Methylphenidate reduces energy intake and dietary fat intake in adults: a mechanism of reduced reinforcing value of food?  

Oleh:

Goldfield, Gary S. ; Lorello, Claudio ; Doucet, Éric

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 86 no. 02 (Aug. 2007), page 308.
Topik: Methylphenidate • dopamine • eating • energy intake • food reinforcement • obesity

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2007.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background: Dopamine mediates the reinforcing value of food, and low concentrations of dopamine are related to increased feeding. Thus, administering a drug that increases dopamine may reduce energy intake, possibly by reducing food reinforcement. Objectives: We tested whether short-acting methylphenidate (MPH), a drug that increases the availability of dopamine by blocking its reuptake, reduces energy intake and alters macronutrient preference and whether these effects are due to a mechanism of reduced hunger or food reinforcement. Design: Fourteen adults were given placebo or short-acting MPH (0.5 mg/kg) in a randomized, double-blind, placebo-controlled crossover fashion. One hour after ingestion, hunger and the relative reinforcing value of snack food were measured, followed immediately by energy intake and macronutrient preference during a buffet-style lunch. Results: MPH reduced energy intake by 11% (P = 0.024) as well as intake of fat by 17% (P = 0.003) relative to placebo. Despite similar levels of prebuffet hunger, subjects taking MPH reduced their energy and fat intakes more than did those taking placebo, which suggests that hunger may not mediate the effects of MPH on energy intake. MPH showed a trend toward reducing the reinforcing value of high-fat food relative to placebo, but reduced food reinforcement was not significantly correlated with energy intake. Conclusion: MPH reduced overall energy intake with a selective reduction in dietary fat. Findings are consistent with a reward deficiency model of obesity whereby low brain dopamine predicts overeating and obesity, and administering agents that increase dopamine results in reduced feeding behavior.

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