Lecture 1: Obesity, Appetite Regulation, Energy Balance Flashcards
What factors influence energy intake?
Longer term (tonic) and shorter term (episodic) factors: genetic, biological, physiological, environmental, behavioural and cognitive influences
What’s the problem with living with obesity?
It is a risk factor for non-communicable diseases (cannot catch it from the other person). Some cancers, musculoskeletal disorders (eg osteoarthritis) and cardiovascular diseases such as heart disease and stroke. But obesity and associated diseases are preventable! Obesity also has economic and national health service impacts.
What is obesity?
Abnormal or excessive fat accummulation that presents a risk to health (WHO, 2020)
What is energy balance?
Implies an interplay between energy intake (EI) and energy expenditure (EE). Energy in: food, carbohydrates, lipids, proteins, alcohol
Energy out: basal metabolism (60-75%); thermogenesis (10%); physical activity (15-30%). Energy balance in humans complies with the first law of thermodynamics- energy cannot be made or destroyed (Hall et al., 2012).
Contribution of organs to BMR: liver 26%, muscle 26%, brain 18%, heart 9%, kidney 7%.
Thermogenesis
Increased rate in metabolism after a meal that occurs due to digestion and the absorption of nutrients
Macronutrients
Fat: most energy dense and in general less satiating than carbohydrates and protein; 9kcal/g
Protein is the most satiating macronutrient; 4kcal/g
Carbs: 4kcal/g
Set point Model (Kennedy, 1963)
Set point model (Kennedy, 1963): individuals have an in-built target of body fatness that the body defends by increasing or decreasing intake and expenditure. But this does not explain the obesity pandemic (people would not gain weight)
Settling Point Model (Wirtshafter & Davis, 1977)
A level of body fatness is not set nor a target but is the consequence of changing intake and expenditure. But it omits any sort of active regulation from fat stores.
Dual Intervention Model
Body defends high and low set points but in between settles at a level of body fatness based on energy intake and expenditure.
General Intake Model
Factors that affect food intake are sorted in two: compensated (primarily physiological, with negative feedback loops affecting and being affected by intake) and uncompensated (primarily environmental, which affect but are not affected by intake).
Tonic factors/ long term influences
Genetics play a part but no single gene is responsible for obesity.
Biological signalling (central / peripheral mechanisms)
Physiological
Environmental, cognitive, behavioural influences
Biological signalling (central mechanisms)
Orexigenic peptides: anabolic effector pathways; search for and consumption of food; decrease energy expenditure; overall aim to lay down fat and increase hunger (eg Neuropeptide Y, Orexin A &B)
Anorexigenic peptides: catabolic effector pathways; decrease intake by inhibiting hunger (eg CRF, 5-HT)
Structures in hypothalamus: lateral hypothalamic area (LHA); arcuate nucleus (ARC); paraventricular nucleus (PVN)
Biological signalling (peripheral)
Leptin; lipostatic (set point) model of energy regulation
Secreted from adipose tissue
Increase in fat mass=increase in leptin=decrease in drive to eat
Decrease in fat mass=decrease in leptin=increase in drive to eat
Physiological Tonic Factor
Fat free mass; main tonic (long term) driver to eat (arising from biological needs)
Environmental, cognitive and behavioural tonic influences
Bronfenbrenner’s Ecological Systemm Theory/Model (1977): change in one system can affect the individual (individual-microsystem-mesosystem-ecosystem-macrosystem); increase in availability, convenience and decrease in price of highly palatable foods; increase in portion size norms
Biological Episodic Factors
(Peripheral); hunger and satiety related hormones before and after eating
Appetite stimulating (orexigenic): ghrelin- hunger hormone (lowers leptin)
Appetite suppressing (anorexigenic): CCK, insulin (suppress drive to eat)
Cephalic stage hormone secretion (eg insulin)
Genetic/behavioural/cognitive & Environmental episodic factors
Reactivity/reaction to specific smells, flavors, nutrients, packaging
Social norms/ influence and distraction
Cognitive/behavioural/biological episodic factors
Decision to eat because of hunger
Decision to choose your food and portion size
Decision to stop eating because of satiation
Satiation: within-meal sensation of fullness that leads to the termination of eating
Satiety: the inhibition of intake after the termination of eating (before the next meal)
Central mechanisms
Orexigenic peptides (Neuropeptide Y, Orexin A & B) Anorexigenic peptides (CRF: corticotrophin releasing factor; 5-HT: serotonin)
Peripheral mechanisms
CCK: cholescystokinin (fullness- released by stretch receptors in stomach, received by brainstem/hypothalamus
Leptin: adipose/satiety hormone
Ghrelin: hunger hormone, stimulates appetite by lowering leptin
Food neophobia
Reluctance to eat or taste novel food (developmental)
Growth faltering
Unsatisfactory growth (weight/height) for healthy development for age and gender
Child food refusal
Persistent refusal to eat food or foods over a sustained period despite repeated offerings
Restrained eating
The intentional restriction of food intake in order to maintain or loose weight -cognitive resources (not natural, not necessarily dieting)
Disinhibited eating
Disruption of habitual restriction/ inhibition of intake resulting in overconsumption (unconscious)
Counterregulatory eating
Cognitively-mediated tendency for restrained eaters to consume more after a preload than do unrestrained eaters, who compensate (regulate) by reducing intake in a subsequent meal (abstinence violation/emotion regulation)
