DNC News

 

Five Reasons why Fructose is bad stuff

 

Introduction:

From a medical point of view consumption of high fructose corn syrup is not a great idea. When first introduced this sugar was promoted as a healthier, more natural alternative to table sugar. Over the years fructose has fallen from grace, and most practitioners consider regular sugar safer than fructose. This does not make the manufacturers of fructose happy and they have begun an aggressive campaign to maintain their rapidly tarnishing public image.

 

Last week a colleague of ours, Dr. Justin Pollack, who practices in Frisco, had an interesting article published in the Summit County News on optimizing children's brain function. In passing he suggested minimizing consumption of high fructose corn syrups. This mention provoked a rapid response from Audrae Erickson, President of the Corn Refiner's Association in Washington, DC. This trade group represents the interests of the industry that makes high fructose corn syrup.

 

Below is my letter to the editor in response:

 

The September 16, 2005 issue of the Summit Daily News contains a short opinion piece by Audrae Erickson, the president of the corn refiners association in Washington, DC. Ms Erickson wrote in response to Dr. Justin Pollack's article on optimizing children's brains with nutrition that appeared just a few days prior on September 12.

 

Ms. Erickson took umbrage at Dr. Pollack's categorization of high fructose corn syrup as “bad stuff” that should be minimized in a child's diet. Rather she would prefer we consider, “high fructose corn syrup (HFCS) (as) a natural, homegrown, sweetener from US corn fields….” She then goes on to attempt to equate fructose corn syrup with honey, suggesting the human body cannot discern a difference between them.

 

Fructose has the same chemical formula as glucose but the atoms are arranged in a different structure. Sucrose, or white sugar, contains fructose and glucose molecules bound together in pairs. In honey, bees have enzymatically broken the sucrose molecules found in flower nectar into their separate molecules. To produce high fructose corn syrup, processors first treat the starch with enzymes to break it down into glucose molecules and then with a second chemical process to convert the glucose to fructose. Fructose is the sweetest of all common sugars and the most soluble in water, absorbing and retaining water. The human body metabolizes fructose more slowly than glucose, producing a slower rise in blood sugar. At one time this was thought to be advantageous for diabetics. Fructose melts and caramelizes at about 220 degrees, only slightly above the boiling point of water, a temperature much lower temperatures than other sugars. Fructose molecules exist in several different shapes and their perceived sweetness varies with shape. In cold solutions, the classic six cornered ring structure of fructose predominates and this is the sweetest tasting form. The perceived sweetness of fructose drops by 50% if the fructose is heated over 140 F. Neither glucose or sucrose lose ‘sweetness' like this when heated. In other words, fructose will work great in iced tea, but have less perceived effect in hot coffee. This also explains fruit pies. A bowl of perfectly deliciously sweet tasting fruit won't taste as sweet when baked in a pie; you need to add sugar to fruit pies.

 

Although Ms. Erickson might argue that fructose has always been a component in the human diet and should be considered safe, it wasn't until the 1960's and the development of the enzymatic processes that allowed corn to be converted to HFCS, that people consumed fructose in any quantity. Until then, the only concentrated source of fructose in the human diet was honey, of which only slightly more than half of its sugar content is fructose. The average American consumes less than one pound of honey per year and has done so since the late 1800's when technological innovations in honey production lowered the price to make it affordable. In 2001, the average American consumed 63 pounds of high fructose corn syrup. It is illogical to trust that fructose is safe based on historic consumption.

 

In the decades since the food industry introduced high fructose corn syrups, published scientific research has pointed out a number of problems with long term consumption of large amounts of fructose.

 

Here are five concerns about the effect HFCS has on the human body which wisely have led Dr. Pollack's advice against excess consumption:

  1. Fructose increases the amount of fat in the blood, increasing triglyceride levels.
  2. Fructose causes insulin resistance, the hallmark symptom of type II diabetes
  3. Fructose over consumption has been postulated as a major cause of the current obesity epidemic. Fructose does not trigger the release of chemicals which cause the feeling of satiety. Syndrome X, also termed the metabolic syndrome, is a cluster of abnormalities including abdominal obesity, hyperinsulinemia, dyslipidemia and hypertension. In order to study this syndrome, scientists give it to rats simply by feeding them fructose. [i]
  4. Fructose increases Maillard Browning reactions, which although desirable on a loaf of bread, are undesirable within our bodies as they may be the chemical basis of aging. [ii]
  5. Fructose is not absorbed well in all people and may cause digestive upsets similar to lactose intolerance. [iii] Fructose malabsorption has been linked to depression in teens. [iv]

 

When Ms. Erickson suggests that honey and high fructose corn syrup have the same effect in the human body, she is incorrect. In a study published in 2004, volunteers were fed either a daily dose of honey or a mixture of glucose and fructose in the same proportions as found in honey for fifteen days. The honey moved cholesterol, triglycerides, insulin, c-reactive protein and other blood measurements in desirable healthy directions. In most instances the artificial honey sugar mixture made of high fructose corn syrup had the opposite effect. [v] Though there are chemical similarities to honey and high fructose corn syrup, the human body does not respond the same way to both substances. Honey appears to have a good effect and fructose a negative effect.

