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      Calorie Anticipation Alters Food Intake After Low-Caloric but Not High-Caloric Preloads

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          Abstract

          Objective

          Cognitive factors and anticipation are known to influence food intake. The current study examined the effect of anticipation and actual consumption of food on hormone (ghrelin, cortisol, and insulin) and glucose levels, appetite and ad libitum intake, to assess whether changes in hormone levels might explain the predicted differences in subsequent food intake.

          Design and Methods

          During four breakfast sessions, participants consumed a yogurt preload that was either low caloric (LC: 180 kcal/300 g) or high caloric (HC: 530 kcal/300 g) and was provided with either consistent or inconsistent calorie information (i.e., stating the caloric content of the preload was low or high). Appetite ratings and hormone and glucose levels were measured at baseline ( t = 0), after providing the calorie information about the preload ( t = 20), after consumption of the preload ( t = 40), and just before ad libitum intake ( t = 60).

          Results

          Ad libitum intake was lower after HC preloads (as compared to LC preloads; P < 0.01). Intake after LC preloads was higher when provided with (consistent) LC information (467±254 kcal) as compared to (inconsistent) HC information (346±210 kcal), but intake after the HC preloads did not depend on the information provided (LC information: 290±178 kcal, HC information: 333±179 kcal; caloric load*information P = 0.03). Hormone levels did not respond in an anticipatory manner, and the post-prandial responses depended on actual calories consumed.

          Conclusions

          These results suggest that both cognitive and physiological information determine food intake. When actual caloric intake was sufficient to produce physiological satiety, cognitive factors played no role; however, when physiological satiety was limited, cognitively induced satiety reduced intake to comparable levels.

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          Most cited references35

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          Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues.

          Ghrelin is an orexigenic hormone that is implicated in meal initiation, in part because circulating levels rise before meals. Because previous human studies have examined subjects fed on known schedules, the observed preprandial ghrelin increases could have been a secondary consequence of meal anticipation. A causal role for ghrelin in meal initiation would be better supported if preprandial increases occurred before spontaneously initiated meals not prompted by external cues. We measured plasma ghrelin levels among human subjects initiating meals voluntarily without cues related to time or food. Samples were drawn every 5 min between a scheduled lunch and a freely requested dinner, and hunger scores were obtained using visual analog scales. Insulin, glucose, fatty acids, leptin, and triglycerides were also measured. Ghrelin levels decreased shortly after the first meal in all subjects. A subsequent preprandial increase occurred over a wide range of intermeal intervals (IMI; 320-425 min) in all but one subject. Hunger scores and ghrelin levels showed similar temporal profiles and similar relative differences in magnitude between lunch and dinner. One subject displayed no preprandial ghrelin increase and was also the only individual whose insulin levels did not return to baseline between meals. This finding, along with a correlation between area-under-the-curve values of ghrelin and insulin, suggests a role for insulin in ghrelin regulation. The preprandial increase of ghrelin levels that we observed among humans initiating meals voluntarily, without time- or food-related cues, and the overlap between these levels and hunger scores are consistent with a role for ghrelin in meal initiation.
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            Postprandial plasma ghrelin is suppressed proportional to meal calorie content in normal-weight but not obese subjects.

            Circulating levels of the gastric hormone ghrelin rise before and decrease after a meal. In normal-weight subjects, postprandial suppression of ghrelin is proportional to calories consumed. Obese individuals have lower fasting ghrelin levels; however, it is unclear whether the obese show normal postprandial suppression. This study aimed to compare postprandial ghrelin responses in normal-weight and obese subjects, using mixed macronutrient meals with varied fat and calorie content. Postprandial ghrelin response was measured in normal-weight insulin-sensitive subjects and obese insulin-resistant subjects, after six test meals with different fat and calorie content (250-3000 kcal). Increasing the calorie content of meals in normal-weight subjects progressively lowered nadir levels of ghrelin. The obese had lower fasting ghrelin levels, and the reduction after the consumption of all test meals was less than the normal-weight subjects. The lowest postprandial levels in the obese were no different to the nadir in normal-weight volunteers after 1000-, 2000-, and 3000-kcal meals. Thus, circulating ghrelin levels decreased in normal-weight subjects after mixed meals. Obese subjects demonstrated a much reduced ghrelin postprandial suppression. This reduced suppression may influence satiety, thus reinforcing obesity.
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              Mind over milkshakes: mindsets, not just nutrients, determine ghrelin response.

              To test whether physiological satiation as measured by the gut peptide ghrelin may vary depending on the mindset in which one approaches consumption of food. On 2 separate occasions, participants (n = 46) consumed a 380-calorie milkshake under the pretense that it was either a 620-calorie "indulgent" shake or a 140-calorie "sensible" shake. Ghrelin was measured via intravenous blood samples at 3 time points: baseline (20 min), anticipatory (60 min), and postconsumption (90 min). During the first interval (between 20 and 60 min) participants were asked to view and rate the (misleading) label of the shake. During the second interval (between 60 and 90 min) participants were asked to drink and rate the milkshake. The mindset of indulgence produced a dramatically steeper decline in ghrelin after consuming the shake, whereas the mindset of sensibility produced a relatively flat ghrelin response. Participants' satiety was consistent with what they believed they were consuming rather than the actual nutritional value of what they consumed. The effect of food consumption on ghrelin may be psychologically mediated, and mindset meaningfully affects physiological responses to food.
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                Author and article information

                Journal
                Obesity (Silver Spring)
                Obesity (Silver Spring)
                oby
                Obesity (Silver Spring, Md.)
                Blackwell Publishing Ltd
                1930-7381
                1930-739X
                August 2013
                02 January 2013
                : 21
                : 8
                : 1548-1553
                Affiliations
                [1 ]Department of Neuroscience, Uppsala University SE-751 24 Uppsala, Sweden
                [2 ]Department of Physiology/Endocrinology, The Sahlgrenska Academy at the University of Gothenburg 405 30 Gothenburg, Sweden
                Author notes
                Correspondence: P.S. Hogenkamp ( pleunie.hogenkamp@ 123456neuro.uu.se )

                Disclosure: The authors declared no conflict of interest.

                The study is registered with http://ClinicalTrials.gov (NCT01680315).

                Funding source: This work was supported by the Swedish Research Council, Åhlens stiftelse, and the Swedish Brain Research Foundation, Tore Nilsons Foundation, Ingrid Thurings Foundation, Brain Foundation, Åke Wiberg Foundation, Novo Nordisk, the Swedish Research Council (Work from HB Schiöth's laboratories), the Swedish Research Council (2009-S266), the Forskning och Utvecklingsarbete/Avtal om Läkarutbildning och Forskning Göteborg (ALFGBG-138741), and German Research Foundation (DFG) (Work from SL Dickson's laboratories).

                Article
                10.1002/oby.20293
                3817524
                23585292
                f1b8e25a-9f0c-4af3-a7f6-93de18af4c90
                Copyright © 2012 The Obesity Society

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                : 14 November 2012
                : 28 November 2012
                Categories
                Clinical Trials: Behavior, Pharmacotherapy, Devices, Surgery

                Medicine
                Medicine

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