with water following consumption of soda. “Both tactics increase saliva flow, which naturally helps to return the acidity levels in the mouth to normal,” he says.

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Could artificial sweetener CAUSE diabetes? Splenda ‘modifies way the body handles sugar’, increasing insulin production by 20%

  • Study found sugar substitute sucralose had  an effect on blood sugar levels
  • Also discovered that insulin production  increased by 20% when consumed
  • Scientists aren’t sure what implications  are, but said that regularly elevated insulin levels could eventually cause  insulin resistance and even diabetes

By  Rachel Reilly

PUBLISHED: 12:27 EST, 30 May  2013 |  UPDATED: 12:27  EST, 30 May 2013

Sugar substitute Splenda is made of sucralose, which has been found to affect blood glucose and insulin levelsSplenda is made of sucralose, which has been found to  affect blood glucose and insulin levels

Splenda can modify how the body handles sugar  and could lead to diabetes, according to a new study.

Scientists found that consuming the sugar  alternative made of sucralose caused a person’s sugar levels to peak at a higher  level and in turn increase the amount of insulin a person produced.

Researchers said that while they did not  fully understand the implications of the findings, they might suggest that  Splenda could raise the risk of diabetes.

This is because regularly elevated insulin  levels can lead to insulin  resistance, which is a known path to type 2  diabetes.

‘Our results indicate that this  artificial  sweetener is not inert – it does have an effect,’ said Yanina Pepino, research  assistant professor of medicine at the  Washington School of Medicine in St. Louis, who led the study.

‘And we need to do more studies to determine  whether this observation  means long-term use could be harmful.’

Sucralose is made from sugar, but once  processed its chemical make up is very different. Gram for gram it is 600 times  sweeter than table sugar.

The scientists analysed  the effects of Splenda in 17 severely obese people who did not have diabetes and  did not use artificial sweeteners regularly.

Participants had an  average body mass index  of just over 42. A person is considered  obese when their BMI reaches 30.

Scientists gave subjects either water or dissolved sucralose to drink before they consumed glucose (sugar).

 

They wanted to understand whether the  combination of sucralose and glucose would affect insulin and blood  sugar  levels.

Every participant was tested twice.  Those  who drank water followed by glucose in one visit drank sucralose  followed by  glucose in the next. In this way, each person served as his or her own control  group.

‘We wanted to study [overweight people] because these sweeteners frequently are recommended to them as a way to  make  their diets healthier by limiting calorie intake,’ Pepino said.

They found that when study participants  drank sucralose, their blood sugar peaked at a higher level than when  they  drank only water before consuming glucose.

Better off with the real thing?: Artificial sweeteners were once thought to be the holy grail for dieters and diabetics 

Better off with the real thing?: Artificial sweeteners  were once thought to be the holy grail for dieters and diabetics, but recent  studies have shown that they could pose dangers to health

Insulin levels also rose about 20 percent  higher. So despite no extra sugar being consumed, the artificial sweetener was  related to an enhanced blood insulin and glucose response.

Professor Yanina explained that they do not  fully understand the implications that these rises could have.

She said: ‘The elevated insulin response  could be a good thing because it shows the person is able to make enough insulin  to deal with spiking glucose levels.

‘But it also might be bad because when people  routinely secrete more insulin, they can become resistant to its effects, a path  that leads to type 2 diabetes.’

It has been thought that artificial  sweeteners, such as sucralose, don’t have an effect on metabolism.

They are used in such small quantities that  they don’t increase calorie intake. Rather, the sweeteners react with receptors  on the tongue to give people the sensation of tasting something sweet without  the calories associated with natural sweeteners, such as table sugar.

While scientists are not sure what the implications of the study are, they said there could be an increased risk of diabetes 

While scientists are not sure what the implications of  the study are, they said there could be an increased risk of diabetes

But recent findings in animal studies suggest  that some sweeteners may be doing more than just making foods and drinks taste  sweeter.

One finding indicates that the  gastrointestinal tract and the pancreas can detect sweet foods and drinks with  receptors that are virtually identical to those in the mouth.

That causes an increased release of hormones,  such as insulin.

Some animal studies also have found that when  receptors in the gut are activated by artificial sweeteners, the absorption of  glucose also increases.

Professor Pepino added: ‘Most  of the studies of artificial sweeteners have been conducted in healthy, lean  individuals. In many of these studies, the artificial sweetener is given by  itself.

But in real life, people rarely consume a  sweetener by itself. They use it in their coffee or on breakfast cereal or when  they want to sweeten some other food they are eating or drinking.’

Just how sucralose influences glucose and  insulin levels in people who are obese is still somewhat of a  mystery.

‘Although we found that sucralose affects the  glucose and insulin response to glucose ingestion, we don’t know the mechanism  responsible,’ said Pepino.

‘We have shown that sucralose is having an  effect. In obese people without diabetes we have shown sucralose is more than  just something sweet that you put into your mouth with no other  consequences.’

She said further studies are needed to learn  more about the mechanism through which sucralose may influence glucose and  insulin levels, as well as whether those changes are harmful.

The study was published in the journal  Diabetes Care.

In a statement, Splenda said: ‘Numerous  clinical studies in people with Type 1 and Type 2 diabetes and non-diabetic  people have shown that Splenda Brand Sweetener (sucralose) does not affect blood  glucose levels, insulin, or HbA1c.

‘FDA and other important safety and  regulatory agencies from around the world have concluded that sucralose does not  adversely affect glucose control, including in people with diabetes.

‘Experts from around the world have found  that Splenda Brand Sweetener is suitable for everyone, including those with  diabetes.’

Read more: http://www.dailymail.co.uk/health/article-2333336/Could-artificial-sweetener-CAUSE-diabetes-Splenda-modifies-way-body-handles-sugar-increasing-insulin-production-20.html#ixzz2UqPXYVsA Follow us: @MailOnline on Twitter | DailyMail on Facebook

Study shows drinking one 12oz sugar-sweetened soft drink a day can increase the risk of type 2 diabetes by 22 percent

Contact: Sam Wong Press Office sam.wong@imperial.ac.uk 44-020-759-42198 Diabetologia

Drinking one (or one extra)* 12oz serving size of sugar-sweetened soft drink a day can be enough to increase the risk of developing type 2 diabetes by 22%, a new study suggests. The research is published in  Diabetologia (the journal of the European Association for the Study of Diabetes) and comes from data in the InterAct consortium**. The research is by Dr Dora Romaguera, Dr Petra Wark and Dr Teresa Norat, Imperial College London, UK, and colleagues.

Since most research in this area has been conducted in North American populations, the authors wanted to establish if a link between sweet beverage consumption and type 2 diabetes existed in Europe. They used data on consumption of juices and nectars, sugar-sweetened soft drinks and artificially sweetened soft drinks collected across eight European cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC study; UK, Germany, Denmark, Italy, Spain, Sweden, France, Italy, Netherlands)***, covering some 350,000 participants.

As part of the InterAct project, the researchers did a study which included 12,403 type 2 diabetes cases and a random sub-cohort of 16,154 identified within EPIC. The researchers found that, after adjusting for confounding factors, consumption of one 12oz (336ml) serving size of sugar-sweetened soft drink per day increased the risk of type 2 diabetes by 22%. This increased risk fell slightly to 18% when total energy intake and body-mass index (BMI) were accounted for**** (both factors that are thought to mediate the association between sugar-sweetened soft drink consumption and diabetes incidence). This could indicate that the effect of sugar-sweetened soft drink on diabetes goes beyond its effect on body weight.

The authors also observed a statistically significant increase in type 2 diabetes incidence related to artificially sweetened soft drink consumption, however this significant association disappeared after taking into account the BMI of participants; this probably indicates that the association was not causal but driven by the weight of participants (i.e. participants with a higher body weight tend to report higher consumption of artificially sweetened drinks, and are also more likely to develop diabetes). Pure fruit juice and nectar***** consumption was not significantly associated with diabetes incidence, however it was not possible using the data available to study separately the effect of 100% pure juices from those with added sugars.

The authors say the increased risk of diabetes among sugar-sweetened soft drink consumers in Europe is similar to that found in a meta-analysis of previous studies conducted mostly in North America (that found a 25% increased risk of type 2 diabetes associated with one 12 oz daily increment of sugar-sweetened beverage consumption).

Dr Romaguera concludes: “Given the increase in sweet beverage consumption in Europe, clear messages on the unhealthy effect of these drinks should be given to the population.”

###

Notes to editors:

*The increased risk of 22% is for each extra 12oz sugar sweetened drink, so would apply to someone who had 1 drink versus someone who had 0, or someone who had 2 drinks versus someone who had 1, etc.

**The InterACT consortium is investigating, among other things, nutritional factors and physical activity to study the association of nutritional, dietary and physical activity behaviours with incident diabetes in the nested case-cohort study and to contribute to the analysis of gene-lifestyle interaction. It is a sub-division of the EPIC study, which was designed to investigate the relationships between diet, nutritional status, lifestyle and environmental factors and the incidence of cancer and other chronic diseases.

***The centres involved were France, Italy, Spain, Denmark, UK (Oxford, Cambridge), Netherlands (Bilthoven, Utrecht), Germany (Heidelberg, Potsdam), Sweden (Umea, Malmo)

****Extra info from Dr Romaguera:  The 22% figure is used as the top line because it is widely accepted by the scientific community that these models should not be adjusted for BMI. In the meta-analysis comparison with other studies from the USA, the risk is those studies is NOT adjusted by BMI. That makes it possible to compare the two sets of results (25% increased risk in North American studies versus 22% in Europe).

*****nectars (UK and USA definition) are fruit juices that have been diluted to some extent and may contain additives (sugar or sweeteners)

Dairy Industry Wants to Put Aspartame in Milk ” would particularly benefit school children “

By NICK MCCANN

WASHINGTON (CN) – Dairy industry groups have asked the Food and Drug Administration to be able to put artificial sweeteners in milk, and not change the label, claiming that it is so consumers can “more easily identify its overall nutritional value”.

Read Courthouse News’ Environmental Law Review.

The Food and Drug Administration is asking for data related to those sweeteners.

The International Dairy Foods Association (IDFA) and the National Milk Producers Federation (NMPF) filed a petition in 2009 requesting that the FDA amend its standard of identity for milk.

The petition asked the agency to allow the use of “any safe and suitable” sweetener for milk and asked to amend the standards of identity for 17 other milk and cream products.

Those products include sweetened condensed milk, whipping cream, yogurt and eggnog, which the groups say should be allowed to have “safe and suitable” sweeteners.

The groups request that the FDA “allow optional characterizing flavoring ingredients used in milk (e.g. chocolate flavoring added to milk) to be sweetened with any safe and suitable sweetener – including non-nutritive sweeteners such as aspartame.”

FDA regulations currently only allow milk products to contain “nutritive sweeteners” (those with calories) which the agency generally recognizes as safe.

The groups say the amendments “would promote more healthful eating practices and reduce childhood obesity by providing for lower-calorie flavored milk products.”

“They state that lower-calorie flavored milk would particularly benefit school children who, according to IDFA and NMPF, are more inclined to drink flavored milk than unflavored milk at school,” the FDA wrote in its notice.

The groups also say they would help with programs that aim to improve nutrition in school meals and argue that the proposed amendments would promote “honesty and fair dealing in the marketplace,” the FDA wrote.

The agency published a notice of the petition on Wednesday requesting comments, data, and information about the proposed amendment to the identity of milk products. The comments are due by May 21

http://www.courthousenews.com/2013/02/21/55075.htm

Sugary soft drinks may raise risk of depression – with diet versions causing the most harm

  • Four cans of pop a day raised depression  risk 30%
  • But drinking four cups of coffee decreased  risk by 10%

By  Fiona Macrae

PUBLISHED: 16:12 EST, 8  January 2013 |  UPDATED: 20:46 EST, 8 January 2013

Cutting out sweetened diet drinks could lower risk of depression, say researchers
Cutting out sweetened diet drinks could lower risk of  depression, say researchers

If you are feeling low, it may be best to lay  off the fizzy drinks and have a cup of coffee instead.

A study has linked soft drinks to depression  – with diet versions particularly problematic.

Coffee, however, appeared to have the  opposite effect.

The finding comes from US researchers who  studied the drink consumption of 265,000 men and women aged 50 to 71.

Ten years into the study, the volunteers were  asked if they had been diagnosed with depression in the previous five  years.

Those who drank more than four cans of soft  drinks a day were 30 per cent more likely to have had depression than those who  drank none, the American Academy of Neurology conference heard. The risk seemed  greater among those who preferred diet drinks.

The researchers said this may be due to the  presence of the artificial sweetener aspartame, which yesterday was  provisionally given a clean bill of health by the European Food Safety  Authority, following a review.

Unsweetened coffee could lower the risk of depression
Unsweetened coffee could lower the risk of  depression

Making the link does not prove soft  drinks  cause depression.

But researcher Honglei Chen said: ‘While our  findings are preliminary and the underlying biological mechanisms are  not  known, they are consistent with a small but growing body of evidence suggesting  that artificially sweetened beverages may be associated with poor health.’

The study found that those who had  four cups  of coffee a day were 10 per cent less likely to become  depressed than  non-coffee drinkers.

Dr Chen said this may be due to the  caffeine  in coffee stimulating the brain.

The British Soft Drinks Association  urged  caution over the findings and pointed out that the scientists  themselves said  that more research is needed.

Previous studies have linked soft drinks to  heart attacks, diabetes, weight gain, brittle bones and pancreatic  cancer.

Read more: http://www.dailymail.co.uk/health/article-2259047/Sugary-soft-drinks-raise-risk-depression–diet-versions-cause-harm.html#ixzz2HScIKApu Follow us: @MailOnline on Twitter | DailyMail on Facebook

Excessive fructose may be making ‘spoiled appetites’ a thing of the past

 

Posted by January 8, 2013

Back in the day, one of the most common admonitions from moms was “don’t eat that, you’ll spoil your appetite.” But if today’s kids are consuming foods and drinks with higher levels of super-sweet fructose, such as are found in high fructose corn syrup, the very opposite may be true.

