Generic placeholder image

Current Pharmaceutical Design

Author(s): Julianna Brutman, Jon F. Davis and Sunil Sirohi*

DOI: 10.2174/1381612826666200206092231

DownloadDownload PDF Flyer Cite As
Behavioral and Neurobiological Consequences of Hedonic Feeding on Alcohol Drinking

Page: [2309 - 2315] Pages: 7

  • * (Excluding Mailing and Handling)

Explore Articles
About Journal
For Authors
For Editors
For Reviewers

Abstract

A complex interplay of peripheral and central signaling mechanisms within the body of an organism maintains energy homeostasis. In addition, energy/food intake is modified by various external factors (e.g., palatability, food availability, social and environmental triggers). Highly palatable foods can provoke maladaptive feeding behavior, which in turn disrupts normal homeostatic regulation resulting in numerous health consequences. Furthermore, neuroendocrine peptides, traditionally considered to regulate appetite and energy homeostasis, also control the intake and reinforcing properties of alcohol and drugs of abuse. Therefore, dysregulated eating as a result of a hedonic/binge-like intake of hyper-palatable food may impact alcohol drinking behavior. Relevant in this case is the fact that eating disorders are highly comorbid with several neuropsychiatric conditions, including alcohol use disorder. The present review is intended to summarize the neurobiological and functional consequences of hedonic feeding on alcohol intake.

Keywords: High-fat diet, alcohol, nutritional contingency, palatable diet, alcohol use disorder, homeostatic, neuroendocrine.

[1]
Abdalla MMI. Central and peripheral control of food intake. Endocr Regul 2017; 51(1): 52-70.
[http://dx.doi.org/10.1515/enr-2017-0006]
[2]
Tracy AL, Hazeltine G, Wee CJM, Benoit SC. Regulation of Energy Intake in Humans MDTextcom, Inc 2013.
[3]
Jodhun BM, Pem D, Jeewon R. A systematic review of factors affecting energy intake of adolescent girls 2016; 16: 910-22.
[4]
Ziauddeen H, Alonso-Alonso M, Hill JO, Kelley M, Khan NA. Obesity and the neurocognitive basis of food reward and the control of intake. Adv Nutr 2015; 6: 474-86.
[http://dx.doi.org/10.3945/an.115.008268]
[5]
McCrickerd K, Forde CG. Sensory influences on food intake control: moving beyond palatability. Obes Rev 2016; 17: 18-29.
[http://dx.doi.org/10.1111/obr.12340]
[6]
Sinha R. Role of addiction and stress neurobiology on food intake and obesity. Biol Psychol 2018; 131: 5-13.
[http://dx.doi.org/10.1016/j.biopsycho.2017.05.001]
[7]
Yeomans MR. Taste, palatability and the control of appetite. Proc Nutr Soc 1998; 57: 609-15.
[http://dx.doi.org/10.1079/PNS19980089]
[8]
Johnson F, Wardle J. Variety, palatability, and obesity. Adv Nutr 2014; 5: 851-9.
[9]
Yeomans MR, Blundell JE, Leshem M. Palatability: response to nutritional need or need-free stimulation of appetite? Br J Nutr 2004; 92(Suppl. 1): S3-S14.
[http://dx.doi.org/10.1079/BJN20041134]
[10]
Davis JF, Melhorn SJ, Shurdak JD, et al. Comparison of hydrogenated vegetable shortening and nutritionally complete high-fat diet on limited access-binge behavior in rats. Physiol Behav 2007; 92: 924.
[http://dx.doi.org/10.1016/j.physbeh.2007.06.024]
[11]
Hudson JI, Hiripi E, Pope HG Jr, Kessler RC. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol Psychiatry 2007; 61: 348-58.
[http://dx.doi.org/10.1016/j.biopsych.2006.03.040]
[12]
Guerdjikova AI, Mori N, Casuto LS, McElroy SL. Update on binge eating disorder. Med Clin North Am 2019; 103: 669-80.
