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Hedonic eating differentiates from homeostatic eating on two main aspects: the first one is that eating occurs when there is no need for calorie ingestion and the second one is that the food is consumed exclusively for its gustatory and rewarding properties. Gastroeneteric hormones such as ghrelin, colecystokinin-33 (CCK) and peptide YY3-36 (PYY3-36) are known to play a pivotal role in the homeostatic control of food intake. To the contrary, their role in hedonic eating has been never investigated. Here we report peripheral responses of CCK, PYY3-36 and ghrelin to the consumption of food for pleasure in well-nourished satiated healthy subjects. Plasma levels of CCK, PYY3-36 and ghrelin were measured in 7 satiated healthy subjects before and after ad libitum consumption of both a highly pleasurable food (hedonic eating) and an isoenergetic non-pleasurable food (non-hedonic eating). The consumption of food for pleasure was associated to a significantly increased production of the hunger hormone ghrelin and a significantly decreased secretion of the satiety hormone CCK. No significant changes in plasma PYY3-36 levels occurred in the two eating conditions. These preliminary data demonstrate that in hedonic eating the peripheral hunger signal represented by ghrelin secretion is enhanced while the satiety signal of CCK production is decreased. This could be responsible for the persistence of peripheral cues allowing a continued eating as well as for the activation of endogenous reward mechanisms, which can drive food consumption in spite of no energy need, only for reward., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Animal studies suggest that the gut-brain peptide ghrelin plays an important role in the neurobiology of alcohol dependence (AD). Human studies show an effect of alcohol on ghrelin levels and a correlation between ghrelin levels and alcohol craving in alcoholics. This investigation consisted of two studies. Study 1 was a 12-week study with alcohol-dependent subjects, where plasma ghrelin determinations were assessed four times (T0-T3) and related to alcohol intake and craving [Penn Alcohol Craving Score (PACS) and Obsessive Compulsive Drinking Scale (OCDS)]. Serum growth hormone levels and assessment of the nutritional/metabolic status were also performed. Study 2 was a pilot case-control study to assess ghrelin gene polymorphisms (Arg51Gln and Leu72Met) in alcohol-dependent individuals. Study 1 showed no significant differences in ghrelin levels in the whole sample, while there was a statistical difference for ghrelin between non-abstinent and abstinent subjects. Baseline ghrelin levels were significantly and positively correlated with the PACS score at T1 and with all craving scores both at T2 and T3 (PACS, OCDS, obsessive and compulsive OCDS subscores). In Study 2, although there was a higher frequency of the Leu72Met ghrelin gene polymorphism in alcohol-dependent individuals, the distribution between healthy controls and alcohol dependent individuals was not statistically significant. This investigation suggests that ghrelin is potentially able to affect alcohol-seeking behaviors, such as alcohol drinking and craving, representing a new potential neuropharmacological target for AD., (© 2011 The Authors, Addiction Biology © 2011 Society for the Study of Addiction.)

Several candidate genes have been associated with antipsychotic-induced body weight (BW) gain. Because the endocannabinoid system is deeply involved in BW regulation, endocannabinoid genes may have a role in the antipsychotic-induced weight gain. Therefore, we investigated the 1359 G/A (rs1049353) single nucleotide polymorphisms (SNP) of the cannabinoid receptor 1 (CNR1) gene, which codes the endocannabinoid CB1 receptor, and the complementary DNA (cDNA) 385C/A (rs324420) SNP of the FAAH gene, which codes the endocannabinoid degrading enzyme, for their role in BW changes induced by antipsychotic drugs. Eighty-three white psychotic patients who underwent a naturalistic treatment with different antipsychotics (clozapine, olanzapine, risperidone, quetiapine, and haloperidol) and completed a 24-week treatment period were included into the study together with 80 age- and sex-matched white healthy controls. At the 24th week of treatment, 41 patients gained more than 7% of their baseline BW. No significant differences between patients and controls emerged in genotype and allele frequencies of both SNPs. Genotype and allele frequencies of the FAAH cDNA 385C/A SNP but not of the CNR1 1359 G/A SNP significantly differed between subjects who gained more than 7% of BW and those who did not, with both AC and AA genotypes and the A allele being significantly more frequent in patients who gained more than 7% of their baseline BW. Present findings, although obtained in a small population and in a naturalistic setting, suggest that the cDNA 385C/A SNP of the FAAH gene may predispose subjects to get a clinically meaningful weight gain after antipsychotic exposure.

