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How does the body deal with energy from alcohol?
... It has been shown that a drinking pattern characterised by frequent consumption of small amounts of alcohol can prevent obesity [43][44][45], diabetes and cardiovascular diseases [46,47]. The likely mechanism involves induction of the microsomal ethanol oxidation system [48,49] and/or inhibition of ghrelin secretion, which is responsible for eating behaviour [50,51]. ...
... Wykazano, że wzór picia charakteryzujący się częstym spożywaniem małych ilości alkoholu może zapobiegać otyłości [43][44][45], cukrzycy, chorobom sercowo-naczyniowym [46,47]. Prawdopodobny mechanizm polega na indukcji mikrosomalnego układu utleniającego etanol [48,49] i/lub hamowaniu wydzielania greliny, która odpowiada za zachowania związane z żywieniem [50,51]. ...
The aim of this review is to present the role of FTO gene sequence variation in determining predisposition to specific forms of alcohol consumption. This systematic review includes studies published in 2011-2013 and 2019 from the PubMed, Science Direct and Wiley Online Library databasis.
The FTO gene is located at locus 16q12.2 and encodes a protein from the AlkB family with nucleic acid demethylase activity. FTO is mainly expressed in the hypothalamus and plays an important role in managing the body’s energetic homeostasis and regulating adipose tissue mass though its exact physiological function is not fully understood.
Observations regarding the association of FTO polymorphic variants with the risk of obesity and depression as well as the results of the GWAS studies on alcohol abuse disorders became the basis for hypothesis on the relationship between the FTO variants and the alcohol consumption. The analysed studies revealed that:
1) FTO genotype is related to the quantity, frequency and the type of consumed alcohol; 2) the relationship between the FTO genotype and the alcohol consumption pattern (amount/frequency/type) is also dependent on the genotype of other genes, including MC4R; 3) the relationship between the FTO genotype and alcohol consumption pattern is population dependent; 4) there are FTO variants correlating with predisposition to consume large amounts of alcohol including rs806289 T; 5) the relationship of the GG genotype of FTO rs17817449 SNP and the amount of alcohol consumed is gender dependent and more strongly expressed in men. These observations indicate a significant participation of genetic variability linked to FTO polymorphism in shaping alcohol consumption patterns.
... The divergent effect of drinking on the indicators between genders may also partly relate to education, income and employment. Highly educated women with better jobs and greater socializing skills may need to drink occasionally and are more likely to pay particular attention to their appearance [35]. In fact, studies on the association between alcohol consumption and abdominal obesity have presented inconsistent findings for either or both genders [36][37][38][39], which may be because alcohol is metabolized differently in men and women. ...
... In fact, studies on the association between alcohol consumption and abdominal obesity have presented inconsistent findings for either or both genders [36][37][38][39], which may be because alcohol is metabolized differently in men and women. However, the insight mechanism has not been well elucidated [35]. With respect to smoking, it generally had a significant negative association with the WC and WHtR in men. ...
Background:
Little is known about the long-term shifts in distributions of three abdominal-obesity-related indicators, waist circumference (WC), waist-to-hip ratio (WHpR) and waist-to-height ratio (WHtR) among Chinese adults. Traditional mean regression models used in the previous analyses were limited in their ability to capture cross-distribution among effects. The current study aims to describe the shift in distribution of WC, WHpR, and WHtR over a period of 18 years (1993-2011) in China, and to reveal quantile-specific associations of the three indicators with key covariates.
Methods:
Longitudinal data from seven waves of the China Health and Nutrition Surveys (CHNS) in 1993, 1997, 2000, 2004, 2006, 2009 and 2011 were analyzed. The LMS method was used to illustrate the gender-specific quantile curves of WC, WHtR and WHpR over age. Separate gender-stratified longitudinal quantile regressions were employed to investigate the effect of important factors on the trends of the three indicators.
Results:
A total of 11,923 participants aged 18-65 years with 49,507 observations were included in the analysis. The density curves of WC, WHtR and WHpR shifted to right and became wider. The three outcomes all increased with age and increased more at upper percentiles. From the multivariate quantile regression, physical activity was negatively associated in both genders; smoking only had a negative effect on male indicators. Education and drinking behavior both had opposite effects on the three indicators between men and women. Marital status and income were positively associated with the shifts in WC, WHtR and WHpR in male and female WC, while urbanicity index had a positive effect on three outcomes in men but inconsistent effect among female outcomes.
Conclusions:
The abdominal-obesity related indicators of the Chinese adults experienced rapid growth according to our population-based, age- and gender-specific analyses. Over the 18-year study period, major increases in WC, WHtR and WHpR were observed among Chinese adults. Specifically, these increases were greater at upper percentiles and in men. Age, physical activity, energy intake, drinking, smoking, education, income and urbanicity index were associated with elevated abdominal obesity indicators, and the effects differed among percentiles and between genders.
... Although definitive data based on family/twin studies are not available, similarities between obesity and addictive disorders, including alcohol dependence, have been suggested [14], pointing to possible common personality characteristics [15][16][17] and neural mechanisms [18]. Conversely, patterns of alcohol consumption characterized by high frequency/low quantity drinking may protect from obesity [19][20][21] as well as from diabetes and cardiovascular diseases [22,23], possibly through induction of the microsomal ethanol-oxidizing system [24,25] and/or inhibition of secretion of ghrelin, which is responsible for food-seeking behaviour [26]. ...
... It has been shown that despite the significant caloric value of ethanol, the correlation between its consumption and BMI is J-shaped rather than linear, so that moderate alcohol use is associated with low risk of obesity [42][43][44][45][46]. Table 6 Parameters of past/present smoking which showed an association/a trend for an association with FTO rs9939609 AA genotype. While solutions of this paradox were proposed based on specific aspects of ethanol metabolism and/or epidemiological confounding factors [24][25][26]42,44,47], our data indicate a novel possibility. The pattern of drinking distilled spirits (and possibly beer) observed by us in those without the FTO AA (i.e. ...
To investigate whether the FTO rs9939609 A allele (a risk factor for obesity) is associated with measures of alcohol consumption.
Population-based cross-sectional study and two case-control studies.
Poland and the Warsaw area.
A total of 6584 subjects from the WOBASZ survey and two cohorts of alcohol-dependent patients (n = 145 and n = 148).
Questionnaire data analysis, rs9939609 typing.
Among individuals drinking alcohol, the obesity-associated AA genotype was also associated with lower total ethanol consumption [sex-, age- and body mass index (BMI)-adjusted difference: 0.21 g/day, P = 0.012] and distinct drinking habits with relatively low frequency of drinks but larger volume consumed at a time as evidenced by (i) association between AA and frequency/amount of typical drinks (P = 0.023, multiple logistic regression analysis); (ii) inverse correlation between AA and drink frequency adjusted for drink size (P = 0.007 for distilled spirits, P = 0.018 for beer); (iii) decreased frequency of AA [odds ratio (OR) = 0.46, P = 0.0004] among those who drank small amounts of distilled spirits (≤ 100 ml at a time) but frequently (≥ 1-2 times/week). A decrease of AA was also found in both cohorts of alcohol-dependent patients versus geographically matched subjects from WOBASZ yielding a pooled estimate of OR = 0.59, confidence interval (CI): 0.40-0.88, P = 0.008. Exploratory analysis showed that those with rs9939609 AA reported lower (by 1.22) mean number of cigarettes/day during a year of most intense smoking (P = 0.003) and were older at start of smoking by 0.44 years (P = 0.016).
The FTO AA genotype, independently from its effect on BMI, is associated with measures of ethanol consumption and possibly tobacco smoking.
... As food, consumption of 30g or 3 units of alcohol can produce up to 10% of daily energy requirement. 1 As a drug, alcohol is psychoactive and can change how we feel, think or behave when consumed. Thus, it may be anxiolytic, mood enhancing, sedating, produce motor incoordination or impair judgement. ...
Objective: Alcohol has become a regular part of social functions in many cultures. Before the advent of alcohol use disorder becoming a nosological entity, many cultures noted the detrimental association with alcohol use, particularly in its excess use. With such observation, many cultures and even medical research, have tried in many ways to either justify or explain away the harmful effects of alcohol use and gone ahead to promote the use for the most mundane effects. Such explanations for alcohol use over time become acceptable in many cultures and can be viewed asmyths. Four of such myths associated with alcohol use in Ghana, are presented here. Methodology: These myths were drawn from a bigger study that looked at the prevalence of alcohol use disorder in an engineering company with mixed methods. A thematic analysis of their responses was used to arrive at these myths. Results: Participants believed that alcohol is sexually potentiating, improves appetite and quality of sleep, and has medicinal qualities like “curing” chicken pox and necessary for successful surgery. Apart from the inconclusive evidence of alcohol, particularly red wine,protecting against cardiovascular death, we could not substantiate any of these claims from medicine. Conclusion: Myths of alcohol use in different cultures need to be incorporated in preventive strategies adopted for alcohol use disorder for a comprehensive public health approach to curb the menace. Such myths should be integrated in the training of health workers to help them understand the addictive behaviour of alcohol users and the anthropological underpinnings to alcohol use.
... First, it can be a significant source of calories in the diet because there is no reduction in other food ingredients in response to energy supplementation from alcohol [161]. Alcohol cannot be stored in the body, so it is quickly metabolized using a variety of mechanisms, such as increased thermogenesis and reduced lipolysis [161][162][163]. Alcohol also causes increased cortisol secretion as well as high levels of androgens in women and androgen reduction in men, which contributes to increased visceral fat accumulation [164][165][166][167][168]. ...
