Too much fructose
Fructose: Too much in diet associated with
INSULIN resistance /T2D/obesity, fatty liver
and CVD
About fructose
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 ~3.5g .
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.
The use of mixed sugars are more metabolically predictive
of dietary consequences than that from single monosaccharides studied individually.
Studies show the greatest absorption rate occurs when glucose and fructose are
administered in equal quantities
Wikipedia
When fructose and glucose are ingested together (e.g. as in sucrose),
the oxidation rates of the mixed sugars are faster than that of either one of them
ingested alone at the same dosage. A
meta-analysis of various studies shown
here:
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%
Oxidation rates (represents conversion)
of fructose & glucose
Sun,
2012
The data of obese or diabetic
subjects were not included in this figure .
Metabolic fate of dietary fructose carbons.
The data obtained within study periods <=
6 hours after 50-150 gm fructose ingestion by non-diabetic or obese persons.
Sun,
2012
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.
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 p er
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)
GROUP
Mean fructose (g/day) % 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)
---Male
--- 63.4
10
---Female
--- 46.2
10.5
2-5 yrs
44.9
11.6
6-11 yrs
54.2
10.9
12--18 yrs
72.8 (vs. 15-18 yrs 54g/day
in 1977-78) 12.1
19-30 yrs
66.6
10.8
31-50 yrs
55
9.7
51-70 yrs
44.1
9.2
>70 yrs
38.4
9.4
Normal weight
56.2
9.9
Obese
51.1
9.8
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
Fruits / 100% fruit juice was the largest
source of fructose for over 51 year olds
Chart: How much fructose in fruit
If
all fructose sources except whole fruit and vegetables were removed: 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
Pie chart of fructose-source consumed by adults (2008)
Dietary Fructose Consumption Among
US Children and Adults: National Health and Nutrition Examination Survey III
(n=21,483)
RTE=Ready to eat
Beverages= sugar-sweetened beverages
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).
Consumed?
Study participants
Effects
Reference
Sucrose
1669 children 6-19 years
TGs ↑
HDL
Morrison, 1980
Increased sugar
12 year old Finnish children
HDL
Kouvalainen, 1982
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
B antle,
2000
12% cals as fructose/12 wks
Adults
TGs ↔
Osei, 1987
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.
High fructose corn
syrup (HFCS)
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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
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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
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PubMed
Osei K, Falko J, Bossetti B, Holland G. (1987) Metabolic
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Pubmed
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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
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Pubmed
