A cautionary tale for health education initiatives in vulnerable populations: Improving nutrition in Haiti prisons.

Introduction: Prisons in low-income countries have barriers to providing adequate nutrition to the incarcerated. This perspective discusses a quality improvement program with health education to improve nutrition provided to men in two prisons in Haiti. Methods: Incarcerated men in the National Penitentiary in Port Au Prince and the prison in Mirebalais were the focus of the program. A culturally competent educational intervention was delivered to the prison cooks. Program evaluation included a baseline and a follow-up assessment in 2021 and 2022 in both prisons. Calories, body composition, and nutrition were assessed at both time points. Results: Among 1,060 men assessed in the baseline time period, the mean number of calories per day was 571. Further, 62.5% had a vitamin C intake insufficient to prevent scurvy and 91.6% had vitamin B1 insufficient to prevent beriberi. In the follow-up period, caloric intake decreased to a mean of 454 per day (p < 0.001). The proportion of incarcerated men who had insufficient vitamin C and vitamin B1 to prevent disease increased in the follow-up period. Discussion: The caloric and nutritional intake of incarcerated men in Haitian prisons is poor and is getting worse. The educational intervention with the cooks was not successful due to civil and political strife in the low-income country of Haiti. Standard interventions to improve nutrition need to consider the social context for accessing food.

Perinatal deficiency in dietary omega-3 fatty acids potentiates sucrose reward and diet-induced obesity in mice.

Insufficient dietary intake of essential omega-3 polyunsaturated fatty acids (N-3), especially during critical stages of development, is well-associated with negative neurological and metabolic consequences. The increased availability and intake of foods rich in saturated fat coincides with reduced N-3 consumption, yet how N-3 dietary deficiency during perinatal development modulates motivation for palatable food and interacts with a high-fat diet to affect body weight and emotional states is not clear. Pregnant C57Bl6 mice and pups were subjected to diets either deficient or adequate (control) in N-3 until postnatal day 21. Adult male N-3 deficient or control offspring were tested in a progressive ratio operant task for sucrose motivated behavior or given prolonged access to a saturated high-fat diet or chow followed by measures of energy balance and anxiety-like behavior in the elevated-plus maze and open field test. Brain fatty acid profiles were measured via gas chromatography mass spectrometry. Perinatal dietary N-3 deficiency lowered brain N-3 levels, augmented the rewarding effects of sucrose, heightened diet-induced weight gain and fat mass accumulation and diminished spontaneous physical activity. Finally, perinatal N-3 deficiency increased anxiety-like behaviour independent of diet in the open field but not in the elevated-plus maze test. Insufficient dietary N-3 during critical periods of developmental can amplify the obesogenic effects of saturated fat intake, enhance motivated behaviour for palatable foods and may elicit negative emotional states that can perpetuate overeating and obesity.

Central Agonism of GPR120 Acutely Inhibits Food Intake and Food Reward and Chronically Suppresses Anxiety-Like Behavior in Mice.

BACKGROUND: GPR120 (FFAR4) is a G-protein coupled receptor implicated in the development of obesity and the antiinflammatory and insulin-sensitizing effects of omega-3 (ω-3) polyunsaturated fatty acids. Increasing central ω-3 polyunsaturated fatty acid levels has been shown to have both anorectic and anxiolytic actions. Despite the strong clinical interest in GPR120, its role in the brain is largely unknown, and thus we sought to determine the impact of central GPR120 pharmacological activation on energy balance, food reward, and anxiety-like behavior. METHODS: Male C57Bl/6 mice with intracerebroventricular cannulae received a single injection (0.1 or 1 µM) or continuous 2-week infusion (1 µM/d; mini-pump) of a GPR120 agonist or vehicle. Free-feeding intake, operant lever-pressing for palatable food, energy expenditure (indirect calorimetry), and body weight were measured. GPR120 mRNA expression was measured in pertinent brain areas. Anxiety-like behavior was assessed in the elevated-plus maze and open field test. RESULTS: GPR120 agonist injections substantially reduced chow intake during 4 hours postinjection, suppressed the rewarding effects of high-fat/-sugar food, and blunted approach-avoidance behavior in the open field. Conversely, prolonged central GPR120 agonist infusions reduced anxiety-like behavior in the elevated-plus maze and open field, yet failed to affect free-feeding intake, energy expenditure, and body weight on a high-fat diet. CONCLUSION: Acute reductions in food intake and food reward suggest that GPR120 could mediate the effects of central ω-3 polyunsaturated fatty acids to inhibit appetite. The anxiolytic effect elicited by GPR120 agonist infusions favors the testing of compounds that can enter the brain to activate GPR120 for the mitigation of anxiety.

Nutritional controls of food reward.

The propensity to select and consume palatable nutrients is strongly influenced by the rewarding effects of food. Neural processes integrating reward, emotional states and decision-making can supersede satiety signals to promote excessive caloric intake and weight gain. While nutritional habits are influenced by reward-based neural mechanisms, nutrition and its impact on energy metabolism, in turn, plays an important role in the control of food reward. Feeding modulates the release of metabolic hormones that have an important influence on central controls of appetite. Nutrients themselves are also an essential source of energy fuel, while serving as key metabolites and acting as signalling molecules in the neural pathways that control feeding and food reward. Along these lines, this review discusses the impact of nutritionally regulated hormones and select macronutrients on the behavioural and neural processes underlying the rewarding effects of food.