This chapter reviews the risks and benefits of lifestyle in relation to abdominal obesity in children and adolescents and indicates that many issues have not yet been exhaustively studied and explained. Analyses indicate the existence of a clear relationship between physical activity and abdominal obesity in children and adolescents. There is little evidence of an increased risk of abdominal obesity resulting from a long time spent in sedentary activities. Most studies, however, show that sleep duration that is too short may be a risk factor. It has been proven that a lower risk of abdominal obesity involves the application of ''healthy'' patterns of diet based on a high intake of fruits, vegetables, fish, milk, and dairy products. Elevated risk is associated with an increased consumption of fast food, sugar and sweets, sweetened beverages, skipping breakfast, and smoking.
... This is why it has absolute priority in metabolism using different pathways, e.g. increasing thermogenesis or decreasing lipolysis (Buemann & Astrup, 2001; Suter, 2005; Yeomans et al., 2003). Alcohol metabolism may also trigger endocrine changes, such as increased cortisol secretion or modified steroid metabolism in the liver (Bjorntorp, 1990; Sarkola et al., 2001; Suter, 2005). ...
Background/objectives:
The relation between lifetime use of alcohol and measures of abdominal and general adiposity is unknown.
Subjects/methods:
Among 99,381 men and 158,796 women of the European Prospective Investigation into Cancer and Nutrition (EPIC) study, means of waist circumference (WC), waist-to-hip-ratio (WHR) and body mass index (BMI), and odds ratios (OR) for a larger WC than predicted for a given BMI (WClp=positive residuals of gender specific linear regression of BMI on WC) across categories of average lifetime use of alcohol (total, from wine and from beer) were calculated, all adjusted for socio-demographic, lifestyle and health factors.
Results:
WC, WHR and BMI in men using lifetime ≤6 g/d alcohol were 95.1 cm, 0.942 and 27.3 kg/m(2), and 96.2 cm, 0.961 and 28.3 kg/m(2) when using >96 g/d. WC and WHR in women was 83.2 cm and 0.813 for ≤6 g/d, and 84.6 cm and 0.830 for >60 g/d, whereas BMI deviated only slightly with the lowest BMI (26.7 kg/m(2)) observed for >6-24 g/d. Compared with ≤6 g/d, OR for a WClp in both genders increased steadily across categories of alcohol use (up to 1.40 (95% confidence interval 1.32, 1.49) in men using >60 g/d and 1.63 (1.54, 1.73) in women using >24 g/d), though increase was higher for alcohol from beer than from wine (P for difference between beer and wine<0.001 (men) and=0.002 (women)).
Conclusion:
Lifetime alcohol use is positively related to abdominal and general adiposity in men, possibly following the male weight gain pattern; in women, it is positively related only to abdominal adiposity. In this context, beer may contribute additionally to abdominal adiposity.
... Our two studies, taken together with a number of prior studies [41], indicate that alcohol selection by rodents involves the sensory and caloric information transduction systems dealing with the recognition, and the satiating and rewarding properties of foodstuffs. Ethanol , unlike other psychoactive drugs, has significant caloric value (seven cal/gm) and these calories have been clearly shown to have relevance to an organism's energy status [42].Figure 3 illustrates that most of the candidate genes that we identified can be related within a neurobiological pathway that was constructed based on analysis of the literature . Many of the candidate genes identified in this study code for products (protein) that have been implicated in regulation of feeding and energy metabolism. ...
We have used a genetical genomic approach, in conjunction with phenotypic analysis of alcohol consumption, to identify candidate genes that predispose to varying levels of alcohol intake by HXB/BXH recombinant inbred rat strains. In addition, in two populations of humans, we assessed genetic polymorphisms associated with alcohol consumption using a custom genotyping array for 1,350 single nucleotide polymorphisms (SNPs). Our goal was to ascertain whether our approach, which relies on statistical and informatics techniques, and non-human animal models of alcohol drinking behavior, could inform interpretation of genetic association studies with human populations.
In the HXB/BXH recombinant inbred (RI) rats, correlation analysis of brain gene expression levels with alcohol consumption in a two-bottle choice paradigm, and filtering based on behavioral and gene expression quantitative trait locus (QTL) analyses, generated a list of candidate genes. A literature-based, functional analysis of the interactions of the products of these candidate genes defined pathways linked to presynaptic GABA release, activation of dopamine neurons, and postsynaptic GABA receptor trafficking, in brain regions including the hypothalamus, ventral tegmentum and amygdala. The analysis also implicated energy metabolism and caloric intake control as potential influences on alcohol consumption by the recombinant inbred rats. In the human populations, polymorphisms in genes associated with GABA synthesis and GABA receptors, as well as genes related to dopaminergic transmission, were associated with alcohol consumption.
Our results emphasize the importance of the signaling pathways identified using the non-human animal models, rather than single gene products, in identifying factors responsible for complex traits such as alcohol consumption. The results suggest cross-species similarities in pathways that influence predisposition to consume alcohol by rats and humans. The importance of a well-defined phenotype is also illustrated. Our results also suggest that different genetic factors predispose alcohol dependence versus the phenotype of alcohol consumption.
... The high DIT after the alcohol meal is presumably related to the reoxidation of cytoplasmic NADH not being tightly linked to ATP generation. Alcohol oxidation starts instantly after intake, and alcohol is eventually completely eliminated by oxidation (22,33). Still, the results of previous studies are not concordant on the magnitude of DIT after alcohol consumption, and reported DIT values range between 9% and 28% (22,(34)(35)(36). ...
It has been suggested that the satiating power of the 4 macronutrients follows the oxidation hierarchy: alcohol > protein > carbohydrate > fat. However, the experimental evidence for this is still scarce.
The goal was to investigate the effects on appetite, energy intake and expenditure, and substrate metabolism of meals rich in 1 of the 4 macronutrients.
Subjective appetite sensations, ad libitum food intake, energy expenditure, substrate metabolism, and hormone concentrations were measured for 5 h after breakfast meals with similar energy density and fiber contents but rich in either protein (32% of energy), carbohydrate (65% of energy), fat (65% of energy), or alcohol (23% of energy). Subjects were normal-weight, healthy women (n = 9) and men (n = 10) studied in a crossover design.
There were no significant differences in hunger or satiety sensations or in ad libitum energy intake after the 4 meals. Diet-induced thermogenesis was larger after the alcohol meal (by 27%; P < 0.01), whereas protein produced an intermediary response (17%; NS) compared with carbohydrate and fat (meal effect: P < 0.01). After the alcohol meal, fat oxidation and leptin concentrations were greatly suppressed (meal effects, P < 0.0001 and P < 0.05) and triacylglycerol concentrations were as high as after the fat meal.
Intake of an alcohol-rich meal stimulates energy expenditure but suppresses fat oxidation and leptin more than do isoenergetically dense meals rich in protein, carbohydrate, or fat. Despite differences in substrate metabolism and hormone concentrations, satiety and ad libitum energy intake were not significantly different between meals. Our data, therefore, do not support the proposed relation between the macronutrient oxidation hierarchy and the satiety hierarchy.
... 36 Also, low doses of alcohol may stimulate energy expenditure since alcohol has an acute thermogenic effect. 37 It is possible that this effect is influenced by drinking pattern, so that an increased thermogenesis induced by a frequent low intake of alcohol is more sufficient in outbalancing the additional energy from the alcohol than for a corresponding less frequent intake of higher amounts per drinking occasion. ...
To study the association between alcohol drinking pattern and obesity.
Cross-sectional population study with assessment of quantity and frequency of alcohol intake, waist and hip circumference, height, weight, and lifestyle factors including diet.
In all, 25 325 men and 24 552 women aged 50-65 y from the Diet, Cancer and Health Study, Denmark, 1993-1997 participated in the study.
Drinking frequency, total alcohol intake, body mass index (BMI), and waist and hip circumference.
Among men, total alcohol intake was positively associated with high BMI (>/=30 kg/m(2)), large waist circumference (>/=102 cm) and inversely associated with small hip circumference (<100 cm). Among women, the total alcohol was associated with high BMI, large waist (>/=88 cm), and small hips only for the highest intake (28+ drinks/week). The most frequent drinkers had the lowest odds ratios (OR) for being obese. Among men, OR for having a high BMI were 1.39 (95% confidence interval: 1.36-1.64), 1.17 (1.02-1.34), 1.00 (reference), 0.87 (0.77-0.98), and 0.73 (0.65-0.82) for drinking 1-3 days/month, 1 day/week, 2-4 days/week, 5-6 days/week, and 7 days/week, respectively. Similar estimates were found for waist circumference. Corresponding results were found for women.
For a given level of total alcohol intake, obesity was inversely associated with drinking frequency, whereas the amount of alcohol intake was positively associated with obesity. These results indicate that frequent drinking of small amounts of alcohol is the optimal drinking pattern in this relation.
... This finding, together with the larger WC of the men in the high-fat, low-carbohydrate diet group, is consistent with the results of prospective studies showing that high dietary fibre levels are associated with a reduction in the risk of coronary heart disease. 54,55 The complex nature of the relationships between alcohol consumption and body weight or fat distribution is suggested by the conflicting findings of observational studies: 56,16 generally, an inverse association between BMI and alcohol intake has been reported for women, and a slight positive relationship for men. 57-60 It is not known why male drinkers are no heavier than abstainers, or why alcohol may even promote leanness in women, 61,62,50 although it has been suggested that the calories from alcohol are added to energy intakes from other sources in men, and that the energy from alcohol intake displaces sucrose in women. ...