[13]
Bahji A, Mazhar MN, Hudson CC, Nadkarni P, MacNeil BA, Hawken E. Prevalence of substance use disorder comorbidity among individuals with eating disorders: A systematic review and meta-analysis. Psychiatry Res 2019; 273: 58-66.
[http://dx.doi.org/10.1016/j.psychres.2019.01.007]
[14]
McDonald CE, Rossell SL, Phillipou A. The comorbidity of eating disorders in bipolar disorder and associated clinical correlates characterised by emotion dysregulation and impulsivity: A systematic review. J Affect Disord 2019; 259: 228-43.
[http://dx.doi.org/10.1016/j.jad.2019.08.070] [PMID: 31446385]
[15]
Miyawaki D, Goto A, Harada T, et al. High prevalence of shoplifting in patients with eating disorders. Eat Weight Disord 2018; 23: 761-8.
[http://dx.doi.org/10.1007/s40519-018-0575-1]
[16]
Udo T, Grilo CM. Psychiatric and medical correlates of DSM-5 eating disorders in a nationally representative sample of adults in the United States. Int J Eat Disord 2019; 52: 42-50.
[http://dx.doi.org/10.1002/eat.23004]
[17]
Holderness CC, Brooks-Gunn J, Warren MP. Co-morbidity of eating disorders and substance abuse review of the literature. Int J Eat Disord 1994; 16: 1-34.
[http://dx.doi.org/10.1002/1098-108X(199407)16:1<1:AID-EAT2260160102>3.0.CO;2-T]
[18]
Ferriter C, Ray LA. Binge eating and binge drinking: an integrative review. Eat Behav 2011; 12: 99-107.
[http://dx.doi.org/10.1016/j.eatbeh.2011.01.001]
[19]
Volkow ND, Wang GJ, Fowler JS, Tomasi D, Baler R. Food and drug reward: overlapping circuits in human obesity and addiction. Curr Top Behav Neurosci 2012; 11: 1-24.
[20]
Blum K, Thanos PK, Wang G-J, et al. The Food and Drug Addiction Epidemic: Targeting Dopamine Homeostasis. Curr Pharm Des 2018; 23(39): 6050-61.
[http://dx.doi.org/10.2174/1381612823666170823101713] [PMID: 28831923]
[21]
Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like behavior. J Nutr 2009; 139: 623-8.
[http://dx.doi.org/10.3945/jn.108.097584]
[22]
Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 2008; 32: 20-39.
[http://dx.doi.org/10.1016/j.neubiorev.2007.04.019]
[23]
Vadnie CA, Park JH, Abdel Gawad N, Ho AMC, Hinton DJ, Choi D-S. Gut-brain peptides in corticostriatal-limbic circuitry and alcohol use disorders. Front Neurosci 2014; 8: 288.
[http://dx.doi.org/10.3389/fnins.2014.00288]
[24]
Jerlhag E, Egecioglu E, Landgren S, et al. Requirement of central ghrelin signaling for alcohol reward. Proc Natl Acad Sci USA 2009; 106: 11318-23.
[http://dx.doi.org/10.1073/pnas.0812809106]
[25]
Hayes MR, Schmidt HD. GLP-1 influences food and drug reward. Curr Opin Behav Sci 2016; 9: 66-70.
[26]
Baker JH, Munn-Chernoff MA, Lichtenstein P, Larsson H, Maes H, Kendler KS. Shared familial risk between bulimic symptoms and alcohol involvement during adolescence. J Abnorm Psychol 2017; 126: 506-18.
[http://dx.doi.org/10.1037/abn0000268]
[27]
Blomquist KK, Masheb RM, White MA, Grilo CM. Parental substance use history of overweight men and women with binge eating disorder is associated with distinct developmental trajectories and comorbid mood disorder. Compr Psychiatry 2011; 52: 693-700.
