effect of alcoholic beverages on postprandial glycemia and insuinemia

8/12/2019 Effect of Alcoholic Beverages on Postprandial Glycemia and Insuinemia

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Effect of alcoholic beverages on postprandial glycemia andinsulinemia in lean, young, healthy adults1–3

Jennie C Brand-Miller, Kaniz Fatima, Christopher Middlemiss, Marian Bare, Vicki Liu, Fiona Atkinson, and Peter Petocz

ABSTRACT

Background: Ethanol’s ability to inhibit gluconeogenesis might

reduce postprandial glycemia in realistic meal settings.

Objective: The objective was to explore the effect of 3 types of

alcoholic beverages consumed alone, with a meal, or 1 h before a

meal on postprandial glycemia in healthy subjects.

Design: In study 1, isoenergetic (1000 kJ) servings of beer, white

wine, and gin were compared witha 1000-kJ portion of white bread.In study 2, the same servings were compared with water as an

accompaniment to a bread meal. In study 3, 20-g alcohol portions

were served as a premeal drink. Fingertip capillary blood samples

were taken at regular intervals over 2–3 h.

Results: In study 1, the mean (SE) glucose scores for beer (58

11), wine (7 3), and gin (10 5) were significantly lower (P

0.001) than those for bread ( 100). In study 2, meals consumed

with beer (84 11; P 0.03), wine (63 6; P 0.001), and gin

(80 12; P 0.007) produced less glycemia than did the meal

consumed with water ( 100). In study 3, all 3 beverages reduced

the postprandial glycemic response to the subsequent meal (67 5,

75 6, and 78 4 with the beer, wine, and gin trials, respectively;

P 0.003).

Conclusion: In realistic settings, alcoholic beverage consumption

lowers postprandial glycemia by 16–37%, which represents an un-

recognized mechanism by which alcohol may reduce the risk of

chronic disease. Am J Clin Nutr 2007;85:1545–51.

KEY WORDS Alcohol, glucose, insulin, postprandial hyper-

glycemia

INTRODUCTION

Large prospective studies and meta-analyses have directly

linked light-to-moderate alcohol intake with a lower risk of cor-

onary heart disease and type 2 diabetes (1–4). Several mecha-nisms have been suggested to underlie the apparent protective

effect, including ethanol’s ability to raise the HDL concentration

and reduce coagulatory activity. Moderate consumption (1–3

drinks/d) has also been associated with lower fasting glucose and

insulin concentrations (5, 6), improved glucose tolerance (6, 7),

and lower insulin resistance estimated indirectly by homeostasis

modeling assessment (6). Some evidence is conflicting. Alco-

holic beverages have decreased glucose utilization in some stud-

ies (8, 9), yet increased insulin sensitivity in others (6, 10, 11).

Ethanol consumption is also known to directly inhibit glu-

coneogenesis (12, 13), which theoretically might contribute to

reductions in postprandial glycemia. In one study, ethanol ad-

ministered every hour in the afternoon before a glucose load at

1700 resulted in substantially reduced blood glucose concentra-

tions (14). Alcohol consumption is a recognized risk factor for

hypoglycemiain individuals withtype 1 diabetes (15,16), but the

effect of alcoholic beverages on postprandial glycemiain healthy

subjects (9) and individuals with type 2 diabetes (17) is thought

to be negligible.In this context, however, most studies have usedforearm venous sampling to detect changes in plasma glucose. It

is now recognized that rapid changes in blood glucose concen-

trations after a meal may be identified more readily at fingertip

sites than at the forearm (18). For this reason, it is possible that

modest, but clinically important, effects of alcohol on postpran-

dial glycemia may have gone undetected.

The aim of the present studies was to investigate the acute

effects of realistic portionsof 3 different alcoholic beverages(not

alcohol per se) consumed alone, before, or with a carbohydrate

meal on postingestive plasma glucose and insulin responses. We

hypothesized that alcohol’s ability to acutely inhibit gluconeo-

genesis and enhance insulin sensitivity might reduce postpran-

dial glycemia on one hand, but that other components in thebeverages, such as the carbohydrates in beer, might increase

postprandial responses on the other.

