Hunger, Eating, and Health

Digestion

Is the gastrointestinal process of breaking down food and absorbing its constituents into the body

Lipids, Amino acids, and Glucose

Energy is delivered to the body in three forms:

Fats

Most efficient for energy storage

Energy metabolism

Chemical changes that make energy available for use Cep

Cephalic phase

Preparatory phase; sight, smell, or even just the thought of food until intake

Absorptive phase

Energy is absorbed into the blood stream

Fasting phase

Usage of all stored energy and withdrawal of energy from its reserves

Insulin

High during cephalic and absorptive

• Triggers glucose use as fuel by body cells

• Triggers conversion of blood-borne energy to fat, glycogen, and protein

• Triggers energy storage in adipose cells, liver, and muscles

Glucagon

High during fasting phase

• Triggers change of stored energy to usable fuel: fat to free fatty acids and then ketone: protein to glucose

Gluconeogenesis

Conversion of protein to glucose

The Set-Point Assumption

Hunger is a response to an energy need; we eat to maintain an energy set point

Set-point mechanism

Defines the set point

Detector mechanism

Detects deviations from the set point

Effector mechanism

Acts to eliminate the deviations

Negative feedback system

Turns on when energy is needed, off when set point is reached

Glucostatic theories

The main purpose of eating is to defend a blood glucose set point, because glucose is the brain’s primary fuel

Lipostatic theories

Deviations from body fat’s set point produce compensatory adjustments in the level of eating that return level of body fat to their set point.

Positive-Incentive Theory

Humans and other animals are not normally driven to eat by internal energy deficits but are drawn to eat by the anticipated pleasure of eating (behavior)

Satiety

May stop a meal, “being full”

Nutritive density

Calories per unit volume of the food; maintaining a single diet

Sham eating

The amount we eat is influenced largely by our previous experience with the food’s physiological effects, not by the immediate effects of the food in the body

Appetizer effect and Satiety

Small amounts of food consumed before a meal actually increase hunger rather than reducing it

Occurs because it elicits cephalic-phase response

Serving size and Satiety

The larger the serving, the more we tend to eat

Cafeteria Diet

Offering of varied diet of highly palatable foods

Hyperphagia (excessive eating)

Lesions produce _______ and extreme obesity in rats

Dynamic phase

Several weeks of grossly excessive eating and rapid weight gain

Static phase

Consumptions declines to a level that is just sufficient to maintain a stable level of obesity

Aphagia & Adipsia

Lesion produce ____ (cessation of eating) and ____ (cessation of drinking)

Cannon and Washburn

Their studies suggested stomach contractions led to hunger, while stomach distention to safety

Gut peptide

Decrease meal size

Hunger peptides

Usually synthesized in the hypothalamus

Diet-Induced thermogenesis

Mechanism by which the body adjusts the efficiency of its energy utilization in response to its levels of body fats

Basal Metabolic Rate

The rate at which energy is utilized to maintain bodily processes when resting

Settling point

The level which the various factors that influence body weight achieve an equilibrium

Leptin

A negative feedback fat signal

Gastric bypass

A surgical treatment for extreme obesity that involves short-circuiting the normal path of food through the digestive tract so that its absorption is reduced.

Adjustable gastric band

Involves surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it

Anorexia

Voluntary self-starvation

Fatal in 10% of patients

underweight

Bulimia

Bingeing & Purging; excessive use of laxatives, enemas, or diuretics; orextreme exercise

Obese or normal weight

Bingeing anorexics

Bulimics who are underweight