According to the results of a new study published at the beginning of January in The Journal of the American Medical Association (JAMA), a brain on fructose just doesn’t know when to stop eating.

Drinking a fructose-sweetened beverage, the researchers found, created no sense of having ‘had enough’ giving a “completely different effect” than did the consumption of a beverage containing glucose (which makes up 50 percent of ‘real’ sugar).

“When we gave participants a fructose drink…there was not that fullness signal getting  up to the appetite control region,” said study co-author Dr. Kathleen Page, Assistant Professor of Clinical Medicine at Keck School of Medicine of University of Southern California (USC).

Glucose, however, had the “opposite” effect, Dr. Page noted, in that it “basically inhibited those regions of the brain called the hypothalamus and reward regions…that regulate motivation for food.”

The study, conducted with 20 volunteers using MRI scans to view brain blood flow, was, Dr. Page said, “exactly” what had previously been seen in lab experiments with animals.

The Corn Refiners Association (CRA), quick to notice any mention of ‘overeating’ and ‘fructose’ in the same sentence, sent out a press release the same day the study was released saying that the study involved “massive doses of sugars” not consumed in “real life.”

“I don’t think that’s a true comment if you look at the amount (of sweetener) in a typical 20-ounce soda, which is 60 grams,” Dr. Page said. “We gave 75 grams so it’s not that much different.”

An ‘unbalanced’ formula with different results

The fructose in sugar, or sucrose, is a set amount of 50 percent with the other half being glucose. In high fructose corn syrup, however, research has shown the amount of fructose varies widely. And even though the CRA doesn’t talk about it, HFCS that is up to 90 percent fructose is apparently being sold for use in some foods and beverages.

“That’s why we are interested, we know there are differences in the way our bodies process fructose and glucose…there are reasons to believe that fructose is worse for us than glucose,”  Dr. Page said, adding “the processing of HFCS, which could be made with higher percentages of fructose…has public health implications.”

While the FDA’s legal limit on the fructose content of HFCS is 55 percent (ten percent higher than sugar), some studies have shown amounts in soft drinks to be as much as 20 percent higher. Research by Dr. Michael Goran, director of the Childhood Obesity Research Center and professor of preventive medicine at the University of Southern California, found some of the HFCS-sweetened beverages he had analyzed coming in as high as 65 percent fructose. And a recent study in the journal Global Public Health by Dr. Goran pegged HFCS as an “additional contributing factor” to the development of diabetes, likely coming from the “more damaging” fructose in HFCS.

(This past September, Citizens for Health filed a petition with the FDA calling for disclosure of the actual amounts of fructose in HFCS. Read about it here, and sign the petition here).

“It’s hard to know (fructose amounts) as foods don’t state their fructose content, just (total) sugars,” Dr. Page said, pointing out “most people aren’t aware of how much fructose they’re getting in these foods. If Dr. Goran’s study is true, we may actually be getting more fructose than we think.

“We know there are very different hormone responses, and these hormones signal to the brain to make us feel full,” said Dr. Page.  “The body is responding differently to fructose than to glucose, we’re pretty confident with that.”

Dr. Page said she tells her patients a good strategy for healthier eating is to follow the recommendations of the American Heart Association, which include consuming fewer processed products. “You don’t find HFCS in natural foods,” she added.

http://foodidentitytheft.com/excessive-fructose-may-be-making-spoiled-appetites-a-thing-of-the-past/

 

High Fructose Corn Syrup Direct Correlation with Autism in the U.S. – Clin Epigenetics. 2012

EEV: Highlights Although there are many potential causes. We chose to highlight HFCS, due to its toxin amplification.

1) Ca, Mg and Zn, or losses or displacement of any of these minerals from the consumption of HFCS

2) mercury (Hg) and fructose may both modulate PON1 activity

3) mercury (Hg) that may occur from the low Hg concentrations sometimes found in HFCS as a result of the manufacturing process

4) HFCS, may further enhance the toxic effects of lead (Pb) on cognitive and behavioral development in children

2nd Source http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378453/

Initial Study date: 10 APR 2012

A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States

Renee Dufault1,2*Walter J Lukiw3Raquel Crider4Roseanne Schnoll5David Wallinga6 and Richard Deth7

Author Affiliations

1 Food Ingredient and Health Research Institute, Ocean View, HI, USA

2 United Tribes Technical College, Bismarck, ND, USA

3 Department of Neuroscience and Ophthalmology, Louisiana State University Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA

4 Shepherd University, Shepherdstown, WV, USA

5 Department of Health and Nutrition Sciences, Brooklyn College of City, University of New York, Brooklyn, NY, USA

6 Institute for Agriculture and Trade Policy, Minneapolis, MN, USA

7 Department of Pharmaceutical Sciences, Northeastern University, Boston, MA, USA

For all author emails, please log on.

Clinical Epigenetics 2012, 4:6 doi:10.1186/1868-7083-4-6

The electronic version of this article is the complete one and can be found online at: http://www.clinicalepigeneticsjournal.com/content/4/1/6

Received: 9 December 2011
Accepted: 10 April 2012
Published: 10 April 2012

© 2012 Dufault et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The number of children ages 6 to 21 in the United States receiving special education services under the autism disability category increased 91% between 2005 to 2010 while the number of children receiving special education services overall declined by 5%. The demand for special education services continues to rise in disability categories associated with pervasive developmental disorders. Neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors, such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as mercury or organophosphate pesticides. Gene expression patterns differ geographically between populations and within populations. Gene variants of paraoxonase-1 are associated with autism in North America, but not in Italy, indicating regional specificity in gene-environment interactions. In the current review, we utilize a novel macroepigenetic approach to compare variations in diet and toxic substance exposure between these two geographical populations to determine the likely factors responsible for the autism epidemic in the United States.

Keywords:

Autism; DNA methylation; Environmental epigenetics; Heavy metals; HFCS; PON1; SAM; Zn

Introduction to macroepigenetics with autism as a case study

Autism is a developmental disorder defined by the American Psychiatric Association (APA) in the Diagnostic and Statistical Manual of Mental Disorders (DSM). The condition is considered a pervasive developmental disorder (PDD) that appears in the first three years of life and affects brain development impacting social and communication skills. Autism is defined by a common set of behaviors, including, but not limited to, observed deficits in nonverbal and verbal communication, lack of social reciprocity, and failure to develop and maintain appropriate peer relationships [1]. Recent estimates suggest that 31% of children with Autism Spectrum Disorder (ASD) also meet diagnostic criteria for Attention-Deficit/Hyperactivity Disorder (ADHD) and another 24% of children with ASD exhibit sub-threshold clinical symptoms for ADHD [2]. The number of children affected by this debilitating disorder remains unknown. As part of this review, we analyze the current United States (U. S.) Department of Education Special Education data to estimate the increase in autism prevalence from 2005 to 2010.

The cause(s) of autism also remain(s) unknown. D’Amelio et al. found paraoxonase-1 (PON1) gene variants associated with autism in subgroups of the U. S. population but not in Italy [3]. They attributed the gene variation to greater household use of organophosphate (OP) pesticides in the U.S. compared to Italy. We think a more plausible explanation may lie in the U. S. food supply. As part of this investigation, we also reviewed and analyzed the U.S. Department of Agriculture (USDA) Food Availability Spreadsheets to identify which foods are most frequently consumed by Americans and of those which most frequently contain OP pesticide residue as reported by the U.S. Pesticide Data Program.

During this investigation, we conducted a literature review of all studies published on autism since we published our first Mercury Toxicity Model [4], which explains how mercury exposure, nutritional deficiencies and metabolic disruptions contribute to the development of autism. We evaluated all of the relevant studies and expanded our Mercury Toxicity Model. We then used the expanded model to compare the U.S. and Italian populations to determine what, if any, factors could explain the difference in PON1 gene variation and autism prevalence between the two countries. We propose the term “macroepigenetics” to describe the process of examining food supplies and their impact on body metabolism and gene function along with what is known about environmental exposures across populations.

In studying the larger factors outside the gene and human body that impact gene expression, we can better explain some of the gene-environment interactions that create disease conditions such as autism. There is agreement among many in the psychiatry profession that gene-environment interaction research is essential to understanding the etiology of autism and the other pervasive developmental disorders found in the ASD category [5]. How the scientific community arrives at this understanding is key to solving the problem of rising autism prevalence. By demonstrating the macroepigenetic approach to determine the factors likely responsible for the autism prevalence in the U.S., we hope more scientists will follow our interdisciplinary lead and use macroepigenetics as a research strategy.

Current U. S. autism prevalence and special education trends

Before the 1980s the prevalence of autism in the U. S. was about 0.05% [6]. In 2006, the Center for Disease Control and Prevention (CDC) reported that the estimated prevalence of autism had increased to between 0.6 and 0.7% of all children [7]. Many scientists and parents believe the autism prevalence rate in the U.S. is much higher than these CDC statistics indicate. U.S. government scientists and collaborators published an article in 2007 indicating that 1.1% of U.S. children aged 3 to 17 years were currently diagnosed with ASD [8].

Special education data have been used in the past to estimate autism prevalence trends in the U.S. [9]. In birth cohorts from 1975 to 1995, increases in autism were greatest for annual cohorts born from 1987 to 1992 [9]. From 1992 to 1995, the autism prevalence increased with each successive year but the increases did not appear as great [9]. Our review of the current special education data indicates the number of children ages 6 to 21 receiving special education services under the Autism category has increased 91% from 2005 to 2010. The number of children in the Developmental Delay category has increased 38% and the number of children receiving special education and related services under the Other Health Impaired (OHI) category has increased 26% from 2005 to 2010. Children with a diagnosis of ADHD are included in the OHI category. These increases are startling given that the overall number of children receiving special education services decreased by 5% from 2005 to 2010. Table 1 provides a graphical representation of the data obtained from the Data Accountability Center and analyzed during this review [10].

Table 1. Number of U.S. students ages 6 to 21 receiving special education services by disability category and year

Data from the 1997 to 2008 National Health Interview Surveys conducted by the CDC confirm these findings of increasing prevalence in autism and developmental disabilities associated with or sharing the diagnostic criteria for autism [11]. Regardless of the source of data it seems clear that autism prevalence is rising in the U.S. compared to other countries, such as Italy, where the autism prevalence in the general population is estimated at only 0.1% [12]. Because autism prevalence rates vary by country, population and geographic location, it is becoming more evident that gene-environment interactions are at play with dietary factors. The influence of environment factors on gene expression is primarily mediated by epigenetic mechanisms, including deoxyribonucleic acid (DNA) methylation along with methylation, acetylation, ubiquitination and phosphorylation of histones. Epigenetic regulation is particularly important during neurodevelopment [13].

A macroepigenetic model to explain gene-environment interactions in autism

In public health, epidemiology arguably has led the way in researching gene-environment interactions by studying how genotypes, environmental exposures and disorder outcomes occur in the human population [5]. However, this epidemiological approach has often resulted in contradictory scientific conclusions when its practitioners do not consider the dietary factors that interact and modulate the molecular and genetic mechanisms underlying human metabolism and brain function [14]. This has been the case despite the existence of literature from the field of “nutrigenomics”, which has specifically studied the effects of food and food ingredients on gene expression. In identifying the public health and the social and/or environmental determinants of disease, it seems invalid to study epidemiology without nutrigenomics, or vice versa. In other words, a more macro-level approach to unraveling the full range of environmental and genetic factors contributing to these kinds of neurological disorders ought to include nutrition factors as a component of the environment. By combining information derived from both nutrigenomic and epidemiology studies, a macroepigenetic model has already been developed to explain some of the gene-environment interactions with dietary factors that lead to the development of autism and ADHD [4].

Figure 1 shows the Mercury Toxicity model that provides a macroepigenetic explanation of how human neurodevelopment can be adversely impacted when gene expression is altered by dietary transcription factors such as zinc insufficiency or deficiency, or by exposure to toxic substances found in our environment, such as the heavy metals mercury and copper [4]. Elimination of heavy metals requires the expression of the metallothionein (MT) gene, which synthesizes the Zn-dependent metal binding protein metallothionein [15]. With dietary zinc (Zn) loss and copper (Cu) gain from the consumption of high fructose corn syrup (HFCS) [16], metabolic processes required to eliminate heavy metals are impaired in children with autism [4]. Mercury has been found in samples of high fructose corn syrup and is allowable in trace amounts in certain food colors so long as the concentration does not exceed one part per million [17,18]. Mercury (Hg) and specific other heavy metals, including lead (Pb), copper (Cu), cadmium (Cd), silver (Ag) and bismuth (Bi), are capable of displacing the Zn atom in the MT protein molecule [15]. This ‘pathogenic’ displacement of Zn impairs the MT molecule and its ability to pick up the heavy metal and carry it out of the body. If the diet is deficient in Zn or the absorption of Zn is impaired, then the body may not produce enough MT protein to carry and excrete the heavy metal load [19,20]. Children with autism may be Zn deficient and often have MT dysfunction [2123]. Because of their diminished capacity to excrete toxic heavy metals, the severity of their condition is associated with their toxic metal burden [24]. This macroepigenetic model proposes that autism prevalence is related to the consumption of HFCS and the overall exposure to Hg in the U.S. [4]. However, other dietary factors associated with the consumption of HFCS may further contribute to the development of autism in the U.S.

                        Figure 1. The original Mercury Toxicity Model. The original Mercury Toxicity Model was published in 2009 by Dufault et al. in the Behavioral and Brain Functions journal. The model is a flow chart of what can happen in the body when there is exposure to mercury (Hg) from ingestion of foods (via HFCS, food colors and fish) or inhalation of air. Human neurodevelopment can be adversely impacted when MT gene expression is altered or suppressed by dietary transcription factors such as zinc (Zn) insufficiency or deficiency. Without proper MT expression and function, mercury excretion may not be possible and oxidative stress in the brain from mercury insult leads to reduced neuronal plasticity and impaired learning. Hg in fish is a problem when there is not enough selenium (Se) in the fish to counteract the Hg and the glutathione (GSH) system is disrupted leading to further oxidative stress.