SUBJECTS AND METHODS

Study design

Postprandialresponses to beer, white wine, and ginwere stud-

ied alone (study 1), with a carbohydrate-containing meal (study

2), and 1 h before a meal (study 3). In all 3 studies, each subject

underwent 5 tests: 3 with the test drinks and 2 with the reference

meal. All tests were given in random order, on separate days3

d apart. Subjects were tested at the same time of the day undersimilar conditions and acted as their own controls. They were

instructed to maintain regular activity patterns, to abstain from

1 From the Human Nutrition Unit, The University of Sydney, NSW, Aus-

tralia.2 Supported by Sydney University’s Glycemic Index Research Service,

Human Nutrition Unit, University of Sydney, NSW, Australia.3 Reprints not available. Address correspondence to JC Brand-Miller,

HumanNutritionUnit, G 08,The University ofSydney,Sydney, NSW, 2006,

Australia. E-mail: [email protected] August 15, 2006.

Accepted for publication January 17, 2007.

1545 Am J Clin Nutr 2007;85:1545–51. Printed in USA. © 2007 American Society for Nutrition

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alcohol on the previous day, and to avoid legumes in the prior

evening meal. The energy, macronutrient, and alcohol contents

of the test foods and reference meals in each study are shown in

Table 1. Nutrient composition was calculated by using FOOD-

WORKS Professional Edition version 3.0 (Xyris Software,Bris-

bane, Australia), which is based on the Australian food-

composition tables and manufacturers’ data.

Subjects

Healthy, nonsmoking volunteers were recruited by advertise-

ment from the University of Sydney student population. Exclu-

sion criteria included a family history of type 2 diabetes or a

recent history of gastrointestinal disease. In study 1, there were

10subjects (7men, 3 women)with a mean(SE)ageof29 3 y

(range: 21–46 y) and a BMI (in kg/m2) of 25 1 (range: 20

27).In study 2,a secondset of10 subjects(5 men, 5 women)with

a mean (SE) age of 23 1 y (range: 19–26 y) and a BMI of

22 1 (range: 18 25) was studied. In study 3, there were 18

subjects (8 men, 10 women) with a mean (SE) age of 22 2 y

(range: 22–32 y) and a BMI of 22.3 2.5 (range: 20 23). The

study protocol was approved by the institutional human ethics

committee, and subjects gave written informed consent.

Study 1

The 3 test foods consisted of 1000-kJ portions of beer (Bud-

weiser regular, 5% wt:vol alcohol; Anheuser-Busch, St Louis,

MO), white wine (Columbard Chardonnay, 11% wt:vol alcohol;

Yalumba Winery, Angaston, South Australia), and gin (Beef-

eater London distilled dry gin, 40% wt:vol alcohol; James Bur-

rough, London, United Kingdom), corresponding to 33, 39, and

47 g alcohol, respectively. We chose energy equivalence, rather

than carbohydrate or alcohol equivalence, because it represented

a “level playing field” for the comparison of the postprandial

effect of all foods, irrespective of nutrient composition, on gly-

cemia and insulinemia. The white wine and beer were consumed

with 250 mLwater and the gin with400 mLwater. The reference

meal consisted of a 1000-kJ portion of white bread (Tip Top

Sunblest Sandwich; Tip Top Bakeries, Chatswood, NSW, Aus-

tralia) with 250mL water.On each test day, subjects attended the

Human Nutrition Unit at 0800 after a 10-h overnight fast. On

arrival, a breakfast consisting of cereal, fruit, and milk was con-

sumed in self-selected amounts held constant within each sub-

ject. Exactly 4 h after breakfast, the test beverage or reference

food was consumed within 25 min. Fingerprick blood samples

(0.5 mL) were collectedfromwarmed hands with an automaticlancet (Autoclix Boehringer Mannheim Australia, Castle Hill,

New South Wales) at 0 min (the start of the test meal) and 15, 30,

45, 60, 90, and 120 min after the test food.

Study 2

The 3 test meals consisted of 1000-kJ portions of beer, white

wine, or gin as in study 1 but were consumed together with a

sandwich consisting of 2000 kJ white bread (Tip Top Sunblest

Sandwich) and 280 kJ margarine (Meadow Lea Original;

Meadow Lea Foods, Macquarie Park, NSW, Australia). The

reference meal, tested twice, consisted of the sandwich and 250

mL water. The study design was identical to study 1, except thatadditional blood samples were taken at 150 and180 min to allow

for the higher total energy content of the meal.

