Fructose is one of only 3 monosaccharides (single sugar molecules; the others being glucose and galactose). Fructose makes up half of the sucrose (table sugar) molecule. In this diagram, that's a glucose molecule on the left, covalently linked (in the case of sugar molecules, called a disaccharide bond) to a fructose molecule (on the right):
Fructose is naturally present in honey, sugar cane, fruits, flowers, berries and most root vegetables (especially sugar beets). Fructose is present both as a single molecule and as 50% of sucrose/ table sugar (bonded to a glucose molecule). A cup of strawberries contains ~4g of fructose, a teaspoon of honey ~g .
Fructose ranks high on the sweetness scale. Rated from 1.2 to 1.8 times sweeter than sucrose.
Fructose ranks low on the glycemic index at 19 (doesn't much raise blood glucose), but it does raise blood fructose levels - which is worse. Fructose binds to cellular proteins 7 times faster than glucose. This creates 100 times more reactive oxygen species (ROS) than glucose, which can cause significant cellular damage. E.g. to arterial or pancreatic cells
Fructose digestion / metabolism
The monsaccharides are directly absorbed into the bloodstream during digestion. If fructose is consumed in sugar (i.e. attached to a glucose molecule), the enzyme sucrase cleaves them apart in the small intestines, ready for individual absorption. Once in the blood, fructose enters the hepatic portal vein en route to the liver to be metabolized. Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities [Link]
The use of mixed sugars are more metabolically predictive of dietary consequences than that from single monosaccharides studied individually. When fructose and glucose are ingested together (including fructose-containing sucrose), the oxidation rates of the mixed sugars were faster than that of either one of them ingested alone at the same dosage. A meta-analysis of various studies shown here:
The data of obese or diabetic subjects were not included in this figure.
Some people are unable to fully metabolize / absorb fructose, which causes digestive gas / discomfort. In these cases fructose is considered a FODMAP (fermentable oligo-, di-, mono-saccharides and polyols) - - -short-chain carbs, which resist digestion.
Meta-analysis study found these results:
Non-exercise subjects: The oxidation rate from fructose to glucose had a mean average of 45% (mean conversion rate 41%) within a period of 3-6 hours after ingestion.
With exercise: The mean average oxidation rate of fructose was about 45.8% within 2-3 hours. Ingesting fructose with glucose, the oxidation rate increased to ~66%
As always, study results depend on the details
Fructose administered on its own (as often the case in studies) is poorly absorbed. It will therefore have little effect, other than causing GI pain, bloating or diarrhea. Dietary fructose is usually present with other sugars and fiber.
Some studies attempt to skew the data, for example, showing that consumed fructose generates liver fat at a slow rate of <5%. This is likely the case for someone who is thin, not INSULIN-resistant, has not consumed anything in the last few hours (i.e. has depleted glycogen /glucose storage in liver), and then consumes only fructose. However, it would be a very different outcome for someone well-fed, INSULIN-resistant, overweight and consuming a more natural combination of fructose together with glucose, which reveals fructose converting to fat at a rate closer to 30%.
The dose matters. E.g. Studies supplying fructose as a high percentage of dietary calories do show increased blood TGs and LDL cholesterol, INSULIN resistance and weight gain
How much fructose are we consuming?
Foods containing the highest amount of fructose per serving include: foods containing sucrose, HFCS, agave nectar, honey, molasses, maple syrup, fruit and their juices.
1977-1978: Estimated that mean fructose consumption in U.S. was 37 g/day (8% of total caloric intake) and 54 g/day among those age 15-18 years (Park &Yetley, 1993)
|1988 to 1994: Mean fructose consumption|
|% total cals|
|2008 Study analyzed data from NHANES III collected from 1988 to 1994|
|All subjects||54.7 (mean average)||10.2|
|(~50% increase vs. 1977-78)|
|12--18 yrs||72.8 (vs. 15-18 yrs 54g/day in 1977-78)||12.1|
Some "food for thought"
• Sugar-sweetened beverages (SSBs) were the source of 30% of fructose for all age groups and almost 50% of fructose for adolescents. Grains (including breads, cereal, cakes, pies, and snacks) were the second-largest source (11-12%).
• 74% of fructose came from foods and beverages other than whole fruits and vegetables.
• Fruits / 100% fruit juice was the largest source of fructose for over 51 year olds
• If all fructose sources except whole fruit and vegetables were removed: children would eliminate 82% dietary fructose, and adults 75%.
• Underreporting of total calorie intake is known to increase as BMI increases. (Neuhouser, 2008)
• Adults ate ~ 50% higher percentage of whole fruit and 33% less percentage of sweetened beverages than teens
So - is consuming fructose harmful or not?
