Body Mass Index and Alcohol Consumption: Family History of Alcoholism as a Moderator

Department of Psychology, Yale University, New Haven, CT 06520-8205, USA.
Psychology of Addictive Behaviors (Impact Factor: 2.09). 07/2009; 23(2):216-25. DOI: 10.1037/a0015011
Source: PubMed


Recent research suggests that excess food consumption may be conceptualized as an addictive behavior. Much of the evidence comes from neurobiological similarities between drug and food consumption. In addition, an inverse relation between alcohol consumption and body mass index (BMI) has been observed. Previous research has hypothesized that this inverse relation is attributable to competition between food and alcohol for similar neurotransmitter receptors. The current study explored this neurobiological hypothesis further by examining the influence of an indicator of biological risk associated with alcohol problems (family history of alcoholism) on the relationship between alcohol and food intake. Data from 37,259 participants in the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were included in the study. BMI, family history of alcoholism, gender, and race/ethnicity were assessed as predictors of typical drinking frequency and estimated blood alcohol concentration (BAC). An inverse relationship between alcohol consumption and BMI was demonstrated. An attenuation of family history effects on drinking behavior was evident for obese compared to nonobese participants. The results suggest a neurobiological link between alcohol use and food consumption, consistent with theories characterizing excess food consumption as an addictive behavior.

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    • "A smaller Akaike's Information Criterion (AIC) indicates a better fit to the data (Heath et al., 1989; Neale and Maes, 1992; Rijsdijk and Sham, 2002). We first ran the ACE and ADE models without adjustment, and then we adjusted for body mass index (BMI) as BMI was a biology-meaningful potential confounder (Elks et al., 2012; Gearhardt and Corbin, 2009; Heath and Martin, 1994). We conducted 2 sensitivity analyses by reclassification of twins who answered " less often " into those who answered " absence " in response to questions " How often do you have an intoxication/ hangover? "
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    ABSTRACT: Background Alcohol consumption is influenced by heritable factors. The genetic influence on usual high-density drinking, including alcohol intoxication and hangover, is unknown. We aim to estimate the heritability of usual high-density drinking.MethodsA total of 13,511 male twins in this cross-sectional study were included from the National Academy of Sciences-National Research Council (NAS-NRC) Twin Registry. Data on the frequency of alcohol intoxication and alcohol hangover over the past year, that is, usual high-density drinking (phenotypes), were collected through a self-administered questionnaire when twins were middle-aged in 1972. Structural equation modeling was used to estimate the variance components of phenotypes.ResultsThe mean of the frequency of usual high-density drinking in the entire twin population was 0.16 times per month for intoxication and 0.18 times per month for hangover. The heritability of usual alcohol intoxication was 50.7% (95% confidence interval [CI] 46.2 to 55.0) before and 49.9% (95% CI 45.3 to 54.2) after the body mass index (BMI) adjustment. The heritability of usual hangover was 55.4% (95% CI 51.2 to 58.6) before and 54.8% (95% CI 50.6 to 58.8) after adjustment for BMI. Unshared environmental factors between co-twins explained the remaining variance in alcohol intoxication and in hangover.Conclusions Both genetic and unshared environmental factors have important influences on usual alcohol intoxication and hangover. These findings are important in understanding the occurrence of and developing interventions for usual high-density drinking.
    Alcoholism Clinical and Experimental Research 08/2014; 38(8). DOI:10.1111/acer.12487 · 3.21 Impact Factor
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    • "bei BN und BES; Calero-Elvira et al., 2009; Gadalla & Piran, 2007; O'Brien, K. M. & Vincent, 2003). Andererseits wurde eine inverse Beziehung zwischen der Höhe des BMI und Alkoholkonsum gezeigt (Gearhardt & Corbin, 2009; Kleiner et al., 2004). Da die Yale Food Addiction Scale-Werte sowohl mit dem selbstberichteten BMI als auch mit erhöhter Esspathologie positiv korrelierten, könnten sich diese Zusammenhänge gegenseitig aufheben. "
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    ABSTRACT: Excessive food consumption is often described as an addictive behavior. Nevertheless, to date in the German literature, there is a lack of instruments specifically assessing the construct of food addiction. For this reason, we translated and validated the Yale Food Addiction Scale (YFAS, Gearhardt, Corbin, & Brownell, 2009). This scale identifies people with distinctive symptoms indicative of addiction to certain foods. Psychometric properties were tested in a sample comprising predominantly university students (N = 752). The one-factorial structure of the YFAS could be replicated and an adequate internal consistency was achieved. Convergent validity revealed medium-to-high correlations with other measures of problematic eating behavior. Discriminant validity was shown for distinct but related constructs, such as alcohol addiction and impulsivity. Furthermore, the YFAS proved to be a significant predictor of binge eating episodes. The YFAS appears to be a useful tool for the assessment of eating behaviors that have an addiction-like character.
    Diagnostica 07/2012; 58(3):115-126. DOI:10.1026/0012-1924/a000047 · 0.72 Impact Factor
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    ABSTRACT: In this thesis several aspects of metabolic syndrome are addressed. The focus involves questions concerning the genetics of obesity, TG and cholesterol and hyperglycemia. Since we hypothesized that obesity is the most important trigger of metabolic impairment, the MetS definition in this thesis was chosen to include the obesity measure waist circumference as an essential component. In the study described in chapter 2, the heritability of the metabolic syndrome was addressed and compared to the heritability of its individual components. Since the individual components of MetS were shown to be more heritable than MetS itself, the studies described in chapter 3 and 4 focused on the genetics of the individual MetS component plasma TG. For this purpose, a candidate gene approach was employed using HTG patients and healthy controls. The involvement of a series of candidate genes was confirmed. The study described in chapter 5 followed a similar approach to that used in the studies described in chapter 3 and 4. Several candidate genes were studied in patients suffering from hyperlipoproteinemia (HLP) type III, which is characterized by elevated levels of total plasma cholesterol and plasma TG. HLP type III is characterized by APOE2 homozygosity. Contributing genetic factors in the (metabolically stressed) APOE2/2 environment were confirmed. Plasma adiponectin, an adipose tissue secreted hormone (adipokine), has been suggested to be a biomarker for MetS. In chapter 6 we describe a study which particularly aimed to determine the effect of menopause on the discriminating accuracy of adiponectin to predict MetS. Especially low levels of plasma adiponectin in postmenopausal women were found to be a risk for MetS. However, the discriminating accuracy of adiponectin for the presence of MetS was exceeded by BMI in men and pre –and post menopausal women. Since plasma adiponectin levels are very well correlated with MetS components or related traits, the study described in chapter 7 addressed the question whether these correlations are caused by a genetic overlap (genetic correlation). The genetic correlation was mono-laterally validated with regard to the adiponectin gene (ADIPOQ). Chapter 8 describes a study towards finding novel loci associated with adiponectin or loci that are possibly involved in the genetic overlap between adiponectin and MetS components or related traits. This study followed a genome-wide association (GWA) approach. The results of this GWA were used in a joined analysis with two other cohorts in a meta-analysis. In addition, a selected proportion of SNPs was submitted for replication in several cohorts. Chapter 9 provides a general discussion by reviewing all previous chapters in the thesis. Furthermore, chapter 9 includes suggestions and proposals for future analyses towards unraveling genetic and environmental factors involved in the expression and manifestation of metabolic risk factors.
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