Study 3

The 3 predinner drinks consisted of 2 standard drinks (two

10-g alcohol portions) of beer (Toohey’s New Lager; Tooheys

Pty Ltd, Lidcombe, NSW, Australia), white wine (Sauvignon

Blanc; Yalumba Winery), and gin (Gordon’s Special London

Dry Gin); the latter was mixed with low-energy, artificially

sweetened “diet” tonic water (Cadbury Schweppes, Sydney,

NSW, Australia). In the reference trial, 250 mL water was con-

sumed in lieu of the alcoholicbeverages. At 0800 on the test day,

TABLE 1

Nutritional composition of the reference meal and test foods in each study

Weight Energy Carbohydrate Fat Protein Alcohol

g kJ g g g g

Study 1

Reference meal (white bread) 97 1000 44 2 8 0

Test foods

Beer 667 1000 13 0 2 33White wine 353 1000 1 0 1 39

Gin 117 1000 0 0 0 47

Study 2

Reference meal ( water)

White bread 198 2000 88 5 16 0

Margarine 10 278 0 8 0 0

Test meals

Beer meal 875 3278 101 13 18 33

Wine meal 561 3278 89 13 17 39

Gin meal 325 3278 89 13 16 47

Study 3

Reference meal (instant mashed potato) 682 1107 48 4 5 0

Test foods (predinner drinks)

Beer 435 808 11 0 2 20

White wine 230 635 3 0 0 20

Gin 54 581 0 0 0 20

1546 BRAND-MILLER ET AL



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after a 10–12 h fast, thesubjects consumed a prepackaged break-

fast consisting of cereal (Just Right, 45 g; Kellogg’s, Battle

Creek, MI),whole milk(250 mL,Dairy Farmer’sLtd, Homebush

Bay, NSW, Australia), toasted white bread (Tip-Top, 35 g), and

orange juice (250 mL, Just Juice; National Foods Ltd, Mel-

bourne, Victoria, Australia). At 1100, the subjects consumed the

predinner beverage and, 1 h later, consumed a standard lunch

meal consisting of a 50-g carbohydrate portion of mashed potato

(Table 1) within 12 min. Fingerprick blood samples were takenat baseline (the start of the meal) and 15, 30, 45, 60, 90, and 120

min after the meal.

Blood samples (0.8 mL) were collected into Eppendorf

tubes previously coatedwith heparin (10IU heparin sodiumsalt;

Sigma Chemical Co, St Louis, MO) and centrifuged at 12 500

g for 1 min. Plasma was pipetted into chilled tubes and stored at

20 °C until assayed (1 mo). Plasma glucose concentrations

were measured in duplicate with a Cobas Fara automatic spec-

trophotometric analyzer (Roche Diagnostica, Basel, Switzer-

land) per the hexokinase/glucose-6-phosphate dehydrogenase

method (Unimate 5 Gluc HK; Roche Diagnostic Systems,

Frenchs Forest, New South Wales). The mean intra- and inter-

assay CVs were both3%. Plasma insulin was measured with acommercial antibody coated tube radioimmunoassay kit (Coat-

a-Count; Diagnostic Products Corporation, Los Angeles, CA).

The mean intraassay CV was 3%, and the mean interassay CV

was3.5%in study1 andstudy 2 and6.3%and 6.6%, respectively,

in study 3.

Data treatment and statistical analysis

Cumulative changes in plasma glucose and insulin responses

were quantified as the incremental area under the 120-min (study

1 andstudy 3) or 180-min (study2) area under thecurves (AUCs)

and were calculated by using the trapezoidal rule with fasting

concentrations representing the baseline truncated at zero. Any

area below the baseline was ignored. For each of interpretations,

glucose scores were calculated by using the following equation:

Glucose score

area under the 120-min (or 180-min)

glucose response curve for the test food/average

area under the 120-min (or 180-min)

glucose response curve for the reference meals

100 (1)

In study 2, the AUC was determined over 180 min (in lieu of 120

min) to allow for the higher total energy content of the meals in

comparison with study 1 and study 3. Insulin scores were calcu-lated by using thesame equation using thecorresponding plasma

insulin AUC values.

For each study separately, the glucose and insulin AUC data

were analyzed by using a general linear model with drink as a

fixed factor and subject as a random factor. When drink was

FIGURE 1. Study 1. Mean (SE) changes in plasma glucose and insulin and incremental areas under the curve (AUCs) in lean healthy subjects (n 10)after consumption of a 1000-kJ portion of white bread, beer, wine, or gin. *Significantly different from white bread, P 0.001 (2-factor ANOVA followed by

pairwise comparisons with Bonferroni adjustment).