To study the relationship between behavioural factors, body adiposity and muscle mass.
A total of 1415 Italian individuals (705 men and 710 women) aged 40-74 years from a population-based survey carried out in the town of Bollate (Milan). Analysis of covariance was used to refine and improve the precision of the comparisons.
Men: Smoking and sedentary behaviour were related to larger waist circumference (WC) and smaller hip circumference (HC). Increased WC was also associated with high-fat diet and moderate-to-heavy drinking (compared to light drinkers). Those more educated (completed high school) were leaner and ex-smokers had higher body mass index (BMI) than non-smokers. Women: BMI was inversely related with education, the more educated having also lower muscle mass. The light drinkers were leaner and moderate-to-heavy drinkers had less muscle mass than abstainers. Moderate-to-heavy drinkers had larger WC than light drinkers. A strong negative trend was found in the relationship between dietary fibre and WC. Overall adiposity (BMI) and, more weakly, HC and peripheral subcutaneous fat increased with more TV watching, whereas BMI lowered, together with WC and muscle mass (as measured by the mid-arm circumference), with more walking/cycling.
Modifiable habits such as smoking (men) and moderate-to-heavy alcohol drinking are associated with a pattern that is particularly deleterious to health: increased intra-abdominal fat and less muscle mass. Prevention strategies should be simultaneously aimed at promoting physical activities and reducing sedentary behaviours. A low-fat, fibre-rich diet seems to be closely related to a healthy distribution of body fat.
... The mechanisms linking alcohol consumption with an enhanced visceral lipid deposition are not completely understood. Alcohol consumption leads to a suppression of fat oxidation and thereby favours lipid storage [34]. Furthermore, alcohol increases the release of glucocorticoids via stimulation of the hypothalamicpituitary-adrenal axis [35]. ...
The high energy content of alcohol makes its consumption a potential contributor to the obesity epidemic.
To determine whether alcohol consumption is a risk factor for abdominal obesity, taking into account energy underreporting.
The subjects were Spanish men (n = 1491) and women (n = 1563) aged 25-74 years who were examined in 1999-2000, in a population-based cross-sectional survey in northeastern Spain (Girona). Dietary intake, including alcohol consumption, was assessed using a food frequency questionnaire. Anthropometric variables were measured.
The mean consumption of alcohol was 18.1 +/- 20.7 g/d in men and 5.3 +/- 10.4 g/d in women. 19.3% of men and 2.3% of women reported alcohol consumption of more than 3 drinks per day. The consumption of alcohol was directly associated with total energy intake in men (P < 0.001) and women (P = 0.001). The proportion of energy underreporting significantly (P < 0.001) decreased with higher amounts of alcohol drinking in both genders. Multiple logistic regression analysis, controlled for energy underreporting, smoking, educational level, leisure-time physical activity, energy, and diet quality, revealed that consuming more than 3 drinks of alcohol (>30 g ethanol) was significantly associated with the risk of abdominal obesity (Odds ratio 1.80; 1.05, 3.09) and exceeding recommended energy consumption (Odds ratio 1.97; 1.32, 2.93) in men. A very small number (2.13%) of women in this population reported high levels of alcohol consumption.
Alcohol consumption in elevated amounts was associated with risk of abdominal obesity in men, independent of energy underreporting.
... If such a cycle is of any physiologic significance, drinking frequency may be important for the degree of MEOS activation and hence for the fraction of energy from alcohol that is lost as heat (33). Another mechanism could be that low doses of alcohol stimulate energy expenditure because alcohol has an acute thermogenic effect (34). It is possible that, for the same weekly alcohol intake, a frequent drinking pattern results in relatively more energy being converted to heat, compared with a less frequent intake. ...
Cross-sectional studies have reported a lower prevalence of abdominal obese persons among frequent drinkers than among nonfrequent drinkers.
We tested the hypothesis that drinking frequency is associated with subsequent changes in waist circumference.
Data come from a prospective cohort study conducted in 1993-1997 (baseline) and 1999-2002 (follow-up) and included 43 543 men and women. Baseline information on alcohol drinking frequency was related to 1) change in waist circumference by linear regression and 2) major gain and major loss in waist circumference (defined as waist change in the lowest or highest quintile of waist changes) by polytomous logistic regression, also taking into account amount of alcohol intake.
Drinking frequency was inversely associated with changes in waist circumference in women and was unassociated with changes in waist circumference in men. Drinking frequency was unassociated with major waist loss but was inversely associated with major waist gain: odds ratios among men were 0.97 (95% CI: 0.73, 1.28), 0.95 (95% CI: 0.81, 1.12), 0.88 (95% CI: 0.77, 0.99), 0.82 (95% CI: 0.71, -0.95), and 0.79 (95% CI: 0.69, 0.9) for never drinking, drinking on 1, 2-4, 5-6, and 7 d/wk, respectively, compared with men who drank alcohol on <1 d/wk (P for trend < 0.0001). Results for women were similar. Adjustment for the amount of alcohol intake or total energy intake did not affect results considerably.
Drinking pattern may be associated with development of abdominal obesity; in this prospective study, drinking frequency was inversely associated with major waist gain and was unassociated with major waist loss.
The presented comprehensive review of current knowledge about genetic factors predisposing to Graves' disease (GD) put emphasis on functional significance of observed associations. In particular, we discuss recent efforts aimed at refining diseases associations found within the HLA complex and implicating HLA class I as well as HLA-DPB1 loci. We summarize data regarding non-HLA genes such as PTPN22, CTLA4, CD40, TSHR and TG which have been extensively studied in respect to their role in GD. We review recent findings implicating variants of FCRL3 (gene for FC receptor-like-3 protein), SCGB3A2 (gene for secretory uteroglobin-related protein 1- UGRP1) as well as other unverified possible candidate genes for GD selected through their documented association with type 1 diabetes mellitus: Tenr-IL2-IL21, CAPSL (encoding calcyphosine-like protein), IFIH1(gene for interferon-induced helicase C domain 1), AFF3, CD226 and PTPN2. We also review reports on association of skewed X chromosome inactivation and fetal microchimerism with GD. Finally we discuss issues of genotype-phenotype correlations in GD.
Based on the fact that energy content in 1 gram of alcohol is 29 kJ or 7.1 kcal, alcohol consumption can lead to weight gain. The present review was conducted to analyze the effects of alcohol consumption on body weight. A search of the Medline database for the period 1984 to March 2010 was conducted to identify cross-sectional, prospective cohort studies and intervention trials investigating the relationship between alcohol consumption and the risk of weight gain. Thirty-one publications were selected on the basis of relevance and quality of design and methods. The findings from large cross-sectional studies as well as from well-powered, prospective, cohort studies with long periods of follow-up were contradictory. Findings from short-term experimental trials also did not show a clear trend. The overall results do not conclusively confirm a positive association between alcohol consumption and weight gain; however, positive findings between alcohol intake and weight gain have been reported, mainly from studies with data on higher levels of drinking. It is, therefore, possible that heavy drinkers may experience such an effect more commonly than light drinkers. Moreover, light-to-moderate alcohol intake, especially wine intake, may be more likely to protect against weight gain, whereas consumption of spirits has been positively associated with weight gain. Further research should be directed towards assessing the specific roles of different types of alcoholic beverages. Studies should also take the effect of consumption patterns into account. In addition, a potential effect modifier that has not been evaluated before but might be important to consider is the subjects' previous tendency to gain weight.
Moderate alcohol consumption is associated with a decreased risk of type 2 diabetes in the general population, but little is known about the effects in individuals at high risk of diabetes.
The objectives were to determine associations between alcohol consumption and diabetes risk factors and whether alcohol consumption was a predictor of incident diabetes in individuals enrolled in the Diabetes Prevention Program (DPP).
DPP participants (n = 3175) had impaired glucose tolerance (2-h glucose: 7.8-11.1 mmol/L), elevated fasting glucose (5.3-7.0 mmol/L), and a body mass index (in kg/m(2)) > or =24. Participants were randomly assigned to placebo, metformin, or lifestyle modification and were followed for a mean of 3.2 y. Alcohol intake was assessed at baseline and year 1 by using a semiquantitative food-frequency questionnaire. Diabetes was diagnosed by annual oral-glucose-tolerance testing and semiannual fasting plasma glucose measurement.
Participants who reported higher alcohol consumption tended to be male, older, white, and less obese and to have a higher calorie intake and a higher HDL-cholesterol concentration. Higher alcohol consumption was associated with lower insulin secretion at any level of insulin sensitivity. We found lower incidence rates of diabetes with higher alcohol consumption in the metformin (P < 0.01 for trend) and lifestyle modification (P = 0.02 for trend) groups, which remained significant after adjustment for multiple baseline covariates. No similar association was observed in the placebo group.
Despite overall low rates of alcohol consumption, there was a reduced risk of incident diabetes in those who reported modest daily alcohol intake and were assigned to metformin or lifestyle modification. Moderate daily alcohol intake is associated with lower insulin secretion-an effect that warrants further investigation. This trial was registered at clinicaltrials.gov as NCT00038727.
Psychological distress and high body mass index (BMI) are linked in adults, especially in females. Effects of social position and behaviour, and whether obesogenic environments affect adolescents and adults equally are unresolved. The aim was to examine associations between psychological distress and being overweight in adolescents, by sex, accounting for social, lifestyle and contextual factors. Correlation of area-level variation in overweight status in adolescents and adults was investigated.
