Heather M. Francis

The longer-term impacts of Western diet on human cognition and the brain.

Animal work over the last three decades has generated a convincing body of evidence that a Western diet - one high in saturated fat and refined carbohydrates (HFS diet) - can damage various brain systems. In this review we examine whether there is evidence for this in humans, using converging lines of evidence from neuropsychological, epidemiological and neuroimaging data. Using the animal research as the organizing principal, we examined evidence for dietary induced impairments in frontal, limbic and hippocampal systems, and with their associated functions in learning, memory, cognition and hedonics. Evidence for the role of HFS diet in attention deficit disorder and in neurodegenerative conditions was also examined. While human research data is still at an early stage, there is evidence of an association between HFS diet and impaired cognitive function. Based upon the animal data, and a growing understanding of how HFS diets can disrupt brain function, we further suggest that there is a causal link running from HFS diet to impaired brain function in humans, and that HFS diets also contribute to the development of neurodegenerative conditions.

Higher reported saturated fat and refined sugar intake is associated with reduced hippocampal-dependent memory and sensitivity to interoceptive signals.

Regulation of energy intake depends in part on both memory for prior food intake and internal signals of hunger and satiety. These functions are both mediated by the hippocampus, a brain structure that animal studies have shown to be impaired after maintenance on high fat and refined sugar (HFS) diets. Study 1, using a cross-sectional design, revealed that self-reported HFS diet was associated with poorer performance on hippocampal sensitive memory tasks but not other neuropsychological control measures. Study 2 replicated this finding in two groups selected to differ in HFS intake, additionally showing that this effect is specific to hippocampal functioning and does not extend to measures of prefrontal cortex function. Furthermore, in a laboratory-based test of food intake, the HFS rich diet groups were less accurate in recalling what they had previously eaten and evidenced reduced sensitivity to internal signals of hunger and satiety, relative to a group consuming less HFS rich diets. Together, these findings reveal an association between HFS consumption and poorer hippocampal function in human participants, consistent with findings from animal-based studies. Moreover, our results suggest that this may be related to impaired regulation of energy intake via less accurate tracking of prior food intake and reduced sensitivity to hunger and satiety signals.

Chemosensory Abilities in Consumers of a Western-Style Diet

People vary in their habitual diet and also in their chemosensory abilities. In this study, we examined whether consumption of a Western-style diet, rich in saturated fat and added sugar, is associated with either poorer or different patterns of chemosensory perception, relative to people who consume a healthier diet. Participants were selected based on a food frequency questionnaire, which established whether they were likely to consume a diet either higher or lower in saturated fat and added sugar. Eighty-seven participants were tested for olfactory ability (threshold, discrimination, and identification), gustatory ability (PROP sensitivity, taste intensity, quality, and hedonics), and flavor processing (using dairy fat-sugar-odor mixtures). A Western-style diet was associated with poorer odor identification ability, greater PROP sensitivity, poorer fat discrimination, different patterns of sweetness taste enhancement, and hedonic differences in taste and flavor perception. No differences were evident for odor discrimination or threshold, in perception of taste intensity/quality (excluding PROP) or the ability of fats to affect flavor perception. The significant relationships were of small to moderate effect size, and would be expected to work against consuming a healthier diet. The discussion focuses on whether these diet-related differences precede adoption of a Western-style diet and/or are a consequence of it.

Thirst interoception and its relationship to a Western-style diet

Less sensitive interoception for hunger and fullness has been observed in people who consume a diet rich in saturated fat and added sugar. In this study we examined whether healthy young people who routinely consume such diets, also demonstrate less sensitive thirst interoception. Participants, varying primarily in diet, were made thirsty by consuming salted chips and later provided with ad libitum access to water, with thirst ratings obtained throughout. A self-report measure of interoceptive awareness was also included plus measures to determine eating habits, memory and executive function. A diet reported as richer in saturated fat and added sugar (an HFS diet) was associated both with less sensitive thirst interoception and with greater attention to somatic signs. Evidence of poorer hippocampal-sensitive learning and memory was also detected. Poorer sensitivity to interoceptive cues appears to be a reliable correlate of an HFS diet and its causal origins are discussed.