ALCOHOL AND POSTPRANDIAL GLYCEMIA 1547



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significant, multiple comparisons were undertaken by using a

Bonferroni adjustment for multiple tests. The effect of sex was

examined instudy 2 and study 3 by using an extended model that

added sex and drink-by-sex interaction as fixed factors. Finally,

the overall effect of sex was investigated across all studies by

including study as a fixed factor. Statistical analyseswere carried

out using STATVIEW Student Software (Abacus Concepts Inc,

Berkley, CA) and the STATISTICAL PACKAGE FOR THE

SOCIAL SCIENCES (SPSS, version 12; SPSS Inc, Chicago,

IL), and (adjusted) P values0.05 were considered significant.

Results are reported as means SEMs.

RESULTS

The protocols in all studies were well tolerated, except in one

subject, in study 2, who consumed only 75% of the gin portion.Within eachstudy, fasting glucose and insulin concentrations did

not differ significantly, averaging 5.2 0.1 mmol/L and 40.9

8.7 pmol/L, respectively, in study 1 and 5.4 0.1 mmol/L and

33.6 8.6 pmol/L, respectively, in study 2. In Study 3, the mean

baseline glucose and insulin concentrations at the start of the

mealwere 5.10.1mmol/Land48.96.0 pmol/L respectively.

There were no significant differences between water and alcohol

trials at this time point.

Study 1

Mean plasma glucose and insulin response curves in response

to the alcoholic beverages and white bread are shown in Figure

1. Taking the reference food as 100, the glucose scores for beer

(58 11), white wine (7 3), and gin (10 5) were all

significantly lower than the reference food (P 0.001 in each

case). Beer produced significantly higher scores than did white

wine and gin (P 0.003 and 0.007, respectively). Similarly,

insulin scores for beer (27 5), white wine (4 2), and gin

(1 1) were all significantly lower than the reference food (P

0.001 in each case). Two hours after each type of alcoholic

beverage, the mean insulin concentration, but not the glucose

concentration, was significantly lower than fasting concentra-

tions (P 0.05).

Study 2

Mean plasma glucose and insulin response curves in responseto the 3 test meals and the average reference meal are shown in

Figure 2. Relative to the white bread and water trial ( 100),

glucose scores for beer, wine, and gin were 84 11, 63 6, and

80 12, respectively, with the white wine and gin meals pro-

ducing significantlylower glucose AUCsthan the reference meal

(P 0.001 and 0.015, respectively). The beer meal showed only

marginal significance (P 0.07). Reductions in glycemia in the

wine trial appeared to be more pronounced in the men (50 3)

than in the women (77 6), but the effect of sex was not statis-

tically significant overall (P 0.22). Insulin scores for the 3

alcohol-containing test meals were not significantly different

from those for the reference meal or each other (Figure 2).

FIGURE 2. Study 2. Mean (SE) changes in plasma glucose and insulin and incremental areas under the curve (AUCs) in lean healthy subjects (n 10)afterconsumptionof a white-breadmeal with wateror 1000-kJ portionsof white bread,beer,wine,or gin. *,†Significantlydifferent fromwater bread(2-factor

ANOVA followed by pairwise comparisons with Bonferroni adjustment): *P 0.001, †P 0.015.




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Study 3

Mean plasma glucose and insulin response curves after the

standard lunch are shown in Figure 3. In each case, glucose

scores (67 5, 75 6, and 78 4 for the beer, wine and gin

trials, respectively) were significantly lower than those in the

water trial (P 0.001 forboth beer andwine; P 0.003 forgin).

The mean peak glucose concentration was also significantly

lower (8.3 0.2, 8.5 0.2 and 8.6 0.2 in the beer, wine and

gin trials respectively) that in the water trial (9.3 0.2; P

0.001). Conversely, insulin scores tended to be higher (111 7,

11411,and13811 forbeer, wine, andgin,respectively),but

the difference was significant only in the gin trial (P 0.007).

There were no differences in peak insulin concentrations. At 120

min after thestart of themeal, glucose andinsulin concentrations

were similar and the alcohol trials did not differ from the watertrial (Figure 3). There were no significant sex differences, and

adding sex to the model left the results essentially unchanged.

When all3 studies were combined,sex wasnot significant forthe

glucose AUC (P 0.13) andwas only marginally significant for

the insulin AUC (P 0.046).

