Study Design:
- Click here for explanation of classification scheme.
Quality Rating:
Research Purpose:
  1. To assess the thermic effect of alcohol in varying concentrations.
  2. In addition, to investigate the impact of alcohol on diet-induced thermogenesis (DIT).


  • Steady state: not discussed
  • Thermic effect of food: difference between the average energy expenditure over a period of 90 min and the corresponding baseline RMR
  • DIT with or witout ETOH: difference between the average hourly and total (4 h) postprandial energy expenditure and the corresponding baseline RMR.
Inclusion Criteria:
  1. Understand and give written consent
  2. Apparently healthy (no past or present evidence of hypo- or hyperthyroidism or diabetes mellitus); assessed by questionnaire, which was then evaluated by a physician
  3. Non-obese (body fat percentage below 25)
  4. Moderate smoking (less than 10 cigarettes/day)
  5. Moderate drinking habits (no more than 5 alcoholic drinks/d)
  6. Did not use medications known to affect energy metabolism
  7. Not on a diet; consuming normal balanced meals
  8. Weight fluctuations within 2.5 kg for at least 6 months before the start of the study.
Exclusion Criteria:
  1. Refusal to consent
  2. Not meeting inclusion criteria.
Description of Study Protocol:

Test 1 (thermic effect of alcohol)

10 subjects received on 3 occasions on different days (randomized and at least 2 d between sessions), an oral dose of 20 g alcohol dissolved in 335 ml water (75 ml/l solution), 140 ml water (180 ml/l solution) or 85 ml water (300 ml/l solution). 1.2 g of non-nutritive sweetener and 0.12 mg aniseed oil were added to the 180 and 300 ml/l solutions to improve sensory characteristics. After the alcohol ingestion, RMR was taken. Subjects received the 3 alcohol solutions either early in the morning after an overnight fast or early in the afternoon after a fasting period of at least 4-5 h after a standardized breakfast of 2 MJ (480 kcals).

Test 2 (Impact of alcohol on DIT)

12 subjects received on 4 different days in the afternoon (randomized; at least 2 d between treatments) 2 treatments—control and test, in duplicate, i.e., either a test treatment (i.e., ingestion of aperitif (containing 20 g ethanol in a 180 ml/l solution) and a yogurt-based mixed liquid test meal [(1.96 MJ (470 kcals), 130 g protein/l, 270 g fat/l, 600 g carbohydrate/l)] or a placebo aperitif (0 kcal) and an isoenergetic yogurt-based liquid diet [(2.55 MJ (612 kcals), 130 g protein, 270 g fat/l, 600 g carbohydrate/l)].

After aperitif ingestion (within 10 min) the hood was replaced. After 15 min, subjects received the liquid test meal through a straw (passed through the hood). Meals were eaten within 5 min.


  • Ht measured? yes, method not provided
  • Wt measured? yes, method not provided
  • Fat-free mass measured? body fat mass and body fat-free mass estimated from total body density using Siri’s (1956) formula. Total body density was measured by hydrostatic weighing.


  • Monitored heart rate? not discussed
  • Body temperature? not discussed
  • Medications administered? No

Resting energy expenditure

  • IC type: ventilated hood system
  • Equipment of Calibration: yes, once every hour
  • Coefficient of variation using std gases: during calibration of gas analysers; used outside fresh air
  • Rest before measure (state length of time rested if available): not discussed
  • Measurement length: Initial RMR was measured for at least 60 min (3 occasions for the 1st study and 4 different days for the 2nd study). Following the alcohol ingestion in the first study, RMR measured continuously for another 90 min. In the second study, after the ingestion of the aperitif (within 10 min) and liquid test meal consumption, RMR continuously measured for 4 hr.
  • Steady state: Not discussed; spontaneous movements monitored by a load cell under hospital bed leg; During calibration (every hour), subjects were allowed to move briefly for 2-3 min.
  • Fasting length: either fasted overnight or period of at least 4.5 h after a standardized breakfast
  • Exercise restrictions: PM measures: “avoid moderate or heavy exercise in AM”
  • Room temp: not discussed
  • No. of measures within the measurement period: 3x for baseline RMR; and 1- 90-min continuously and 1 4-hr continuous
  • Were some measures eliminated? not discussed
  • Were a set of measurements averaged? Hourly DIT values were averaged for the 2 treatments.
  • Coefficient of variation in subjects measures? not discussed
  • Training of measurer? not discussed
  • Subject training of measuring process? yes, subjects received a letter in which the purpose and nature of the experiments were explained.


