The effect of appetite on pain

Hunger and pain are powerful homeostatic drives, which compete for a behavioural response when experienced simultaneously. This thesis set out to explore neural mechanisms underpinning this competition, and how appetitive visual and olfactory stimuli may modulate the effect of homeostatic energy man...

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Main Author: Wright, H. J.
Published: University of Liverpool 2016
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616
Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706762
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spelling ndltd-bl.uk-oai-ethos.bl.uk-7067622018-07-24T03:15:31ZThe effect of appetite on painWright, H. J.2016Hunger and pain are powerful homeostatic drives, which compete for a behavioural response when experienced simultaneously. This thesis set out to explore neural mechanisms underpinning this competition, and how appetitive visual and olfactory stimuli may modulate the effect of homeostatic energy manipulations on pain. Using well-established techniques including EEG source analysis and resting state fMRI, we consistently employed a within-subjects fasting vs. satiation paradigm to investigate the effects of appetite on subjective pain perception and neural pain processing. Pain stimuli which selectively activated nociceptive Aδ fibres were presented concurrently with appetitive stimuli, and the neural nociceptive responses were mapped with high-density (128-channel) EEG recordings and fMRI functional connectivity. Based on the results of previous research, we hypothesised that fasting would suppress subjective and neural pain processing, and that visual and olfactory appetitive stimuli may augment this effect. We first found that a relatively short overnight fast was sufficient to induce significant changes in resting state functional connectivity in areas that underlie both hunger/satiety and pain: insula cortex, hypothalamus, and regions of prefrontal cortex. Source analysis of EEG data revealed a small group of brain regions whose pain-related activation was suppressed by hunger and/or appetitive stimuli: anterior cingulate cortex, operculo-insular cortex, parahippocampal cortex, and cerebellum. Functional connectivity analysis of fMRI data further uncovered a widely-distributed network of brain areas whose pain-induced connectivity was enhanced by fasting or satiety. Of particular interest was a small network of areas involved in stimulus saliency processing (anterior insula, anterior cingulate cortex, and prefrontal cortex), which was stronger during fasting; presumably advantageous when searching for food. Lastly, in an experiment using a bread odour, we found that the suppressive effect of appetitive stimuli on nociception is not just confined to the visual modality. Brief, strong pain can also be suppressed by an appetitive odour during fasting. We conclude that fasting reliably interferes with pain processing, and that ambient appetitive stimuli might be of use in situations where short-lasting pain is likely to occur.616University of Liverpoolhttp://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706762http://livrepository.liverpool.ac.uk/3001070/Electronic Thesis or Dissertation
collection NDLTD
sources NDLTD
topic 616
spellingShingle 616
Wright, H. J.
The effect of appetite on pain
description Hunger and pain are powerful homeostatic drives, which compete for a behavioural response when experienced simultaneously. This thesis set out to explore neural mechanisms underpinning this competition, and how appetitive visual and olfactory stimuli may modulate the effect of homeostatic energy manipulations on pain. Using well-established techniques including EEG source analysis and resting state fMRI, we consistently employed a within-subjects fasting vs. satiation paradigm to investigate the effects of appetite on subjective pain perception and neural pain processing. Pain stimuli which selectively activated nociceptive Aδ fibres were presented concurrently with appetitive stimuli, and the neural nociceptive responses were mapped with high-density (128-channel) EEG recordings and fMRI functional connectivity. Based on the results of previous research, we hypothesised that fasting would suppress subjective and neural pain processing, and that visual and olfactory appetitive stimuli may augment this effect. We first found that a relatively short overnight fast was sufficient to induce significant changes in resting state functional connectivity in areas that underlie both hunger/satiety and pain: insula cortex, hypothalamus, and regions of prefrontal cortex. Source analysis of EEG data revealed a small group of brain regions whose pain-related activation was suppressed by hunger and/or appetitive stimuli: anterior cingulate cortex, operculo-insular cortex, parahippocampal cortex, and cerebellum. Functional connectivity analysis of fMRI data further uncovered a widely-distributed network of brain areas whose pain-induced connectivity was enhanced by fasting or satiety. Of particular interest was a small network of areas involved in stimulus saliency processing (anterior insula, anterior cingulate cortex, and prefrontal cortex), which was stronger during fasting; presumably advantageous when searching for food. Lastly, in an experiment using a bread odour, we found that the suppressive effect of appetitive stimuli on nociception is not just confined to the visual modality. Brief, strong pain can also be suppressed by an appetitive odour during fasting. We conclude that fasting reliably interferes with pain processing, and that ambient appetitive stimuli might be of use in situations where short-lasting pain is likely to occur.
author Wright, H. J.
author_facet Wright, H. J.
author_sort Wright, H. J.
title The effect of appetite on pain
title_short The effect of appetite on pain
title_full The effect of appetite on pain
title_fullStr The effect of appetite on pain
title_full_unstemmed The effect of appetite on pain
title_sort effect of appetite on pain
publisher University of Liverpool
publishDate 2016
url http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.706762
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