Experimental data suggest that the endogenous cannabinoid system is involved in mood regulation, but no study has been performed so far to investigate the role of endocannabinoid genes in the susceptibility to major depression (MD) and/or bipolar disorder (BD). We assessed the CB1 receptor gene (CNR1) single nucleotide polymorphism (SNP) rs1049353 (1359 G/A) and the fatty acid amide hydrolase (FAAH) gene rs324420 SNP (cDNA 385C to A) for their associations with MD and/or BD in 83 Caucasian patients with recurrent MD, 134 Caucasian individuals with BD, and 117 Caucasian healthy subjects. The distribution of the CNR1 1359 G/A genotypes and alleles significantly differed among the groups (chi(2)=12.595; df=4, P=0.01 for genotypes; chi(2)=13.773; df=2, P=0.001 for alleles) with MD patients showing a higher frequency of both AG, GG genotypes and A allele as compared to healthy controls. The distribution of the FAAH cDNA 385C to A genotypes, according to the CC dominant model (AA+AC vs. CC), significantly differed among the groups (chi(2)=6.626; df=2, P=0.04), with both BD patients and MD patients showing a non-significant slightly higher frequency of the AC genotype. These findings, although preliminary, suggest that the CNR1 1359 G/A and the FAAH cDNA 385C to A gene variants may contribute to the susceptibility to mood disorders., ((c) 2010 Elsevier Ltd. All rights reserved.)

Endocannabinoids are involved in the modulation of eating behavior; hence, alterations of this system may play a role in obesity. Recently, a single nucleotide polymorphism (cDNA 385C to A) of the gene coding for fatty acid amide hydrolase (FAAH), the major degrading enzyme of endocannabinoids, has been found to be associated with obesity. However, the possibility that the FAAH gene cDNA 385C to A single nucleotide polymorphism (SNP) is associated to binge eating disorder (BED), a condition that frequently occurs in obese individuals, has not been investigated. In order to address this issue, we assessed the distribution of the cDNA 385C to A SNP in 115 overweight/obese subjects with BED, 74 non-BED patients with obesity and 110 normal weight healthy controls. As compared to healthy controls, the whole group of overweight/obese BED and non-BED patients had a significantly higher frequency of the CA genotype and the A allele of the FAAH gene cDNA 385C to A SNP. Moreover, the SNP resulted significantly correlated to the presence of overweight/obesity (F(2, 296)=3.58, P=0.02), but not to the occurrence of BED (F(2, 296)=0.98; P=0.3). The present study confirms previously published significant over-representations of the FAAH 385 A allele in overweight/obese subjects and presents new data in BED patients that the 385 mutation is not significantly associated with BED-related obesity.

Loss of circadian patterning of metabolism-related functions seems to play a role in the pathogenesis of obesity; therefore, it is reasonable to hypothesize that the functional 3111T/C single nucleotide polymorphism (SNP) of the (Circadian locomotor output cycles kaput) CLOCK gene may have a part in the genetic susceptibility to obesity. The aim of this study was to assess the frequencies of 3111T/C CLOCK gene SNP in overweight/obese subjects with or without binge eating disorder (BED) as compared to normal weight healthy controls. A total of 284 Caucasian subjects, including 92 normal weight healthy subjects and 192 overweight/obese patients (107 with BED) participated into the study. Genotype and allele frequencies did not significantly differ between normal weight controls and overweight/obese patients with and/or without BED. However, overweight/obese patients carrying the CC genotype had significantly higher values of body mass index (BMI) as compared to those carrying the CT and/or TT genotypes. Moreover, obese class III individuals had a significantly higher frequency of both the CC genotype and the C allele as compared to individuals with BMI<40 kg/m(2). Present findings show for the first time that the 3111T/C SNP of the CLOCK gene is not associated to human obesity and/or BED, but it seems to predispose obese individuals to a higher BMI.

The brain-derived neurotrophic factor (BDNF) is involved not only in promoting neuronal outgrowth and differentiation, synaptic connectivity and neuronal repair, but also in modulating eating behavior. Since genetic factors likely contribute to the biological vulnerability to bulimia nervosa (BN) and binge eating disorder (BED), we investigated whether the functional 196G/A single nucleotide polymorphism (SNP) of the BDNF gene was associated to BN and/or BED or to some phenotypic aspects of the disordered eating. Two hundred and ten Caucasian women (126 with BN, 84 with BED and 121 healthy controls) participated into the study. No significant differences were found in the frequencies of the 196G/A variants of the BDNF gene among patients with BN or BED and healthy controls. In both BN and BED groups, subjects carrying the 196A/A genotype exhibited a weekly frequency of bingeing and a severity of binge eating (as assessed by the Bulimia Investigation Test Edinburgh) significantly higher than those with the 196A/G and 196G/G genotypes. These results suggest that the 196G/A SNP of the human BDNF gene does not contribute to the genetic susceptibility to BN and BED, but may predispose those patients to a more severe binge eating behavior.