2019
DOI: 10.1093/nutrit/nuz089
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The Western diet: a blind spot of eating disorder research?—a narrative review and recommendations for treatment and research

Abstract: Over the last 50 years, in parallel with the obesity epidemic, the prevalence of eating disorders has increased and presentations have changed. In this narrative review, we consider recent research exploring the implications of changing patterns of food consumption on metabolic and neurobiological pathways, a hitherto neglected area in eating disorder research. One of the major changes over this time has been the introduction of ultra-processed (NOVA-4) foods, which are gradually replacing unprocessed and mini… Show more

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Cited by 24 publications
(17 citation statements)
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“…Proposed mechanisms include a poor nutritional profile (i.e., UPFs are vectors for added sugars, sodium and trans-fats) and displacement of MPFs in the diet [ 33 , 34 , 35 , 58 , 108 , 109 , 110 , 111 , 112 , 113 , 114 ], higher glycaemic load and reduced gut–brain satiety signalling resulting from altered physical properties created by the processing of foods [ 115 , 116 , 117 , 118 ], carcinogens formed during high-temperature cooking (e.g., carbohydrate-rich foods with acrylamide) [ 119 , 120 ], and inflammatory responses linked with acellular nutrients and industrial food additives, gut microflora dysbiosis and increased intestinal permeability [ 98 , 121 , 122 ]. Certain properties of UPFs may promote overconsumption [ 123 ], including their often ubiquitous availability and convenience [ 124 , 125 , 126 ], palatability and quasi-addictiveness [ 127 , 128 ] and intensive marketing practices used to promote purchasing and consumption, especially among children and adolescents [ 129 , 130 , 131 ].…”
Section: Discussionmentioning
confidence: 99%
“…Proposed mechanisms include a poor nutritional profile (i.e., UPFs are vectors for added sugars, sodium and trans-fats) and displacement of MPFs in the diet [ 33 , 34 , 35 , 58 , 108 , 109 , 110 , 111 , 112 , 113 , 114 ], higher glycaemic load and reduced gut–brain satiety signalling resulting from altered physical properties created by the processing of foods [ 115 , 116 , 117 , 118 ], carcinogens formed during high-temperature cooking (e.g., carbohydrate-rich foods with acrylamide) [ 119 , 120 ], and inflammatory responses linked with acellular nutrients and industrial food additives, gut microflora dysbiosis and increased intestinal permeability [ 98 , 121 , 122 ]. Certain properties of UPFs may promote overconsumption [ 123 ], including their often ubiquitous availability and convenience [ 124 , 125 , 126 ], palatability and quasi-addictiveness [ 127 , 128 ] and intensive marketing practices used to promote purchasing and consumption, especially among children and adolescents [ 129 , 130 , 131 ].…”
Section: Discussionmentioning
confidence: 99%
“…Another important characteristic of UPF pertains to food additives, such as colors, emulsifiers, flavor enhancers, sugar substitutes, etc. The expanding UPF consumption worldwide has been linked to deleterious metabolic outcomes via various endocrine, neurobiological and microbiome pathways ( Ayton & Ibrahim, 2020 ). Artificial non-nutritive sweeteners, for example, were initially marketed as healthy sweetener alternatives yet have been implicated in overeating owing to potentiation of sugar-cravings and potential sugar dependence ( Onaolapo & Onaolapo, 2018 ).…”
Section: Discussionmentioning
confidence: 99%
“…Causality is not always easily established, but lack of dietary fat, for instance, has been repeatedly associated with specific physical and cognitive deficits found in underweight or post-underweight individuals ( Mayer et al, 2012 ; Nguyen et al, 2019 ; for an overview, see Troscianko, 2020 ). Ultra-processed high-sugar foods are implicated in binging behaviors ( Ayton and Ibrahim, 2020 ), while diets higher in fat and protein may offer psychological and physical benefits post-recovery from a restrictive eating disorder ( Troscianko, 2012 ). Higher-fat and -protein diets may also align neatly with the neural and hormonal mechanisms by which eating-rate interventions are effective for overweight, by modulating ghrelin and leptin levels ( Lomenick et al, 2009 ; Ebbeling et al, 2018 ) and secretion of glucagon-like peptide ( Gibbons et al, 2013 ).…”
Section: Discussion: Putting It All Togethermentioning
confidence: 99%