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Transcript
Fructose and its effect
on alcohol elimination
from blood following
alcoholic beverage consumption
FERNANDO SCHVED
Galam ltd., Mobile Post Menashe
Kibutz Maanit, 37855, Israel
Fernando Schved
AgroFood industry hi-tech - September/October 2009 - vol 20 n 5
Sweeteners
ABSTRACT: Fructose is a naturally occurring simple carbohydrate that successfully found its way into a myriad range of food
and beverage applications. This paper will describe a possible different use of fructose as a detoxification agent, by
examining the ability of fructose to accelerate the elimination of alcohol in blood following alcoholic beverage
consumption .The recommended dosage ranges between 0.25 g/ kg body weight to 2 g/kg body weight.
74
Fructose, also known as “fruit Sugar”, is a naturally-occurring,
simple bulk sweetener used in the food industry, and is
characterized by “clean” non-lingering sweet taste. Fructose
is highly soluble, and is characterized by a Relative
Sweetening Value (RSV) of 1.1-1.7 (where sucrose = 1.0),
depending on temperature and pH (1).
Fructose’s advantages are prominent in products consumed
at refrigeration temperatures and acid pH (~ 2.5-4.5). Fructose
is GRAS and non-allergenic sweetener, and its use is not
restricted by official regulatory bodies (2). Additional
beneficial trait of fructose includes its ability to reduce the
glycemic loads of food (2). Fructose is characterized by a GI
~20 (sucrose GI ~ 60). Fructose also works as a “masking
agent” for undesirable aftertastes of some artificial
sweeteners. Combinations of fructose with aspartame, Ace K,
cyclamate, saccharin allow a reduction in the caloric content
up to 60 percent. Moreover, fructose also exhibits sweetening
synergy effects with several bulk sugars. In this article, a unique
feature of fructose, namely its ability to accelerate the
elimination of alcohol in blood, following alcoholic beverage
consumption, will be discussed, suggesting a potential
application.
Following its ingestion, about 20 percent of alcohol consumed
is absorbed in the stomach with rest (~ 80 percent) more
rapidly and at a constant rate through the intestine. Ninety
percent of the alcohol consumed is metabolized in the liver
(small quantity that is not metabolized can be measured in
breath and urine). About 90 to 98 percent of ingested alcohol
is eliminated from the body through oxidative metabolism,
and the basic pathways involve the progressive oxidation of
ethanol to ethanoic acid via ethanol (3). The major site of this
oxidation is the liver parenchyma cells, but other potential
sites include the stomach (4), vascular tissues, and the brain
(5). Thus the metabolic rate of alcohol is a two-step process; -1
the enzyme alcohol dehydrogenase (ADH) metabolizes
alcohol to acetaldehyde, -2 acetaldehyde is converted by
acetaldehyde dehydrogenase to either acetate or into water
+ acetic acid.
The liver can metabolize only a certain amount of alcohol per
hour, regardless of the amount that has been consumed. The
rate of alcohol metabolism depends, in part, on the amount
of metabolizing enzymes in the liver, which varies among
individuals and appears to have genetic determinants (7, 8).
In general, after the consumption of one standard drink, the
amount of alcohol in the drinker’s blood (blood alcohol
concentration: BAC) peaks within 30 to 45 minutes. (A
standard drink is defined as 12 ounces of beer, 5 ounces of
wine, or 1.5 ounces of 80-proof distilled spirits, all of which
contain the same amount of alcohol.) The BAC curve, shown
below provides an estimate of the time needed to absorb
and metabolize different amounts of alcohol (9). Since the
metabolism of alcohol is slow, consumption needs to be
controlled to prevent accumulation in the body and
intoxication.
Time needed to absorb and metabolize different
amounts of alcohol*
Factors such as food intake and its constituent profile, gender
and age have been reported to influence the kinetics of
alcohol absorption and metabolism. It is widely accepted
that the rate of alcohol absorption can be decreased by
consuming food along with the alcoholic drink (10-12). The
rate at which alcohol is absorbed depends on how quickly
the stomach empties its contents into the intestine. The higher
the dietary fat content, the more time this emptying will
require and the longer the process of absorption will take.
One study found that subjects who drank alcohol after a meal
that included fat, protein, and carbohydrates, absorbed the
alcohol about three times more slowly than when they
consumed alcohol on an empty stomach (13). In another
work (14) Rogers et al. showed that carbohydrates
significantly increased the rate of alcohol metabolism in
fasting humans while protein and fat failed to show the same
effect.