  • See Test 1 & 2 descriptions above
  • Intervening factor: Physical activity was not assessed.
Data Collection Summary:

Outcome(s) and other measures

  1. Measured REE [(VO2 l/min), VCO2 (l/min; ml/kg/min), RQ, ventilation (l/min)]
  2. Independent variables of weight, height, age, BMI
  3. Total VO2and CO2were corrected for the volumes of VO2and CO2associated with alcohol oxidation.

Blinding used: No

Description of Actual Data Sample:
  • N=22 males
  • Average age, y: 27 (SEM: ±1.5)
  • Range, y: 21-41

[Analyst note: 4 males participated in both experiments.]

Average body fat percentage was 16.5 (s.e. 1.2); 3 subjects had a body fat percentage between 20 and 25, but none were obese.

Statistical tests

Two-sided T-tests, ANOVA was used to test differences among the three treatments (75, 180, and 300 ml/l solutions) in thermic effect. A two-way ANOVA with repeated measures on the (within-subject) factors meal ±alcohol and time period (duplicates). Standard errors and P <0.05 was significant.

Summary of Results:


Men (Study 1) Mean±SE    Range

Wt, kg

76.8±3.2 66.2-102.0


not provided

Body fat content (%)

17.0±1.1 13.0-24.7

Habitual alcohol use (number drinks/d)

1.2±0.2 0-3

Men (Study 2) Mean±SE Range

Wt, kg

78.3±3.0 58.8-101.8

Body fat content (%)

16.0±1.2 7.9-22.5

Habitual alcohol use (number drinks/d)

1.4±0.4 0-5

Thermic Effect of Alcohol

  • Alcohol induced a significant thermic effect from baseline, which varied between 0.22-0.30 kJ/min (0.05-0.072 kcals/min)
  • Alcohol ingestion induced a significant increase in metabolic rate and O2consumption, but not in CO2production (P<0.05) RQs decreased significantly after alcohol use.
  • Group mean RQ before consumption of 20 g alcohol was 0.84±0.02 (se) and a 90 min average after ingestion was 0.77±0.01 (se) (P<0.05).
  • Metabolic rate was elevated on average by 3.4% (75 ml/l), 4.6% (180 ml/l) and 6.2% (300 ml/l). However, there were no significant differences in thermic effect among alcohol solutions of varying concentrations.

Impact of alcohol on DIT

  • No significant difference was found between treatments (different concentrations) in the increase in metabolic rate or in O2consumption.
  • On average, DIT was about 16% higher on the test treatment in comparison with the control treatment; however the difference in DIT between treatments was not significant.
  • In regard to average hourly DIT values for the 2 treatments, during the second, third and fourth hour DIT was higher on the test treatment compared with the control treatment, but only for the second hour was the difference statistically significant (p = 0.03).
  • No systematic difference in DIT (diet induced thermogenesis) was observed among the different alcohol concentrations. DIT was not significantly affected (P>0.05) by the ingestion of alcohol.
  • Total DIT was 219±SE 14 kJ (52±3.3 kcals) for the alcohol treatment and 185±SE 20 kJ (44±4.8) for the control treatment.
  • Glucose and fat oxidation rates were significantly lower (p<0.001) on the test treatment in comparison with the control treatment. Protein oxidation was not significantly affected by alcohol ingestion. On the control treatment, subjects oxidized on average about 50% of the carbohydrate and fat intake.
  • Energy and carbohydrate and fat storage were not significantly different between treatments.
Author Conclusion:

As stated by the author in body of report

“The results of the present study show that alcohol in a moderate amount of 20 g induces a significant increase in O2consumption and metabolic rate, but not in CO2production in fasting individuals [and] not significantly related to alcohol concentration”

“Alcohol induced an [RMR] increase of ~ 4-6% of the ingested energy load (about 0.6 MJ or 144 kcals). And results support the findings of Perman (1962) and Rosenberg & Durnin (1978), but are in contrast with the observations of Stock & Stuart (1974) and Barnes et al. (1965) [and have] differences in experimental design, technique for assessing alcohol-induced thermogenesis (including amount and concentration of alcohol given.)”

“We did not find a significant relationship between the thermic effect of alcohol at lower alcohol concentrations; at (75 and 180 ml/l) the thermic effect of alcohol was on average 4.6 v. 6.2% [with a] relative difference of 30%

“Alcohol ingestion and its subsequent oxidation significantly reduced basal respiratory quotients.”