DISCUSSION

The findings of these 3 studies suggest that, under realistic

conditions, moderate quantities of beer, wine, and gin reduce

postprandialglycemia by up to 37% in leanhealthysubjects. This

applies when isoenergetic portions (1000 kJ, or 240 calories) are

consumed as an accompaniment to a high-carbohydrate meal or

as the equivalent of 2 predinner drinks (20 g alcohol). Surpris-ingly, beer was effective in reducing glycemia, despite its having

a higher carbohydrate content than wine or gin. By themselves,

the alcoholic beverages producedmuch lessglycemia thandid an

isoenergetic portion of a starchy food. The physiologic basis of

these findings is likely to be ethanol’s ability to acutely inhibit

gluconeogenesis and hepatic glucoseoutput (12). Reducing post-

prandial hyperglycemia may therefore be an additional mecha-

nism, hitherto unrecognized, through which moderate alcohol

consumption may improve glucose homeostasis and conse-

quently lower the risk of chronic disease.

Relatively few studies have systematically investigated the

acute metabolic effects of alcoholic beverages (not alcohol per

se) on postprandial glycemia. Moreover, to our knowledge, nonehas specifically studied the effect of predinner drinks consumed

in the hour or so before a meal. Although suppression of hepatic

glucose output would largely explain the findings (13), beer,

wine, and spirits contain components other than ethanol, which

means thatadditional effects are possible. Standardbeers contain

a small amount of rapidly digested carbohydrate as small-

molecular-weight dextrins (3–5% wt:vol, representing the

breakdown products of starch digestion by the enzymes in ger-

minated grains) that could potentially contribute to postprandial

glycemia and insulinemia. The relative glycemic potency of car-

bohydrates in differentfoods canbe compared by using GI tables

(19), but alcoholic beverages contain too little carbohydrate to be

FIGURE 3. Study 3. Mean (SE) changes in plasma glucose and insulin and incremental areas under the curve (AUCs) in lean healthy subjects (n 18)after consumption of a mashed potato meal, which was preceded (1 h before) by the consumption of 250 mL water or 20-g portions of beer, wine, or gin.*,†,**Significantlydifferent fromwater (2-factorANOVA followed by pairwise comparisonswith Bonferroniadjustment): *P 0.001, †P0.003, **P0.007.




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tested by standard methodology. Even in the case of beer, a 25-g

or 50-g carbohydrate portion represents an unrealistically large

amount for consumption within a 12 min period (ie, 750

and 1500 mL, respectively). Using a nonstandard 10-g carbohy-

drate portion size for testing, our group found that the GI of

beer (Toohey New Draft, 4.6% wt:vol alcohol) was 66 on the

glucose 100 scale (Sydney University’s Glycemic Index Re-

search Service, unpublished observations, 2003). Surprisingly,

however, when consumed with or before a carbohydrate meal,

we found that beer tended to reduce, rather than increase, post-

prandial glycemia. This implies that alcohol inhibits hepatic glu-

cose output quickly, counteracting the glycemic effect of glu-

cose absorption from the gut and thereby reducing the overall

glycemic response. Prior carbohydrate and alcohol consumption

probably “primes” the liver (inhibits gluconeogenesis), which

reduces the hepatic glucose output and up-regulates the enzymes

involved in glucose uptake.

In type 1 diabetic individuals, alcohol consumption, specifi-

cally gin, is known to predispose individuals to hypoglycemia

(20, 21). This is corroboratedby thefindingsof study 3, in which

all 3 alcoholic beverages produced lower peak glucose concen-

trations than did water. None of the concentrations, however,

were indicative of “true” hypoglycemia, defined as a plasma

glucose concentration3.0 mmol/L in these young healthy sub-

jects. Interestingly, all the beverages tended to result in higher

insulin concentrations, but only gin was statistically significant

(38%). It is probable that the stepwise increase in plasma insu-

linemia, although not statistically significant, was related to the

stepwise reduction in glycemia. This implies that the increased

insulin response is effective in driving faster glucose uptake into

the tissues. Last, although there are differences in alcohol me-

tabolism between men and women (22), we found no significant

effect of sex. Because the number of subjects of each sex was

small, further studies with largernumbersof men andwomenare

needed.Pure alcohol acutely improves insulin sensitivity, as demon-

strated with the euglycemic, hyperinsulinemic clamp technique

(15, 23, 24) and the homeostatic model (6). In study 2, wine

produced the greatest reduction in the postprandial glucose re-

sponse, despite contributing less alcohol than the gin (39 g com-

pared with 47 g). This suggests the possibility that wine contains

substances other than alcohol that are physiologically relevant.