Additional dietary factors associated with consumption of HFCS

U.S. per capita consumption of HFCS in 2009 was 35.7 pounds per year [25]. The peak years for annual consumption of HFCS coincided with the peak growth rates of ASD in California, the only state that reports number of cases of ASD dating back to the mid-1980s [4]. The Mercury Toxicity Model shows the HFCS characteristics most likely contributing to autism include the zinc-depleting effect that comes from consuming HFCS and certain food colors found in processed foods, and the additional Hg exposure that may occur from the low Hg concentrations sometimes found in HFCS as a result of the manufacturing process [4,17]. This model can be expanded to include additional adverse effects associated with the consumption of HFCS that likely contribute to the development of autism through PON1 gene modulation and lead intoxication.

U.S. Department of Agriculture (USDA) scientists warn that when dietary intake of magnesium (Mg) is low, consumption of HFCS leads to lower calcium (Ca) and phosphorus (P) balances adversely affecting macromineral homeostasis in humans [26]. This is an unfortunate finding because there is evidence to suggest that dietary intake of Mg is low among Americans, most of whom consume a high fructose diet. In 2003, CDC scientists reported that substantial numbers of U.S. adults fail to consume adequate Mg in their diets [27]. Children with autism were found to have significantly lower plasma Mg concentrations than normal subjects [28]. Adams et al. found significant reductions in red blood cell (RBC) Ca, serum and white blood cell (WBC) Mg and an increase in RBC copper in autistic children as compared to controls [29]. Recently, USDA scientists reported that the National Health and Nutrition Examination Survey (NHANES) data for 2005 to 2006 indicate that overall, nearly one half of all individuals one year and over had inadequate intakes of dietary Mg [30]. With a substantial number of Americans consuming inadequate amounts of dietary Mg along with HFCS diets, one may predict that substantial numbers of Americans are likely experiencing a calcium (Ca) deficit as well.

Insufficient intake of dietary Ca, Mg and Zn, or losses or displacement of any of these minerals from the consumption of HFCS, may further enhance the toxic effects of lead (Pb) on cognitive and behavioral development in children [31]. A significant and independent inverse relationship between dietary Ca intake and blood Pb concentrations was found in 3,000 American children examined as part of NHANES II [32]. Elevated blood Pb levels are indicative of Pb intoxication, which is found in some children diagnosed with autism and associated with the development of ADHD [33,34]. It may be that inadequate intake of Ca or Mg combined with a HFCS zinc-depleting diet increases the risk of developing autism and ADHD from Pb intoxication.

Inadequate intake of Ca or Mg may further contribute to these developmental disorders by impacting human serum paraoxonase-1 (PON1) gene expression. PON1 is a calcium dependent enzyme responsible for OP pesticide detoxification as well as hydrolysis of the thiolactone form of homocysteine [35,36]. PON1 is synthesized in the liver and secreted in blood where it is incorporated into high density lipoproteins (HDL). The availability and catalytic activity of PON1 are impaired in many children with ASD making them more susceptible to the toxic effects of OP pesticide residues which are most frequently found in grain [37,38]. Figure 2 shows the expanded Mercury Toxicity Model that includes changes both in Pb toxicity and PON1 activity when dietary intake of Mg is low and consumption of HFCS leads to greater loss of calcium (Ca) and phosphorus (P), thereby adversely affecting macromineral homeostasis.

Figure 2. The expanded Mercury Toxicity Model. Figure 2 shows the expanding Mercury Toxicity Model that includes changes both in lead (Pb) toxicity and human serum paraoxonase (PON1) activity when dietary intake of Mg is low and consumption of high fructose corn syrup (HFCS) leads to lower calcium (Ca) and phosphorus (P) balances, adversely affecting macromineral homeostasis. With insufficient dietary intake of Ca and/or Mg, children become more susceptible to Pb intoxication and OP exposures with decreasing PON1 activity. Pb intoxication and OP exposures can both lead to oxidative stress in the brain reducing neuronal plasticity.

PON1 activity and organophosphate exposure in U.S

One can assert that with the consumption of a HFCS intensive diet and inadequate Mg intakes, PON1 activity may decrease, along with resulting Ca losses in genetically predisposed individuals. Although there are no human data yet to support this assertion, PON1 activity in rats decreased when fed a HFCS diet to mimic the human metabolic syndrome [39]. PON1 activity has been extensively studied in humans and there are a number of factors known to modulate or alter PON1 expression including, but not limited to, Hg exposure, sex and age [40,41]. Age plays the most relevant role, as PON1 activity is very low before birth and gradually increases during the first few years of life in humans [41]. In one study, scientists at UC Berkeley found the PON1 levels in many children may remain lower than those of their mothers for several years, especially those with genotypes associated with decreased PON1 activities [42]. The scientists concluded that these children may be more susceptible to OP pesticides throughout their childhood and more vulnerable to conditions associated with oxidative stress such as autism [42]. In a different study, scientists at UC Berkeley found that two-year-old children were less likely to display symptoms of PDD when their mothers had higher paraoxonase levels during their pregnancy [43]. Proper function and adequate expression of the PON1 gene is essential both for prenatal development and child health because exposure to OP pesticides is a common occurrence in the U.S.

The CDC tracks exposure to OP pesticides or their metabolites through the National Biomonitoring Program (NBP). Exposure data are reported for the population as a whole and for subgroups. While most American groups are exposed to OP pesticides, children ages 6 to 11 have significantly higher exposures than adults and are at greatest risk from OP neurotoxicity [44]. Harvard University researchers recently reported finding OP pesticide residues in a number of foods frequently consumed by children [45]. The researchers expressed concern that the children were at times being exposed to multiple pesticide residues in single food commodities. OP pesticide exposures occur primarily from the consumption of foods containing pesticide residues.

It is well known that pesticide exposure can impair neurodevelopment in children, but recent studies have found that pesticide exposure during pregnancy can also cause delayed mental development in children [46]. A review of epidemiological studies in 2008 found that prenatal and childhood exposure to OPs impairs neurobehavioral development [47]. Higher concentrations of urinary dialkyl phosphate (DAP) measured during pregnancy was significantly associated with lower cognitive scores in children at seven years of age. Those children in the highest quintile of maternal DAP concentrations had an IQ score seven points lower than those children in the lowest quintile [48]. In a group of newborns with the highest levels of the organophosphate chlorpyrifos measurable in their umbilical cord blood, birth weight averaged 150 grams less than the group with the lowest exposure [49]. Prenatal pesticide exposure showed deficits consistent with developmental delays of 1.5 to 2 years [49].

Diet is the main source of OP exposure in children. Under the 1996 Food Quality Protection Act, the U.S. Secretary of Agriculture is directed to collect pesticide residue data on commodities frequently consumed by infants and children. USDA Pesticide Data Program (PDP) provides the residue data to comply with this law [50]. We reviewed the PDP data from 2004 to 2008 and identified the foods most frequently found to contain organophosphate insecticide residues. In addition, we obtained the per capita availability data from the USDA to determine the amount of each food commodity the average American consumes [25]. The results of our review indicate that wheat and corn are the commodities most likely contributing to OP exposure in U. S. children. Estimated per capita wheat consumption was approximately 95 pounds per year while estimated per capita corn consumption was approximately 23 pounds per year. The primary use of corn is for the production of corn sweeteners, such as HFCS; however, pesticide residue data were not gathered for this commodity by the PDP. Table 2 provides a complete breakdown of the results of this data review.

Table 2. PDP residue detections by year sampled wi th U.S. per capita consumption data

From Table 2 it is clear consumers are at risk of exposure to multiple OP pesticide residues from consuming the very same commodity. Cumulative exposures will continue to occur in the U.S. where OP pesticide use is widespread by the agricultural industry. Although OP pesticide use is equally widespread in other countries, there is genetic variation across populations that determine degree of susceptibility to OP exposure. The PON1 gene variants associated with autism in subgroups of the U.S. population but not in Italy could be attributed to the fact that HFCS consumption rarely occurs in Italy, thereby lessening the conditions for PON1 modulation.

HFCS consumption and PON1 modulation in autism in the U.S

In the 27-member European Union (EU), of which Italy is an original participant, HFCS is known as “isoglucose” and currently it is rarely consumed by Italians. Americans on the other hand consume on average 35.7 pounds per year, which may increase their overall Hg exposure [17,25]. Figure 3 shows U.S. per capita food consumption in pounds per year for HFCS beginning in the early 1970s and increasing throughout the 1980s to reach a peak between 1999 and 2002. In our previous publication, we reported the peak years for annual consumption of HFCS in the U.S. occurred within the same period as when the annual growth rates of autism peaked in California [4].

Figure 3. U.S. per capita consumption of high fructose corn syrup 1966-2004. Figure 3 shows the United States (US) per capita consumption of high fructose corn syrup (HFCS) in pounds per year as calculated by the United States Department of Agriculture (USDA)/Economic Research Service.

American per capita consumption of HFCS has exceeded 20 pounds per year since 1980 while Italians consume negligible amounts of the same ingredient. As was previously mentioned, mercury (Hg) and fructose may both modulate PON1 activity [3941]. While excessive fructose exposure in the U.S. may primarily occur through the consumption of foods containing HFCS, mercury exposure may occur in a number of ways. A comparison of common sources of mercury exposure in the U.S. and Italy may offer a further explanation of the PON1 gene variation associated with autism in the U.S. but not in Italy.

In addition to HFCS, primary sources of inorganic and elemental Hg exposure may occur from consumption of food colors and preservatives made with mercury-cell chlorine or chlor-alkali products, seafood consumption, Hg in dental amalgam, thimerosal in vaccines, and depending on geographic location, inhalation of Hg contaminated air [4,5154]. Children living near coal-fired power plants are often exposed to higher levels of Hg in their breathing air and have a higher prevalence of autism [55]. Because Hg emissions from coal-fired power plants are not yet regulated in either the U.S. or Italy, this particular source of Hg exposure is unlikely to explain the overall difference in autism prevalence between these two countries. With respect to the consumption of seafood, use of Hg dental amalgam, thimerosal in vaccines or Hg-containing food colors and preservatives, there is also no appreciable difference between Italy and the U.S. [5658]. The only remaining variable in our model is the excessive consumption of HFCS by Americans, which results in greater chronic exposures to both inorganic Hg and, by definition, fructose [4].

Inorganic Hg may interact with cysteine residues on PON1 preventing its activation in the liver and impairing the body’s ability to protect itself against OP pesticides and oxidative stressors involved in autism [41]. As noted above, PON1 is responsible for hydrolysis of homocysteine thiolactone, and plasma PON1 activity is negatively correlated with homocysteine levels [36,59]. Homocysteine is a metabolic biomarker for oxidative stress and impaired methylation capacity. A recent study of the Inuit population found a significant inverse correlation between PON1 activity and Hg levels, as well as a direct correlation with selenium levels [60]. With increasing Hg and fructose exposure and reductions in dietary Ca, one can expect to see reduced PON1 activity and increasing homocysteine levels in children with ASD.

Indeed, Pasca et al. recently reported finding that both PON1 arylesterase and PON1 paraoxonase activities were decreased in children with autism [61,62]. James et al. found that children with autism had higher plasma homocysteine levels than controls but demonstrated significant improvements in transmethylation metabolites and glutathione (GSH) after receiving folate and vitamin B12 [63]. Patel and Curtis found that in addition to glutathione and B12 injections one to three times per week, children with autism and ADHD showed significant improvement in many areas of social interaction, concentration, writing, language and behavior when fed an organic diet low in fructose and free of food additives and food colors [64].

Mothers of autistic children in the U.S. were also found to have significant increases in mean plasma homocysteine levels compared to controls [65]. Schmidt et al. found that women who took vitamin supplements during the periconceptional period reduced the risk of autism in their children [66]. Those women who did not take vitamins during this period were more likely to have a child with autism and were at even greater risk when they had specific genetic variants within one-carbon metabolism pathways. This suggests that folate and other dietary methyl donors may alter epigenetic regulation of gene expression in their children, thereby reducing the risk of autism [66].

Methionine synthase links oxidation to epigenetics

Epigenetic regulation of gene expression is highly dependent upon methylation of both DNA and histones, and methylation capacity is in turn dependent upon activity of the folate and vitamin B12-dependent enzyme methionine synthase, which converts homocysteine to methionine. Lower methionine synthase activity decreases the level of the methyl donor S-adenosylmethionine (SAM) while simultaneously increasing the level of the methylation inhibitor S-adenosylhomocysteine (SAH) [67]. The combined effect of changes in the SAM to SAH ratio, therefore, exerts a powerful influence over more than 200 methylation reactions, including DNA and histone methylation [68].

Methionine synthase activity is inhibited by oxidative stress, and its inhibition results in the diversion of homocysteine to produce the antioxidant glutathione (GSH), providing an important adaptive response [69]. However, oxidative inhibition of methionine synthase leads to epigenetic effects via the resultant decrease in the SAM to SAH ratio and decreased DNA and histone methylation. Epigenetic changes in gene expression can recruit further adaptive responses to oxidative stress. Figure 4 illustrates how these changes may occur when the body is under oxidative stress from exposure to OP pesticides, heavy metals, and calcium depleting substances, such as HFCS. Decreased methionine synthase activity during oxidative stress also increases homocysteine thiolactone formation [70], raising the importance of PON1. As was previously mentioned, PON1 is essential for reducing homocysteine levels, which are thought to be harmful. Elevated plasma homocysteine (tHcy) levels are associated with genome-wide DNA hypomethylation that may carry over from one generation to the next, increasing the risk of autism [71]. Epigenetic changes affecting germline cells can give rise to these transgenerational effects [72]. James et al. found that parents share similar metabolic deficits in methylation capacity and glutathione-dependent antioxidant/detoxification capacity with their children with autism [71].

Figure 4. Methionine synthase links oxidative stress to epigenetic regulation. Figure 4 shows how exposure to toxic substances, such as OP pesticides, HFCS, or heavy metals, inhibits methionine synthase through effects of oxidative stress. As a result, decrease of SAM to SAH ratio will lead to a decrease in DNA methylation and consequently to altered PON1 gene expression.

