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High fructose corn syrup and health

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The chemical structures of fructose (left) and glucose (right), the main components of HFCS

The consumption of high fructose corn syrup (HFCS or glucose–fructose syrup) and its relationship to a healthy diet is a subject of investigation. Concerns center around excessive sugar intake and its contribution to obesity, type-2 diabetes, metabolic syndrome, and cardiovascular disease. Evidence does not indicate it is less healthy than sugar consumption in general[1].

Background

The term high fructose corn syrup was developed to distinguish it from all-glucose corn syrups that existed in the past, and does not accurately describe the composition of the syrup (which is composed of a mixture of 42-55% fructose, 41-45% glucose and 0-5% glucose polymers depending on the specific blend),[2] and from 0.293 to 1.130 gram/liter α-dicarbonyl decomposition products.[3] In the 1980s it replaced sucrose as the main sweetener of soft drinks in the United States. Sucrose is a disaccharide that when consumed, is hydrolysed into 50% glucose and 50% fructose. This step takes extra time and creates a lower rate of fructose release. Rates of obesity subsequently rose, paralleling an increase in the consumption of soft drinks in general. Additional concerns have been raised due to laboratory research that suggested a link between consuming large amounts of fructose and changes to various proxy health measures including elevated blood triglycerides, size and type of low-density lipoproteins and uric acid levels.[2]

United States guidelines regarding sugar consumption

Numerous agencies in the United States recommend reducing the consumption of all sugars, including HFCS, without singling it out as presenting extra concerns. The Mayo Clinic cites the American Heart Association's recommendation that women limit the added sugar in their diet to 100 calories a day (~6 teaspoons) and that men limit it to 150 calories a day (~9 teaspoons), noting that there is not enough evidence to support HFCS having more adverse health effects than excess consumption of any other type of sugar.[4] The United States departments of Agriculture and Health and Human Services recommendations for a healthy diet state that consumption of all types of added sugars be reduced.[5]: p.27 

Obesity and metabolic syndrome

A 2004 commentary in The American Journal of Clinical Nutrition suggested that the altered metabolism of fructose when compared to glucose may be a factor in increasing obesity rates since, as compared to glucose, fructose may be more readily converted to fat and the sugar causes less of a rise in insulin and leptin, both of which increase feelings of satiety. Fructose, in contrast to glucose, was shown to potently stimulate lipogenesis (creation of fatty acids, for conversion to fat).[6] The review in Trends in Endocrinology and Metabolism concluded: 'dietary fructose might promote the development of nonalcoholic fatty liver disease, which in and of itself, can result in hepatic insulin resistance, a key feature of type 2 diabetes mellitus.'[6] The authors suggested reducing intake of sugars by using sugar substitutes instead.[7] In subsequent interviews, two of the study's authors stated the article was distorted to place emphasis solely on HFCS when the actual issue was the overconsumption of any type of sugar.[8][9] While fructose absorption and modification by the intestines and liver does differ from glucose initially, the majority of the fructose molecules are converted to glucose or metabolized into byproducts identical to those produced by glucose metabolism. Consumption of moderate amounts of fructose has also been linked to positive outcomes, including reducing appetite if consumed before a meal, lower blood sugar increases compared to glucose, and (again compared to glucose) delaying exhaustion if consumed during exercise.[2]

In 2007 an expert panel assembled by the University of Maryland's Center for Food, Nutrition and Agriculture Policy reviewed the links between HFCS and obesity and concluded there was no ecological validity in the association between rising body mass indexes (a measure of obesity) and the consumption of HFCS. The panel stated that since the ratio of fructose to glucose had not changed substantially in the United States since the 1960s when HFCS was introduced, the changes in obesity rates were probably not due to HFCS specifically but rather a greater consumption of calories overall, and recommended further research on the topic.[10] In 2009 the American Medical Association published a review article on HFCS and concluded that based on the science available at the time it appeared unlikely that HFCS contributed more to obesity or other health conditions than sucrose, and there was insufficient evidence to suggest warning about or restricting use of HFCS or other fructose-containing sweeteners in foods. The review did report that studies found direct associations between high intakes of fructose and adverse health outcomes, including obesity and the metabolic syndrome.[1]