Wine’s acidity may slow down gastric emptying (25), and spe-

cific components may inhibit-amylase or-glucosidase activ-

ity and, therefore, the rate of starch digestion. Interestingly, a

recent prospective observational study of 37 000 adults found

wine consumption, but not beer or spirit consumption, was as-

sociated with a significantly lower risk of type 2 diabetes (19).We conclude that alcoholic beverages consumed alone, with

or before a carbohydrate-containing meal, are capable of reduc-

ing peakblood glucose concentrations or the overall postprandial

glucose response in young, lean, healthy subjects. In contrast,

insulin concentrations were largely unchanged, which suggests

an acute enhancement of glucose metabolism. These effects may

provide a hithertounrecognizedbenefit of moderatealcoholcon-

sumption for cardiovascular health.

The authors’ responsibilities were as follows—JCB-M: designed the

study, obtained funding, and drafted the manuscript; KF, CM, and VL:

recruited subjects, managed the testing sessions, and performed data entry;

MB, FA, and PP: interpreted the data and performed the statistical analysis.

All authors reviewed and commented on the manuscript. JCB-M serves on

the board of directors of Glycemic Index Limited, a not-for-profit company

that managesthe Glycemic Index Symbolfoodlabelingprogram in Australia

(Internet: www.gisymbol.com.au); is the director of a glycemic index testing

service at the Universityof Sydney(Internet: www.glycemicindex.com);and

is the coauthor of a series of books under the general title The New Glucose

Revolution (published by Marlowe and Co in North America), which ex-

plains the theory and practice of the glycemic index to the lay public. None

of the other authors declared a conflict of interest.

REFERENCES1. Grøenbæk M. Alcohol, type of alcohol, andall-causeand coronary heart

disease mortality. Ann N Y Acad Sci 2002;957:16–20.

2. Rimm E, Williams P, Fosher K, Criqui M, Stampfer M. Moderate

alcohol consumption and lower risk of coronary heart disease: meta-analysis of effects on lipids and hemostatic factors. BMJ 1999;319:

1523–8.

3. Hu F, Manson J, Stampfer M, et al. Diet, lifestyle, and the risk of type 2

diabetes mellitus in women. N Engl J Med 2001;345:790–7.

4. Beulens J, Stolk R, van der Schouw Y, et al. Alcohol consumption and

risk of type 2 diabetes among older women. Diabetes Care 2005;28:2933–8.

5. Davies M, Baer D, Judd J, Brown E, Campbell W, Taylor P. Effects of moderate alcohol intake on fasting insulin and glucose concentrations

and insulin sensitivity in postmenopausal women: a randomised con-trolled trial. JAMA 2002;287:2559– 62.

6. Kiechl S, Willeit J, Rungger G, et al. Insulin sensitivity and regular

alcohol consumption: large, prospective, cross-sectional populationstudy (Bruneck Study). BMJ 1996;313:1040 – 4.

7. Mayer E, NewmanB, Quesenberry C Jr,Friedman GD,SelbyJ. Alcoholconsumption and insulin concentrations. Role of insulin in associations

of alcohol intake with high-density lipoprotein cholesterol and triglyc-erides. Circulation 1993;88:2190–7.

8. Yki-Jarvinen H, Nikkila J. Ethanol decreases glucose utilization in

healthy man. J Clin Endocrinol Metab 1985;61:941–5.

9. Avogaro A, Duner F, Marescotti C, et al. Metabolic effects of moderate

alcohol intake with meals in insulin-dependent diabetics controlled byartificial endocrine pancreas (AEP) and normal subjects. Metabolism

1983;32:463–70.10. Bell R, Mayer-Davis E, Martin M, D’Agostino RJ, Haffner S. Associ-

ations between alcohol consumption and cardiovascular disease risk

factors: the Insulin Resistance and Atherosclerosis Study.Diabetes Care2000;23:1630–6.

11. Facchini F, Chen Y, Reaven G. Light-to-moderate alcohol intake isassociated withenhanced insulin sensitivity(1994). Diabetes Care1994;

17:115–9.