A four-day Western-style dietary intervention causes reductions in hippocampal-dependent learning and memory and interoceptive sensitivity

In animals, a Western style diet–high in saturated fat and added sugar–causes impairments in hippocampal-dependent learning and memory (HDLM) and perception of internal bodily state (interoception). In humans, while there is correlational support for a link between Western-style diet, HDLM, and interoception, there is as yet no causal data. Here, healthy individuals were randomly assigned to consume either a breakfast high in saturated fat and added sugar (Experimental condition) or a healthier breakfast (Control condition), over four consecutive days. Tests of HDLM, interoception and biological measures were administered before and after breakfast on the days one and four, and participants completed food diaries before and during the study. At the end of the study, the Experimental condition showed significant reductions in HDLM and reduced interoceptive sensitivity to hunger and fullness, relative to the Control condition. The Experimental condition also showed a markedly different blood glucose and triglyceride responses to their breakfast, relative to Controls, with larger changes in blood glucose across breakfast being associated with greater reductions in HDLM. The Experimental condition compensated for their energy-dense breakfast by reducing carbohydrate intake, while saturated fat intake remained consistently higher than Controls. This is the first experimental study in humans to demonstrate that a Western-style diet impacts HDLM following a relatively short exposure–just as in animals. The link between diet-induced HDLM changes and blood glucose suggests one pathway by which diet impacts HDLM in humans.

Proteomic analysis of the dorsal and ventral hippocampus of rats maintained on a high fat and refined sugar diet.

The typical Western diet, rich in high saturated fat and refined sugar (HFS), has been shown to increase cognitive decline with aging and Alzheimers disease, and to affect cognitive functions that are dependent on the hippocampus, including memory processes and reversal learning. To investigate neurophysiological changes underlying these impairments, we employed a proteomic approach to identify differentially expressed proteins in the rat dorsal and ventral hippocampus following maintenance on an HFS diet. Rats maintained on the HFS diet for 8 weeks were impaired on a novel object recognition task that assesses memory and on a Morris Water Maze task assessing reversal learning. Quantitative label‐free shotgun proteomic analysis was conducted on biological triplicates for each group. For the dorsal hippocampus, 59 proteins were upregulated and 36 downregulated in the HFS group compared to controls. Pathway ana‐lysis revealed changes to proteins involved in molecular transport and cellular and molecular signaling, and changes to signaling pathways including calcium signaling, citrate cycle, and oxidative phosphorylation. For the ventral hippocampus, 25 proteins were upregulated and 27 downregulated in HFS fed rats. Differentially expressed proteins were involved in cell‐to‐cell signaling and interaction, and cellular and molecular function. Changes to signaling pathways included protein ubiquitination, ubiquinone biosynthesis, oxidative phosphorylation, and mitochondrial dysfunction. This is the first shotgun proteomics study to examine protein changes in the hippocampus following long‐term consumption of a HFS diet, identifying changes to a large number of proteins including those involved in synaptic plasticity and energy metabolism. All MS data have been deposited in the ProteomeXchange with identifier PXD000028.

The use of pulse oximetry as a screening assessment for paediatric neurogenic dysphagia

Purpose: Early screening and intervention for dysphagia is crucial to offset potential outcomes such as compromised nutrition or reduced respiratory function. Current paediatric dysphagia screening tests are subjective with poor sensitivity and specificity. The present study examined whether an objective method, pulse oximetry (measuring oxygen saturation (SpO2) levels), could differentiate between children with and without dysphagia, in relation to (1) Average pre-feeding baseline SpO2 levels; (2) Average feeding SpO2 levels; (3) Average post-feeding SpO2 levels; and (4) The number of events of oxygen desaturation pre-, during and after feeding. Methods: Nine participants with chronic neurological disability (CND) (7 F, 2 M) (9;7–15;11 years) and nine control participants matched for age (9;5–16;0 years) and sex were assessed using a clinical bedside evaluation (CBE) and pulse oximetry. Results: A statistically significant difference was found in SpO2 levels between the two groups (p < 0.001) during oral feeding only (sensitivity, 88.9%; specificity, 88.9%). Only three children with dysphagia experienced ‘events’ of SpO2 desaturation during feeding. Conclusion: Pulse oximetry may provide a useful adjunct to the CBE for dysphagia screening, with average SpO2 levels during feeding predicting those with and without dysphagia with moderate levels of sensitivity and specificity. The finding of individual variation in desaturation ‘events’, however, warrants the provision of further data on large homogenous populations to provide definitive criterion for pathological SpO2 levels associated with dysphagia during oral feeding. Propósito: El estudio y la intervención temprana de la disfagia es crucial para tener potencial offset resultados tales como la nutrición comprometida, o la reducción de la función respiratoria. Las pruebas de estudio de la disfagia en pacientes pediátricos son subjetivas y con una especificidad y sensibilidad pobres. El presente estudio evaluó sí un método objetivo como la oximetría de pulso (midiendo los niveles de saturación de oxígeno(SpO2) podría diferenciar entre niños con y sin disfagia, en base a: 1. Promedio de los niveles baasales de SpO2 antes de la alimentación. 2. Promedio de los niveles de SpO2 durante la alimentación. 3. Promedio de niveles de SpO2 después de la alimentación. 4. El número de eventos de desaturación de oxígeno antes, durante y después de la alimentación. Métodos: Se evaluaron a nueve participantes con una discapacidad neurológica crónica (CND) (7F, 2M)(9;7 A 15;11 años) y a nueve participantes de grupo control de igual género y con edades similares (9;5 a 16;0 años); usando una evaluación clínica para pacientes encamados (CBE) junto con la oximetría de pulso. Resultados: Se encontró una diferencia estadísticamente significativa en los niveles de SpO2 entre los dos grupos (p < 0.001) solamente durante la alimentación oral (sensiblidad, 88.9%; especificidad, 88,9%). Solamente tres niños con disfagia experimentaron “eventos” de desaturación de SpO2 durante la alimentación. Conclusión: La oximetría de pulso puede ser útil para la evaluación de la disfagia en CBE, utilizando el promedio de los niveles de SpO2 durante la alimentación, y prediciendo con niveles moderados de sensibilidad y especificidad quienes cursarán con disfagia y quienes no. El resultado de variaciones individuales en los “eventos “de desaturación, asegurará la obtención subsecuente de datos en grandes poblaciones homogéneas y brindará los criterios definitivos para determinar los niveles de SpO2 patológicos asociados a disfagia durante la alimentación oral. Palabras claves: Discapacidad neurológica, discapacidad intelectual, niño, disfagia, alteraciones en la deglución, oximetría de pulso