[http://dx.doi.org/10.1016/j.comppsych.2010.12.007]
[28]
Gorrell S, Walker DC, Anderson DA, Boswell JF. Gender differences in relations between alcohol-related compensatory behavior and eating pathology. Eat Weight Disord 2019; 24: 715-21.
[http://dx.doi.org/10.1007/s40519-018-0545-7]
[29]
Baker JH, Mazzeo SE, Kendler KS. Association between broadly defined bulimia nervosa and drug use disorders: common genetic and environmental influences. Int J Eat Disord 2007; 40: 673-8.
[http://dx.doi.org/10.1002/eat.20472]
[30]
Kaye WH, Lilenfeld LR, Plotnicov K, et al. Bulimia nervosa and substance dependence: association and family transmission. Alcohol Clin Exp Res 1996; 20: 878-81.
[http://dx.doi.org/10.1111/j.1530-0277.1996.tb05266.x]
[31]
Kendler KS, Walters EE, Neale MC, Kessler RC, Heath AC, Eaves LJ. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women. Phobia, generalized anxiety disorder, panic disorder, bulimia, major depression, and alcoholism. Arch Gen Psychiatry 1995; 52: 374-83.
[http://dx.doi.org/10.1001/archpsyc.1995.03950170048007]
[32]
Wiseman CV, Sunday SR, Halligan P, Korn S, Brown C, Halmi KA. Substance dependence and eating disorders: impact of sequence on comorbidity. Compr Psychiatry 1999; 40(5): 332-6.
[http://dx.doi.org/10.1016/S0010-440X(99)90136-0]
[33]
Baker JH, Mitchell KS, Neale MC, Kendler KS. Eating disorder symptomatology and substance use disorders: prevalence and shared risk in a population based twin sample. Int J Eat Disord 2010; 43: 648-58.
[34]
Rolland B, Naassila M, Duffau C, Houchi H, Gierski F, André J. Binge eating, but not other disordered eating symptoms, is a significant contributor of binge drinking severity: findings from a cross-sectional study among french students. Front Psychol 2017; 8: 1878.
[35]
Constant A, Gautier Y, Coquery N, Thibault R, Moirand R, Val-Laillet D. Emotional overeating is common and negatively associated with alcohol use in normal-weight female university students. Appetite 2018; 129: 186-91.
[http://dx.doi.org/10.1016/j.appet.2018.07.012]
[36]
Yung L, Gordis E, Holt J. Dietary choices and likelihood of abstinence among alcoholic patients in an outpatient clinic. Drug Alcohol Depend 1983; 12: 355-62.
[http://dx.doi.org/10.1016/0376-8716(83)90007-8]
[37]
Stickel A, Rohdemann M, Landes T, et al. changes in nutrition-related behaviors in alcohol-dependent patients after outpatient detoxification: the role of chocolate. Subst Use Misuse 2016; 51(5): 545-52.
[http://dx.doi.org/10.3109/10826084.2015.1117107] [PMID: 27050118]
[38]
Anonymous A. Living Sober 2007.
[39]
Tench T, Brown O, Byrd-Bredbenner C, et al. Racial differences in anthropometric measures and dietary intake of college students. J Acad Nutr Diab 2014; 114: A85.
[40]
Carrillo CA, Leibowitz SF, Karatayev O, Hoebel BG. A high-fat meal or injection of lipids stimulates ethanol intake. Acad Nutr Diab 2004; 34: 197-202.
[http://dx.doi.org/10.1016/j.alcohol.2004.08.009]
[41]
Pekkanen L, Eriksson K, Sihvonen ML. Dietarily-induced changes in voluntary ethanol consumption and ethanol metabolism in the rat. Br J Nutr 1978; 40: 103-13.
[http://dx.doi.org/10.1079/BJN19780100]
[42]
Krahn DD, Gosnell BA. Fat-preferring rats consume more alcohol than carbohydrate-preferring rats. Alcohol 1991; 8: 313-6.