Studies

Part of the concern over fructose arises from animal testing in which the injection of fructose directly into the brain of rats led to increased eating and subsequent research in mice seemed to confirm this effect.[2] Re-examination of the results suggested that the results in rodents would have little meaning in humans due to the strict control over the amount of fructose that crosses the blood–brain barrier.[2] Subsequent testing with humans using both short- and long-term experiments found no important differences between the consumption of HFCS versus other sugars.[2] Most of the studies linking fructose consumption to higher blood triglycerides have been in rodents through mechanisms different from those in humans, and therefore it is unlikely that high-fructose diets would have comparable effects in humans. Tests in humans suggest that for people with insulin resistance, diets with 50 grams or more per day (high consumption) may result in elevated triglycerides, but there is no effect with normal levels of fructose consumption.[2]

Epidemiological research has suggested that the increase in obesity is linked to increased consumption of sugars and/or calories in general, and not due to any special effect of HFCS[11][2]

Other issues

Consumption of HFCS has been associated with non-alcoholic fatty liver disease, as it is thought that fructose may cause increased fat deposits in the abdomen[12] though it has also been suggested that this association is not unique to fructose and may be due to glucose consumption as well.[13]

High fructose consumption has been linked to high levels of uric acid in the blood, though this is only thought to be a concern for patients with gout.[2]

The possibility that significant consumption of products containing high fructose corn syrup with detectable levels of mercury could result in neurotoxicity was raised by studies in 2009.[14][15][16] In 2011 the Corn Refiners Association announced that “no mercury or mercury-based technology is used in the production of high fructose corn syrup in North America.”[17] By the end of 2012, most chlor-alkali plants in the United States had phased out older "mercury cell" technology linked to mercury contamination of HFCS, except for two chlor-alkali plants - one in Ohio and one in West Virginia, run by ASHTA Chemicals and PPG Industries, respectively.[18][19][20] Mercury cell technology is still widely used outside of the United States and there are no restrictions on importing mercury-grade caustic soda for use in HFCS production.[16][21]

HFCS consumption can be problematic in those with fructose malabsorption.[22]

α-dicarbonyl degradation products

While some high-fructose corn syrup advocates may claim the product contains all-natural ingredients, multiple toxic dicarbonyl degradation products have been detected, created during the processing steps.[23] The seven major dicarbonyls are: 3-deoxyglucosone, glucosone, 3-deoxygalactosone, 1-deoxyglucosone, 3,4-dideoxyglucosone-3-ene, methylglyoxal, and glyoxal. 3-Deoxyglucosone was identified as the major α-DC with concentrations up to 730 μg/mL HFCS. The total α-DC content ranged from 0.293 to 1.130 gram/liter HFCS. These compounds react with amino acids to form advanced glycation end-products. The α-dicarbonyls and AGEs are inducing and compounding factors of diabetes and its complications, e.g. nephropathy, Alzheimer's disease and cataracts,[24] and vascular complications.[25] AGEs affect nearly every type of cell and molecule in the body and are thought to be one factor in aging and some age-related chronic diseases.[26][27][28]