Synergistic effect of multiple neurotoxins

Based upon the discussion above, it is clear that methionine synthase activity is crucial for translating changes in oxidative status into epigenetic effects, and this role is confirmed by the improved metabolic profile in autistic subjects given folate and vitamin B12 [63]. This relationship has given rise to the “Redox/Methylation Hypothesis of Autism”, which proposed that oxidative insults arising from environmental exposures, such as Hg and pesticides, can cause neurodevelopmental disorders by disrupting epigenetic regulation [73]. The macroepigenetic Mercury Toxicity Model expanded in this paper provides additional support for the “Redox/Methylation Hypothesis of Autism” while contributing important insight into the oxidative stress feedback mechanisms that may occur as a result of malnutrition resulting from dietary exposures to toxins. The delivery of children exhibiting autistic behaviors might be associated with the prenatal diet of their mothers. The severity of these behaviors can be further exacerbated by toxic dietary exposures of the children, which can improve with dietary changes aimed at eliminating these exposures. Children with autism could well be exhibiting an epigenetic response to several neurotoxic substances at once, including, but not limited to, inorganic Hg, Pb, OP pesticides and/or HFCS. The combined effect of these substances acting together is likely greater than the sum of the effects of the substances acting by themselves. This effect likely reduces neuronal plasticity and impairs learning capacity in autistic children.

Conclusion

The number of children ages 6 to 21 in the U.S. receiving special education services under the autism disability category increased 91% between 2005 to 2010 despite fewer children receiving special education services overall during the same time period. A comparison of autism prevalence between the U.S. and Italy using the Mercury Toxicity Model suggests the increase in autism in the U.S. is not related to mercury exposure from fish, coal-fired power plants, thimerosal, or dental amalgam but instead to the consumption of HFCS. Consumption of HFCS may lead to mineral imbalances, including Zn, Ca and P loss and Cu gain and is a potential source of inorganic mercury exposure. These mineral imbalances create multiple pathways for oxidative stress in the brain from exposure to OP pesticides and heavy metals, such as Pb or Hg. Inorganic mercury and fructose exposure from HFCS consumption may both modulate PON1 gene expression. With a reduction in PON1 activity, there is a potential for increasing homocysteine levels which are associated with genome-wide DNA hypomethylation that may carry over from one generation to the next, affecting both neurodevelopment and autism prevalence.

Abbreviations

ADHD: Attention-Deficit-Hyperactivity-Disorder; Ag: Silver; APA: American Psychiatric Association; ASD: Autism Spectrum Disorder; Bi: Bismuth; Ca: Calcium; Cd: Cadmium; CDC: Center for Disease Control and Prevention; Cu: Copper; DAP: Dialkyl phosphate; DSM: Diagnostic and Statistical Manual of Mental Disorders; EU: European Union; GSH: Glutathione; HDL: High density lipoprotein; HFCS: High fructose corn syrup; Hg: Mercury; Mg: Magnesium; MT: Metallothionein; NBP: National Biomonitoring Program; NHANES: National Health and Nutrition Examination Survey; OHI: Other Health Impaired; OP: organophosphate pesticide; P: phosphorus; Pb: lead; PDD: Pervasive Developmental Delay; PDP: Pesticide Data Program; PON1: paraoxonase-1; RBC: red blood cell; SAH: S-adenosylhomocysteine; SAM: S-adenosylmethionine; tHcy: total plasma homocysteine; USDA: United States Department of Agriculture; WBC: White blood cell; Zn: Zinc.

Competing interests

RDeth has in the past received compensation as an expert witness on the topic of autism. All of the other authors declare that they have no competing interests.

Authors’ contributions

RDufault spearheaded the review and recruited interdisciplinary collaborators to contribute to the development of the manuscript. RDufault was the lead investigator and literature reviewer for the expansion of the mercury toxicity model. RDufault acquired, analyzed and interpreted the new data sets. WJL, RS and RDeth helped revise the manuscript critically for important intellectual content. RDeth provided Figure 4 and was the primary author of the methionine synthase section. All authors read and approved the final manuscript. RS validated all of the references. RC validated the data in Table 1 to ensure it was correctly gathered from existing data bases. RC also double checked the calculations in Table 1 to ensure they were error free. DW helped draft and edit the manuscript.

Lead author’s information

After retiring with honors from her position as an environmental health officer with the U.S. Public Health Service, R. Dufault obtained her teaching license and taught elementary special education for 3.5 years at which time she gained an understanding of how children with autism and ADHD in the U.S. receive special education services. As a volunteer, she currently teaches an epigenetics course on-line through the Food Ingredient and Health Research Institute.

Acknowledgements

The authors would like to thank Drs. Robert Lustig, Blaise LeBlanc and Steven Gilbert for the feedback each provided on this manuscript and/or the concepts therein. Funding for this research project was provided primarily by donations to the Food Ingredient and Health Research Institute. Research in the Lukiw laboratory is supported through Grant Number P20RR016456 from the National Center for Research Resources, a Translational Research Initiative Grant from LSU Health Sciences Center New Orleans, an Alzheimer Association Investigator-Initiated Research Grant IIRG-09-131729, and NIH NIA Grants AG18031 and AG038834.

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Eating Foods High in Fructose from Added Sugars Linked to Hypertension

 

 

 

Washington, DC (June 25, 2010) — People who eat a diet high in fructose, in the form

of added sugar, are at increased risk of developing high blood pressure, or

hypertension, according to a study appearing in an upcoming issue of the Journal of the

American Society Nephrology (JASN). The results suggest that cutting back on foods

and beverages containing a lot of fructose (sugar) might decrease one’s risk of

developing hypertension.

 

Hypertension is the most common chronic condition in developed countries and a major

risk factor for heart and kidney diseases. Researchers are striving to identify

environmental factors that might be responsible for the development of hypertension,

and they suspect that fructose may play a role. Over the past century, a dramatic

increase in the consumption of this simple sugar, which is used to sweeten a wide

variety of processed foods, mirrors the dramatic rise in the prevalence of hypertension.

 

To examine whether increased fructose consumption has contributed to rising rates of

hypertension, Diana Jalal, MD (University of Colorado Denver Health Sciences Center)

and her colleagues analyzed data from the National Health and Nutrition Examination

Survey (2003-2006). The study involved 4,528 US adults 18 years of age or older with no

prior history of hypertension. Study participants answered questions related to their

consumption of foods and beverages such as fruit juices, soft drinks, bakery products,

and candy. Dr. Jalal’s team found that people who consumed a diet of 74 grams or more

per day of fructose (corresponding to 2.5 sugary soft drinks per day) had a 26%, 30%,

and 77% higher risk for blood pressure levels of 135/85, 140/90, and 160/100 mmHg,

respectively. (A normal blood pressure reading is below 120/80 mmHg.)

 

“Our study identifies a potentially modifiable risk factor for high blood pressure.

However, well-planned prospective randomized clinical studies need to be completed to

see if low fructose diets will prevent the development of hypertension and its

complications,” said Dr. Jalal.

Princeton researchers find that high-fructose corn syrup prompts considerably more weight gain

2010 study posted for filing

Contact: Kitta MacPherson
kittamac@princeton.edu
609-258-5729
Princeton University

A sweet problem

IMAGE:A Princeton University research team, including (from left) undergraduate Elyse Powell, psychology professor Bart Hoebel, visiting research associate Nicole Avena and graduate student Miriam Bocarsly, has demonstrated that rats with…

Click here for more information. 

A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.

In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.

“Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn’t true, at least under the conditions of our tests,” said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. “When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they’re becoming obese — every single one, across the board. Even when rats are fed a high-fat diet, you don’t see this; they don’t all gain extra weight.”

In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.

The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.

IMAGE:When male rats were given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow, the animals gained much more weight than male rats that…

Click here for more information. 

The second experiment — the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals — monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet. In humans, this would be equivalent to a 200-pound man gaining 96 pounds.

“These rats aren’t just getting fat; they’re demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides,” said Princeton graduate student Miriam Bocarsly. “In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes.” In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.

High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars — it is 50 percent fructose and 50 percent glucose — but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.

This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.

In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.

“Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic,” Avena said.

The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.

In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet — the equivalent of a typical fast-food meal containing a hamburger, fries and soda — and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.

 

###

 

The research was supported by the U.S. Public Health Service.

Radio and TV News Broadcasts: Princeton University maintains at its Broadcast Center on campus both an ISDN line for conducting radio interviews with its faculty and experts and also a state-of-the-art, high definition video studio for conducting TV interviews with members of its campus community. The radio service is available during regular business hours free of charge to representatives of news organizations, while the TV studio is available to the news media on a fee basis. For more information, please: e-mail bctv@princeton.edu; call (609) 258-7872; or visit the center’s website at http://www.princeton.edu/bc/.

For Princeton University breaking news, visit: www.princeton.edu.

High fructose corn syrup: A recipe for hypertension

2009 study posted for filing

Contact: Shari Leventhal
sleventhal@asn-online.org
202-558-8423
American Society of Nephrology

Elevated dietary fructose linked to high blood pressure

A diet high in fructose increases the risk of developing high blood pressure (hypertension), according to a paper being presented at the American Society of Nephrology’s 42nd Annual Meeting and Scientific Exposition in San Diego, California. The findings suggest that cutting back on processed foods and beverages that contain high fructose corn syrup (HFCS) may help prevent hypertension.

Over the last 200 years, the rate of fructose intake has directly paralleled the increasing rate of obesity, which has increased sharply in the last 20 years since the introduction of HFCS. Today, Americans consume 30% more fructose than 20 years ago and up to four times more than 100 years ago, when obesity rates were less than 5%. While this increase mirrors the dramatic rise in the prevalence of hypertension, studies have been inconsistent in linking excess fructose in the diet to hypertension.

Diana Jalal, MD (University of Colorado Denver Health Sciences Center), and her colleagues studied the issue in a large representative population of US adults. They examined 4,528 adults 18 years of age or older with no prior history of hypertension. Fructose intake was calculated based on a dietary questionnaire, and foods such as fruit juices, soft drinks, bakery products, and candy were included. Dr. Jalal’s team found that people who ate or drank more than 74 grams per day of fructose (2.5 sugary soft drinks per day) increased their risk of developing hypertension. Specifically, a diet of more than 74 grams per day of fructose led to a 28%, 36%, and 87% higher risk for blood pressure levels of 135/85, 140/90, and 160/100 mmHg, respectively. (A normal blood pressure reading is below 120/80 mmHg.)

“These results indicate that high fructose intake in the form of added sugars is significantly and independently associated with higher blood pressure levels in the US adult population with no previous history of hypertension,” the authors concluded. Additional studies are needed to see if low fructose diets can normalize blood pressure and prevent the development of hypertension.

Study co-authors include Richard Johnson, MD, Gerard Smits, PhD, and Michel Chonchol, MD (University of Colorado Denver Health Sciences Center). Dr. Richard Johnson reports a conflict of interest as the author of “The Sugar Fix”. The authors report no other financial disclosures.

 

###

 

EDITOR: The study abstract, “Increased Fructose Intake is Independently Associated with Elevated Blood Pressure. Findings from the National Health and Nutrition Examination Survey (2003-2006),” (TH-FC037) will be presented as part of a Free Communications Session during the American Society of Nephrology’s 42nd Annual Meeting and Scientific Exposition on Oct. 29 at 4:24 pm in Room 2 of the San Diego Convention Center in San Diego, CA and on Oct. 30 at 12:30 pm in Room 12.

ASN Renal Week 2009, the largest nephrology meeting of its kind, will provide a forum for 13,000 professionals to discuss the latest findings in renal research and engage in educational sessions related to advances in the care of patients with kidney and related disorders. Renal Week 2009 will take place October 27 – November 1 at the San Diego Convention Center in San Diego.

Founded in 1966, the American Society of Nephrology (ASN) is the world’s largest professional society devoted to the study of kidney disease. Comprised of 11,000 physicians and scientists, ASN continues to promote expert patient care, to advance medical research, and to educate the renal community. ASN also informs policymakers about issues of importance to kidney doctors and their patients. ASN funds research, and through its world-renowned meetings and first-class publications, disseminates information and educational tools that empower physicians.

Heat forms potentially harmful substance in high-fructose corn syrup: Hydroxymethylfurfural (HMF)

2009 study posted for filing

Contact: Michael Woods m_woods@acs.org 202-872-6293 American Chemical Society

Researchers have established the conditions that foster formation of potentially dangerous levels of a toxic substance in the high-fructose corn syrup (HFCS) often fed to honey bees. Their study, which appears in ACS’ bi-weekly Journal of Agricultural and Food Chemistry, could also help keep the substance out of soft drinks and dozens of other human foods that contain HFCS. The substance, hydroxymethylfurfural (HMF), forms mainly from heating fructose.

In the new study, Blaise LeBlanc and Gillian Eggleston and colleagues note HFCS’s ubiquitous usage as a sweetener in beverages and processed foods. Some commercial beekeepers also feed it to bees to increase reproduction and honey production. When exposed to warm temperatures, HFCS can form HMF and kill honeybees. Some researchers believe that HMF may be a factor in Colony Collapse Disorder, a mysterious disease that has killed at least one-third of the honeybee population in the United States.

The scientists measured levels of HMF in HFCS products from different manufacturers over a period of 35 days at different temperatures. As temperatures rose, levels of HMF increased steadily. Levels jumped dramatically at about 120 degrees Fahrenheit. “The data are important for commercial beekeepers, for manufacturers of HFCS, and for purposes of food storage. Because HFCS is incorporated as a sweetener in many processed foods, the data from this study are important for human health as well,” the report states. It adds that studies have linked HMF to DNA damage in humans. In addition, HMF breaks down in the body to other substances potentially more harmful than HMF.