Height, weight, General Health Questionnaire 12 (GHQ12) of psychological distress, physical activity, smoking, alcohol consumption, area deprivation and social class were available on 635 male and 618 female adolescents (13-15 years) from two cross-sectional population health surveys conducted in Scotland in 1998-99/2003-04. Multilevel logistic regression modelled overweight (including obese) status accounting for intraclass correlation of adolescents in households within postcode sector areas in health board regions. Univariable analysis examined effects of high (4 or more) GHQ12 score; multivariable analysis further allowed for covariates. Adult data were used to assess the importance of correlation between adolescent and adult area-level variation.
Univariably, there was significantly increased risk of being overweight associated with high GHQ12 score for girls but not boys; adolescent and adult area-level variation correlation did not impact. Results remained significant for girls in multivariable analyses (OR = 2.44, 95% confidence interval (CI): 1.33-4.50) and non-significant for boys (OR = 1.31, 95% CI: 0.56-3.05).
Findings indicate being overweight is associated with psychological distress in adolescent girls, but not boys. Effects are not mediated by social, lifestyle or contextual factors.
Moderate alcohol consumption protects against type 2 diabetes and cardiovascular disease. Because humans spend most of their time in the postprandial state, we examined the effect of 15 g alcohol on postprandial metabolic factors in 20 postmenopausal women over 6 h. We measured 1) glucose, insulin, lipids, C-reactive protein, and adiponectin levels; 2) augmentation index by applanation tonometry; and 3) energy expenditure and substrate oxidation by indirect calorimetry. Subjects received low carbohydrate (LC; visits 1 and 2) and high carbohydrate (HC; visits 3 and 4) high fat meals with and without alcohol. Alcohol augmented the postprandial increment in insulin (P = 0.07) and reduced the postprandial increment in glucose (P = 0.04) after the LC meal only. Triglycerides were increased by alcohol after the LC (P = 0.002) and HC (P = 0.008) meals. Total and high-density lipoprotein cholesterol, fatty acids, and total adiponectin responses were unaffected. C-reactive protein levels decreased postprandially; reductions were enhanced by alcohol after the HC meal, but were attenuated after the LC meal. Postprandial reductions in the augmentation index were increased by alcohol after the LC meal only (P = 0.007). Alcohol enhanced the postprandial increase in energy expenditure 30-60 min after the LC meal (increase, 373 +/- 49 vs. 236 +/- 32 kcal/d; P = 0.02) and HC meal (increase, 362 +/- 36 vs. 205 +/- 34 kcal/d; P = 0.0009), but suppressed fat and carbohydrate oxidation. Some of our findings may be mechanisms for lower diabetes and cardiovascular risks in moderate drinkers.
Alcohol is a caloric compound that can contribute to energy intake. Therefore, peptides that regulate energy balance likely modify the motivation to consume alcohol. Melanin-concentrating hormone (MCH) regulates energy homeostasis and has been implicated in other behaviors that impact alcohol consumption (i.e., anxiety, fluid balance, and reward). We tested the hypothesis that MCH would decrease the motivation to consume alcohol secondarily to reducing anxiety.
Rats were trained to drink 10% ethanol or an isocaloric concentration of sucrose with use of a sucrose-fading technique. MCH (1, 5, or 10 microg) or its saline vehicle was administered into the third cerebral ventricle (i3vt), and intake of ethanol or sucrose and chow was assessed for 2 hr. Alcohol-naïve rats were evaluated in an elevated plus maze after i3vt MCH (10 microg), neuropeptide Y, or saline administration.
Contrary to the hypothesis, MCH dose-dependently increased alcohol intake: saline = 0.7 +/- 0.1 g/kg, 1 microg MCH = 1.0 +/- 0.1 g/kg, 5 microg MCH = 1.2 +/- 0.1 g/kg, and 10 microg MCH = 1.8 +/- 0.3 g/kg (p < 0.01), and this was true whether water was simultaneously available or not. MCH also significantly increased sucrose intake (saline = 1.0 +/- 0.3 g/kg, 10 mug MCH = 1.4 +/- 0.5 g/kg; p < 0.05). MCH had no effect on time spent in the open arms (54.3 +/- 11.5 sec) relative to saline (58.2 +/- 23.8 sec), whereas neuropeptide Y, a known anxiolytic, increased time spent on the open arms (119.2 +/- 22 sec, p < 0.05).
We conclude that MCH nonspecifically increases ingestive behavior. Furthermore, MCH had no apparent effect on anxiety. The ability of MCH to increase alcohol and/or sucrose intake may be explained by the effect of MCH on energy balance and/or reward processes.
Cross-sectional associations between body fat and its distribution and environmental factors influencing energy balance were examined in 5115 young adults. Protein was directly associated with body mass index (BMI) in all race and sex groups (P less than 0.01) after age, education, cigarette-smoking status, alcohol intake, and physical activity were adjusted for. Carbohydrate intake was inversely associated with BMI in males (P = 0.02). Total physical activity was inversely associated with BMI in white women and with skinfold-thickness measures (P less than 0.01) in all groups. Waist-to-hip-circumference ratio (WHCR) was positively associated with total kilojoules (kilocalories) in women, inversely associated with percent of kilojoules (kilocalories) from carbohydrates in whites, grams of crude fiber/4184 kJ (1000 kcal) (except in black men), and physical activity (except in white women). WHCR was directly associated with cigarette smoking except in black men, and with total alcohol intake in men. Beer was consistently associated with WHCR in all race and sex groups.
The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DIT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/l water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 MJ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/l solution) or an isoenergetic meal of food alone (2.55 MJ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) kJ for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates.
Alcohol's effects on eating were investigated by paying 92 adult humans to maintain 7-d diaries of everything they ingested, the time of ingestion, their subjective state at the time of ingestion, and the number of people present at the time of ingestion. Total intakes, meal sizes, meal compositions, pre- and postmeal intervals, and deprivation and satiety ratios were compared between nondrinkers and drinkers and between meals associated with alcohol ingestion and those without. Univariate and multivariate prediction of meal size and of postmeal interval were also calculated to ascertain alcohol's contribution to the regulation. The results suggest that alcohol supplements rather than displaces macronutrient-supplied calories, that alcohol is associated with prolonged meal durations, and that alcohol calories may be unregulated. Other apparent changes in the meal pattern appear to be artifacts of time of day and meal duration.
To investigate the mechanism by which ethanol lowers plasma free fatty acids, we tested the ability of two products of alcohol metabolism, acetate and lactate, to lower free fatty acids in man. Sodium acetate was given orally to five healthy fasting volunteers and caused a significant fall in plasma free fatty acids. After amounts of ethanol and acetate that produced similar reductions in free fatty acids, plasma acetate increased 3- to 4-fold within 20 min. In each of three subjects the fall of free fatty acids observed after acetate ingestion occurred at plasma acetate levels less than or equal to those reached after ethanol. In all studies plasma glucose remained stable. Oral administration of sodium lactate to another volunteer in amounts sufficient to raise plasma lactate concentrations to a level similar to that found after ethanol administration failed to lower plasma free fatty acids.
Thus acetate, a metabolite of ethanol, reduces plasma free fatty acids at plasma acetate levels comparable to those resulting from ethanol metabolism, which suggests that the lowering of plasma free fatty acids produced by ethanol is mediated, at least in part, by acetate.
One hundred years of research about the metabolism of alcohol have provided many details, but some general aspects of the physiologic value of alcohol remain uncertain or inadequately proven. Results from epidemiologic studies appear to be in conflict with interpretations based on results from indirect calorimetric studies. The apparent inability of body mass index to be maintained in women when alcohol is consumed with food may indicate impaired metabolic processes that need to be better understood. Current evidence on the effects of alcohol are summarized to identify experimental approaches that may provide information needed to resolve the current contradictions.
Energy expenditure and macronutrient balances were assessed in normal healthy men by whole-body indirect calorimetry after meals consumed with and without ethanol to test the theory that alcohol energy is not fully available because of futile cycling. Alcohol addition (A) or isoenergetic substitution (S) caused fat retention by significantly suppressing its oxidation when the alcohol was actively metabolized (0-6h). However, on protocol S, fat balance was later reestablished due to raised fat oxidation (6-20.5 h) secondary to a relative carbohydrate deficiency. On protocol A, fat balance remained significantly raised. The thermogenic effect of alcohol was similar to that of carbohydrate, providing no evidence for futile cycling. Short-term studies that fail to account for later readjustments of macronutrient balance can be misleading. We conclude that alcohol has a fat-sparing effect similar to that of carbohydrate and will only cause fat gain when consumed in excess of normal energy needs.