References

  1. ^ a b Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 20516261, please use {{cite journal}} with |pmid= 20516261 instead. "Because the composition of HFCS and sucrose is so similar, particularly on absorption by the body, it appears unlikely that HFCS contributes more to obesity or other conditions than sucrose does. ... few studies have evaluated the potentially differential effect of various sweeteners."
  2. ^ a b c d e f g h i Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 21050460 , please use {{cite journal}} with |pmid= 21050460 instead.
  3. ^ Gensberger Sabrina, Mittelmaier Stefan, Glomb Marcus A, Pitschetsrieder Monika (July 2012). "Identification and quantification of six major α-dicarbonyl process contaminants in high-fructose corn syrup". Analytical and Bioanalytical Chemistry. 403 (10): 2923–2931.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ "High-fructose corn syrup: What are the health concerns?". Mayo Clinic. 2012-09-27. Retrieved 2012-10-17.
  5. ^ Dietary Guidelines for Americans, 2010. 7th Edition (pdf). United States Department of Agriculture and United States Department of Health and Human Services. December 2010. Retrieved 2012-10-17.
  6. ^ a b Samuel VT (February 2011). "Fructose induced lipogenesis: from sugar to fat to insulin resistance". Trends Endocrinol. Metab. 22 (2): 60–5. doi:10.1016/j.tem.2010.10.003. PMID 21067942.
  7. ^ Bray, GA (2004). "Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity". American Journal of Clinical Nutrition. 79 (4): 537–543. PMID 15051594. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  8. ^ Parker-Pope, Tara (September 20, 2010). "In Worries About Sweeteners, Think of All Sugars". The New York Times. Retrieved 2011-04-20.
  9. ^ Warner, M (2006-07-02). "A Sweetener With a Bad Rap". The New York Times. Retrieved 2012-05-02.
  10. ^ Forshee RA; Storey, ML; et al. (2007). "A critical examination of the evidence relating high-fructose corn syrup and weight gain" (pdf). Critical Reviews in Food Science and Nutrition. 47 (6): 561–82. doi:10.1080/10408390600846457. PMID 17653981. {{cite journal}}: Explicit use of et al. in: |last3= (help)
  11. ^ Stanhope, Kimber L.; Schwarz, Jean-Marc; Havel, Peter J. (June 2013). "Adverse metabolic effects of dietary fructose". Current Opinion in Lipidology. 24 (3): 198–206. doi:10.1097/MOL.0b013e3283613bca.
  12. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 20518077 , please use {{cite journal}} with |pmid= 20518077 instead.
  13. ^ Allocca, M; Selmi C (2010). "Emerging nutritional treatments for nonalcoholic fatty liver disease". Nutrition, diet therapy, and the liver. CRC Press. pp. 131–146. ISBN 1-4200-8549-2. {{cite book}}: Unknown parameter |editors= ignored (|editor= suggested) (help)
  14. ^ Dufault R, Schnoll R, Lukiw WJ, Leblanc B, Cornett C, Patrick L, Wallinga D, Gilbert SG, Crider R (Oct 27, 2009). "Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children". Behav Brain Funct. 5: 44. doi:10.1186/1744-9081-5-44. PMC 2773803. PMID 19860886.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  15. ^ Wallinga D, Sorensen J, Mottl P, Yablon B (January 2009). "Not So Sweet: Missing Mercury and High Fructose Corn Syrup" (PDF). Institute for Agriculture and Trade Policy. Retrieved 2012-09-20.{{cite web}}: CS1 maint: multiple names: authors list (link) (self-published)
  16. ^ a b Connie Howard (February 2010). "Mercury confusion: What's being done about mercury in our food?". VueWeekly.com. Retrieved 2013-01-08.
  17. ^ http://www.sweetsurprise.com/2011/06/08/5-reasonshighfructosecornsyrupwillkillyou
  18. ^ Rob Pavey (July 2012). "Olin prepares for mercury free future after 47 years". Augusta Chronicle. Retrieved 2013-01-08.
  19. ^ Bradley J. Westfall, ASHTA Chemicals; John McIntosh, Olin Chlor Alkali Products; and Michael H. McGarry, PPG Industries Inc. (September 2009). "Letter to EC Committee". regulations.gov. Retrieved 2013-01-08.{{cite web}}: CS1 maint: multiple names: authors list (link)
  20. ^ Olin (October 2012). "Olin Announces Third Quarter Earnings". Olin. Retrieved 2013-01-08.
  21. ^ World Chlorine Council (January 2011). "Reduction of Mercury Emissions and Use from the Chlor-Alkali Sector Partnership" (PDF). EuroChlor.org. Retrieved 2013-01-08.
  22. ^ "Fructose intolerance: Which foods should I avoid?". Mayo Clinic. Retrieved 2012-09-15.
  23. ^ Gensberger Sabrina, Mittelmaier Stefan, Glomb Marcus A, Pitschetsrieder Monika (July 2012). "Identification and quantification of six major α-dicarbonyl process contaminants in high-fructose corn syrup". Analytical and Bioanalytical Chemistry. 403 (10): 2923–2931.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  24. ^ Wang, Yu (January 2009). "Roles of Reactive Carbonyl Species in Health and Flavor Generation". New Brunswick Rutgers, The State University of New Jersey.
  25. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 18331228, please use {{cite journal}} with |pmid=18331228 instead.
  26. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 19409449, please use {{cite journal}} with |pmid=19409449 instead.
  27. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 19448391, please use {{cite journal}} with |pmid=19448391 instead.
  28. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1038/ajh.2008.320, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1038/ajh.2008.320 instead.
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