“In the present study, postprandial measurements were carried out over a period of 4 h and energy expenditure averaged over the fourth hour of the postprandial period was on average 4.5% elevated above the corresponding pre-meal baseline energy expenditure on the control treatment and 6.5% on the test treatment.”

“After alcohol consumption, maximum blood alcohol concentrations occur about 30-45 min in fasting subjects and most of the alcohol will have been eliminated within 30-150 min after ingestion of the meal (given 15 min after the aperitif). During this period, alcohol oxidation contributed on average 3.8 kJ/min (i.e., 3.5 kcal/min) to total energy expenditure. Between 55 and 65% of total energy expended was derived from alcohol oxidation [and] during this period more fats and carbohydrates were stored on the test treatment when compared with the control treatment.”

“The results of the present study on the thermic effect of alcohol and the impact of alcohol on DIT do not indicate that moderate amounts of alcohol are less efficiently used as an energy source in comparison with fats or carbohydrates.”

“In conclusion, alcohol consumed in a moderate amount has a significant thermic effect, probably similar to fats or carbohydrates [and there is ] no significant DIT potentiation Alcohol given in combination with a mixed liquid meal had a substantial impact on substrate oxidation and storage rates, in particular during the period at which alcohol oxidation was at its maximum [but] postprandial energy retention was similar for an isoenergetic food + alcohol meal vs. food alone.”
Funding Source:
Government: Associazione Italiana per la Ricerca sul Cancro
Reviewer Comments:


  • Conditions before IC measurements established such that RMR and DIT measured in the afternoon did not differ systematically from RMR and DIT measured in the morning.
  • Treatments assigned to subjects in randomized order.
  • Between treatments there was a time interval of at least 2 d to minimize effects of prior treatment.
  • Control and test treatments were carried out in duplicate
  • Postprandial measurements were carried out over a 4 hour period
  • ETHO elimination measurements for each subject were made repeatedly under different conditions to not bias conclusions on within-person treatment comparisons.


