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Definitions
Hunger : The internal or physiological drive to find and eat food (energy) Appetite : The external or psychological influences that encourage us to find and eat specific food (pleasure) Palatable : Food that is pleased to the senses. This may include taste, smell and texture Satiety : A physiological state in which there is no longer desire to eat
WHY DO WE EAT?
Socioeconomic Factors Eg. Income, food price Biological and Physiological factors Cultural and religious factors Eg. Invitation, fasting, halal, belief
Food choice
Hypothalamic neurons
Two subpopulations of hypothalamic neurons, whose activations have opposing effects on food intake, has provided some insights into the functions of the hypothalamic centres. Activation of one subpopulation of neurons, which produce the neurotransmitters neuropeptide Y (NPY) and agouti-related peptide (AgRP), induces hunger sensations leading to increased food intake; these neurons are referred to as the orexigenic NPY/AgRP neurons. In contrast, activation of another subpopulation of neurons, which produce propiomelanocortin (POMC), cocaine and amphetamine-related transcript (CART), leads to the formation of -melanocytestimulating hormone (-MSH) which, via melanocortin receptors, induces satiety and reduces food intake; they are referred to as the anorexigenic POMC/CART neurons
Aminostatic signals
Dietary protein induces satiety in the short term, and consumption of low protein diets leads to increased appetite for protein containing foods. Atkins diet? Aminostatic theory: Food intake is determined by the level of plasma amino acids, and that this could be related to the regulation of lean body mass, which is known to be rigorously defended against experimental or dietary manipulation.
The various signals from the periphery can be integrated in a model in which the control of food intake is considered in three phases, each with a distinct goal:
1. short-term (hour) blood glucose homeostasis by dampening episodes of hypoglycaemia or hyperglycaemia. 2. medium-term (day) maintenance of adequate hepatic stores of glycogen which, consistent with Flatts glycogenostatic theory, would imply corrective responses to offset deviations from carbohydrate balance during the previous day. 3. long-term (> weeks) maintenance of the bodys fat and protein compartments,. Periods of food deprivation that lead to substantial reductions in body weight are normally followed by increased food intake (hyperphagia). Reanalysis of data on food intake and body composition in humans subjected to experimental semistarvation and refeeding in the classic Minnesota Experiment (Keys et al 1950) suggested that the duration and magnitude of such compensatory hyperphagia is determined by (i) the magnitude of fat loss, (ii) the magnitude of fat-free mass loss and (iii) the severity of energy deprivation (Dulloo et al 1998). These findings are consistent with the existence of powerful signals that relate food intake to body composition as well as to psycho-biological reaction to the state of food deprivation. Conversely, in overfeeding trials, subjects often report great difficulty in maintaining high levels of food intake over long periods of time, and they spontaneously lose weight over subsequent weeks and months, apparently by eating less.