Outcome instruments in moderate-to-severe adult traumatic brain injury: recommendations for use in psychosocial research

ABSTRACT Background: Traumatic brain injury (TBI) can reduce psychosocial functioning, causing relationship, family, and employment difficulties. The present study by Moving Ahead: Centre for Research Excellence (CRE) in Brain Recovery aimed to identify a set of adult outcome instruments for moderate-to-severe TBI psychosocial research. Procedure: A review of 115 instruments (identified through nomination, literature search, and international expert opinion) was conducted over a 15-month period. Eleven psychosocial areas were examined: Global Outcome, Communication, Social Cognition, Behavioural and Executive Function, Other Neuropsychological Functioning, Psychological Status, TBI-related Symptoms, Activities and Participation, Support and Relationships, Sense of Self, and Health-related Quality of Life. Individual instruments were considered against selection guidelines, and specific measures that best met the guidelines were identified as core (common across all studies), supplemental (dependent on study type) or emerging. Results: The final recommendations, organised in accordance with the World Health Organisation’s International Classification of Functioning taxonomy, comprised 56 instruments for use in early recovery, outcome, and intervention studies. Conclusion: These recommendations provide a coherent framework along with identified outcome instruments to guide psychosocial research in moderate-to-severe TBI. Adherence to the recommendations will enable data-pooling and comparison across studies and research settings facilitating consistent measurement across the lifespan.

The hippocampus and the regulation of human food intake

Human and animal data suggest that the hippocampus plays certain roles in regulating food intake. However, its actual role may be far broader than currently envisaged, a claim suggested by the centrality of the hippocampus to so many aspects of human/animal cognition. Understanding these ingestion-related functions is especially significant. This is because some degree of hippocampal impairment may be quite common, resulting for example from a Western-style diet, insomnia, diabetes, and depression-among many other causes. One potential consequence of hippocampal impairment could be a loosening of food intake regulation, leading in the longer-term to weight gain and its health-related impacts. Here we review known, suspected and newly hypothesized hippocampal-dependent functions involved in regulating human food intake: (a) declarative memory processes, and their use in explicitly evaluating when, what and how much to eat; (b) interoception, as it relates to hunger, fullness and thirst; (c) inhibitory processes, especially as applied to physiological state, place, and time, and their role in modulating memory retrieval; (d) craving and imagery for food; (e) perception of time and its role in preparing the body for food intake and estimating meal length; (f) trace conditioning and nutrient-related learning; and (g) inhibition of the hypothalamic-pituitary-adrenal stress response and stress-related eating. For each we present evidence for hippocampal involvement, describe the putative regulatory role, and the hypothesized effects of hippocampal impairment. We conclude that the hippocampus is intimately involved in regulating human food intake via multiple interconnected pathways, many of which are unstudied and understudied. (PsycINFO Database Record

Potential for diet to prevent and remediate cognitive deficits in neurological disorders

The pathophysiology of many neurological disorders involves oxidative stress, neuroinflammation, and mitochondrial dysfunction. There is now substantial evidence that diet can decrease these forms of pathophysiology, and an emerging body of literature relatedly suggests that diet can also prevent or even remediate the cognitive deficits observed in neurological disorders that exhibit such pathology (eg, Alzheimers disease, multiple sclerosis, age-related cognitive decline, epilepsy). The current review summarizes the emerging evidence in relation to whole diets prominent in the scientific literature-ketogenic, caloric restriction, high polyphenol, and Mediterranean diets-and provides a discussion of the possible underlying neurophysiological mechanisms.