We have examined the effect of alcohol on the gastric emptying rate of a liquid meal in 10 volunteers. Each volunteer was
allocated randomly to receive, on three occasions, no alcohol, 3 units or 6 units of alcohol. Gastric emptying was measured
using applied potential tomography. The rate of gastric emptying as measured by the time to 50% emptying (T50) was delayed significantly (P < 0.01) after alcohol 6 units (median 45.0 mm (range 19–90 min)) compared with control (23.0
min (13–36 min)) and there was little change after alcohol 3 units (25.5 min (10–41 min)). (Br. J. Anaesth. 1993; 71: 674–676)
The effect of alcohol on overnight energy expenditure and substrate disposal was studied in eleven subjects (five men, six women) using whole-body indirect calorimetry for 15.5 h after test meals. Three test meals were studied in random order with at least 48 h between treatments: control, 50% of maintenance energy needs provided as 14, 40 and 46% energy from protein, fat and carbohydrate respectively; alcohol addition, control plus 23% energy as alcohol; alcohol substitution, control with alcohol replacing 23% of carbohydrate energy. ANOVA revealed no significant sex effects. Alcohol-induced thermogenesis dissipated only 15 (SD 14)% of the alcohol energy. Alcohol addition had no significant effect on protein or carbohydrate oxidation but fat oxidation was suppressed (P < 0.0005) to an extent equivalent to storing 74 (SD 51)% of the alcohol energy as fat. Alcohol substitution reduced carbohydrate oxidation (P < 0.009) to an equivalent of 42 (SD 41)% and also spared fat (P < 0.005) to an equivalent of 59 (SD 37)% of the alcohol energy. It is concluded that alcohol has no special thermogenic capacity, and that its energy can be accounted for in a similar way to carbohydrate.
Although previous studies have clearly demonstrated that energy from alcohol may not be efficiently utilized to maintain body weight when it comprises 20% or more of the daily caloric intake, there is considerable debate regarding the influence of moderate alcohol consumption (< or = 5% of the total daily caloric intake) upon metabolism, substrate utilization and body weight regulation. Consequently, the objectives of this study were to determine whether moderate alcohol consumption could influence body weight via changes in substrate utilization, oxygen consumption or alterations in dietary macronutrient content.
Fourteen male subjects (mean age = 32.1 years) participated in a 12-week, free-living, crossover trial in which they either drank red wine (270 ml; 13% v/v ethanol) daily for 6 weeks and then abstained for the next 6 weeks or vice-versa.
Whether wine was imbibed or not, no significant differences (p > 0.05) were demonstrated for any of the following variables: body weight, body fat percentage, skinfold thickness, resting metabolic rate, respiratory quotient, caloric intake, dietary macronutrient content, or fasting insulin or glucose concentrations.
In free-living subjects over a 6-week period, the addition of two glasses of red wine to the evening meal does not appear to influence any measured variable which may adversely affect body weight or promote the development of obesity during this time period.
Daily alcohol intake may amount to a substantial input of calories in Western world consumers. Epidemiological and experimental studies indicate that consumption of alcohol does not inhibit the spontaneous intake of nonalcoholic calories. There is also no relationship between habitual alcohol intake and body weight. This has been attributed to an inefficient use of alcoholic calories (concept of 'empty alcohol calories'). This hypothesis however is not supported by recent studies showing that the thermic effect of acute alcohol administration (about 16%) is close to the theoretical energy cost of alcohol metabolism. This indicates that the absence of relationship between alcohol consumption and body weight is explained by other, yet unidentified factors.
The thermogenic response induced by ethanol ingestion in humans has not been extensively studied. This study was designed to determine the thermic effect of ethanol added to a normal diet in healthy nonalcoholic subjects, using indirect calorimetry measurements over a 24-h period in a respiration chamber. The thermic effect of ethanol was also measured when ethanol was ingested in the fasting state, using a ventilated hood system during a 5-h period. Six subjects ingested 95.6 +/- 1.8 (SE) g ethanol in 1 day partitioned over three meals; there was a 5.5 +/- 1.2% increase in 24-h energy expenditure compared with a control day in which all conditions were identical except that no ethanol was consumed. The calculated ethanol-induced thermogenesis (EIT) was 22.5 +/- 4.7% of the ethanol energy ingested. Ingestion of 31.9 +/- 0.6 g ethanol in the fasting state led to a 7.4 +/- 0.6% increase in energy expenditure over baseline values, and the calculated EIT was 17.1 +/- 2.2%. It is concluded that in healthy nonalcoholic adults ethanol elicits a thermogenic response equal to similar to 20% of the ethanol energy. Thus the concept of the apparently inefficient utilization of ethanol energy is supported by these results which show that only similar to 80% of the ethanol energy is used as metabolizable energy for biochemical processes in healthy nonalcoholic moderate ethanol consumers.
A nasogastric formula infusion method was used to evaluate the steady-state fuel value of ethanol relative to that of glucose in eight chronically alcoholic men undergoing a 4- or 5-week balance experiment. Each subject received a maintenance infusion of the formula diet throughout the study. When control formula glucose (week 1) was isocalorically replaced with ethanol [week 2, 30% of kcal; week 3 or 4 (5-week experiment) 40% to 60% of kcal], the following was observed: weight loss; zero energy balance and reduced or negative balances of N, K, P, Mg, and Na; increased urinary urea N and 3-methylhistidine; lowered urinary C-peptide; no change in indirectly or directly measured thermal energy losses; and a blood level related rise in breath and urinary ethanol losses. All of these changes promptly reversed during the middle (week 3 in 5-week experiment) and final control weeks. Accounting for all diet-related energy losses (urine, breath, thermal), the fuel value of the ethanol-containing diet relative to the glucose control formula varied between 0.95 and 0.99, depending upon the blood alcohol level. Hence weight loss during short-term (seven-day) ethanol infusion is unrelated to overall negative energy balance, stems primarily from decrements in protein, minerals, and fluid, and may in part be mediated by the reduction in insulin secretion that accompanies switching from dietary glucose to ethanol.
Alcohol contributes more than 10 per cent of the total caloric intake of adult drinkers in the United States. However, the effect of alcohol on body weight has not been adequately studied in the general population. The association between weight and frequency of alcohol consumption was examined in two national cross-sectional surveys: the Second National Health and Nutrition Examination Survey (HANESII; n = 10,929) and the Behavioral Risk Factor Surveys (BRFS; n = 18,388). Linear multiple regression was used to estimate the independent effect of alcohol on weight, adjusting for smoking, age, diet practices, physical activity, race, education, and height. Among men, alcohol had only a slight effect on weight in either survey. However, among women, alcohol was associated with a substantial reduction in weight, which was as large as the effect of smoking. Compared with nondrinkers, women who consumed alcohol 7-13 times per week had the greatest reduction in weight: -3.6 kg (95% confidence limits [CL] = -5.6, -1.5 kg) in HANESII and -3.2 kg (95% CL = -4.9, -1.5 kg) in BRFS. Alcohol confounded the association between smoking and weight, and among women it accounted for nearly 45 per cent of the weight-lowering effect of smoking. Alcohol also diminished the weight-lowering effect of smoking in men, while in women the smoking effect was slightly enhanced. Further studies are needed to understand the causal mechanisms by which alcohol is associated with body weight.
Specific alcoholic beverage associations with the waist-to-hip ratio were characterized in 12,145 African-American and white men and women ages 45–64 years. Estimated waist-to-hip ratios of those consuming more than six nonwine alcohol drinks/week and more than six wine drinks/week (vs. nondrinkers) were 0.007 larger ( p <0.001) and 0.009 smaller ( p <0.05), respectively. In similar comparisons, the odds ratios for a large waist-to-hip ratio were 1.4 (95% confidence interval 1.1–1.7) for nonwine and 0.45 (95% confidence interval 0.21–0.95) for wine intake. The opposite direction in adjusted associations for wine and nonwine (mainly beer) drinking supports the popular concept of the “beer belly.” Am J Epidemiol 1995;142:1034–8.
Plasma acetate turnover and oxidation were determined in 11 healthy subjects by the constant infusion of a trace amount of [1-14C]acetate for 6 h. The subjects ages ranged from 22 to 57 yr. There was a positive correlation (P less than 0.001) between plasma acetate concentration and turnover rate, and a negative correlation (P less than 0.001) between turnover and age. The plasma acetate concentration in the subjects 22--28 yr old was 0.17 vs. 0.13 mM (P less than 0.02) in subjects 40--57 yr old. The plasma acetate turnover rate was also greater in the younger age group (8.23 +/- 0.66 vs. 4.98 +/- 0.64 mumol/min . kg, P less than 0.01). Approximately 90% of the plasma acetate turnover was immediately oxidized to CO2 in both age groups, however, 13.2 +/- 0.89% of the CO2 output in the younger group was derived from plasma acetate oxidation compared to 7.9 +/- 0.94% in the older group (P less than 0.01). The mean plasma acetate concentration, turnover, and oxidation in six cancer patients 47--63 yr old were similar to the values observed in the age-matched healthy subjects. Uptake or output of acetate by various tissues was measured by arterial-venous plasma acetate concentration differences. In seven of eight subjects undergoing elective surgery, the arterial-portal venous concentration difference was negative, which indicated that the gastrointestinal tract can contribute to plasma acetate production. Uptake of plasma acetate by both the leg and liver appeared to be dictated by the arterial acetate concentration. Net production of acetate by both the leg and liver was most often observed at arterial plasma acetate concentrations less than 0.08 mM.
There are implications in the literature that wine is different from other alcoholic beverages and that it may even have a beneficial effect on the nutritional process. A metabolic study was undertaken in an attempt to document the effects of wine versus ethanol on absorption of various nutrients. Nitrogen and caloric data are presented here. During each of four 18-day experimental periods, six healthy, young men were given, in random order, a liter per day of the following test beverages: Zinfandel wine (9.3% w/v alcohol); dealcoholized Zinfandel wine; pure ethanol (9.3% w/v aqueous alcohol solution); and deionized water. These beverages were divided into four equal feedings and administered with a carefully controlled isocaloric diet over a 12-hr period. The subjects tended to lose weight on alcohol-containing regimens, suggesting that calories from alcohol may not be as efficient as those from fat and carbohydrate. Urinary excretion of nitrogen was significantly greater during wine and ethanol administration than during feeding of the other test beverages. This was reflected in an increase in uric acid and urea nitrogen output, primarily, the latter, suggesting that alcohol may directly affect protein catabolism. There was no significant difference in fecal nitrogen excretion between experimental periods.
