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dc.contributor.authorPagoto, Sherry L.
dc.contributor.authorSpring, Bonnie
dc.contributor.authorMcChargue, Dennis
dc.contributor.authorHitsman, Brian
dc.contributor.authorSmith, Malaina
dc.contributor.authorAppelhans, Bradley
dc.contributor.authorHedeker, Donald
dc.date2022-08-11T08:09:39.000
dc.date.accessioned2022-08-23T16:38:48Z
dc.date.available2022-08-23T16:38:48Z
dc.date.issued2009-01-28
dc.date.submitted2010-03-29
dc.identifier.citation<p>Eat Behav. 2009 Jan;10(1):36-41. Epub 2008 Oct 30. <a href="http://dx.doi.org/10.1016/j.eatbeh.2008.10.010">Link to article on publisher's site</a></p>
dc.identifier.issn1471-0153 (Linking)
dc.identifier.doi10.1016/j.eatbeh.2008.10.010
dc.identifier.pmid19171315
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39328
dc.description.abstractSerotonergic involvement has been implicated in preferential consumption of treat foods. We tested the effect of acute tryptophan depletion (ATD) on food consumption by overweight and lean adults with and without a history of recurrent major depressive disorder (MDD). ATD and taste-matched placebo challenges were administered double-blind in counter-balanced order. Participants were classified as lean (n=36) or overweight (n=19) on the basis of body mass index (BMI). Total calorie, carbohydrate, protein, and sweet food consumption were assessed via a test meal 8-h following ATD. Four food items of comparable palatability were offered as a part of the test: two sweet (one carbohydrate-rich, and one protein-rich) and two non-sweet (one carbohydrate-rich, and one protein-rich). As compared to the placebo challenge, ATD significantly increased sweet calorie intake among overweight participants and increased their propensity to consume sweet food first before any other type of food. Lean participants' sweet calorie intake and food preference were unaffected by ATD. Findings suggest serotonergic involvement in the sweet food consumption by overweight individuals.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=19171315&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663793/
dc.subjectAdult
dc.subject*Body Mass Index
dc.subjectDietary Carbohydrates
dc.subjectDietary Proteins
dc.subjectDouble-Blind Method
dc.subjectFemale
dc.subject*Food
dc.subject*Food Preferences
dc.subjectHumans
dc.subjectMale
dc.subjectOverweight
dc.subjectSweetening Agents
dc.subjectTryptophan
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleAcute tryptophan depletion and sweet food consumption by overweight adults
dc.typeJournal Article
dc.source.journaltitleEating behaviors
dc.source.volume10
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2128
dc.identifier.contextkey1250261
html.description.abstract<p>Serotonergic involvement has been implicated in preferential consumption of treat foods. We tested the effect of acute tryptophan depletion (ATD) on food consumption by overweight and lean adults with and without a history of recurrent major depressive disorder (MDD). ATD and taste-matched placebo challenges were administered double-blind in counter-balanced order. Participants were classified as lean (n=36) or overweight (n=19) on the basis of body mass index (BMI). Total calorie, carbohydrate, protein, and sweet food consumption were assessed via a test meal 8-h following ATD. Four food items of comparable palatability were offered as a part of the test: two sweet (one carbohydrate-rich, and one protein-rich) and two non-sweet (one carbohydrate-rich, and one protein-rich). As compared to the placebo challenge, ATD significantly increased sweet calorie intake among overweight participants and increased their propensity to consume sweet food first before any other type of food. Lean participants' sweet calorie intake and food preference were unaffected by ATD. Findings suggest serotonergic involvement in the sweet food consumption by overweight individuals.</p>
dc.identifier.submissionpathoapubs/2128
dc.contributor.departmentDepartment of Medicine, Division of Preventive and Behavioral Medicine
dc.source.pages36-41


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