###

ARTICLE FOR IMMEDIATE RELEASE “Formation of Hydroxymethylfurfural in Domestic High-Fructose Corn Syrup and Its Toxicity to the Honey Bee (Apis mellifera)”

DOWNLOAD FULL TEXT ARTICLE http://pubs.acs.org/stoken/presspac/presspac/full/10.1021/jf9014526

CONTACT: Blaise W. LeBlanc, Ph.D. Carl Hayden Bee Research Center
Agricultural Research Service U.S. Department of Agriculture Tucson, Ariz. 85719 Phone: 520-792-1296 Fax: 520-792-1296 Email: blaise_LL@hotmail.com

Mercyhurst study aims to identify sucralose levels in beach water

Oct 10, 2012 | Posted in News Releases

Faculty and student researchers at Mercyhurst University continue to investigate the presence of potentially harmful chemicals in the beach waters of Presque Isle State Park and have added a new one to their list: sucralose.  A chlorinated form of sucrose found in artificial sweeteners, sucralose is used in an estimated 4,500 products ranging from Halloween candies to diet sodas.

Studies suggest that approximately 95 percent of ingested sucralose is not metabolized by the body and is excreted into the water supply, said Dr. Amy Parente, assistant professor of chemistry and biochemistry at Mercyhurst.

Many chlorinated compounds have been found to be toxic to humans and, while sucralose appears to have limited toxicity, the long-term effects of exposure have yet to be determined. Common practices aimed at removing contaminants from wastewater have not been shown to be successful at reducing levels of sucralose, Parente said.

Parente’s preliminary research has identified detectable levels of sucralose in local Lake Erie waters, which may pose concerns for the environment. She has received a grant from the Regional Science Consortium at the Tom Ridge Environmental Center to confirm these levels, with the ultimate goal of understanding the impact on the local aquatic ecosystem.

Sucralose in the water can have repercussions like altered water taste and biological health effects, she said. Another problem is that sucralose in the environment can provide a false signal for nutrient availability so organisms feeling that their food supply is adequate show decreased foraging behavior, which can ultimately affect their ability to survive.
Five undergraduate students are assisting in the research project. They are Erin Cox, Juliane Harmon, Michael Gigliotti, Gregg Robbins-Welty and Kristen Vidmar.

http://www.mercyhurst.edu/news/news-releases/article/?article_id=2730

 

Eating lots of carbs, sugar may raise risk of cognitive impairment, Mayo Clinic study finds

Contact: Nick Hanson newsbureau@mayo.edu 507-284-5005 Mayo Clinic

Those 70-plus who ate food high in fat and protein fared better cognitively, research showed

ROCHESTER, Minn. — People 70 and older who eat food high in carbohydrates have nearly four times the risk of  developing mild cognitive impairment, and the danger also rises with a diet heavy in sugar, Mayo Clinic researchers have found. Those who consume a lot of protein and fat relative to carbohydrates are less likely to become cognitively impaired, the study found. The findings are published in the Journal of Alzheimer’s Disease.

The research highlights the importance of a well-rounded diet, says lead author Rosebud Roberts, M.B., Ch.B., a Mayo Clinic epidemiologist.

“We think it’s important that you eat a healthy balance of protein, carbohydrates and fat, because each of these nutrients has an important role in the body,” Dr. Roberts says.

Researchers tracked 1,230 people ages 70 to 89 who provided information on what they ate during the previous year. At that time, their cognitive function was evaluated by an expert panel of physicians, nurses and neuropsychologists. Of those participants, only the roughly 940 who showed no signs of cognitive impairment were asked to return for follow-up evaluations of their cognitive function. About four years into the study, 200 of those 940 were beginning to show mild cognitive impairment, problems with memory, language, thinking and judgment that are greater than normal age-related changes.

Those who reported the highest carbohydrate intake at the beginning of the study were 1.9 times likelier to develop mild cognitive impairment than those with the lowest intake of carbohydrates. Participants with the highest sugar intake were 1.5 times likelier to experience mild cognitive impairment than those with the lowest levels.

But those whose diets were highest in fat — compared to the lowest — were 42 percent less likely to face cognitive impairment, and those who had the highest intake of protein had a reduced risk of 21 percent.

When total fat and protein intake were taken into account, people with the highest carbohydrate intake were 3.6 times likelier to develop mild cognitive impairment.

“A high carbohydrate intake could be bad for you because carbohydrates impact your glucose and insulin metabolism,” Dr. Roberts says. “Sugar fuels the brain — so moderate intake is good. However, high levels of sugar may actually prevent the brain from using the sugar — similar to what we see with type 2 diabetes.”

###

The study was funded by the National Institute on Aging.

About Mayo Clinic

Mayo Clinic is a nonprofit worldwide leader in medical care, research, and education for people from all walks of life. For more information, visit www.mayoclinic.org/about/ and www.mayoclinic.org/news.

Nick Hanson 507-284-5005 (days) 507-284-2511 (evenings) Email: newsbureau@mayo.edu

MULTIMEDIA ALERT: For audio and video of Dr. Roberts talking about the study, visit Mayo Clinic News Network.

Fructose-sweetened but not glucose-sweetened beverages can adversely affect both sensitivity to the hormone insulin and how the body handles fats

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation

Too much sugar is bad, but which sugar is worse: Fructose or glucose?

In 2005, the average American consumed 64kg of added sugar, a sizeable proportion of which came through drinking soft drinks. Now, in a 10-week study, Peter Havel and colleagues, at the University of California at Davis, Davis, have provided evidence that human consumption of fructose-sweetened but not glucose-sweetened beverages can adversely affect both sensitivity to the hormone insulin and how the body handles fats, creating medical conditions that increase susceptibility to heart attack and stroke.

In the study, overweight and obese individuals consumed glucose- or fructose-sweetened beverages that provided 25% of their energy requirements for 10 weeks. During this period, individuals in both groups put on about the same amount of weight, but only those consuming fructose-sweetened beverages exhibited an increase in intraabdominal fat. Further, only these individuals became less sensitive to the hormone insulin (which controls glucose levels in the blood) and showed signs of dyslipidemia (increased levels of fat-soluble molecules known as lipids in the blood). As discussed in an accompanying commentary by Susanna Hofmann and Matthias Tschöp, although these are signs of the metabolic syndrome, which increases an individual’s risk of heart attack, the long-term affects of fructose over-consumption on susceptibility to heart attack remain unknown.

###

TITLE: Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

AUTHOR CONTACT:
Peter J. Havel
University of California at Davis, Davis, California, USA.
Phone: (530) 752-6553; Fax: (530) 752-2474; E-mail: pjhavel@ucdavis.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=37385

ACCOMPANYING COMMENTARY

TITLE: Dietary sugars: a fat difference

AUTHOR CONTACT:
Matthias H. Tschöp
University of Cincinnati-College of Medicine, Cincinnati, Ohio, USA.
Phone: (513) 558-8648; Fax: (513) 558-8658; E-mail: tschoemh@ucmail.uc.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=39332

Not so sweet: Over-consumption of sugar linked to aging

2009 study posted for filing

Contact: Sylvain-Jacques Desjardins
sylvain-jacques.desjardins@umontreal.ca
514-343-7593
University of Montreal

University of Montreal scientists explain how sugar shortens lifespan in PLoS Genetics

This release is available in French.

From left to right: Antoine Roux, Pascal Chartrand, Gerardo Ferbeyre and Luis Rokeach.

Click here for more information.

Montreal, March 6, 2009 – We know that lifespan can be extended in animals by restricting calories such as sugar intake. Now, according to a study published in the journal PLoS Genetics, Université de Montréal scientists have discovered that it’s not sugar itself that is important in this process but the ability of cells to sense its presence.

Aging is a complex phenomenon and the mechanisms underlying aging are yet to be explained. What researchers do know is that there is a clear relationship between aging and calorie intake. For example, mice fed with half the calories they usually eat can live 40 percent longer. How does this work?

As part of the PLoS Genetics study, Université de Montréal Biochemistry Professor Luis Rokeach and his student Antoine Roux discovered to their surprise that if they removed the gene for a glucose sensor from yeast cells, they lived just as long as those living on a glucose-restricted diet. In short, the fate of these cells doesn’t depend on what they eat but what they think they’re eating.

There are two obvious aspects of calorie intake: tasting and digestion. By the time nutrients get to our cells there is an analogous process: sensors on the surface of the cell detect the presence of, for example, the sugar glucose and molecules inside the cell break down the glucose, converting it to energy. Of these processes, it is widely thought that the by-products of broken down sugars are the culprits in aging. The study by Rokeach and Roux suggests otherwise.

To understand aging, Rokeach and Roux in collaboration with Université de Montréal Biochemistry Professors Pascal Chartrand and Gerardo Ferbeyre used yeast as a model organism. At a basic level, yeast cells are surprisingly similar and age much like human cells, as well as being easy to study.

The research team found that the lifespan of yeast cells increased when glucose was decreased from their diet. They then asked whether the increase in lifespan was due to cells decreasing their ability to produce energy or to the decrease in signal to the cells by the glucose sensor.

The scientists found that cells unable to consume glucose as energy source are still sensitive to the pro-aging effects of glucose. Conversely, obliterating the sensor that measures the levels of glucose significantly increased lifespan.

“Thanks to this study, the link between the rise in age-related diseases and the over-consumption of sugar in today’s diet is clearer. Our research opens a door to new therapeutic strategies for fighting age-related diseases,” says Professor Rokeach.

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Partners in research:
Professor Rokeach’s research is supported by the Canadian Institutes of Health Research (www.cihr-irsc.gc.ca) and by the National Science and Engineering Research Council (www.nserc-crsng.gc.ca). Professor Ferbeyre’s and Professor Chartrand’s research are funded by the Canadian Institutes of Health Research (www.cihr-irsc.gc.ca)

On the web:
About PLoS Genetics: http://www.plosgenetics.org/home.action
About the Université de Montréal: www.umontreal.ca/english/index.html
About the Department of Biochemistry www.bcm.umontreal.ca
About Professor Rokeach www.mapageweb.umontreal.ca/rokeach/index-en.html
About Professor Ferbeyre http://www.mapageweb.umontreal.ca/ferbeyre/index-en.htm
About Professor Chartrand: http://www.bcm.umontreal.ca/bottin/chartrand.html

US researchers find traces of toxic mercury in high-fructose corn syrup

2009 report posted for filing

 

• Mercury linked to learning disabilities and heart disease
• Study published in peer-reviewed journal Environmental Health

 

A swig of soda or bite of a candy bar might be sweet, but a new study suggests that food made with corn syrup also could be delivering tiny doses of toxic mercury.

 

For the first time, researchers say they have detected traces of the silvery metal in samples of high-fructose corn syrup, a widely used sweetener that has replaced sugar in many processed foods. The study was published yesterday in the peer-reviewed journal Environmental Health.

 

Eating high-mercury fish is the chief source of exposure for most people. The new study raises concerns about a previously unknown dietary source of mercury, which has been linked to learning disabilities in children and heart disease in adults.

 

The source of the metal appears to be caustic soda and hydrochloric acid, which manufacturers of corn syrup use to help convert corn kernels into the food additive.

 

A handful of plants across the US still make the soda and acid by mixing a briny solution in electrified vats of mercury. Some of the toxic metal ends up in the final product, according to industry documents cited in the study.

 

Corn syrup manufacturers insisted their products are mercury-free. But the study noted that at least one maker of caustic soda that has used the mercury-based technology listed the corn syrup industry as a client.

 

“This seems like an avoidable source of mercury that we didn’t know was out there,” said David Wallinga, one of the study’s co-authors and a researcher at the Institute for Agriculture and Trade Policy, a Minnesota-based advocacy group.

 

The researchers cautioned that their study was limited. Only 20 samples were analyzed; mercury was detected in nine.

 

Still, the impact of the findings could be significant. High-fructose corn syrup has become such a staple in processed foods that the average American consumes about 12 teaspoons of it daily, according to federal estimates. Teenagers and young children tend to eat more of it than adults.

 

There is no established safe dose for elemental mercury, the type discovered in corn syrup. But the US Environmental Protection Agency says an average-sized woman should limit her exposure to 5.5 micrograms a day of methylmercury, the kind found in fish.

 

If that same woman regularly ate corn syrup contaminated at the highest level detected in the study – 0.57 micrograms per gram – the researchers estimated that she could end up consuming an amount of mercury that is five times higher than the EPA’s safe dose.

 

One former EPA scientist who reviewed the paper said more study is needed to establish the risk, if any, posed by contaminated corn syrup. She urged the Food and Drug Administration to conduct a review of food made with the sweetener.

 

“For the most part, previous studies haven’t found mercury in foods other than fish,” said Kathryn Mahaffey, a former EPA scientist who co-wrote a landmark report to Congress on the perils of mercury contamination. “Is this an outlier or something we didn’t know about before?”

 

In response to a 2005 Chicago Tribune series about mercury hazards, then-senator Barack Obama introduced legislation that would force chlorine plants to phase out its use or shut down. One plant in Wisconsin later vowed to switch to a mercury-free process by this year, leaving four others – in Georgia, Ohio, Tennessee and West Virginia – that still use the older technology.

 

The new study’s lead author, Renee Dufault, began her research while investigating the Wisconsin plant for the FDA in the mid-2000s. But her results weren’t published until now, a year after she retired from the agency.

 

An FDA spokesman said he still was waiting for a response to the study. Industry representatives, meanwhile, said the study was outdated.

 

“It is important that Americans are provided accurate, science-based information,” Audrae Erickson, president of the Corn Refiners Association, said in a statement. “They should know that high-fructose corn syrup is safe.”

 

In another statement, the Chlorine Institute said: “It is conceivable that measurable mercury content can be found in high-fructose corn syrup regardless of how it is processed.”

Genes remember sugar hit: Australian research: ” capable of permanently altering DNA “

2009 study posted for filing

Genes remember sugar hit: Australian research

 

SYDNEY (AFP) – Human genes remember a sugar hit for two weeks, with prolonged poor eating habits capable of permanently altering DNA, Australian research has found.

A team studying the impact of diet on human heart tissue and mice found that cells showed the effects of a one-off sugar hit for a fortnight, by switching off genetic controls designed to protect the body against diabetes and heart disease.

“We now know that chocolate bar you had this morning can have very acute effects, and those effects can continue for up to two weeks,” said lead researcher Sam El-Osta, from the Baker IDI Heart and Diabetes Institute.

“These changes continue beyond the meal itself and have the ability to alter natural metabolic responses to diet,” he told Australian Associated Press Friday.