Ethanol can account for up to 10 percent of the energy intake of persons who consume moderate amounts of ethanol. Its effect on energy metabolism, however, is not known.
We studied the effect of ethanol on 24-hour substrate-oxidation rates in eight normal men during two 48-hour sessions in an indirect-calorimetry chamber. In each session, the first 24 hours served as the control period. On the second day of one session, an additional 25 percent of the total energy requirement was added as ethanol (mean [+/- SD], 96 +/- 4 g per day); during the other session, 25 percent of the total energy requirement was replaced by ethanol, which was isocalorically substituted for lipids and carbohydrates.
Both the addition of ethanol and the isocaloric substitution of ethanol for other foods reduced 24-hour lipid oxidation. The respective mean (+/- SE) decreases were 49.4 +/- 6.7 and 44.1 +/- 9.3 g per day (i.e., reductions of 36 +/- 3 percent and 31 +/- 7 percent from the oxidation rate during the control day; P less than 0.001 and P less than 0.0025). This effect occurred only during the daytime period (8:30 a.m. to 11:30 p.m.), when ethanol was consumed and metabolized. Neither the addition of ethanol to the diet nor the isocaloric substitution of ethanol for other foods significantly altered the oxidation of carbohydrate or protein. Both regimens including ethanol produced an increase in 24-hour energy expenditure (7 +/- 1 percent with the addition of ethanol, P less than 0.001; 4 +/- 1 percent with the substitution of ethanol for other energy sources, P less than 0.025).
Ethanol, either added to the diet or substituted for other foods, increases 24-hour energy expenditure and decreases lipid oxidation. Habitual consumption of ethanol in excess of energy needs probably favors lipid storage and weight gain.
The administration of a single, 100-300 mg/kg ip, dose of a B6 vitamer to rats resulted in an almost immediate and gradual mobilization of the liver glycogen and a concomitant elevation of the serum glucose, with the order of potency being pyridoxal greater than pyridoxamine greater than pyridoxine. Since the B6 vitamer also stimulated the secretion of adrenal catecholamines and the accumulation of liver cAMP, and a pretreatment with selected blocking agents conferred significant protection against the glycogen depletion in the order of potency propranolol + phentolamine greater than propranolol greater than verapamil greater than phentolamine, a role for an adrenomedullary catecholamine-stimulated, beta-adrenoceptor-mediated, activation of the glycogen cascade system was suggested. This assumption was confirmed by verifying pyridoxal to possess virtually no effect on the liver glycogen of adrenalectomized rats.
We determined the site at which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) acts to increase food intake in rats. Rats began eating sooner and ate more food during hepatic portal than during jugular infusions of 2,5-AM (50, 100, or 150 mg/h). After rats were intubated with 2,5-[14C]AM (1.15 microCi in 200 mg/kg), significant quantities of radioactivity were found in liver but not in brain. Hepatic vagotomy prevented the eating response to 200 mg/kg 2,5-AM without altering the effect of the analogue on plasma fuels. These results indicate that low doses of 2,5-AM act in the liver to increase food intake and suggest that the signal for feeding generated in the liver is transmitted to the brain through the hepatic vagus nerve. Taken together, this work provides the strongest evidence to date that a signal initiating feeding behavior originates in the liver.
Until two decades ago, dietary deficiencies were considered to be the only reason for alcoholics to develop liver disease. As the overall nutrition of the population improved, more emphasis was placed on secondary malnutrition and direct hepatotoxic effects of ethanol were established. Ethanol is hepatotoxic through redox changes produced by the NADH generated in its oxidation via the alcohol dehydrogenase pathway, which in turn affects the metabolism of lipids, carbohydrates, proteins, and purines. Ethanol is also oxidized in liver microsomes by an ethanol-inducible cytochrome P-450 (P-450IIE1) that contributes to ethanol metabolism and tolerance, and activates xenobiotics to toxic radicals thereby explaining increased vulnerability of the heavy drinker to industrial solvents, anesthetic agents, commonly prescribed drugs, over-the-counter analgesics, chemical carcinogens, and even nutritional factors such as vitamin A. In addition, ethanol depresses hepatic levels of vitamin A, even when administered with diets containing large amounts of the vitamin, reflecting, in part, accelerated microsomal degradation through newly discovered microsomal pathways of retinol metabolism, inducible by either ethanol or drug administration. The hepatic depletion of vitamin A is strikingly exacerbated when ethanol and other drugs were given together, mimicking a common clinical occurrence. Microsomal induction also results in increased production of acetaldehyde. Acetaldehyde, in turn, causes injury through the formation of protein adducts, resulting in antibody production, enzyme inactivation, decreased DNA repair, and alterations in microtubules, plasma membranes and mitochondria with a striking impairment of oxygen utilization. Acetaldehyde also causes glutathione depletion and lipid peroxidation, and stimulates hepatic collagen production by the vitamin A storing cells (lipocytes) and myofibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)
Six healthy young men were studied by indirect calorimetry for 6 h after eating a meal composed of glucose or manioc starch (equivalent to 50 g dextrose). Blood was drawn every 30 min for 6 h to measure plasma glucose, free fatty acid (FFA), and insulin concentrations. The glycemic index of the starch was 57%. Plasma insulin and glucose concentrations were significantly higher from 150 to 210 min and FFA concentrations remained significantly lower from 210 to 360 min after starch than after glucose. Carbohydrate oxidation rose from a similar initial concentration for glucose and starch, to a constant concentration until 200 min before becoming significantly higher for the starch load until the end of the test. Total glucose oxidation was significantly higher with starch. Total fat oxidation did not differ after the two loads. A negative correlation was found between glucose oxidation and plasma FFA concentrations. Use of low-glycemic-index carbohydrates increases carbohydrate oxidation because of lower plasma FFA concentrations and fat oxidation.
We studied relations between alcohol intake, body mass index, and diet in 89,538 women and 48,493 men in two cohort studies. Total energy increased with alcohol consumption (partial r = 0.11, P less than 0.001), and carbohydrate intake decreased from 153 g/d in abstainers to 131 g/d in women drinking 2.5.0-49.9 g alcohol/d. The decrease in carbohydrate intake was due mainly to decreased sugar consumption with higher alcohol intake (partial r = -0.05, P less than 0.001), reflecting decreased energy consumption from sources excluding alcohol. In men total energy increased with alcohol consumption (partial r = 0.19, P less than 0.001), from 7575.6 (abstainers) to 9821.5 kJ/d (greater than 50 g alcohol/d). Energy intake excluding alcohol varied little with alcohol intake (partial r = 0.003, P = 0.48) but sucrose intake decreased with higher alcohol intake. These data suggest that calories from alcohol were added to energy intake from other sources in men, and that in women, energy from alcohol intake displaced sucrose. The consumption of candy and sugar is inversely related to alcohol intake, raising the possibility that it is related to appetite for alcohol.
We studied correlates of wine, hard liquor or beer preference among 53,172 white men and women in a Northern California prepaid health plan. Preference for a beverage type was reported by 51% of drinkers; 22% of persons with a preference reported exclusive use of the preferred beverage. Persons who prefer wine are likely to be women, temperate, young or middle-aged, non-smokers, better educated and free of symptoms or risk of illness. Persons who prefer liquor are likely to be men, heavier drinkers, middle-aged or older, less educated and afflicted with symptoms or risk factors for major illnesses. Persons who prefer beer are likely to be young men who are intermediate between wine and liquor preferrers for most traits. The traits of persons reporting exclusive use of a beverage type were similar. These data identify correlates of beverage choice which need to be controlled for in alcohol-health studies.
The short-term effects of moderate alcohol consumption on energy balance, serum lipids, and lipoproteins were studied in eight healthy middle-aged men (age 30 to 47 years and body mass index 23.1 to 27.7 w/h2). A crossover dietary trial included two isocaloric periods without (20% protein, 50% carbohydrate, 30% fat) or with alcohol (12% protein, 29% carbohydrate, 25% fat, 75 g of alcohol as red wine). Each period lasted 2 weeks. The body weight of the subjects remained stable over the study. Fasting blood glucose, serum insulin, total cholesterol, and LDL cholesterol were similar at the end of both dietary periods. Mean values of serum total triglyceride (108 +/- 18 v 85 +/- 24 mg/dL, P less than 0.05), VLDL-Tg (88 +/- 24 v 73 +/- 16 mg/dL, NS), and total HDL cholesterol (49.4 +/- 6.0 v 43.4 +/- 5.5 mg/dL, P less than 0.05) were higher after the diet with alcohol than without alcohol. The increase of HDL cholesterol was primarily due to that of HDL2 cholesterol (10.4 +/- 5.1 v 5.7 +/- 3.9 mg/dL, P less than 0.05). The concentration of apoprotein A-I, A-II, and B averaged 104 +/- 17 v 89 +/- 16 mg/dL, 33 +/- 4 v 28 +/- 8 mg/dL, P less than 0.02, and 111 +/- 24 v 105 +/- 33 mg/dL after the diets with and without alcohol, respectively. Adipose tissue LPL activity increased in six of the eight volunteers during the diet with alcohol. Resting metabolic rate, postprandial energy expenditure, and postprandial responses of blood glucose, serum insulin, triglyceride, and plasma FFA were similar after the both diets.(ABSTRACT TRUNCATED AT 250 WORDS)
A review of 144 published studies of the relationship between socioeconomic status (SES) and obesity reveals a strong inverse relationship among women in developed societies. The relationship is inconsistent for men and children in developed societies. In developing societies, however, a strong direct relationship exists between SES and obesity among men, women, and children. A review of social attitudes toward obesity and thinness reveals values congruent with the distribution of obesity by SES in different societies. Several variables may mediate the influence of attitudes toward obesity and thinness among women in developed societies that result in the inverse relationship between SES and obesity. They include dietary restraint, physical activity, social mobility, and inheritance.