 

Ms. Erickson as a representative of the industry that makes high fructose corn syrup is paid to increase sales of fructose. Dr. Pollack, the generous and caring man that he is, simply told you the truth about what is good for your children.

 

 

 

 

 

 

 

[i] Am J Hypertens. 2005 Mar;18(3):372-8

Risk reduction therapy for syndrome X: comparison of several treatments.

 

Oron-Herman M, Sela BA, Rosenthal T.

 

Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. mor.orn@sheba.health.gov.il

 

BACKGROUND: Syndrome X, also termed the metabolic syndrome, is a cluster of physiologic and metabolic abnormalities including abdominal obesity, hyperinsulinemia, dyslipidemia and hypertension. Severe cardiovascular morbidity is associated with this pre-diabetic syndrome. We recently suggested that hyperhomocysteinemia is affiliated with this syndrome and thereby contributes to the vascular risk accompanying this condition. The present study compared the effects of antihypertensive, lipid-lowering, and insulin-sensitizing agents on the above-mentioned components of this metabolic syndrome. METHODS: Experimental metabolic syndrome was induced in Sprague-Dawley rats by feeding them a fructose-enriched diet (FED) for 5 weeks. During the last 2 weeks, the rats were treated with amlodipine, captopril, bezafibrate, or rosiglitazone in addition to FED. The control group did not receive any medication. Another control group was fed standard rat chow for 5 weeks. Post- and pretreatment measurements of body weight, systolic blood pressure (SBP), fasting plasma insulin, triglycerides, and total homocysteine concentrations were compared. RESULTS: Amlodipine reduced SBP but did not show metabolic impact. Bezafibrate improved SBP, triglycerides, and insulin but induced elevation of homocysteine levels. Captopril and rosiglitazone remarkably improved SBP, insulin, triglycerides, and total homocysteine levels. In addition, rosiglitazone alone promoted weight gain. CONCLUSIONS: The results indicate that captopril and rosiglitazone have a greater cardiovascular protective potential than amlodipine or bezafibrate. Captopril would be the best choice for patients with metabolic syndrome in whom hypertension and obesity are prominent, whereas rosiglitazone would be the preferred drug when glucose and other metabolic parameters are disturbed.

 

PMID: 15797656 [PubMed - indexed for MEDLINE

 

 

[ii] Ann Univ Mariae Curie Sklodowska [Med]. 2003;58(2):159-62.

The Maillard reaction and its consequences for a living body.

 

Sztanke K, Pasternak K.

 

Department of Synthesis and Technology of Drugs, Medical University of Lublin.

 

The Maillard reaction (nonenzymatic browning) leads through early stage products such as Schiff base and Amadori adduct to advanced glycation end products (AGEs). AGE crosslinks of the Maillard reaction are formed under physiological conditions in a living organism on a variety of blood constituents, on long-lived connective tissues and matrix components. Recently evidence has accumulated that AGE crosslinks as the final products of the Maillard reaction have been suggested as factors in diabetic complications and the ageing process.

 

Publication Types:

Review

Review, Tutorial

 

PMID: 15323185 [PubMed - indexed for MEDLINE]

 

 

[iii] Nutr Clin Care. 2004 Jul-Sep;7(3):92-7.   

Dietary fructose intolerance: diet modification can impact self-rated health and symptom control.

 

Johlin FC Jr, Panther M, Kraft N.

 

Division of Gastroenterology, Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, IA 52242, USA. frederick-johlin@uiowa.edu

 

Carbohydrate intolerance to lactose is widely accepted as a cause of gastrointestinal symptoms, but controversy persists on how important dietary fructose intolerance (DFI) is in causing gastrointestinal pain and suffering and if an elimination diet can control the presenting complaints. The objective of this study was to identify a group of well-defined DFI patients and explore whether dietary education followed by dietary compliance could control symptoms and improve quality of life. During a 5-year period, patients referred to a pancreato-biliary clinic were evaluated for dietary carbohydrate intolerances if they presented with gastrointestinal pain and/or gas and/or bloating and/or diarrhea. Patients were tested with a standardized mixture of glucose, fructose, and lactose diluted in sterile water. End-expiratory breath samples were collected for hydrogen and methane measurement. Symptoms were scored using a 9-point symptom questionnaire. The patients underwent in-depth education by a dietician, and were provided with access to a cookbook, a newsletter, and a support group. A dietary questionnaire was used to evaluate compliance with the fructose-restricted diet. DFI can cause significant gastrointestinal symptoms that may not respond to medications or surgical interventions. Symptoms can improve and self-rated health does improve in DFI patients willing to adhere to a low fructose diet.

