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”

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 )”

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

Health Research Report (Video) 8 JUL 2013

High Fructose Corn Syrup Causes Rapid Liver Damage
Number of Americans taking prescription drugs at 7 out of 10
Anti-depressants may keep PTSD patients in a constant state of fear.
Anti-Bacterial Soaps may contribute to infant deaths

New study finds neither HFCS nor table sugar increases liver fat under ‘real world’ conditions !!! STUDY designed to FAIL !!!

EEV: This study must be faulted in two area’s immediately:

1. Length of Study 10 Weeks, like Huh?

2. “Not only is it safe to consume caloric sweeteners at recommended levels, it is important for consumers to understand that high fructose corn syrup and table sugar have the same amount of calories and studies like this indicate your body metabolizes them about the same.” Huh, Huh?

3. Study Participants had to be disease free between 25 and 35 kg yet consume no more than more than 14 alcoholic beverages per week.

4. HFCS was based upon percentage of calories required for weight maintenance, not real world caloric intake.

5. Even though all caloric intake equal, the 30% sweetener group gained weight, but no fat?

6. Lots of holes in this partial blind study, but the researches did report honestly. Even though the study sucked and open to experimenter bias in its reporting and design.

7. Oh and the COI’s

Steve Bravo: Has received consulting fees and equipment support from Siemens Inc.

James M. Rippe: Dr. Rippe’s research organization has received funding and Dr. Rippe has received consulting fees from ConAgra Foods, PepsiCo International,

Kraft Foods, the Corn Refiners Association and Weight Watchers Internationals

Contact: Carol Moreau cmoreau@rippelifestyle.com 508-756-1228 Rippe Lifestyle Institute

Adds to scientific evidence that the sweeteners are metabolically equivalent

SHREWSBURY, MA — A study published today in the Journal of Applied Physiology, Nutrition, and Metabolism presented compelling data showing the consumption of both high fructose corn syrup (HFCS) and sucrose (table sugar) at levels consistent with average daily consumption do not increase liver fat in humans, a leading cause of non-alcoholic fatty liver disease (NAFLD). The findings also add to an already well-established body of science that high fructose corn syrup and table sugar are metabolically equivalent.

Increased fat levels in the liver and muscle tissue have also shown to contribute to insulin resistance, a key factor in the development of type 2 diabetes.

The study, conducted by James Rippe, MD, Founder and Director of the Rippe Lifestyle Institute and Professor of Biomedical Sciences at the University of Central Florida, examined sixty-four individuals who consumed low-fat milk sweetened with either HFCS or sucrose with the added sugar matching the 25th, 50th and 90th percentile population consumption levels of fructose for ten weeks.

The results showed fat content of the liver remained unchanged when the six HFCS and sucrose groups were averaged. Fat content in muscle tissue was also unchanged over the 10 weeks when the six HFCS and sucrose groups were averaged.

“The study’s results are compelling because this is the first study of its kind to test the effects of HFCS and sucrose on liver fat levels in humans using real world conditions,” said Dr. Rippe, who received a grant from the Corn Refiners Association (CRA) to conduct the study. “Previous studies that sought to find a link between caloric sweeteners and diseases such as type 2 diabetes and liver disease often subjected individuals to unrealistically high levels of fructose or had subjects consume fructose independent of glucose, which is just not how fructose is consumed in our daily diet.  Using real world conditions, we find that HFCS and other caloric sweeteners do not appear to increase liver fat or contribute to insulin resistance.”

The two largest sources of fructose in the human diet are sucrose (containing 50% fructose and 50% glucose) and HFCS which is present in the human diet in two forms:  HFCS-55 (which consists of 55% fructose, 42% glucose and 3% other carbohydrates) and HFCS-42 (which consists of 42% fructose and 58% glucose).

“This study seems to confirm what physicians, registered dietitians and healthcare associations such as the American Medical Association have been saying for decades,” said Dr. Mark Haub, Associate Professor in the Department of Nutrition at Kansas State University. “Not only is it safe to consume caloric sweeteners at recommended levels, it is important for consumers to understand that high fructose corn syrup and table sugar have the same amount of calories and studies like this indicate your body metabolizes them about the same.”

For further information or to obtain a copy of this study, please visit www.nrcresearchpress.com/journal/apnm

###

Dr. Rippe is a cardiologist and graduate of Harvard College and Harvard Medical School. His research laboratory has conducted numerous studies and published widely in the areas of nutrition and weight management. He is an advisor to the food and beverage industry and has received unrestricted educational grants from the Corn Refiners Association. He is the Founder and Director of the Rippe Lifestyle Institute, and Professor of Biomedical Sciences at the University of Central Florida.