To study the mechanism of the diabetogenic action of ethanol, ethanol (0.75 g/kg over 30 min) and then glucose (0.5 g/kg over 5 min) were infused intravenously into six normal males. During the 4-h study, 21.8 +/- 2.1 g of ethanol was metabolized and oxidized to CO2 and H2O. Ethanol decreased total body fat oxidation by 79% and protein oxidation by 39%, and almost completely abolished the 249% rise in carbohydrate (CHO) oxidation seen in controls after glucose infusion. Ethanol decreased the basal rate of glucose appearance (GRa) by 30% and the basal rate of glucose disappearance (GRd) by 38%, potentiated glucose-stimulated insulin release by 54%, and had no effect on glucose tolerance. In hyperinsulinemic-euglycemic clamp studies, ethanol caused a 36% decrease in glucose disposal. We conclude that ethanol was a preferred fuel preventing fat, and to lesser degrees, CHO and protein, from being oxidized. It also caused acute insulin resistance which was compensated for by hypersecretion of insulin.
To study the effect of alcohol on glucose and insulin metabolism, a simultaneous infusion of glucose and insulin was given for 150 min to healthy volunteers, once during alcohol and once during calorie-free gingerale (control) ingestion. During alcohol intake, the average steady-state (between 100 and 150 min) glucose of 5.44 +/- 0.39 mmol/l. and the average steady-state insulin of 6.3 +/- 1.1 ng/ml were significantly higher than those (4.0 +/- 0.39 mmol/l. of glucose and 4.4 +/- 0.6 ng/ml of insulin) observed during the control state. Despite the higher steady-state insulin concentrations, the glucose metabolism was significantly less during alcohol ingestion. These findings suggest alcohol-induced impairment in glucose metabolism is caused by a decreased tissue sensitivity to insulin.
Data from the first National Health and Nutrition Examination Survey (HANES I) were analyzed for differences in nutrient intakes based on the amounts of alcohol consumed by US adults, and for relationships between alcohol consumption, calorie intake, and relative body weight. Drinkers had significantly higher intakes of total calories than nondrinkers, but only because of their intakes of alcoholic calories. Among drinkers, the intakes of nonalcoholic calories decreased as alcohol intakes increased, and it was estimated that between 15 and 41% of the alcoholic calories replaced nonalcoholic calories. Despite their higher caloric intakes, drinkers were not more obese than nondrinkers, suggesting that alcoholic calories may be less efficiently utilized than nonalcoholic calories, or may interfere with utilization of nonalcoholic calories. The most salient difference in nutrient intake between drinkers and nondrinkers was the substantially lower carbohydrate intake of drinkers.
Hepatic microsomes contain an ethanol-oxidizing system distinct from alcohol dehydrogenase. In vitro, it has characteristics comparable to those of microsomal drug-detoxifying enzymes and, in vivo, it is capable of adaptation to the administration of ethanol. The existence of this microsomal ethanol-oxidizing system may explain ultrastructural, pharmacological, and biochemical effects of ethanol.
Observations of changes in body weight in man and rats indicate that the administration of high doses of ethanol results in an inefficient utilization of calories. It is postulated that this is due, at least in part, to activation of energy wasteful metabolic pathways such as microsomal ethanol oxidizing system (MEOS) in the hepatic endoplasmic reticulum, that this effect is increased by microsomal enzyme proliferation induced by ethanol consumption, and that the energy balance may be similarly disturbed by administration of other drugs. The proposed mechanism for these changes is an increase in the microsomal oxidation of both substrates (such as ethanol) and of NADPH, a process which does not appear to be linked to energy conservation such as the production of ATP. In the case of ethanol, these effects would be expected to be most obvious during ingestion of moderately high doses because of the much higher Km of ethanol for MEOS than for ADH. Because of the ability of ethanol feeding to induce various microsomal enzyme activities, the metabolism of substrates other than ethanol may also be involved in the energy wasting process.
The effect of preprandial alcohol on gastric emptying was investigated with the use of ⁵¹Cr chloride as the marker and external counting of radioactivity. Eight healthy men, who received a balanced test meal containing about 60 g fat, showed an exponential decrease of radioactivity from the gastric area with an average half-time of 105 min. Ingestion of 4 oz. whiskey before the meal increased the emptying time by 99 min.
Specific alcoholic beverage associations with the waist-to-hip ratio were characterized in 12,145 African-American and white men and women ages 45-64 years. Estimated waist-to-hip ratios of those consuming more than six nonwine alcohol drinks/week and more than six wine drinks/week (vs. nondrinkers) were 0.007 larger (p < 0.001) and 0.009 smaller (p < 0.05), respectively. In similar comparisons, the odds ratios for a large waist-to-hip ratio were 1.4 (95% confidence interval 1.1-1.7) for nonwine and 0.45 (95% confidence interval 0.21-0.95) for wine intake. The opposite direction in adjusted associations for wine and nonwine (mainly beer) drinking supports the popular concept of the "beer belly."
A gender difference in alcohol pharmacokinetics has been suggested to explain why women are more vulnerable to ethanol's toxic effects. The results of animal experiments suggest that females exhibit higher alcohol metabolic rates than males as a result of hormonal differences. Experimental results examining gender differences in human alcohol metabolism have been inconsistent; the diversity of experimental protocols and variety of pharmacokinetic parameters reported have made comparisons of these studies very difficult. Variability in alcohol metabolic rate between individuals of the same sex is often significant, preventing an assessment of gender differences in some studies. This chapter attempts to summarize the findings of studies from the last decade that examined the role of gender and sex hormone differences on ethanol metabolism in men and women. The role of body composition, genetic factors, gastric and hepatic alcohol dehydrogenase, and gastric absorption in creating gender differences in alcohol metabolism is discussed. Suggestions are offered that may result in better cross-study comparisons and more consistent experimental results.
Moderate alcohol consumers obtain excess calories from alcohol and these additional calories do not result in weight gain. This study examined the contribution of alcohol to the total caloric intakes and expenditures of light to moderate alcohol consumers and compared the data to soda drinkers. Physical activity levels were measured by employing continuous heart rate monitoring for a 6-day normal phase and a 6-day abstinence phase. The normal food intake of both groups was recorded in diet diaries. Subjects' overall intake of food energy during the alcohol week was significantly higher than during any of the other three phases (an excess of 241 kcal/day). This study suggests that excess alcohol calories are compensated by an increase in energy expenditure, as evidenced indirectly by increased heart rates occurring between the hours of 2300 and 0700 h, increased self-reported nightly restlessness, increased wake time, and exercise.
Little is known about the role of alcohol in determining change in body weight. In this paper, the authors examine the relation between alcohol intake and body weight in 7,230 US adults aged 25-74 years who participated in the First National Health and Nutrition Examination Survey (1971-1975) and who were reweighed 10 years later (1982-1984). Both cross-sectional and prospective analyses were adjusted for age, race, height, education, health status, smoking status, diet status, physical activity, and total nonalcoholic caloric intake. At baseline, women who reported at least one drink per day weighed 2.3 kg less than nondrinkers (95% confidence interval (CI) -0.4 to -4.2). Little relation was observed between body weight and alcohol intake cross-sectionally among men. Prospectively, both men and women drinkers tended to gain less weight than did nondrinkers (p = 0.006 for trend in women, p = 0.11 for trend in men). Drinkers also had more stable weight over the 10-year follow-up period. Drinkers were less likely to have major weight gain or loss (gaining or losing > or = 10 kg) than were nondrinkers. Compared with nondrinkers, for those who consumed 1-6.9 drinks per week, women had an odds ratio (OR) = 0.7 (95% CI 0.5 to 0.9) for major weight gain and an OR = 0.7 (95% CI 0.5 to 1.1) for major weight loss, while men had an OR = 1.0 (95% CI 0.6 to 1.6) for major weight gain and an OR = 0.7 (95% CI 0.5 to 1.2) for major weight loss. For those who consumed > or = 2 drinks per day, women had an OR = 0.5 (95% CI 0.3 to 1.0) for major weight gain and an OR = 0.8 (95% CI 0.4 to 1.6) for major weight loss, while men had an OR = 0.9 (95% CI 0.5 to 1.6) for major weight gain and an OR = 1.0 (95% CI 0.6 to 1.7) for major weight loss. These data suggest that alcohol intake does not increase the risk of obesity.
