Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic

Yung, Lillian; Gordis, Enoch; Holt, James

doi:10.1016/0376-8716(83)90007-8

Cited by 74 publications

(30 citation statements)

References 16 publications

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“…Men add alcohol to the daily ingestion of calories, while women have a tendency to use alcohol as a substitute to other energy sources [30,59], such as reducing the consumption of carbohydrates [16,18] without an increase of the total calorie ingestion. These differences must be included when considering the energetic balance, as they may generate different results regarding bodyweight.…”

Section: Could Alcohol Be a Risk Factor For Obesity?mentioning

confidence: 99%

Alcohol: Effects on Nutritional Status, Lipid Profile and Blood Pressure

Toffolo

2012

J Endocrinol Metab

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Alcohol consumption can be the cause of several diseases. Depending on the frequency and quantity, the consumption of alcohol may increase the risk of malnutrition, weight-gain, obesity and cardiovascular diseases. The aim of this study was to review the influence of alcohol intake on nutritional status, lipid profile and blood pressure. The review shows that the additional consumption of ethanol calories will favor weight gain and metabolic changes and may engrave the risk of cardiovascular diseases, altering the lipid profile and promoting hypertension. Recommending a moderate use of alcohol with the purpose of taking advantage of its health benefits must not be done.

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Section: Could Alcohol Be a Risk Factor For Obesity?mentioning

confidence: 99%

Alcohol: Effects on Nutritional Status, Lipid Profile and Blood Pressure

Toffolo

2012

J Endocrinol Metab

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“…In animal studies, rats maintained on a high-fat diet or exhibiting a preference for fat are found to consume more ethanol (Carrillo et al, 2004;Krahn and Gosnell, 1991;Pekkanen et al, 1978). Also, clinical studies show that fat intake is elevated in ethanol drinkers, with bingeing on fat-rich foods associated with high rates of alcoholism (Herbeth et al, 1988;Swinburn et al, 1998), and drinkers maintained on a fat-rich diet compared with a carbohydrate-rich diet exhibit shorter periods of ethanol abstinence (Forsander, 1998;Yung et al, 1983). A direct and possibly causal relationship between dietary fat and ethanol intake is demonstrated by the finding that a high-fat meal, compared with a low-fat/high-carbohydrate meal, can significantly increase ethanol intake right after the meal (Carrillo et al, 2004).…”

Section: Role Of Pvn Peptides In the Relationship Between Fat And Ethmentioning

confidence: 99%

Effect of Ethanol on Hypothalamic Opioid Peptides, Enkephalin, and Dynorphin: Relationship With Circulating Triglycerides

Chang

Karatayev

Ahsan

et al. 2007

Alcoholism Clin & Exp Res

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Background: Recent evidence has demonstrated that ethanol intake can stimulate the expression and production of the feeding-stimulatory peptide, galanin (GAL), in the hypothalamic paraventricular nucleus (PVN), and that PVN injection of this peptide, in turn, can increase the consumption of ethanol. To test the hypothesis that other feeding-related systems are involved in ethanol intake, this study examined the effect of ethanol on the hypothalamic opioid peptides, enkephalin (ENK), and dynorphin (DYN).Method: Adult, male Sprague-Dawley rats were trained to voluntarily drink increasing concentrations of ethanol, up to 9% v/v, on a 12-hour access schedule or were given a single injection of ethanol (10% v/v) versus saline vehicle. The effect of ethanol on GAL, ENK, and DYN mRNA was measured using real-time quantitative polymerase chain reaction and radiolabeled in situ hybridization, while radioimmunoassay was used to measure peptide levels. In addition to blood alcohol, circulating levels of triglycerides (TG), leptin, and insulin were also measured.Results: The data demonstrated that: (1) rats voluntarily drinking 9% v/v ethanol (approximately 2.0 g/kg/d) show a significant increase in GAL, ENK, and DYN mRNA in the PVN compared with water-drinking rats; (2) voluntary consumption of ethanol also increases peptide levels of ENK and DYN in the PVN; (3) acute injection of 10% ethanol (1.0 g/kg of 10% v/v) similarly increases the expression of GAL, ENK, and DYN in the PVN; and (4) ethanol consumption and injection, while having little effect on leptin and insulin, consistently increase circulating levels of TG as well as alcohol, both of which are strongly, positively correlated with peptide expression in the PVN.Conclusions: These findings, together with published studies, suggest a possible role for hypothalamic opioid peptides in the drinking of ethanol. Based on evidence that dietary fat and lipid injections stimulate the PVN peptides and injection of the opiates and GAL increase ethanol intake, it is proposed that both TG and alcohol in the circulation, which are elevated by the ingestion or injection of ethanol, are involved in stimulating these peptides in the PVN, which in turn promote further consumption of ethanol.

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“…Direct positive correlations between alcohol and sweetener consumption are also observed in randomly bred rats (Kampov-Polevoy et al 1990), inbred mice (Belknap et al 1993) and the F 2 progeny of ethanol-preferring and -avoiding lines/strains (Bachmanov et al 1996;Overstreet et al 1993). Further, human alcoholics prefer more highly concentrated sucrose solutions than nonalcoholic control subjects (Kampov-Polevoy et al 1997), and abstinent alcoholics may substitute ingestion of sweets for alcohol (Yung et al 1983).…”

Section: Introductionmentioning

confidence: 96%

Alcohol Activates a Sucrose-Responsive Gustatory Neural Pathway

Lemon

Brasser

Smith

2004

Journal of Neurophysiology

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Lemon, Christian H., Susan M. Brasser, David V. Smith. Alcohol activates a sucrose-responsive gustatory neural pathway. J Neurophysiol 92: 536 -544, 2004. First published February 25, 2004 10.1152/jn.00097.2004. A strong positive association exists between the ingestion of alcohol and sweet-tasting solutions. The neural mechanisms underlying this relationship are unknown, although recent data suggest that gustatory substrates are involved. Here, we examined the role of sweet taste receptors and central neural circuits for sugar taste in the gustatory processing of ethanol. Taste responses to ethanol (3, 5, 10, 15, 25, and 40% vol/vol) and stimuli of different taste qualities (e.g., sucrose, NaCl, HCl, and quinine-HCl) were recorded from neurons of the nucleus of the solitary tract in anesthetized rats prior to and after oral application of the sweet receptor blocker gurmarin. The magnitude of ethanol-evoked activity was compared between sucroseresponsive (n ϭ 21) and sucrose-unresponsive (n ϭ 20) neurons and the central neural representation of ethanol taste was explored using multivariate analysis. Ethanol produced robust concentration-dependent responses in sucrose-responsive neurons that were dramatically larger than those in sucrose-unresponsive cells. Gurmarin selectively and similarly inhibited ethanol and sucrose responses, leaving NaCl, HCl, and quinine responses unaltered. Across-neuron patterns of response to ethanol were most similar to those evoked by sucrose, becoming increasingly more so as the ethanol concentration was raised. Results implicate taste receptors for sucrose as candidate receptors for ethanol and reveal that alcohol and sugar taste are represented similarly by gustatory activity in the CNS. These findings have important implications for the sensory and reward properties of alcohol.

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Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic

Cited by 74 publications

References 16 publications

Alcohol: Effects on Nutritional Status, Lipid Profile and Blood Pressure

Alcohol: Effects on Nutritional Status, Lipid Profile and Blood Pressure

Effect of Ethanol on Hypothalamic Opioid Peptides, Enkephalin, and Dynorphin: Relationship With Circulating Triglycerides

Alcohol Activates a Sucrose-Responsive Gustatory Neural Pathway

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