[http://dx.doi.org/10.1016/0741-8329(91)90465-9]
[43]
Takase K, Tsuneoka Y, Oda S, Kuroda M, Funato H. High-fat diet feeding alters olfactory-, social-, and reward-related behaviors of mice independent of obesity. Obesity (Silver Spring) 2016; 24: 886-94.
[44]
Prasad A, Abadie JM, Prasad C. Can dietary macronutrient preference profile serve as a predictor of voluntary alcohol consumption? Alcohol 1993; 10: 485-9.
[http://dx.doi.org/10.1016/0741-8329(93)90070-5]
[45]
Gelineau RR, Arruda NL, Hicks JA, Monteiro De Pina I, Hatzidis A, Seggio JA. The behavioral and physiological effects of high-fat diet and alcohol consumption: Sex differences in C57BL6/J mice. Brain Behav 2017; 7: e00708
[46]
DiBattista D, Joachim D. The effect of fat and carbohydrate content of the diet on voluntary ethanol intake in golden hamsters. Alcohol 1999; 18: 153-7.
[http://dx.doi.org/10.1016/S0741-8329(98)00078-0]
[47]
Cook JB, Hendrickson LM, Garwood GM, Toungate KM, Nania CV, Morikawa H. Junk food diet-induced obesity increases D2 receptor autoinhibition in the ventral tegmental area and reduces ethanol drinking. PLoS One 2017; 12: e0183685
[http://dx.doi.org/10.1371/journal.pone.0183685]
[48]
Mirone L. Dietary deficiency in mice in relation to voluntary alcohol consumption. Quarterly J Studies Alcohol 1957; 18: 552-60.
[49]
Sirohi S, Van Cleef A, Davis JF. Binge-like intake of HFD attenuates alcohol intake in rats. Physiol Behav 2017; 178: 187-95.
[http://dx.doi.org/10.1016/j.physbeh.2016.10.006]
[50]
Blanco-Gandía MC, Ledesma JC, Aracil-Fernández A. Navarrete F, Montagud-Romero S, Aguilar MA, et al. The rewarding effects of ethanol are modulated by binge eating of a high-fat diet during adolescence. Neuropharmacology 2017; 121: 219-30.
[http://dx.doi.org/10.1016/j.neuropharm.2017.04.040]
[51]
Pian JP, Criado JR, Walker BM, Ehlers CL. Milk consumption during adolescence decreases alcohol drinking in adulthood. Pharmacol Biochem Behavior 2009; 94: 179-85.
[http://dx.doi.org/10.1016/j.pbb.2009.08.006]
[52]
Tracy AL, Wee CJM, Hazeltine GE, Carter RA. Characterization of attenuated food motivation in high-fat diet-induced obesity: Critical roles for time on diet and reinforcer familiarity. Physiol Behav 2015; 141: 69-77.
[53]
Krishna S, Lin Z, de La Serre CB, et al. Time-dependent behavioral, neurochemical, and metabolic dysregulation in female C57BL/6 mice caused by chronic high-fat diet intake. Physiol Behav 2016; 157: 196-208.
[54]
Sirohi S, Van Cleef A, Davis JF. Intermittent access to a nutritionally complete high-fat diet attenuates alcohol drinking in rats. Pharmacol Biochem Behav 2017; 153: 105-15.
[http://dx.doi.org/10.1016/j.pbb.2016.12.009]
[55]
Villavasso S, Shaw C, Skripnikova E, Shah K, Davis JF, Sirohi S. Nutritional contingency reduces alcohol drinking by altering central neurotransmitter receptor gene expression in rats. Nutrients 2019; 11
[http://dx.doi.org/10.3390/nu11112731]
[56]
Forsander OA, Sinclair JD. Protein, carbohydrate, and ethanol consumption: interactions in AA and ANA rats. Alcohol 1988; 5: 233-8.