The thermogenic response induced by ethanol ingestion in humans has not been extensively studied. This study was designed to determine the thermic effect of ethanol added to a normal diet in healthy nonalcoholic subjects, using indirect calorimetry measurements over a 24-h period in a respiration chamber. The thermic effect of ethanol was also measured when ethanol was ingested in the fasting state, using a ventilated hood system during a 5-h period. Six subjects ingested 95.6 +/- 1.8 (SE) g ethanol in 1 day partitioned over three meals; there was a 5.5 +/- 1.2% increase in 24-h energy expenditure compared with a control day in which all conditions were identical except that no ethanol was consumed. The calculated ethanol-induced thermogenesis (EIT) was 22.5 +/- 4.7% of the ethanol energy ingested. Ingestion of 31.9 +/- 0.6 g ethanol in the fasting state led to a 7.4 +/- 0.6% increase in energy expenditure over baseline values, and the calculated EIT was 17.1 +/- 2.2%. It is concluded that in healthy nonalcoholic adults ethanol elicits a thermogenic response equal to approximately 20% of the ethanol energy. Thus the concept of the apparently inefficient utilization of ethanol energy is supported by these results which show that only approximately 80% of the ethanol energy is used as metabolizable energy for biochemical processes in healthy nonalcoholic moderate ethanol consumers.
We examined the association of fat distribution with a number of personality attributes and behaviours in a sample of 5115 young blacks and whites. Body fat distribution, measured by the ratio of waist-to-hip circumferences (WHR), was significantly and positively associated with cigarette smoking and negatively associated with education in all of the race and sex groups. WHR was positively associated with alcohol consumption in men and black women and with marijuana use in women. A number of psychosocial factors assessing personality attributes and behaviours were also examined, including the Cook-Medley hostility score, type A/B behaviour pattern, life events, social support, financial situation, and diagnosis of a nervous, emotional or mental disorder. In age- and BMI-adjusted analyses, only the Cook-Medley hostility score and a financial situation score were significantly and positively associated with WHR in all race and sex groups. In multivariate linear regression, these psychosocial factors were associated with WHR in some of the race and sex groups, accounting for less than 1% of the variation in WHR in any one group. These results suggest that fat distribution is weakly associated with these personality attributes and behaviours.
Ethanol-induced perturbations in the energy metabolism and in the catabolism of adenine nucleotides were investigated by 31P NMR spectroscopy and HPLC analyses in perfused rat liver. Ethanol oxidation reduced the redox potential of the hepatocyte, leading to an intracellular accumulation of sn-glycerol 3-phosphate. This accumulation, in turn, led to a cytosolic P(i) depletion with stoichiometric relationship close to 1/1 for an initial period of 2 min. The concentration of nucleoside 5'-triphosphates (83 +/- 4% of ATP) was decreased during ethanol oxidation, reaching about 66% of its control value [2.88 +/- 0.02 mumol.(g of liver wet wt)-1] at high ethanol doses (10 and 70 mM). The depletion of P(i) relieved the inhibition exerted by this compound on AMP deaminase, key enzyme in the catabolism of adenine nucleotides. The degradation of AMP was monitored by HPLC analyses of the adenine nucleosides and bases released in the effluents. Integration over time of the total release of these metabolites accounted for the depletion of ATP recorded in the same time by 31P NMR spectroscopy. This result suggests that ATP depletion occurring during ethanol oxidation originated from an enhanced degradation of adenine nucleotides. There was a strong linear correlation (r2 = 0.92) between cytosolic P(i) level and allantoin release rate during ethanol perfusion. Cytosolic P(i) and allantoin release exhibited biphasic behavior, the recovery toward the initial levels being related to the release of P(i) in the cytoplasm during the complete catabolism of adenine nucleotides. Finally, the depletion of P(i) affected the glycogenolysis pathway, with a maximal inhibition of ca. 19% of the initial level.
Six subjects participated in a residential study assessing the effects of consuming beverages containing energy derived from ethanol or dextrose on total energy and macronutrient intake. On certain days, subjects had to consume four beverages containing a total of approximately 2400 or 4600 kJ, equivalent to 22% and 42% of energy intake under conditions in which no-beverages were required. Each of four conditions (2400 kJ ethanol, dextrose; 4600 kJ ethanol, dextrose), and a no-beverage control condition was examined for 2 days. Subjects compensated for approximately 37% of the energy contained in the beverages such that total intake increased by 13% under the 2400 kJ conditions and 27% under the 4600 kJ conditions. There was no differential effect of ethanol content on energy intake. Cumulative intake curves indicated that caloric compensation was minimal following the consumption of beverages in the evening. While all of the beverage conditions significantly decreased energy intake derived from carbohydrate, the proportion of energy derived from fat, carbohydrate, and protein without the energy content of the beverages was essentially unaffected by dextrose- or ethanol-containing beverages. These results suggest that the effects of ethanol on intake of other foods can be accounted for by the energy content of ethanol as a beverage and by ethanol consumption in the evening when there is little time for daily caloric compensation, rather than by the pharmacological effects of ethanol.
We investigated the effects of an equal-energetic substitution of ethanol for dietary carbohydrate in high-and low-fat diets on energy expenditure and body composition. During the controlled feeding study, subjects maintained their weights and consumed only food and drink provided by the US Department of Agriculture Beltsville Human Nutrition Research Center's Diet Study Facility. Subjects (16 men and 32 women) were divided equally into two groups and consumed either a high-or low-fat diet for 16 wk. The feeding period was divided into two 8-wk periods during which either ethanol or carbohydrate was added to the diet (5% of total daily energy intake) in a crossover design. The metabolizable energy content of the diets (with supplements) was determined for all subjects through measurement of total food intake and fecal and urinary losses for 7 d during both 8-wk periods. Energy expenditure, measured for 24 h in a room calorimeter at the end of each 8-wk period, was the same for both periods. Metabolizable energy intake and changes in total-body energy content were used to calculate the total amount of energy expended by each subject for 7 wk during each 8-wk period. Total energy expenditure for 7 wk was the same when subjects consumed either ethanol or carbohydrate. These data clearly show that on an energy basis ethanol and carbohydrate are utilized in the diet with the same efficiency. These data are consistent with the efficiency of use of alcohol for maintenance of metabolizable energy being the same as that for carbohydrate.
The study was carried out to determine associations of reported alcohol intake with diet and body mass index. Type and frequency of consumed alcohol were also considered.
A cross-sectional study.
The baseline examination of the participants of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in 1985-1988.
27215 middle-aged Finnish male smokers.
The diet was assessed by a self-administered food use questionnaire: Subject's habitual diet and alcohol intake over the previous 12 months were asked. Body mass index was used as the measure of adiposity.
Energy intake from food was not related to alcohol intake. Although alcohol consumption was associated with food selection (eg berry and coffee consumption), this only slightly influenced daily nutrient intakes. Intake of spirits was more consistently related to higher body mass index than that of other alcoholic beverages. Daily alcohol intake had a much smaller association with body mass index than less frequent use, independently of the total consumption.
The differences in nutrient intake between abstainers, light and moderate alcohol consumers were small although the consumption of many foods varied with alcohol consumption. Even if alcohol consumption is one noteworthy factor associated with weight, the energy from alcohol increases body weight less than expected; both the type and frequency of consumed alcohol may explain why energy from alcohol is utilized less efficiently than non-alcoholic energy.
Dietary compensation for energy provided as ethanol is reportedly limited. Whether this is a function of the ethanol or other aspect of the medium in which it is ingested is not known. Eight male and eight female adults ingested 1.08 liters of beer (5.0% ethanol w/v, 1891kJ), light beer (2.9% ethanol w/v, 1197kJ), no-alcohol beer (0.1% ethanol w/v, 816kJ), cola (1749kJ) or carbonated water (0kJ) every 3-4 days with a midday meal. Diet records were kept the preceding day and day of beverage ingestion. Energy intake was significantly higher each day an energy-bearing beverage was consumed relative to its preceding day. A literature review revealed dietary compensation for modifications of energy intake via fluids is less precise than when solid foods are manipulated. These findings demonstrate dietary adjustment for energy derived from ethanol is imprecise, but also indicate energy from carbohydrate elicits little dietary response when ingested in a beverage.
The relationship between alcohol intake and obesity remains uncertain. Evidence suggesting that alcohol-derived energy may be unregulated points to an inability to maintain appetite, energy balance and, hence, body weight when alcohol is introduced to the diet. This study investigated the short-term effects of alcohol on hunger and energy intake in 20 lean women. On 4 occasions, subjects were given a randomised preload drink ('alcohol', 'no alcohol', 'carbohydrate', 'water') followed by visual analogue scales (VAS) rating hunger and an ad lib test meal. There was no difference in hunger ratings (p > 0.05) nor in the amount of energy consumed during the test meal (F = 1.66, p > 0.05) following any of the 4 preloads. Consumption of the 2 high energy preload drinks ('alcohol', 0.91 MJ; 'CHO', 0.72 MJ) did not result in a compensatory decrease in the amount of energy subsequently eaten (ad lib intake: 'alcohol' = 2.62 MJ, 0.32 SEM; 'no alcohol' = 2.98 MJ, 0.28 SEM; 'CHO' = 2.93 MJ, 0.21 SEM; 'water' = 2.82 MJ, 0.25 SEM), suggesting either no physiological recognition or no regulation of energy consumed within a drink in quantities of less than 1 MJ. The addition of either alcoholic or CHO-containing carbonated beverages into the diet will result, in the short-term, to an overall increase in energy intake.
Control of energy intake, either in response to changes in the energy content of food or in energy expenditures and storage, is based on the detection of a feedback signal generated in the processing of metabolic fuels for energy. Evidence from studies of the fructose analogue, 2,5-AM, indicates a sensor in liver responds to changes in intracellular ATP or some closely associated event and communicates this information to the brain via vagal afferent neurons. Such a mechanism could serve as the energy sensor which controls energy intake.