Regular poor eating would amplify the effect, said El-Osta, with genetic damage lasting months or years, and potentially passing through bloodlines.

The study’s findings were reported in the Journal of Experimental Medicine.

 

Splenda may damage gut bacteria, boost weight gain: study

2008 study posted for filing

 

By Stephen Daniells

 

25-Sep-2008 – Consumption of the sweetener Splenda at doses within the US FDA’s Acceptable Daily Intake may suppress beneficial bacteria in the gut, and cause weight gain, says a new rat study.

 

According to findings published in the peer-reviewed Journal of Toxicology and Environmental Health, Part A, a 12-week feeding study with the sweetener also affected the expression of certain enzymes known to interfere with the absorption of nutrients and pharmaceuticals.

 

The study, performed by researchers from Duke University in North Carolina and co-sponsored by the Sugar Association, may raise questions about the safety profile of the sweetener, reported to be used as an ingredient in over 4,000 products worldwide.

 

McNeil Nutritionals, the company behind Splenda, was quick to dismiss the study and draw attention to a number of other studies supporting the safety of the sweetener. The company questioned the methodology and the conclusions drawn by the researchers. Emphasis was also placed on the involvement of the Sugar Association as partial sponsor of the study.

 

Study methodology

 

The Duke University researchers separated 50 male Sprague-Dawley rats into five equal groups. One group was administered only water with its diet, thereby acting as the control group, while the other four groups had the diet supplemented with different doses of Splenda in water. The doses used were 100, 300, 500, and 1,000 mg of Splenda per kg of body weight per day, equivalent to sucralose doses of 1.1, 3.3, 5.5, and 11 mg per kg per day.

 

“These dosage levels were selected because they span the range of values below and above the accepted daily intake (ADI) for sucralose of 5 mg/kg/d established by the U.S. Food and Drug Administration (FDA),” wrote the researchers, led by Professor Mohammed Abou-Donia.

 

Moreover, Professor Abou-Donia told FoodNavigator.com that the study was performed with rats because they are the animal of choice for such studies. “The studies that were submitted for the approval of Splenda to the FDA were mostly performed in rats,” he said. “The Acceptable Daily Limit (ADI) approved by the FDA, was based on studies in rats.”

 

The study protocol was approved by the Duke University Institutional Animal Care and Use Committee (IACUC).

 

After 12 weeks, half of the animals in each group were sacrificed and the cytochrome P-450 (CYP) metabolism system and membrane efflux transporter P-glycoprotein (P-gp) were measured. Both P-gp and CYP are known to impact on the bioavailability of orally consumed compounds, such as drugs and nutrients.

 

The remaining animals spent a further 12 weeks without any Splenda in the diet.

 

Results

 

Professor Abou-Donia and his co-workers report that, at the end of the initial 12 weeks, significant reductions in the levels of so-called beneficial bacteria were observed. Specifically, the numbers of total anaerobes was decreased by 50 per cent, relative to the control animals, while bifidobacteria, lactobacilli, and Bacteroides were reduced by 37, 39, and 67.5 per cent respectively.

 

The body weight of the animals in all the groups increased, but significant increases were observed in animals receiving Splenda, said the researchers. Control animals experienced an increase in body weight of 93 per cent over the 12 weeks. Body weight increases in the 100, 300, 500, and 1,000 mg of Splenda per kg per day groups were 104, 101, 102, and 88.5 per cent, respectively.

 

“The lack of a dose-response effect of Splenda on body weight is likely due to the combined elevation of both intestinal P-gp and CYP that affected the bioavailability of Splenda,” stated the researchers. “At the higher concentrations, less Splenda was absorbed due to the increase in the expression of both P-gp and CYP proteins.”

 

Concerning P-gp and types of CYP, expression of P-gp increased by 2.43- fold, CYP3A4 by 2.51-fold, and CYP2D1 by 3.49-fold, over the course of the 12 weeks.

 

Low beneficial bacteria levels, and elevated P-gp and CYP levels were maintained after the 12 week recovery period, said the researchers.

 

“Evidence indicates that a 12 week administration of Splenda exerted numerous adverse effects, including a reduction in beneficial faecal microflora, an increased faecal pH, and enhanced expression levels of P-gp, CYP3A4, and CYP2D1, which are known to limit the bioavailability of orally administered drugs,” concluded the researchers.

 

Both industry and academia has responded to the results of the study. To read this reaction, click here.

 

Source: Journal of Toxicology and Environmental Health, Part A

Volume 71, Issue 21, Pages 1415-1429

“’Splenda Alters Gut Microflora and Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Male Rats”

Authors: M.B. Abou-Donia, E.M. El-Masry, A.A. Abdel-Rahman, R.E. McLendon, S.S. Schiffman

 

 

High Fructose Sets Table For Weight Gain Without Warning: Leptin Resistance

2008 study posted for filing

 

Common sweetener found in many foods leads to leptin resistance  and exacerbates obesity when paired with high-calorie, high-fat diet

 

BETHESDA, Md. (Oct. 16, 2008) – Eating too much fructose can induce leptin resistance, a condition that can easily lead to becoming overweight when combined with a high-fat, high-calorie diet, according to a new study with rats.

 

Although previous studies have shown that being leptin resistant can lead to rapid weight gain on a high-fat, high-calorie diet, this is the first study to show that leptin resistance can develop as a result of high fructose consumption. The study also showed for the first time that leptin resistance can develop silently, that is, with little indication that it is happening.

 

The study, “Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding,” was carried out by Alexandra Shapiro, Wei Mu, Carlos Roncal, Kit-Yan Cheng, Richard J. Johnson and Philip J. Scarpace, all at the University of Florida College of Medicine in Gainesville. The study appears in the American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, published by The American Physiological Society.

 

Leptin as regulator

 

Leptin is a hormone that plays a role in helping the body to balance food intake with energy expenditure. When leptin isn’t working — that is, when the body no longer responds to the leptin it produces — it’s called leptin resistance. Leptin resistance is associated with weight gain and obesity in the face of a high-fat, high-calorie diet.

 

Obesity has been a growing problem in the U.S. and in other parts of the world and fructose has been suspected of playing a role. Fructose is the sugar found in fruit, but it’s not the normal consumption of fruit that is the problem. Table sugar and high-fructose corn syrup are about 50% fructose and these ingredients have become increasingly common in many foods and beverages. With sugar and high-fructose corn syrup being added to many foods, people now eat much more fructose than ever before.

 

The University of Florida researchers hypothesized that a high-fructose diet could lead to leptin resistance, which in turn could lead to exacerbated weight gain in the face of a high-fat, high-calorie diet, a typical diet in industrialized countries. To test their hypothesis, the research team performed a study with two groups of rats. They fed both groups the same diet, with one important exception: one group consumed a lot of fructose while the other received no fructose.

 

Two groups similar over six months

 

During these six months, there were no differences in food intake, body weight, and body fat between rats on the high-fructose and the rats on the fructose-free diets. In addition, there was no difference between the two groups in the levels of leptin, glucose, cholesterol or insulin found in their blood. There was only one difference at the end of the six months: The rats on the high-fructose diet had higher levels of triglycerides in their blood.

 

The researchers next tested the animals to see if they were leptin resistant. They injected all the animals with leptin, to see if they would respond by eating less. Animals whose leptin response is functioning normally will lower their food intake. The researchers discovered that the rats on the high-fructose diet were leptin resistant, that is, they did not lower their food intake when given leptin. The no-fructose animals responded normally to leptin by eating less.

 

This first six months of the study showed that leptin resistance can develop silently. “Usually, leptin resistance is associated with obesity, but in this case, leptin resistance developed without obesity,” Shapiro said. “This was very surprising.”

 

Role of diet

 

Having seen that leptin resistance could develop silently, the researchers next wanted to find out what would happen if they switched the rats to a high-fat, high-calorie diet — the kind many Americans eat. They found that the animals exposed to the high-fructose diet, the leptin resistant rats, ate more and gained much more weight and fat than the leptin responsive animals on the fructose-free diet. All told, this study showed that leptin resistance can:

 

develop by eating a lot of fructose

 

develop silently, that is, with very little indication it is happening

 

result in weight gain when paired with a high fat, calorie dense diet

 

Scarpace said the study suggests it is the interaction between consumption of large amounts of fructose-containing foods and eating a high-fat, high-calorie diet that produces the weight gain. “This study may explain how the global increase in fructose consumption is related to the current obesity epidemic,” Shapiro said.

 

How it happens

 

Other studies have shown that elevated triglycerides impair the transport of leptin across the blood brain barrier. The researchers hypothesize that the elevation in triglycerides produced by fructose prevented leptin from reaching the brain. If leptin does not reach the brain, the brain will not send out the signal to stop eating.

 

“The presence of high fructose alters the way leptin works, fooling the brain so that it ignores leptin,” Scarpace said. Consumers should be cautious about what they eat, checking labels to see how much sugar the items contain, Shapiro said.

 

The researchers hope to perform future studies to find out if leptin resistance can be reversed by removing or reducing the fructose content of the diet.

Regular consumption of sugary beverages linked to increased genetic risk of obesity

Contact: Todd Datz
tdatz@hsph.harvard.edu
617-432-8413
Harvard School of Public Health

 

Researchers from Harvard School of Public Health have found that greater consumption of sugar-sweetened beverages (SSBs) is linked with a greater genetic susceptibility to high body mass index (BMI) and increased risk of obesity. The study reinforces the view that environmental and genetic factors may act together to shape obesity risk.

The study appears September 21, 2012 in an advance online edition of the New England Journal of Medicine.

“Our study for the first time provides reproducible evidence from three prospective cohorts to show genetic and dietary factors—sugar-sweetened beverages—may mutually influence their effects on body weight and obesity risk. The findings may motivate further research on interactions between genomic variation and environmental factors regarding human health,” said Lu Qi, assistant professor in the Department of Nutrition at HSPH and senior author of the study.

In the past three decades, consumption of SSBs has increased dramatically worldwide. Although widespread evidence supports a link between SSBs, obesity and chronic diseases such as diabetes, there has been little research on whether environmental factors, such as drinking sugary beverages, influence genetic predisposition to obesity.

The research was based on data from three large cohorts, 121,700 women in the Nurses’ Health Study, 51,529 men in the Health Professionals Follow-up Study and 25,000 in the Women’s Genome Health Study. All of the participants had completed food-frequency questionnaires detailing their food and drink consumption over time.

The researchers analyzed data from 6,934 women from NHS, 4,423 men from HPFS, and 21,740 women from WGHS who were of European ancestry and for whom genotype data based on genome-wide association studies were available. Participants were divided into four groups according to how many sugary drinks they consumed: less than one serving of SSB per month, between 1-4 servings per month, between 2-6 servings per week, and one or more servings per day. To represent the overall genetic predisposition, a genetic predisposition score was calculated on the basis of the 32 single-nucleotide polymorphisms known to be associated with BMI (weight in kilograms divided by the square of the height in meters).

The results showed that the genetic effects on BMI and obesity risk among those who drank one or more SSBs per day were about twice as large as those who consumed less than one serving per month. The findings suggest that regular consumption of sugary beverages may amplify the genetic risk of obesity. In addition, individuals with greater genetic predisposition to obesity appear to be more susceptible to harmful effects of SSBs on BMI. “SSBs are one of the driving forces behind the obesity epidemic,” says Frank Hu, professor of nutrition and epidemiology at HSPH and a coauthor of this study. “The implication of our study is that the genetic effects of obesity can be offset by healthier food and beverage choices.”

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Support for the study was provided by grants DK091718, HL071981, HL073168, CA87969, CA49449, CA055075, HL34594, HL088521, U01HG004399, DK080140, 5P30DK46200, U54CA155626, DK58845, U01HG004728-02, EY015473, DK70756, and DK46200 from the National Institutes of Health (NIH); and Merck Research Laboratories. The WGHS is supported by NIH grants HL043851, HL69757, and CA047988.

“Sugar-Sweetened Beverages and Genetic Risk of Obesity,” Qibin Qi, Audrey Y. Chu, Jae H. Kang, Majken K. Jensen, Gary C. Curhan, Louis R. Pasquale, Paul M. Ridker, David J. Hunter, Walter C. Willett, Eric B. Rimm, Daniel I. Chasman, Frank B. Hu, Lu Qi, New England Journal of Medicine, online Sept. 21, 2012

Increased dietary fructose (high fructose corn syrup) linked to elevated uric acid levels and lower liver energy stores

Contact: Dawn Peters sciencenewsroom@wiley.com 781-388-8408 Wiley

Obese patients with type 2 diabetes who consume higher amounts of fructose display reduced levels of liver adenosine triphosphate (ATP)—a compound involved in the energy transfer between cells. The findings, published in the September issue of Hepatology, a journal of the American Association for the Study of Liver Diseases, indicate that elevated uric acid levels (hyperuricemia) are associated with more severe hepatic ATP depletion in response to fructose intake.

This exploratory study, funded in part by grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), also suggests that uric acid levels may serve as a marker for increased fructose consumption and hepatic ATP depletion. Uric acid is produced by the breakdown of purines, natural substances commonly found in foods. According to the authors, increased dietary fructose can alter the body’s metabolism and energy balance. Energy depletion in the liver may be associated with liver injury in patients with non-alcoholic fatty liver disease (NAFLD) and in those at risk for developing this metabolic condition.

Fructose is a simple sugar that fuels the body, and is found in fruits and vegetables. High fructose corn syrup—a mixture of glucose and fructose—is used as a sweetener in consumer food products such as bread, cereal, and soda. Prior research reports that fructose consumption in the U.S. has more than doubled in the past 30 years. In fact, studies have shown that Americans’ fructose intake climbed from 15 grams per day in the early 1900s to 55 grams per day in 1994, which experts believe stems from an increase in soft drink consumption.

“There is an alarming trend of increased rates of obesity, type 2 diabetes and NAFLD in the U.S.,” said lead author Dr. Manal Abdelmalek from Duke University Medical Center. “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.”