[http://dx.doi.org/10.1016/0741-8329(88)90058-4]
[57]
Hanig JP, Yoder P, Krop S, Lao C. Effect of long-term restriction of protein intake, from gestation onward, on free-choice consumption of ethanol by rats. Life Sci 1978; 23: 275-81.
[58]
Avena NM, Carrillo CA, Needham L, Leibowitz SF, Hoebel BG. Sugar-dependent rats show enhanced intake of unsweetened ethanol. Alcohol 2004; 34: 203-9.
[http://dx.doi.org/10.1016/j.alcohol.2004.09.006]
[59]
Meisch RA, Thompson T. Ethanol intake as a function of concentration during food deprivation and satiation. Pharmacol Biochem Behav 1974; 2: 589-96.
[http://dx.doi.org/10.1016/0091-3057(74)90025-2]
[60]
Samson HH, Roehrs TA, Tolliver GA. Ethanol reinforced responding in the rat: a concurrent analysis using sucrose as the alternate choice. Pharmacol Biochem Behav 1982; 17: 333-9.
[http://dx.doi.org/10.1016/0091-3057(82)90088-0]
[61]
Curtis GR, Coudriet JM, Sanzalone L, et al. Short- and long-access palatable food self-administration results in different phenotypes of binge-type eating. Physiol Behav 2019.: 112700
[62]
Carvalho LM, de, Gonçalves JL, et al. High-fat diet withdrawal modifies alcohol preference and transcription of dopaminergic and GABAergic receptors. J Neurogenet 2019; 33: 10-20.
[63]
Marshall SA, Rinker JA, Harrison LK, Fletcher CA, Herfel TM, Thiele TE. Assessment of the effects of 6 standard rodent diets on binge-like and voluntary ethanol consumption in male C57BL/6J mice. Alcohol Clin Exp Res 2015; 39: 1406-16.
[64]
de Macedo IC, de Freitas JS, da Silva Torres IL. The influence of palatable diets in reward system activation: a mini review. Adv Pharmacol Sci 2016.Available from: . https://www.hindawi.com/ journals/aps/2016/7238679/
[65]
Barson JR, Morganstern I, Leibowitz SF. Similarities in hypothalamic and mesocorticolimbic circuits regulating the overconsumption of food and alcohol. Physiol Behav 2011; 104: 128-37.
[http://dx.doi.org/10.1016/j.physbeh.2011.04.054]
[66]
Morganstern I, Barson JR, Leibowitz SF. Regulation of drug and palatable food overconsumption by similar peptide systems. Curr Drug Abuse Rev 2011; 4: 163-73.
[http://dx.doi.org/10.2174/1874473711104030163]
[67]
Barry RL, Byun NE, Williams JM, et al. Brief exposure to obesogenic diet disrupts brain dopamine networks. PLoS One 2018; 13: e0191299
[http://dx.doi.org/10.1371/journal.pone.0191299]
[68]
Wang GJ, Volkow ND, Logan J, et al. Brain dopamine and obesity. Lancet 2001; 357: 354-7.
[http://dx.doi.org/10.1016/S0140-6736(00)03643-6]
[69]
Davis JF, Tracy AL, Schurdak JD, et al. Exposure to elevated levels of dietary fat attenuates psychostimulant reward and mesolimbic dopamine turnover in the rat. Behav Neurosci 2008; 122: 1257-63.
[http://dx.doi.org/10.1037/a0013111]
[70]
Wise RA. Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond B Biol Sci 2006; 361: 1149-58.
[http://dx.doi.org/10.1098/rstb.2006.1854]
[71]
Hernandez L, Hoebel BG. Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis. Life Sci 1988; 42: 1705-12.
[http://dx.doi.org/10.1016/0024-3205(88)90036-7]
[72]
Valdivia S, Cornejo MP, Reynaldo M, De Francesco PN, Perello M. Escalation in high fat intake in a binge eating model differentially engages dopamine neurons of the ventral tegmental area and requires ghrelin signaling. Psychoneuroendocrinology 2015; 60: 206-16.
