There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean meat, is associated with reduced risk of depression. To date, only one randomised controlled trial (RCT) has been conducted with elevated depression symptoms being an inclusion criterion, with results showing that a diet intervention can reduce clinical levels of depression. No such RCTs have been performed in young adults. Young adults with elevated levels of depression symptoms and who habitually consume a poor diet were randomly allocated to a brief 3-week diet intervention (Diet Group) or a habitual diet control group (Control Group). The primary and secondary outcome measures assessed at baseline and after the intervention included symptoms of depression (Centre for Epidemiological Studies Depression Scale; CESD-R; and Depression Anxiety and Stress Scale– 21 depression subscale; DASS-21-D), current mood (Profile of Mood States), self-efficacy (New General Self-Efficacy Scale) and memory (Hopkins Verbal Learning Test). Diet compliance was measured via self-report questionnaires and spectrophotometry. One-hundred-and-one individuals were enrolled in the study and randomly assigned to the Diet Group or the Control Group. Upon completion of the study, there was complete data for 38 individuals in each group. There was good compliance with the diet intervention recommendations assessed using self-report and spectrophotometry. The Diet group had significantly lower self-reported depression symptoms than the Control Group on the CESD-R (p = 0.007, Cohen’s d = 0.65) and DASS-21 depression subscale (p = 0.002, Cohen’s d = 0.75) controlling for baseline scores on these scales. Reduced DASS-21 depression subscale scores were maintained on follow up phone call 3 months later (p = .009). These results are the first to show that young adults with elevated depression symptoms can engage in and adhere to a diet intervention, and that this can reduce symptoms of depression. The findings provide justification for future research into the duration of these benefits, the impacts of varying diet composition, and their biological basis.

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.

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.

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