For the present study, 244 obese and diabetic adults from the Look AHEAD Study were evaluated, with dietary fructose consumption estimated by the food frequency questionnaire. Liver ATP and uric acid levels were measured in 105 patients who participated in the Look AHEAD Fatty Liver Ancillary Study. Researchers assessed the change in liver ATP content using an IV fructose challenge in 25 subjects, comparing patients with low fructose consumption (less than 15 grams per day) to those with high fructose consumption (greater than 15 grams per day).

The team found that participants with a high intake of dietary fructose had lower liver ATP levels at baseline and a greater change in ATP content following the fructose challenge than those who consumed a lower amount of fructose. Patients with high uric acid levels (5.5 mg/dL or more) displayed lower ATP stores in response to fructose.

Dr. Abdelmalek concludes, “High fructose consumption and elevated levels of uric acid are associated with more severe depletion of liver ATP. Our findings suggest that increased dietary fructose intake may impair liver “energy balance.” Further research to define the clinical implications of these findings on metabolism and NAFLD is necessary.” The authors highlight the importance of public awareness of the risks associated with a diet high in fructose.

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This study is published in Hepatology. Media wishing to receive a PDF of this articles may contact sciencenewsroom@wiley.com.

Full Citation: “Higher Dietary Fructose Is Associated with Impaired Hepatic ATP Homeostasis in Obese Individuals with Type 2 Diabetes.” Manal F. Abdelmalek, Mariana Lazo, Alena Horska, Susanne Bonekamp, Edward W. Lipkin, Ashok Balasubramanyam, John P. Bantle, Richard J. Johnson, Anna Mae Diehl, Jeanne M. Clark, and the Fatty Liver Subgroup of the Look AHEAD Research Group. Hepatology; (DOI: 10.1002/hep.25741); Print Issue Date: September, 2012. URL: http://onlinelibrary.wiley.com/doi/10.1002/hep.25741/abstract

Author Contact:

To arrange an interview with Dr. Abdelmalek, please contact Rachel Bloch with Duke University at rachel.bloch@duke.edu or at +1 919-419-5069.

About the Journal:

Hepatology is the premier publication in the field of liver disease, publishing original, peer-reviewed articles concerning all aspects of liver structure, function and disease. Each month, the distinguished Editorial Board monitors and selects only the best articles on subjects such as immunology, chronic hepatitis, viral hepatitis, cirrhosis, genetic and metabolic liver diseases and their complications, liver cancer, and drug metabolism. Hepatology is published on is published by Wiley on behalf of the American Association for the Study of Liver Diseases (AASLD). For more information, please visit http://wileyonlinelibrary.com/journal/hep.

About Wiley

Founded in 1807, John Wiley & Sons, Inc. has been a valued source of information and understanding for more than 200 years, helping people around the world meet their needs and fulfill their aspirations. Wiley and its acquired companies have published the works of more than 450 Nobel laureates in all categories: Literature, Economics, Physiology or Medicine, Physics, Chemistry, and Peace.

Our core businesses publish scientific, technical, medical, and scholarly journals, encyclopedias, books, and online products and services; professional/trade books, subscription products, training materials, and online applications and Web sites; and educational materials for undergraduate and graduate students and lifelong learners. Wiley’s global headquarters are located in Hoboken, New Jersey, with operations in the U.S., Europe, Asia, Canada, and Australia. The Company’s Web site can be accessed at http://www.wiley.com. The Company is listed on the New York Stock Exchange under the symbols JWa and JWb

Princeton researchers find that high-fructose corn syrup prompts considerably more weight gain: rats became obese by drinking high-fructose corn syrup, but not by drinking sucrose

Contact: Kitta MacPherson kittamac@princeton.edu 609-258-5729 Princeton  University

A sweet problem

IMAGE:A Princeton University research team, including (from left) undergraduate Elyse Powell, psychology professor Bart Hoebel, visiting research associate Nicole Avena and graduate student Miriam Bocarsly, has demonstrated that rats with…Click here for more information.

A Princeton University research team has demonstrated that all sweeteners are not equal when it comes to weight gain: Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same.

In addition to causing significant weight gain in lab animals, long-term consumption of high-fructose corn syrup also led to abnormal increases in body fat, especially in the abdomen, and a rise in circulating blood fats called triglycerides. The researchers say the work sheds light on the factors contributing to obesity trends in the United States.

“Some people have claimed that high-fructose corn syrup is no different than other sweeteners when it comes to weight gain and obesity, but our results make it clear that this just isn’t true, at least under the conditions of our tests,” said psychology professor Bart Hoebel, who specializes in the neuroscience of appetite, weight and sugar addiction. “When rats are drinking high-fructose corn syrup at levels well below those in soda pop, they’re becoming obese — every single one, across the board. Even when rats are fed a high-fat diet, you don’t see this; they don’t all gain extra weight.”

In results published online March 18 by the journal Pharmacology, Biochemistry and Behavior, the researchers from the Department of Psychology and the Princeton Neuroscience Institute reported on two experiments investigating the link between the consumption of high-fructose corn syrup and obesity.

The first study showed that male rats given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow gained much more weight than male rats that received water sweetened with table sugar, or sucrose, in conjunction with the standard diet. The concentration of sugar in the sucrose solution was the same as is found in some commercial soft drinks, while the high-fructose corn syrup solution was half as concentrated as most sodas.

IMAGE:When male rats were given water sweetened with high-fructose corn syrup in addition to a standard diet of rat chow, the animals gained much more weight than male rats that…Click here for more information.

The second experiment — the first long-term study of the effects of high-fructose corn syrup consumption on obesity in lab animals — monitored weight gain, body fat and triglyceride levels in rats with access to high-fructose corn syrup over a period of six months. Compared to animals eating only rat chow, rats on a diet rich in high-fructose corn syrup showed characteristic signs of a dangerous condition known in humans as the metabolic syndrome, including abnormal weight gain, significant increases in circulating triglycerides and augmented fat deposition, especially visceral fat around the belly. Male rats in particular ballooned in size: Animals with access to high-fructose corn syrup gained 48 percent more weight than those eating a normal diet. In humans, this would be equivalent to a 200-pound man gaining 96 pounds.

“These rats aren’t just getting fat; they’re demonstrating characteristics of obesity, including substantial increases in abdominal fat and circulating triglycerides,” said Princeton graduate student Miriam Bocarsly. “In humans, these same characteristics are known risk factors for high blood pressure, coronary artery disease, cancer and diabetes.” In addition to Hoebel and Bocarsly, the research team included Princeton undergraduate Elyse Powell and visiting research associate Nicole Avena, who was affiliated with Rockefeller University during the study and is now on the faculty at the University of Florida. The Princeton researchers note that they do not know yet why high-fructose corn syrup fed to rats in their study generated more triglycerides, and more body fat that resulted in obesity.

High-fructose corn syrup and sucrose are both compounds that contain the simple sugars fructose and glucose, but there at least two clear differences between them. First, sucrose is composed of equal amounts of the two simple sugars — it is 50 percent fructose and 50 percent glucose — but the typical high-fructose corn syrup used in this study features a slightly imbalanced ratio, containing 55 percent fructose and 42 percent glucose. Larger sugar molecules called higher saccharides make up the remaining 3 percent of the sweetener. Second, as a result of the manufacturing process for high-fructose corn syrup, the fructose molecules in the sweetener are free and unbound, ready for absorption and utilization. In contrast, every fructose molecule in sucrose that comes from cane sugar or beet sugar is bound to a corresponding glucose molecule and must go through an extra metabolic step before it can be utilized.

This creates a fascinating puzzle. The rats in the Princeton study became obese by drinking high-fructose corn syrup, but not by drinking sucrose. The critical differences in appetite, metabolism and gene expression that underlie this phenomenon are yet to be discovered, but may relate to the fact that excess fructose is being metabolized to produce fat, while glucose is largely being processed for energy or stored as a carbohydrate, called glycogen, in the liver and muscles.

In the 40 years since the introduction of high-fructose corn syrup as a cost-effective sweetener in the American diet, rates of obesity in the U.S. have skyrocketed, according to the Centers for Disease Control and Prevention. In 1970, around 15 percent of the U.S. population met the definition for obesity; today, roughly one-third of the American adults are considered obese, the CDC reported. High-fructose corn syrup is found in a wide range of foods and beverages, including fruit juice, soda, cereal, bread, yogurt, ketchup and mayonnaise. On average, Americans consume 60 pounds of the sweetener per person every year.

“Our findings lend support to the theory that the excessive consumption of high-fructose corn syrup found in many beverages may be an important factor in the obesity epidemic,” Avena said.

The new research complements previous work led by Hoebel and Avena demonstrating that sucrose can be addictive, having effects on the brain similar to some drugs of abuse.

In the future, the team intends to explore how the animals respond to the consumption of high-fructose corn syrup in conjunction with a high-fat diet — the equivalent of a typical fast-food meal containing a hamburger, fries and soda — and whether excessive high-fructose corn syrup consumption contributes to the diseases associated with obesity. Another step will be to study how fructose affects brain function in the control of appetite.

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The research was supported by the U.S. Public Health Service.

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Reposted for filing

Heat forms potentially harmful substance in high-fructose corn syrup: hydroxymethylfurfural (HMF),

Contact: Michael Woods
m_woods@acs.org
202-872-6293
American Chemical Society

Researchers have established the conditions that foster formation of potentially dangerous levels of a toxic substance in the high-fructose corn syrup (HFCS) often fed to honey bees. Their study, which appears in ACS’ bi-weekly Journal of Agricultural and Food Chemistry, could also help keep the substance out of soft drinks and dozens of other human foods that contain HFCS. The substance, hydroxymethylfurfural (HMF), forms mainly from heating fructose.

In the new study, Blaise LeBlanc and Gillian Eggleston and colleagues note HFCS’s ubiquitous usage as a sweetener in beverages and processed foods. Some commercial beekeepers also feed it to bees to increase reproduction and honey production. When exposed to warm temperatures, HFCS can form HMF and kill honeybees. Some researchers believe that HMF may be a factor in Colony Collapse Disorder, a mysterious disease that has killed at least one-third of the honeybee population in the United States.

The scientists measured levels of HMF in HFCS products from different manufacturers over a period of 35 days at different temperatures. As temperatures rose, levels of HMF increased steadily. Levels jumped dramatically at about 120 degrees Fahrenheit. “The data are important for commercial beekeepers, for manufacturers of HFCS, and for purposes of food storage. Because HFCS is incorporated as a sweetener in many processed foods, the data from this study are important for human health as well,” the report states. It adds that studies have linked HMF to DNA damage in humans.  In addition, HMF breaks down in the body to other substances potentially more harmful than HMF.

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ARTICLE FOR IMMEDIATE RELEASE “Formation of Hydroxymethylfurfural in Domestic High-Fructose Corn Syrup and Its Toxicity to the Honey Bee (Apis mellifera)”

DOWNLOAD FULL TEXT ARTICLE http://pubs.acs.org/stoken/presspac/presspac/full/10.1021/jf9014526

CONTACT: Blaise W. LeBlanc, Ph.D. Carl Hayden Bee Research Center Agricultural Research Service U.S. Department of Agriculture Tucson, Ariz. 85719 Phone: 520-792-1296 Fax: 520-792-1296 Email: blaise_LL@hotmail.com

Reposted at Request

High-fructose corn syrup sugar makes maturing human fat cells fatter, less insulin-sensitive

Contact: Aaron Lohr alohr@endo-society.org 240-482-1380 The Endocrine Society

Fructose, the sugar widely used as high-fructose corn syrup in soft drinks and processed foods, often gets some of the blame for the widespread rise in obesity. Now a laboratory study has found that when fructose is present as children’s fat cells mature, it makes more of these cells mature into fat cells in belly fat and less able to respond to insulin in both belly fat and fat located below the skin.

The results will be presented Sunday at The Endocrine Society’s 92nd Annual Meeting in San Diego by lead author Georgina Coade, a PhD student at the University of Bristol in the U.K.

“Our results suggest that high levels of fructose, which may result from eating a diet high in fructose, throughout childhood may lead to an increase in visceral [abdominal] obesity, which is associated with increased cardiometabolic risk,” Coade said.

Defined by a large waistline, abdominal obesity raises the risk of heart disease and Type 2 diabetes. The abdominal cavity contains one of two major types of fat in the body: visceral fat. The other type, subcutaneous fat, is found below the surface of the skin.

Although researchers have shown the negative effects of fructose on the fat distribution of rodents, the effects of this sugar on human adipocytes, or fat cells, are not clear, according to Coade. Therefore, she and her fellow researchers studied biopsy specimens of both subcutaneous and visceral fat from 32 healthy-weight children who had not yet gone through puberty.

From the biopsy samples, the investigators obtained preadipocytes—the precursors to fat cells that have the potential to differentiate, or mature, into fat-containing adipocytes. They then allowed the precursor cells to mature for 14 days in culture media containing normal glucose (the main sugar found in the bloodstream and the principal source of energy in the body), high glucose or high fructose. The researchers assessed cell differentiation by measuring activity of an enzyme (GPDH) and the abundance of the adipocyte fatty acid binding protein, which are both present only in mature fat cells.

Fructose, the research team found, had different effects to that of glucose and caused the fat cells to differentiate more—that is, to form more mature fat cells—but only in visceral fat.

For both types of fat cells, maturation in fructose decreased the cells’ insulin sensitivity, which is the ability to successfully take up glucose from the bloodstream into fat and muscles. Decreased insulin sensitivity is a characteristic of Type 2 diabetes.

Although prolonged exposure to fructose had a negative effect on insulin sensitivity, when Coade and her co-workers exposed mature fat cells, rather than preadipocytes, to fructose for 48 hours, the cells’ insulin sensitivity increased. The reason why is unknown. However, she said, “Fructose alters the behavior of human fat cells if it is present as the fat cells mature. We can maybe compare this [timing] to periods in children when they are making their fat.”

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The London-based organization Diabetes UK helped fund this study.

Pancreatic cancers use high fructose corn syrup (HFCS), common in the Western diet to fuel their growth

Contact: Kim Irwin
kirwin@mednet.ucla.edu310-206-2805
University of California – Los Angeles Health Sciences

Pancreatic cancers use the sugar fructose, very common in the Western diet, to activate a key cellular pathway that drives cell division, helping the cancer to grow more quickly, a study by researchers at UCLA’s Jonsson Comprehensive Cancer Center has found.