12. Siler S, Neese R, Christiansen M, Hellerstein M. The inhibition of glu-coneogenesis following alcohol in humans. Am J Physiol Endocrinol

Metab 1998;275:E897–907.

13. Mathews C, vanHoldeK, AhernK, eds. Biochemistry.In: Carbohydrate

metabolism II: biosynthesis. Boston, MA: Addison Wesley Longman,Inc, 2000.

14. McMonagle J, Felig P. Effectsof ethanol ingestion on glucosetolerance

and insulin secretion in normal and diabetic subjects. Metabolism 1975;

24:625–32.15. Avogaro A, Fontana P, Valerio A, et al. Alcohol impairs insulin sensi-

tivity in normal subjects. Diabetes Res 1987;5:23–7.

16. TurnerB, Jenkins E,KerrD, Sherwin R, Cavan D.The effect ofeveningalcohol consumptionon next-morning glucose control in type1 diabetes.

Diabetes Care 2001;24:1888–93.

17. Christiansen C, Thomsen C, Rasmussen O, et al. Acute effects of graded alcohol intake on glucose, insulin and free fatty acid levels in

non-insulin-dependent diabetic subjects. Eur J Clin Nutr 1993;47:648–52.

18. Ellison J, Stegmann J, Colner S, et al. Rapid changes in blood glucoseproduce concentrationdifferences at finger, forearm, and thighsampling

sites. Diabetes Care 2002;25:961– 4.

19. Foster-Powell K, Holt SH, Brand-Miller JC. International table of gly-cemic index and glycemic load values: 2002. Am J Clin Nutr 2002;76:

5–56.




D ow

nl o a d e df r om























20. Flanagan D, Wood P, Sherwin R, Debrah K, Kerr D. Gin and tonic andreactive hypoglycemia: what is important—the gin, the tonic or both.

J Clin Endocrinol Metab 1998;83:796 – 800.21. O’Keefe S, Marks V. Lunchtime gin and tonic a cause of reactive hy-

poglycaemia. Lancet 1977;18:1286– 8.22. Frezza M, DiPadova C, Pozzato G, Terpin M, Baraona E, Lieber C.

High blood alcohol levels in women: the role of decreased gastric

alcohol dehydrogenase and first-pass metabolism. N Engl J Med1990;322:95–99.

23. Goude D, Fagerberg B, Hulthe J, for the AIR study group. Alcoholconsumption, the metabolic syndrome and insulin resistance in 58-year-old

clinically healthy men (AIR Study). Clin Sci (Lond) 2002;102:345–52.24. Flanagan D, Moore V, Godsland I, Cockington R, Robinson J, Phillips

D. Alcohol consumption and insulin resistance in young adults. EurJ Clin Invest 2000;30:297–301.

25. Liljeberg HG, Lonner CH, Bjorck IM. Sourdough fermentation or ad-

dition of organic acids or corresponding salts to bread improves nutri-tional properties of starch in healthyhumans. J Nutr 1995;125:1503–11.




D ow

nl o a d e df r om























Erratum

Riedt CS, Schlussel Y, von Thun N, et al. Premenopausal overweight women do not lose bone during moderate

weight loss with adequate or higher calcium intake. Am J Clin Nutr 2007;85:972–80.

On page 977, Table 3, an error exists in the third sentence of footnote 1. The sentence should read as follows:

“Does not include 48 mg phosphorus, 10 g vitamin D, 100 mg magnesium, or 10 g vitamin K from

multivitamin-minerals or salt from shaker.”

Erratum

Brand-Miller JC, Fatima K, Middlemiss C, et al. Effect of alcoholic beverages on postprandial glycemia and

insulinemia in lean, young, healthy adults. Am J Clin Nutr 2007;85:1545–51.

The second author’s last name was misspelled. The correct spelling is “Fatema.”

Erratum

Zivkovic AM,German JB. Individual variation in the metabolic syndrome: a new perspectiveon the debate.Am J

Clin Nutr 2007;85:240–1.

An incorrect e-mail address was provided for Angela M Zivkovic. The correct address is as follows:

[email protected].

Erratum

Peters U, Foster CB, Chatterjee N, et al. Serum seleniumand riskof prostatecancer—a nested case-controlstudy.

Am J Clin Nutr 2007;85:209–17.

On page 211, footnote 2 to Table 1 is incorrect. It should read as follows: “2 x SD (all such values).”

808 LETTERS TO THE EDITOR

effect of alcoholic beverages on postprandial glycemia and insuinemia

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