 

PMID: 15624540 [PubMed - indexed for MEDLINE]

 

[iv] J Pediatr Gastroenterol Nutr. 2005 May;40(5):561-5.   

Malabsorption of carbohydrates and depression in children and adolescents.

 

Varea V, de Carpi JM, Puig C, Alda JA, Camacho E, Ormazabal A, Artuch R, Gomez L.

 

Department of Pediatric Gastroenterology, Hepatology and Nutrition, Hospital Sant Joan de Deu, Barcelona, Spain. varea@hsjdbcn.org

 

BACKGROUND: Previous studies have shown an association between sugar malabsorption and depressive symptoms in adult women. Incompletely absorbed sugars may form nonabsorbable complexes with tryptophan, an amino acid precursor of serotonin, decreasing its availability. As serotonin is the most important neurotransmitter involved in depressive disorders, its depletion could lead to the onset of depression. METHODS: The authors' aim was to study the possible association between malabsorption of sugars (lactose and fructose) and depressive symptoms in adolescent patients of Spanish origin. The authors studied two groups of patients. Group G included 14 patients previously diagnosed with sugar intolerance. In these, the authors assessed depressive symptoms. Group P consisted of seven patients suffering from major depression. In these, the authors performed functional sugar absorption tests. The authors studied the metabolic pathway of tryptophan in both groups. RESULTS: In the group with sugar malabsorption, there was a 28.5% prevalence of depressive symptoms that was higher than expected in our population. In the group with depression, the authors found a higher than expected prevalence of sugar intolerance (71.42% versus 15% in controls). CONCLUSIONS: The unexpected prevalences obtained for the groups studied suggest that there may be an association between sugar intolerance and depressive symptoms during adolescence.

 

PMID: 15861016 [PubMed - indexed for MEDLINE]

 

[v] J Med Food. 2004 Spring;7(1):100-7.   

Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose.

 

Al-Waili NS.

 

Dubai Specialized Medical Center and Medical Research Laboratories, Islamic Establishment for Education, Dubai, United Arab Emirates. noori786@yahoo.com

 

This study included the following experiments: (1) effects of dextrose solution (250 mL of water containing 75 g of dextrose) or honey solution (250 mL of water containing 75 g of natural honey) on plasma glucose level (PGL), plasma insulin, and plasma C-peptide (eight subjects); (2) effects of dextrose, honey, or artificial honey (250 mL of water containing 35 g of dextrose and 40 g of fructose) on cholesterol and triglycerides (TG) (nine subjects); (3) effects of honey solution, administered for 15 days, on PGL, blood lipids, C-reactive protein (CRP), and homocysteine (eight subjects); (4) effects of honey or artificial honey on cholesterol and TG in six patients with hypercholesterolemia and five patients with hypertriglyceridemia; (5) effects of honey for 15 days on blood lipid and CRP in five patients with elevated cholesterol and CRP; (6) effects of 70 g of dextrose or 90 g of honey on PGL in seven patients with type 2 diabetes mellitus; and (7) effects of 30 g of sucrose or 30 g of honey on PGL, plasma insulin, and plasma C-peptide in five diabetic patients. In healthy subjects, dextrose elevated PGL at 1 (53%) and 2 (3%) hours, and decreased PGL after 3 hours (20%). Honey elevated PGL after 1 hour (14%) and decreased it after 3 hours (10%). Elevation of insulin and C-peptide was significantly higher after dextrose than after honey. Dextrose slightly reduced cholesterol and low-density lipoprotein-cholesterol (LDL-C) after 1 hour and significantly after 2 hours, and increased TG after 1, 2, and 3 hours. Artificial honey slightly decreased cholesterol and LDL-C and elevated TG. Honey reduced cholesterol, LDL-C, and TG and slightly elevated high-density lipoprotein-cholesterol (HDL-C). Honey consumed for 15 days decreased cholesterol (7%), LDL-C (1%), TG (2%), CRP (7%), homocysteine (6%), and PGL (6%), and increased HDL-C (2%). In patients with hypertriglyceridemia, artificial honey increased TG, while honey decreased TG. In patients with hyperlipidemia, artificial honey increased LDL-C, while honey decreased LDL-C. Honey decreased cholesterol (8%), LDL-C (11%), and CRP (75%) after 15 days. In diabetic patients, honey compared with dextrose caused a significantly lower rise of PGL. Elevation of PGL was greater after honey than after sucrose at 30 minutes, and was lower after honey than it was after sucrose at 60, 120, and 180 minutes. Honey caused greater elevation of insulin than sucrose did after 30, 120, and 180 minutes. Honey reduces blood lipids, homocysteine, and CRP in normal and hyperlipidemic subjects. Honey compared with dextrose and sucrose caused lower elevation of PGL in diabetics.

 

Publication Types:

•   Clinical Trial

•   Randomized Controlled Trial

 

PMID: 15117561 [PubMed - indexed for MEDLINE


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