Low dietary intakes of then-3 long-chain PUFA (LCPUFA) EPA and DHA are thought to be associated with increased risk for a variety of adverse outcomes, including some psychiatric disorders. Evidence from observational and intervention studies for a role ofn-3 LCPUFA in depression is mixed, with some support for a benefit of EPA and/or DHA in major depressive illness. The present study was a double-blind randomised controlled trial that evaluated the effects of EPA+DHA supplementation (1·5 g/d) on mood and cognitive function in mild to moderately depressed individuals. Of 218 participants who entered the trial, 190 completed the planned 12 weeks intervention. Compliance, confirmed by plasma fatty acid concentrations, was good, but there was no evidence of a difference between supplemented and placebo groups in the primary outcome – namely, the depression subscale of the Depression Anxiety and Stress Scales at 12 weeks. Mean depression score was 8·4 for the EPA+DHA group and 9·6 for the placebo group, with an adjusted difference of − 1·0 (95 % CI − 2·8, 0·8;P = 0·27). Other measures of mood, mental health and cognitive function, including Beck Depression Inventory score and attentional bias toward threat words, were similarly little affected by the intervention. In conclusion, substantially increasing EPA+DHA intake for 3 months was found not to have beneficial or harmful effects on mood in mild to moderate depression. Adding the present result to a meta-analysis of previous relevant randomised controlled trial results confirmed an overall negligible benefit ofn-3 LCPUFA supplementation for depressed mood.

We investigated the contribution of hunger and food liking to food reward, and the relationship between food reward and food intake. We defined liking as the pleasantness of taste of food in the mouth, and food reward as the momentary value of a food to the individual at the time of ingestion. Liking and food reward were measured, respectively, by ratings of the pleasantness of the taste of a mouthful, and ratings of desire to eat a portion, of the food in question. Hunger, which we view as primarily the absence of fullness, was rated without food being present. Study 1 provided evidence that hunger and liking contribute independently to food reward, with little effect of hunger on liking. Food intake reduced liking and reward value more for the eaten food than uneaten foods. The results were ambiguous as to whether this food-specific decline in reward value ('sensory-specific satiety') involved a decrease in 'wanting' in addition to the decrease in liking. Studies 2 and 3 compared desire to eat ratings with work-for-food and pay-for-food measures of food reward, and found desire to eat to be equal or superior in respect of effects of hunger and liking, and superior in predicting ad libitum food intake. A further general observation was that in making ratings of food liking participants may confuse the pleasantness of the taste of food with the pleasantness of eating it. The latter, which some call 'palatability,' decreases more with eating because it is significantly affected by hunger/fullness. Together, our results demonstrate the validity of ratings of desire to eat a portion of a tasted food as a measure of food reward and as a predictor of food intake.

Findings from epidemiological and observational studies have indicated that diets high in omega-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may reduce the risk of cognitive decline and Alzheimer’s disease (AD). To determine if increasing intake of DHA and EPA through supplementation is beneficial to cognition and mood in individuals with cognitive impairment no dementia (CIND) or Alzheimer’s disease (AD) a four month, randomised, double-blind, placebo controlled study was conducted. Fifty-seven participants with CIND and nineteen with AD were randomised to receive either omega-3 PUFAs (600 mg EPA and 625 mg DHA per day) or placebo (olive oil) over a four month period. Elevating depleted levels of EPA and DHA through supplementation in individuals with CIND or AD was found to have negligible beneficial effect on their cognition or mood. These findings confirm an overall negligible benefit of omega-3 PUFA supplementation for those with cognitive impairment and dementia. More intervention studies need to be undertaken with longer study durations and larger sample sizes. It may prove fruitful to examine effects of different doses as well as effects in other dementia subtypes.

The idea that food intake is motivated by (or in anticipation of) 'hunger' arising from energy depletion is apparent in both public and scientific discourse on eating behaviour. In contrast, our thesis is that eating is largely unrelated to short-term energy depletion. Energy requirements meal-to-meal are trivial compared with total body energy stores, and energy supply to the body's tissues is maintained if a meal or even several meals are missed. Complex and exquisite metabolic machinery ensures that this happens, but metabolic regulation is only loosely coupled with the control of energy intake. Instead, food intake needs to be controlled because the limited capacity of the gut means that processing a meal presents a significant physiological challenge and potentially hinders other activities. We illustrate the relationship between energy (food) intake and energy expenditure with a simple analogy in which: (1) water in a bathtub represents body energy content, (2) water in a saucepan represents food in the gut, and (3) the bathtub is filled via the saucepan. Furthermore, (4) it takes hours to process and pass the full energy (macronutrient) content of the saucepan to the bathtub, and (5) both the saucepan and bathtub resist filling, representing negative feedbacks on appetite (desire to eat). This model is consistent with the observations that appetite is reduced acutely by energy intake (a meal added to the limited capacity of the saucepan/gut), but not increased by an acute increase in energy expenditure (energy removed from the large store of energy in the bathtub/body). The existence of relatively very weak but chronic negative feedback on appetite proportional to body fatness is supported by observations on the dynamics of energy intake and weight gain in rat dietary obesity. (We use the term 'appetite' here because 'hunger' implies energy depletion.) In our model, appetite is motivated by the accessibility of food and the anticipated and experienced pleasure of eating it. The latter, which is similar to food reward, is determined primarily by the state of emptiness of the gut and food liking related to the food's sensory qualities and macronutrient value and the individual's dietary history. Importantly, energy density adds value because energy dense foods are less satiating kJ for kJ and satiation limits further intake. That is, energy dense foods promote energy intake by virtue (1) of being more attractive and (2) having low satiating capacity kJ for kJ, and (1) is partly a consequence of (2). Energy storage is adapted to feast and famine and that includes unevenness over time of the costs of obtaining and ingesting food compared with engaging in other activities. However, in very low-cost food environments with energy dense foods readily available, risk of obesity is high. This risk can be and is mitigated by dietary restraint, which in its simplest form could mean missing the occasional meal. Another strategy we discuss is the energy dilution achieved by replacing some sugar in the diet with low-calorie sweeteners. Perhaps as or more significant, though, is that belief in short-term energy balancing (the energy depletion model) may undermine attempts to eat less. Therefore, correcting narratives of eating to be consistent with biological reality could also assist with weight control.