Excessive fructose intake elevates plasma triglycerides (TGs) and LDL cholesterol, and lowers HDL cholesterol
"Our study shows for the first time the surprising speed with which humans make body fat from fructose. Once you start the process of fat synthesis from fructose, it's hard to slow it down. The bottom line of this study is that fructose very quickly gets made into fat in the body."
- Dr. Elizabeth Parks, associate professor of clinical nutrition,UT Southwestern Medical Center
Author of a fructose study reported in the Journal of Nutrition (2008).
Several short-term studies show association between fructose intake and dyslipidemia
|Several short-term studies show association between fructose intake and dyslipidemia|
|Sucrose||1669 children 6-19 years||TGs ↑||HDL
|Increased sugar||12 year old Finnish children||HDL
|Varied diet||Swiss children. Tot. fructose was only significant dietary factor as predictor;||LDL size ↓||Aeberli, 2007|
|Fructose||Adults. Effect significant with fructose compared to glucose; persisted for 12 hours||TGs ↑||Teff, 2004|
|25% cals as fructose / 6 days||Healthy men||Mean fasting TGs ↑ x2||Faeh, 2005|
|17% cals as fructose / 6 wks||TGs
|12% cals as fructose/12 wks||Adults||TGs ↔
|25% cals as fructose/10 wks||TGs ↑||Havel, 2003|
|7.5% & 15% cals as fructose/8 wks||LDL & total chol. ↑||Hallfrisch, 1983|
• Observation: Increased TGs may only occur when fructose reaches a threshold percentage of total calorie intake
High fructose intake short-circuits appetite control
High fructose consumption fails to stimulate the normal production of the long-term energy-balancing hormone LEPTIN. This hormone goes up when we have sufficient calories/energy and down when we don't, indicating whether to stop or start eating. Insufficient LEPTIN can have adverse effects on regulating food intake and lead to extra body fat.
Excessive fructose consumption can create fats in the liver
In short, consuming excessive amounts of fructose-containing sweeteners can lead to some serious health issues
• Metabolic syndrome, type 2 diabetes and weight gain / obesity
• Non-alcoholic fatty liver disease
• Cardiovascular disease (CVD)
• Dental caries. The case with all caloric sweeteners
The main sources of oral fructose in the U.S. are:
Sucrose (table sugar). 50% fructose. 1 glucose molecule attached to a fructose molecule via a disaccharide bond;
High fructose corn syrup (HFCS). Either 42% or 55% fructose. The inclusion of this cheap sweetener source in commercial food products and ready-made drinks has escalated since its introduction in the early 1970's.
Aeberli I, Zimmermann M, Molinari L, et al. (2007) Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr.86:1174-1178. Pubmed
Bantle JP, Raatz SK, Thomas W, Georgopoulos A. (2000) Effects of dietary fructose on plasma lipids in healthy subjects. Am J Clin Nutr. 2000;72:1128-1134. Pubmed
Faeh D, Minehira K, Schwarz J-M, Periasami R, Seongsu P, Tappy L. (2005) Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men. Diabetes. 54:1907-1913. Pubmed
Hallfrisch J, Reiser S, Prather E. (1983) Blood lipid distribution of hyperinsulinemic men consuming three levels of fructose. Am J Clin Nutr:740-748. Pubmed
Havel PJ, Elliott S, Keim NL, Krauss RM, Teff K. (2003) Short-term and long-term consumption of high fructose, but not high glucose, diets increases postprandial triglycerides and apo-lipoprotein-B in women. J Invest Med.;52(suppl):S163. Google scholar
Kouvalainen K, Uhari M, Akerblom H, et al. (1982) Nutrient intake and blood lipids in children. Klin Padiatr. 194:307-309 Pubmed
Morrison J, Larsen R, Glatfelter L, et al. (1980) Interrelationships between nutrient intake and plasma lipids and lipoproteins in schoolchildren aged 6 to 19: The Princeton School District study. Pediatrics. 65:727-734 PubMed
Neuhouser ML, Tinker L, Shaw PA, et al. (2008) Use of recovery biomarkers to calibrate nutrient consumption self-reports in the Women's Health Initiative. Am J Epidemiol. 167:1247-1259. PubMed
Osei K, Falko J, Bossetti B, Holland G. (1987) Metabolic effects of fructose as a natural sweetener in the physiologic meals of ambulatory obese patients with type II diabetes. Am J Med.;83:249-255. Pubmed
Park YK, Yetley EA, (Nov 1993) Review intakes and food sources of fructose in the United States. Am J Clin Nutr. 58(5 Suppl):737S-747S. PubMed
Sun, S. Z., & Empie, M. W. (2012). Fructose metabolism in humans - what isotopic tracer studies tell us. Nutrition & metabolism, 9(1), 89. PubMed
Teff KL, Elliott SS, Tschop MH, et al. (2004) Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 89:2963-2972. Pubmed
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