[http://dx.doi.org/10.1016/j.psyneuen.2015.06.018]
[73]
Bello NT, Hajnal A. Dopamine and binge eating behaviors. Pharmacol Biochem Behav 2010; 97: 25-33.
[http://dx.doi.org/10.1016/j.pbb.2010.04.016]
[74]
Lee MR, Hinton DJ, Song JY, et al. Neurotensin receptor type 1 regulates ethanol intoxication and consumption in mice. Pharmacol Biochem Behav 2010; 95: 235-41.
[http://dx.doi.org/10.1016/j.pbb.2010.01.012]
[75]
Lee MR, Hinton DJ, Unal SS, Richelson E, Choi D-S. Increased ethanol consumption and preference in mice lacking neurotensin receptor type 2. Alcohol Clin Exp Res 2011; 35: 99-107.
[76]
Klenowski PM. Emerging role for the medial prefrontal cortex in alcohol-seeking behaviors. Addict Behav 2018; 77: 102-6.
[http://dx.doi.org/10.1016/j.addbeh.2017.09.024]
[77]
Carnell S, Grillot C, Ungredda T, et al. Morning and afternoon appetite and gut hormone responses to meal and stress challenges in obese individuals with and without binge eating disorder. Int J Obes (Lond) 2018; 42: 841-9.
[http://dx.doi.org/10.1038/ijo.2017.307]
[78]
Munsch S, Biedert E, Meyer AH, Herpertz S, Beglinger C. CCK, ghrelin, and PYY responses in individuals with binge eating disorder before and after a cognitive behavioral treatment. Physiol Behav (CBT) 2009; 97: 14-20.
[79]
Landgren S, Jerlhag E, Zetterberg H, et al. Association of pro-ghrelin and GHS-R1A gene polymorphisms and haplotypes with heavy alcohol use and body mass. Alcohol Clin Exp Res 2008; 32: 2054-61.
[http://dx.doi.org/10.1111/j.1530-0277.2008.00793.x]
[80]
Tschöp M, Weyer C, Tataranni PA, Devanarayan V, Ravussin E, Heiman ML. Circulating ghrelin levels are decreased in human obesity. Diabetes 2001; 50: 707-9.
[http://dx.doi.org/10.2337/diabetes.50.4.707]
[81]
Bailer UF, Kaye WH. A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa. Curr Drug Targets CNS Neurol Disord 2003; 2: 53-9.
[http://dx.doi.org/10.2174/1568007033338689]
[82]
Monteleone AM, Castellini G, Volpe U, et al. Neuroendocrinology and brain imaging of reward in eating disorders: A possible key to the treatment of anorexia nervosa and bulimia nervosa. Prog Neuropsychopharmacol Biol Psychiatry 2018; 80: 132-42.
[http://dx.doi.org/10.1016/j.pnpbp.2017.02.020]
[83]
Jerlhag E, Egecioglu E, Landgren S, et al. Requirement of central ghrelin signaling for alcohol reward. Proc Natl Acad Sci USA 2009; 106: 11318-23.
[http://dx.doi.org/10.1073/pnas.0812809106]
[84]
Leggio L, Ferrulli A, Cardone S, et al. Ghrelin system in alcohol-dependent subjects: role of plasma ghrelin levels in alcohol drinking and craving. Addict Biol 2012; 17: 452-64.
[http://dx.doi.org/10.1111/j.1369-1600.2010.00308.x]
[85]
Menzies JRW, Skibicka KP, Leng G, Dickson SL. Ghrelin, reward and motivation. Endocr Dev 2013; 25: 101-11.
[http://dx.doi.org/10.1159/000346058]
[86]
Shirazi RH, Dickson SL, Skibicka KP. Gut peptide GLP-1 and its analogue, Exendin-4, decrease alcohol intake and reward. PLoS One 2013; 8: e61965
[87]
Alhadeff AL, Rupprecht LE, Hayes MR. GLP-1 neurons in the nucleus of the solitary tract project directly to the ventral tegmental area and nucleus accumbens to control for food intake. Endocrinology 2012; 647-58.