100 mg percent BAC is the legal level of intoxication in most States. 50 mg
percent is the level at which deterioration of driving skills begins. (Adapted
from JAMA, 255, pp. 522-527 (1986)).
Among foods, the special effect of fructose on alcohol
metabolism has been reported as early as from 1937 (15).
of oral fructose treatment on alcohol metabolism, was
internally conducted (20-28). In those reviewed studies,
fructose was provided to participants (N= 5-109) who were
non-alcoholics as well as alcoholics characterized by
different degrees of consumptions habits. Protocols included
participants groups of females, males or mix. Fructose was
provided either as a single dose or as a multiple dose, along
with the alcohol or after its consumption. A review of the
studies shows that reported administered levels of fructose
ranged from 0.25-2.0 g /kg body weight or 62-135 g /
participant (total provided to participants, not on a basis of
g/kg body weight). The reported increase in values of “Blood
Ethanol Elimination Rate” (BEER), as a percentage above the
basic rate (range: 100-110 mg/kg/hr) for all treatments, was
between 6-100 percent. Shortening longitudes of intoxication
was decreased also by up to 40 percent (19, 20).
In conclusion, the accumulated data originating from the
above clinical studies shows that fructose while being
formulated into beverage products may provide a simple
way aiming to help dealing with alcohol intoxication. The
mechanism supporting the above is based upon the ability
of fructose to accelerate the rate of ethanol elimination from
blood following consumption of alcoholic beverages.
References and notes
*
1.
2.
3.
4.
5.
If the same number of drinks is consumed over a longer period
of time, BAC's will be lower.
F.W. Schenck, R.E. Hebeda, Starch Hydrolysis Products, p. 201
(1992), publisher: VCH, ISBN=3527281509.
F. Schved, B. Hassidov, “Fructose: a high quality sweetener,
flavor enhancing, clorie-reduction and impact on glycemic
index”, Agro Food Industry Hi-Tech, 19(3), pp. 26-27 (2008).
T.J. Peters, V.R. Preedy, “Metabolic consequences of alcohol
ingestion”, Novartis Found Symp., 216, pp. 19-24 (1998).
E. Baraona, A. Yokoyama et al., “Lack of alcohol
dehydrogenase isoenzyme activities in the stomach of
Japanese subjects”, Life Sci., 49, pp. 1929-1934 (1991).
C.S.
Lieber,
“ E t h a n o l
metabolism,
cirrhosis and
alcoholism”,
Clin Chim
Acta, 257,
pp. 59-84
(1977).
Sweeteners
In this context it is interesting to mention that for a long time
(prior to controlled scientific interventions) a common nonscientific experience existed claiming that consumption of
honey may shorten the period of alcohol intoxication (honey
is an excellent rich source of nutritional fructose). Nowadays
the above observation is also supported up by wellcontrolled documented studies such as that of Onyesom
(16). Onyesom demonstrated that honey significantly
increased blood alcohol disappearance and elimination
rates by 32.4 and 28.6 percent, respectively, and reduced
the intoxication time (that is, the time taken to attain zero
blood alcohol level) and its degree (the peak blood alcohol
level) by 30 and 4.4 percent.
With regards to the possible mechanism by which fructose
accelerates ethanol metabolism, a literature review
indicates a possible shift in the metabolism of fructose in the
presence of alcohol. This shift has been linked to the
production in the liver of NAD+ which facilitates alcohol
oxidation (17, 18, 20). Therefore, in the presence of alcohol,
the metabolism of fructose in the liver is diverted from NAD+
to NADH requiring pathways, which in turn generates the
NAD+ needed for alcohol oxidation.
Several clinical intervention studies on humans have been
reported demonstrating the ability of either intravenous or
oral fructose treatment to enhance alcohol metabolism
following its ingestion i.e. namely increasing the speed of its
clearance from blood. While intravenous treatment with
fructose has been reported a possible practice in health
care institutions, oral consumption of fructose may be more
adequate for accelerating the rate of alcohol
disappearance from blood in the case of occasional or light
drinkers (< 20 g alcohol/day).
Various clinical interventions studies were conducted to
check the oral ability of fructose to speed up the elimination
of alcohol from blood. For example, Onyesom & Anosike (19)
checked the effect of fructose on blood ethanol peak levels
and elimination rates within a group of 10 healthy adults (3
males and 7 females, average age 23.3 years). Four hours
after breakfast the volunteers were orally given a moderate
dose 0.55g (20 percent) ethanol/kg body weight, on two
different occasions separated by 2 weeks. They were
instructed to consume the alcohol single dose within 10
minutes after diluting to 20 percent with orange squash. On
both occasions, the experiments were conducted in a similar
manner, with the exception of fructose use. During the first
occasion, alcohol was consumed alone, but during the
second, 0.25g fructose/kg body weight was administered
orally after about 40 minutes of ingesting the alcohol. Blood
alcohol level (BAL) was determined every 30 minutes for 90
minutes using whole blood obtained from the vein.