  • Small sample size (10 in first study and 12 in second study); possibility of a type 2 error
  • Limited generalizability; sample consisted of young, healthy, non-obese males; may not be generalizable to older individuals-male or female or to overweight/obese subjects
  • Physical activity could be a confounder-intensity not measured
  • Convenience sample; self-selection bias
  • Individuals were moderate drinkers and smokers; results may not be generalizable to heavy drinkers(alcoholics) or smokers
  • Details of the measurement procedure and conditions were not described (indicated previously published).
[Analyst note: the group mean RQ before control meal given is reported as 0.88 and 0.88 after a meal with P<0.01 statistical significance. Text on page 417 indicates there was a significant increase and Figure 2 reports baseline mean RQ of ~0.81 thus interpreted as a typo in Table 3.]
Quality Criteria Checklist: Primary Research
Relevance Questions
  1. Would implementing the studied intervention or procedure (if found successful) result in improved outcomes for the patients/clients/population group? (Not Applicable for some epidemiological studies) Yes
  2. Did the authors study an outcome (dependent variable) or topic that the patients/clients/population group would care about? Yes
  3. Is the focus of the intervention or procedure (independent variable) or topic of study a common issue of concern to dieteticspractice? Yes
  4. Is the intervention or procedure feasible? (NA for some epidemiological studies) Yes
Validity Questions
1. Was the research question clearly stated? Yes
  1.1. Was (were) the specific intervention(s) or procedure(s) [independent variable(s)] identified? N/A
  1.2. Was (were) the outcome(s) [dependent variable(s)] clearly indicated? N/A
  1.3. Were the target population and setting specified? N/A
2. Was the selection of study subjects/patients free from bias? Yes
  2.1. Were inclusion/exclusion criteria specified (e.g., risk, point in disease progression, diagnostic or prognosis criteria), and with sufficient detail and without omitting criteria critical to the study? N/A
  2.2. Were criteria applied equally to all study groups? N/A
  2.3. Were health, demographics, and other characteristics of subjects described? N/A
  2.4. Were the subjects/patients a representative sample of the relevant population? N/A
3. Were study groups comparable? Yes
  3.1. Was the method of assigning subjects/patients to groups described and unbiased? (Method of randomization identified if RCT) N/A
  3.2. Were distribution of disease status, prognostic factors, and other factors (e.g., demographics) similar across study groups at baseline? N/A
  3.3. Were concurrent controls or comparisons used? (Concurrent preferred over historical control or comparison groups.) N/A
  3.4. If cohort study or cross-sectional study, were groups comparable on important confounding factors and/or were preexisting differences accounted for by using appropriate adjustments in statistical analysis? N/A
  3.5. If case control study, were potential confounding factors comparable for cases and controls? (If case series or trial with subjects serving as own control, this criterion is not applicable.) N/A
  3.6. If diagnostic test, was there an independent blind comparison with an appropriate reference standard (e.g., "gold standard")? N/A
4. Was method of handling withdrawals described? No
  4.1. Were follow-up methods described and the same for all groups? N/A
  4.2. Was the number, characteristics of withdrawals (i.e., dropouts, lost to follow up, attrition rate) and/or response rate (cross-sectional studies) described for each group? (Follow up goal for a strong study is 80%.) N/A
  4.3. Were all enrolled subjects/patients (in the original sample) accounted for? N/A
  4.4. Were reasons for withdrawals similar across groups? N/A
  4.5. If diagnostic test, was decision to perform reference test not dependent on results of test under study? N/A
5. Was blinding used to prevent introduction of bias? No
  5.1. In intervention study, were subjects, clinicians/practitioners, and investigators blinded to treatment group, as appropriate? N/A
  5.2. Were data collectors blinded for outcomes assessment? (If outcome is measured using an objective test, such as a lab value, this criterion is assumed to be met.) N/A
  5.3. In cohort study or cross-sectional study, were measurements of outcomes and risk factors blinded? N/A
  5.4. In case control study, was case definition explicit and case ascertainment not influenced by exposure status? N/A
  5.5. In diagnostic study, were test results blinded to patient history and other test results? N/A
6. Were intervention/therapeutic regimens/exposure factor or procedure and any comparison(s) described in detail? Were interveningfactors described? Yes
  6.1. In RCT or other intervention trial, were protocols described for all regimens studied? N/A
  6.2. In observational study, were interventions, study settings, and clinicians/provider described? N/A
  6.3. Was the intensity and duration of the intervention or exposure factor sufficient to produce a meaningful effect? N/A
  6.4. Was the amount of exposure and, if relevant, subject/patient compliance measured? N/A
  6.5. Were co-interventions (e.g., ancillary treatments, other therapies) described? N/A
  6.6. Were extra or unplanned treatments described? N/A
  6.7. Was the information for 6.4, 6.5, and 6.6 assessed the same way for all groups? N/A
  6.8. In diagnostic study, were details of test administration and replication sufficient? N/A
7. Were outcomes clearly defined and the measurements valid and reliable? No
  7.1. Were primary and secondary endpoints described and relevant to the question? N/A
  7.2. Were nutrition measures appropriate to question and outcomes of concern? N/A
  7.3. Was the period of follow-up long enough for important outcome(s) to occur? N/A
  7.4. Were the observations and measurements based on standard, valid, and reliable data collection instruments/tests/procedures? N/A
  7.5. Was the measurement of effect at an appropriate level of precision? N/A
  7.6. Were other factors accounted for (measured) that could affect outcomes? N/A
  7.7. Were the measurements conducted consistently across groups? N/A
8. Was the statistical analysis appropriate for the study design and type of outcome indicators? No
  8.1. Were statistical analyses adequately described and the results reported appropriately? N/A
  8.2. Were correct statistical tests used and assumptions of test not violated? N/A
  8.3. Were statistics reported with levels of significance and/or confidence intervals? N/A
  8.4. Was "intent to treat" analysis of outcomes done (and as appropriate, was there an analysis of outcomes for those maximally exposed or a dose-response analysis)? N/A
  8.5. Were adequate adjustments made for effects of confounding factors that might have affected the outcomes (e.g., multivariate analyses)? N/A
  8.6. Was clinical significance as well as statistical significance reported? N/A
  8.7. If negative findings, was a power calculation reported to address type 2 error? N/A
9. Are conclusions supported by results with biases and limitations taken into consideration? No
  9.1. Is there a discussion of findings? N/A
  9.2. Are biases and study limitations identified and discussed? N/A
10. Is bias due to study's funding or sponsorship unlikely? Yes
  10.1. Were sources of funding and investigators' affiliations described? N/A
  10.2. Was the study free from apparent conflict of interest? N/A