[88]
Sirohi S, Schurdak JD, Seeley RJ, Benoit SC, Davis JF. Central & peripheral glucagon-like peptide-1 receptor signaling differentially regulate addictive behaviors. Physiol Behav 2016; 161: 140-4.
[http://dx.doi.org/10.1016/j.physbeh.2016.04.013]
[89]
Davis JF, Schurdak JD, Magrisso IJ, et al. Gastric bypass surgery attenuates ethanol consumption in ethanol-preferring rats. Biol Psychiatry 2012; 72: 354-60.
[http://dx.doi.org/10.1016/j.biopsych.2012.01.035]
[90]
Thompson-Memmer C, Glassman T, Diehr A. Drunkorexia: A new term and diagnostic criteria. J AM COLL HEALTH 2019; 67: 620-6.
[http://dx.doi.org/10.1080/07448481.2018.1500470]
[91]
Hunt TK, Forbush KT. Is “drunkorexia” an eating disorder, substance use disorder, or both? Eat Behav 2016; 22: 40-5.
[http://dx.doi.org/10.1016/j.eatbeh.2016.03.034]
[92]
Cummings JR, Tomiyama AJ. Bidirectional associations between eating and alcohol use during restricted intake. Food Addict 2018; 5: 243-50.
[93]
Lieber CS. ALCOHOL: its metabolism and interaction with nutrients. Annu Rev Nutr 2000; 20: 395-430.
[http://dx.doi.org/10.1146/annurev.nutr.20.1.395] [PMID: 10940340]
[94]
Addolorato G, Capristo E, Greco AV, Stefanini GF, Gasbarrini G. Influence of chronic alcohol abuse on body weight and energy metabolism: is excess ethanol consumption a risk factor for obesity or malnutrition? J Intern Med 1998; 244: 387-95.
[http://dx.doi.org/10.1046/j.1365-2796.1998.00381.x]
[95]
Sarin SK, Dhingra N, Bansal A, Malhotra S, Guptan RC. Dietary and nutritional abnormalities in alcoholic liver disease: a comparison with chronic alcoholics without liver disease. American J Gastroenterol 1997; 92: 777-83.
[96]
Glória L, Cravo M, Camilo ME, et al. Nutritional deficiencies in chronic alcoholics: relation to dietary intake and alcohol consumption. American J Gastroenterol 1997; 92: 485-9.
[97]
Cummings JR, Ray LA, Tomiyama AJ. Food-alcohol competition: As young females eat more food, do they drink less alcohol? J Health Psychol 2017; 22: 674-83.
[98]
Sirohi S, Bakalkin G, Walker BM. Alcohol-induced plasticity in the dynorphin/kappa-opioid receptor system 2012; 5: 95
[99]
Kissler JL, Sirohi S, Reis DJ, et al. The one-two punch of alcoholism: role of central amygdala dynorphins/kappa-opioid receptors. Biol Psychiatry 2014; 75: 774-82.
[100]
Egan AE, Seemiller LR, Packard AEB, Solomon MB, Ulrich-Lai YM. Palatable food reduces anxiety-like behaviors and HPA axis responses to stress in female rats in an estrous-cycle specific manner. Horm Behav 2019; 115: 104557
[http://dx.doi.org/10.1016/j.yhbeh.2019.07.005]
[101]
Otsuka A, Shiuchi T, Chikahisa S, Shimizu N, Séi H. Sufficient intake of high-fat food attenuates stress-induced social avoidance behavior. Life Sci 2019; 219: 219-30.
[http://dx.doi.org/10.1016/j.lfs.2019.01.012]
[102]
Dencker D, Molander A, Thomsen M, et al. Ketogenic diet suppresses alcohol withdrawal syndrome in rats. Alcohol Clin Exp Res 2018; 42(2): 270-7.