Although it’s widely known that cancers use glucose, a simple sugar, to fuel their growth, this is the first time a link has been shown between fructose and cancer proliferation, said Dr. Anthony Heaney, an associate professor of medicine and neurosurgery, a Jonsson Cancer Center researcher and senior author of the study.

“The bottom line is the modern diet contains a lot of refined sugar including fructose and it’s a hidden danger implicated in  a lot of modern diseases, such as obesity, diabetes and fatty liver,” said Heaney, who also serves as director of the Pituitary Tumor and Neuroendocrine Program at UCLA. “In this study, we show that cancers can use fructose just as readily as glucose to fuel their growth.”

The study appeared in the Aug. 1 issue of the peer-reviewed journal Cancer Research.

The source of fructose in the Western diet is high fructose corn syrup (HFCS), a corn-based sweetener that has been on the market since about 1970. HFCS accounts for more than 40 percent of the caloric sweeteners added to foods and beverages, and it is the sole sweetener used in American soft drinks.

Between 1970 and 1990, the consumption of HFCS in the U.S. has increased over 1,000 percent, according to an article in the April 2004 issue of the American Journal of Clinical Nutrition. Food companies use HFCS – a mixture of fructose and glucose – because it’s inexpensive, easy to transport and keeps foods moist. And because it is so sweet, it’s cost effective for companies to use small quantities of HCFS in place of more expensive sweeteners or flavorings.

In his study, Heaney and his team took pancreatic tumors from patients and cultured and grew the malignant cells in Petri dishes. They then added glucose to one set of cells and fructose to another. Using mass spectrometry, they were able to follow the carbon-labeled sugars in the cells to determine what exactly they were being used for and how.

Heaney found that the pancreatic cancer cells could easily distinguish between glucose and fructose even though they are very similar structurally, and contrary to conventional wisdom, the cancer cells metabolized the sugars in very different ways. In the case of fructose, the pancreatic cancer cells used the sugar in the transketolase-driven non-oxidative pentose phosphate pathway to generate nucleic acids, the building blocks of RNA and DNA, which the cancer cells need to divide and proliferate.

“Traditionally, glucose and fructose have been considered as interchangeable monosaccharide substrates that are similarly metabolized, and little attention has been given to sugars other than glucose,” the study states. “However, fructose intake has increased dramatically in recent decades and cellular uptake of glucose and fructose uses distinct transporters … These findings show that cancer cells can readily metabolize fructose to increase proliferation. They have major significance for cancer patients, given dietary refined fructose consumption.”

As in anti-smoking campaigns, a federal effort should be launched to reduce refined fructose intake, Heaney said.

“I think this paper has a lot of public health implications,” Heaney said. “Hopefully, at the federal level there will be some effort to step back on the amount of HFCS in our diets.”

Heaney said that while this study was done in pancreatic cancer, these finding may not be unique to that cancer type.

Going forward, Heaney and his team are exploring whether it’s possible to block the uptake of fructose in the cancer cells with a small molecule, taking away one of the fuels they need to grow. The work is being done in cell lines and in mice, Heaney said.

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The study was funded by the National Institutes of Health, the Hirschberg Foundation and the Jonsson Cancer Center.

UCLA’s Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation’s largest comprehensive cancer centers, the Jonsson center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2010, the Jonsson Cancer Center was named among the top 10 cancer centers nationwide by U.S. News & World Report, a ranking it has held for 10 of the last 11 years. For more information on the Jonsson Cancer Center, visit our website at http://www.cancer.ucla.edu.

Resposted from 2010

Too much sugar turns off gene that controls the effects of sex steroids

 

 

Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, shows a new study in mice and human cell cultures that’s published this month in the Journal of Clinical Investigation. This discovery reinforces public health advice to eat complex carbohydrates and avoid sugar. Table sugar is made of glucose and fructose, while fructose is also commonly used in sweetened beverages, syrups, and low-fat food products. Estimates suggest North Americans consume 33 kg of refined sugar and an additional 20 kg of high fructose corn syrup per person per year.

 

Glucose and fructose are metabolized in the liver. When there’s too much sugar in the

diet, the liver converts it to lipid. Using a mouse model and human liver cell cultures, the

scientists discovered that the increased production of lipid shut down a gene called

SHBG (sex hormone binding globulin), reducing the amount of SHBG protein in the

blood. SHBG protein plays a key role in controlling the amount of testosterone and

estrogen that’s available throughout the body. If there’s less SHBG protein, then more

testosterone and estrogen will be released throughout the body, which is associated with

an increased risk of acne, infertility, polycystic ovaries, and uterine cancer in overweight

women. Abnormal amounts of SHBG also disturb the delicate balance between estrogen

and testosterone, which is associated with the development of cardiovascular disease,

especially in women.

 

“We discovered that low levels of SHBG in a person’s blood means the liver’s metabolic

state is out of whack – because of inappropriate diet or something that’s inherently wrong

with the liver – long before there are any disease symptoms,” says Dr. Geoffrey

Hammond, the study’s principal investigator, scientific director of the Child & Family

Research Institute in Vancouver, Canada, and professor in the Department of Obstetrics

& Gynecology at the University of British Columbia.

* Requested Repost 2007

 

Fizzical harm: Drinking sugary drinks doesn’t just pile on the pounds – it changes your body so it’s harder to lose weight

By Rob Waugh

  • Drinking sugary drinks for just a month  alters body chemistry
  • More difficult to lose weight
  • Body grows to ‘prefer’ sugar to digesting  own fat

Drinking sugared fizzy drinks for just a  month changes the body permanently so it’s more difficult to lose  weight.

The soft drinks don’t just pile on the pounds  because of the calories in them – they alter the way your body burns  fuel.

Your muscles grow to ‘prefer’ sugar to fat as  a fuel, and thus losing weight becomes harder.

Drinking sugary drinks could be even more  harmful than previously thought.

Soft drinks alter the way our muscles burn  fuel preferring sugar over fat which makes the pounds harder to  shift.

And worryingly this effect lasts long-term  which can raise levels of blood glucose leading to diabetes.

Dr Hans-Peter Kubis, of Bangor University,  said: ‘This study proves our concerns over sugary drinks have been  correct.

‘Not only can regular sugar intake acutely  change our body metabolism; in fact it seems that our muscles are able to sense  the sugars and make our metabolism more inefficient, not only in the present but  in the future as well.

‘This will lead a reduced ability to burn fat  and to fat gain. Moreover, it will make it more difficult for our body to cope  with rises in blood sugar.’

Dr Kubis warned the drinks can compromise  long term health and, when in need of refreshment, people should reach for water  instead.

His researchers also showed isolated muscle  cells identify and respond to the sugary diet, and switch how they use the  fuel.

‘Together with our findings about how  drinking soft drinks dulls the perception of sweetness, our new results  give a  stark warning against regularly drinking sugar sweetened  drinks.’

The move to an inefficient metabolism was  seen in male and female participants who were lightly active, and drinking soft  drinks for just four weeks.

These factors show that regular use of sugar  sweetened soft drinks drives alterations in muscles similar to those found in  people with obesity problems and type 2 diabetes.

Dr Kubis said: ‘What is clear is our body  adjusts to regular soft drink consumption and prepares itself for the future  diet by changing muscle metabolism via altered gene activity – encouraging  unhealthy adaptations similar to those seen in people with obesity problems and  type 2 diabetes.

‘Together with our findings about how  drinking soft drinks dulls the perception of sweetness, our new results  give a  stark warning against regularly drinking sugar sweetened drinks.’

In the study 11 people in their twenties took  part in a sugar sweetened soft drink supplementation for a month and before and  after had their blood and muscle tissue as well as their whole body metabolism  and composition tested.

Genes and proteins important for fat and  sugar metabolism were analysed and blood sugar and fats assessed.

As it turned out metabolism shifted towards  sugar away from using fat and genes for inefficient sugar metabolism were  activated and a particular factor which is known to be crucial for genes of  aerobic metabolism was reduced. Moreover the subjects gained fat and blood sugar  was elevated.

Dr Kubis said: ‘What we found is that it is  not the sugar in itselt that puts on weight but the way it gets the body to  store more. ‘This would relate to all  kinds of soft drinks with a high sugar content, including fruit juices.

‘It was a small study because it is difficult  to find young people who have not previously been exposed to a lot of soft  drinks and who are willing to undergo muscle biopsies.

‘But we are now hoping to carry out a bigger  study with more particpants over a longer period of time.’

He has been campaigning for the government to  take action to address the problem of soft drink consumption.

Added Dr Kubis: ‘Clearly taxation on sugary  drinks is overdue. This money could be invested in the NHS where it is urgently  needed to treat people with obesity problems and diabetes.’

Read more: http://www.dailymail.co.uk/sciencetech/article-2176549/Drinking-sugary-drinks-doesnt-just-pile-pounds–changes-body-difficult-lose-weight.html#ixzz21PD8GBFb

High fructose consumption by adolescents may put them at cardiovascular risk

 

 

Evidence of cardiovascular disease and diabetes risk is present in the blood of adolescents who consume a lot of fructose, a scenario that worsens in the face of excess belly fat, researchers report.

An analysis of 559 adolescents age 14-18 correlated high-fructose diets with higher blood pressure, fasting glucose, insulin resistance and inflammatory factors that contribute to heart and vascular disease.

Heavy consumers of the mega-sweetener also tend to have lower levels of cardiovascular protectors such as such as HDL cholesterol and adiponectin, according to researchers at the Medical College of Georgia at Georgia Health Sciences University.

These dangerous trends are exacerbated by fat around their midsection, called visceral adiposity, another known risk factor for cardiovascular disease and diabetes. The association did not hold up for adolescents with more generalized, subcutaneous fat.

“It is so very important to provide a healthy balance of high-quality food to our children and to really pay close attention to the fructose and sucrose they are consuming at their home or anyone else’s,” said Dr. Vanessa Bundy, an MCG pediatric resident. Drs. Bundy and Norman Pollock, bone biologist at MCG’s Georgia Prevention Institute are co-first authors on the study published in The Journal of Nutrition.

“The nutrition that caregivers provide their children will either contribute to their overall health and development or potentially contribute to cardiovascular disease at an early age,” Bundy said. The best way caregivers can support healthy nutrition is to be good role models, she said. A healthy diet with plenty of physical activity – not dieting – is the best prescription for growing children.

“Adolescents consume the most fructose so it’s really important to not only measure the levels of fructose but to look at what it might be doing to their bodies currently and, hopefully, to look at cardiovascular disease outcomes as they grow,” Pollock said.

While animal studies have had similar findings, evidence in children is needed to support dramatic steps to curb consumption, such as asking schools to remove soda and other vending machines or, at least, to limit access, Pollock said. The researchers noted that more study is needed to flesh out the relationship between high fructose consumption and cardiovascular risk and whether these early associations forebode adult disease.

Fructose, or fruit sugar, is found in fruits and veggies but also in high fructose corn syrup, the sweetener used liberally in processed foods and beverages. Researchers suspect growing bodies crave the cheap, strong sweetener and companies often target young consumers in ads.

“Fructose itself is metabolized differently than other sugars and has some byproducts that are believed to be bad for us,” Bundy said. “The overall amount of fructose that is in high fructose corn syrup is not much different than the amount in table sugar but it’s believed there’s something in the syrup processing that plays a role in the bad byproducts of metabolism.”

The study took a “snapshot” of the adolescents’ lives, looking at overall fructose consumption, general diet history and body fat.

“A unique aspect of our study design is that we took into account the fructose released from sucrose during digestion along with the fructose found in foods and beverages,” Pollock said. “Because sucrose is broken down into fructose and glucose before it arrives at the liver for metabolism, it is important to consider the additional fructose from sucrose when determining the overall health effect of fructose.”

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CU School of Medicine researchers look at effects of 2 common sweeteners on the body

CU School of Medicine researchers look at effects of 2 common sweeteners on the body

AURORA, Colo. (Jan. 23, 2012)  – With growing concern that excessive levels of fructose may pose a great health risk – causing high blood pressure, kidney disease and diabetes – researchers at the University of Colorado School of Medicine, along with their colleagues at the University of Florida, set out to see if two common sweeteners in western diets differ in their effects on the body in the first few hours after ingestion.  The study, recently published in the journal Metabolism, took a closer look at high fructose corn syrup (HFCS) and table sugar (sucrose) and was led by Dr MyPhuong Le (now a postdoctoral fellow at the University of Colorado) and Dr Julie Johnson, a Professor of Pharmacogenomics at the University of Florida.

Both HFCS and sucrose have historically been considered to have nearly identical effects on the body.   But this study finds that indeed there is a difference between the two.  They found that the makeup of the sugars resulted in differences in how much fructose was absorbed into the circulation, and which could have potential impact on one’s health.  Sucrose is 50 percent fructose and 50 percent glucose that is bonded together as a disaccharide (complex carbohydrate) and HFCS is a mixture of free fructose (55%) and free glucose (45%). It’s the difference in fructose amount that appears to create the ill health effects on the body.

Their study was conducted at the University of Florida, where they evaluated 40 men and women who were given 24 ounces of HFCS- or sugar-sweetened soft drinks.   Careful measurements showed that the HFCS sweetened soft drinks resulted in significantly higher fructose levels than the sugar-sweetened drinks.  Fructose is also known to increase uric acid levels that have been implicated in blood pressure, and the HFCS-sweetened drinks also resulted in a higher uric acid level and a 3 mm Hg greater rise in systolic blood pressure.

Dr Richard Johnson, a coauthor in the study and Chief of the Division of Renal Diseases and Hypertension at the University of Colorado, commented  “Although both sweeteners are often considered the same in terms of their biological effects, this study demonstrates that there are subtle differences.  Soft drinks containing HFCS result in slightly higher blood levels of fructose than sucrose-sweetened drinks, “said Johnson.   “The next step is for new studies to address whether the long-term effects of these two sweeteners are different.”