Abstract
Purpose of review
Alcohol is commonly consumed around mealtimes, and both the immediate pharmacological actions of ethanol and the energy generated by metabolism of alcohol have the potential to modify food intake. Effects of moderate alcohol consumption on food intake in humans will be reviewed, and potential mechanisms considered.
Recent findings
Unlike other macronutrients, there is minimal evidence for any reduction in food intake to compensate for the potential energy in alcohol. In contrast, moderate alcohol consumption prior to a test meal leads to a short-term increase in food intake. This stimulatory effect of alcohol is not apparent beyond acute administration, but the inability to reduce voluntary energy intake in response to energy from alcohol metabolism is evident over extended periods. Alcohol suppresses fatty acid oxidation, increases short-term thermogenesis and stimulates a number of neurochemical and peripheral systems implicated in appetite control, including inhibitory effects on leptin, glucagon-like peptide-1, and serotonin, and enhancement of γ-aminobutyric acid, endogenous opioids and neuropeptide Y. All of these effects could lead to overeating, and mechanisms underlying appetite stimulation through alcohol require further substantiation.
Summary
Alcohol is a complex component of the diet, and appears to have multiple effects on appetite. Failure to reduce food intake in response to energy from alcohol makes moderate alcohol consumption a risk factor for obesity. Further integration of evidence from nutrition and neuroscience will be crucial to our understanding of effects of alcohol on appetite.
Alcohol is commonly consumed around mealtimes, and both the immediate pharmacological actions of ethanol and the energy generated by metabolism of alcohol have the potential to modify food intake. Effects of moderate alcohol consumption on food intake in humans will be reviewed, and potential mechanisms considered.
Recent findings
Unlike other macronutrients, there is minimal evidence for any reduction in food intake to compensate for the potential energy in alcohol. In contrast, moderate alcohol consumption prior to a test meal leads to a short-term increase in food intake. This stimulatory effect of alcohol is not apparent beyond acute administration, but the inability to reduce voluntary energy intake in response to energy from alcohol metabolism is evident over extended periods. Alcohol suppresses fatty acid oxidation, increases short-term thermogenesis and stimulates a number of neurochemical and peripheral systems implicated in appetite control, including inhibitory effects on leptin, glucagon-like peptide-1, and serotonin, and enhancement of γ-aminobutyric acid, endogenous opioids and neuropeptide Y. All of these effects could lead to overeating, and mechanisms underlying appetite stimulation through alcohol require further substantiation.
Summary
Alcohol is a complex component of the diet, and appears to have multiple effects on appetite. Failure to reduce food intake in response to energy from alcohol makes moderate alcohol consumption a risk factor for obesity. Further integration of evidence from nutrition and neuroscience will be crucial to our understanding of effects of alcohol on appetite.
| Original language | English |
|---|---|
| Pages (from-to) | 639-644 |
| Number of pages | 6 |
| Journal | Current Opinion in Clinical Nutrition and Metabolic Care |
| Volume | 6 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 1 Nov 2003 |
| Externally published | Yes |
Keywords
- alcohol
- food intake
- compensatory eating
- leptin
- neuropeptide Y
- fatty acid oxidation