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

64th Health Research Report 01 SEP 2009 – Reconstruction

 

 

Editors Top Five:

1. H1N1 Pandemic Virus Does Not Mutate Into ‘Superbug’ in UMd. Lab Study

2. Natural compounds, chemotherapeutic drugs may become partners in cancer therapy

3. Heat forms potentially harmful substance in high-fructose corn syrup

4. Daily aspirin does more harm than good: study

5. Heat forms potentially harmful substance in high-fructose corn syrup

 

In this issue:

1. Off-label use: Oft not evidence base

2. Research shows why low vitamin D raises heart disease risks in diabetics

3. Long-term tamoxifen use increases risk of an aggressive, hard to treat type of second breast cancer

4. Hormone therapy for prostate cancer patients with heart conditions linked to increased death risk

5. More obesity blues

6. Unlocking the body’s defenses against cancer

7. Discovery of natural odors could help develop mosquito repellents

8. Bird flu leaves the nest — adapting to a new host

9. Heat forms potentially harmful substance in high-fructose corn syrup

10. Healthy food obsession sparks rise in new eating disorder

11. Natural compounds, chemotherapeutic drugs may become partners in cancer therapy

12. Daily aspirin does more harm than good: study

13. H1N1 Pandemic Virus Does Not Mutate Into ‘Superbug’ in UMd. Lab Study

 

Health Research Report

64th  Issue Date 01 SEP 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/engineeringevil

www.engineeringevil.com

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

52nd Health Research Report 17 MAR 2009 – Reconstruction

 

 

Editors top five:

1. NCRP Report No. 160 on increased average radiation exposure of the US population

2. Grape Extracts May be Effective Against Harmful Gut Bacteria

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

4. Support for adjunctive vitamin C treatment in cancer

5. A diet rich in calcium aids weight loss

 

 

In this Issue:

1. Moderate alcohol intake associated with bone protection

2. NCRP Report No. 160 on increased average radiation exposure of the US population

3. Half in US see another country emerging as world’s technological leader

4. New study shows how spikes in nitrite can have a lasting impact on the heart

5. Normal Human Gut Bacteria May Inhibit Shiga Toxin Development Following Infection with E. coli O157:H7

6. Grape Extracts May be Effective Against Harmful Gut Bacteria

7. Pure fructose frequently confused with high fructose corn syrup

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

9. Support for adjunctive vitamin C treatment in cancer

10.’Holy powder’ ingredient makes membranes behave for better health

11. Teenage boys who eat fish at least once a week achieve higher intelligence scores

12. May supplementation of docosahexaenoic acid (DHA)suppress colon tumor cell growth?

13. Vitamin C intake associated with lower risk of gout in men

14. UI study suggests salt might be ‘nature’s antidepressant’

15. Low vitamin D levels associated with several risk factors in teenagers

16. AMERICAN ADULTS FLUNK BASIC SCIENCE

17.Older patients with 1 type of heart failure may receive little or no benefit from drugs

18.A diet rich in calcium aids weight loss

 

Health Research Report

52nd Issue Date 17 MAR 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/engineeringevil

www.engineeringevil.com

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.”

50th Health Research Report 17 FEB 2009 – Reconstruction

 

 

 

Editors Top Five:

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

2. Arginine discovery could help fight human obesity

3. Even natural perfumes may cause allergies

4. Vigorous Exercise May Help Prevent Vision Loss

5. Indoor plants can reduce formaldehyde levels

 

In this issue:

 

1. Even natural perfumes may cause allergies

2.Researchers Disprove 15-year-old Theory about the Nervous System

3.Plan offers guidance for evaluating menopause-like condition in girls and young women

4. Arginine discovery could help fight human obesity

5. Pharmaceuticals sold in Sweden cause serious environmental harm in India

6. Gut bacteria can manufacture defenses against cancer and inflammatory bowel disease

7. Mutant rats resist warfarin

8. Vigorous Exercise May Help Prevent Vision Loss

9. BGU researchers identify vitamin B12 as an effective canker sore therapy

10. New lab evidence suggests preventive effect of herbal supplement in prostate cancer

11. Herpesvirus: To Vaccinate or Not To Vaccinate Scientists Weigh Risks and Benefits

12. Food counterfeiting, contamination outpace international regulatory systems

13. Arab-American women need supplement to boost dangerously low vitamin D levels

14. Supplement of probiotics provides a new therapy for ulcerative colitis

15. Indoor plants can reduce formaldehyde levels

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

Health Research Report

50th Issue Date  17 FEB 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/engineeringevil

www.engineeringevil.com

 

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.

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.

###

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.

###

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

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

Reposted for filing

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.”

###

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.

###

 

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

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.”