Oral administration of fructose however, changed
the kinetics of alcohol absorption and elimination
in both male and female subjects. Total
intoxication time, i.e. the time needed to gain zero
BAL was reduced by 41.7 percent (from 5.4 to 3.15
hours) in the men and by 40 percent (from 4.75 to
2.85 hours) in the women. Blood ethanol clearance
rate, an index of blood ethanol metabolic rate, in
both the male and female
subjects was
increased by 66.7 percent
and 92.3 percent,
respectively, in the
presence of fructose.
The increases in both
genders
were
demonstrated to be
statistically significant
(p<0.05).
A review, reporting the effect
75
6.
7.
8.
9.
10.
11.
12.
Sweeteners
13.
14.
15.
AgroFood industry hi-tech - September/October 2009 - vol 20 n 5
16.
76
17.
C.S. Lieber, “Metabolic consequences of ethanol”, The
Endocrinologist, 4(2), pp. 127-139 (1994).
W.F. Bosron, T. Ehrig et al., “Genetic factors in alcohol
metabolism and alcoholism”, Seminars in Liver Disease, 13(2),
pp. 126-135 (1993).
L.Z. Benet, D.L. Kroetz et al., “Pharmacokinetics: The dynamics of
drug absorption, distribution, and elimination”, P.B. Molinoff, R.W.
Ruddon, eds, Goodman and Gillman’s The Pharmacological
Basis of Therapeutics, 9th ed. New York: McGraw-Hill, pp. 3-27
(1996).
Wilkinson et al., "Pharmacokinetics of Ethanol After Oral
Administration in the Fasting State", Journal of Pharmacokinetics
and Biopharmaceutics, 5(3), pp. 207-224 (1977).
M. Horowitz, A. Maddox et al., “Relationships between gastric
emptying of solid and caloric liquid meals and alcohol
absorption”, Am J Physiol Gastrointest Liver Physiol., 257,
G291-G298 (1989).
H. Wallgren, “Absorption, diffusion, distribution and elimination of
ethanol: Effect on biological membranes”, International
Encyclopedia of Pharmacology and Therapeutics, Oxford:
Pergamon, 1, pp. 161-188 (1970).
A.G. Fraser, S.B. Rosalki et al., “Inter-individual and intraindividual variability of ethanol concentration-time profiles:
Comparison of ethanol ingestion before or after an evening
meal”, British Journal of Clinical Pharmacology, 40, pp. 387-392
(1995).
A.W. Jones, K.A. Jönsson, “Food-induced lowering of bloodethanol profiles and increased rate of elimination immediately
after a meal”, Journal of Forensic Sciences, 39(4), pp. 1084-1093
(1994).
J.O. Rogers, J. Smith et al., “Differing Effects of Carbohydrate, Fat
And Protein On The Rate Of Ethanol Metabolism”, Alcohol &
Alcoholism, 22, pp. 245-353 (1987).
T.M. Carpenter, R.C. Lee, “The effect of fructose on the
metabolism of ethyl alcohol in man”, J. Pharmacol. Exp. Ther.,
60, pp. 286-295 (1937).
I. Onyesom:, “Honey induced stimulation of blood ethanol
elimination and its influence on serum TG and blood pressure in
man”, Ann Nutr Metab., 49, pp. 319-324 (2005).
N. Tygstrup, K. Winkler et al., “The mechanism of the fructose
18.
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R. Scholz, H. Nohl, “Mechanism of the stimulatory effect of
fructose on ethanol oxidation in perfused rat liver”, Eur J
Biochem., 63, pp. 449-58 (1976).
I. Onyesom, E.O. Anosike, “Oral fructose-induced changes in
blood ethanol oxidokinetic data among healthy Nigerians”,
Southeast Asian Journal Of Tropical Medicine And Public Health,
35(3), pp. 476-480 (2004).
E. Ugochukwu Uzuegbu, “Innocent Onyesom. Fructose-induced
increase in ethanol metabolism and the risk of Syndrome X in
man”, C. R. Biologies, 18 March 2009.
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R.H. Ylikahri, T. Leino et al., “Effects of Fructose and Glucose on
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Alcohol Intoxication and Hangover”, European Journal of
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blood with oral fructose and sucrose”, American Journal of
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