Principles of Behavioral Neuroscience: Hunger
Chapter 6: Hunger
Homeostasis
Definition: Homeostasis refers to the action of a system to maintain internal stability when faced with a disturbance of its normal condition.
Examples of Homeostatic Processes:
Hunger
Thirst
Thermoregulation
Function: These systems allow organisms to maintain energy in a safe range and operate primarily automatically.
Illustration: Refer to Figure 6-1 for a graphical representation of homeostatic mechanisms.
Digestion of Food
Energy Requirement: The human body requires energy to function, which comes from multiple sources:
Water
Oxygen
Minerals
Vitamins
Carbohydrates
Fats
Proteins
Illustration: Refer to Figure 6-2 for an overview of the energy sources.
Digestive Process
In the Stomach:
The stomach uses acid to break down food.
In the Small Intestine:
Enzymes play a critical role in digesting fats, carbohydrates, and proteins.
Nutrient Absorption:
Nutrients from digested food enter the bloodstream and are transported to cells throughout the body.
Water and select minerals are absorbed in the large intestine.
Basal Metabolism:
Definition: Energy used to keep the body functioning and to maintain body temperature.
Illustration: Refer to Figure 6-2 for a visual depiction.
Short-Term Energy Storage
Glucose:
A simple sugar that primarily originates from carbohydrates.
Insulin:
A hormone present in the bloodstream that facilitates the entry of glucose into cells.
ATP (Adenosine Triphosphate):
The energy currency produced when glucose is metabolized inside cells, providing necessary energy for cellular processes.
Illustration: Refer to Figure 6-3A for more details on short-term energy mechanisms.
Glucose & Glycogen
Glycogen Storage:
Excess glucose is stored in the liver as glycogen.
Function of Glucagon: When blood glucose levels decline, glucagon is released to convert glycogen back into glucose, providing additional energy.
Note: Insulin is not required for glucose to enter neurons.
Illustration: Refer to Figure 6-3B for pathways of glucose storage and release.
Long-Term Energy Storage
Primary Source: Most long-term energy is stored as fat.
Triglycerides:
Composed of fatty acids and a glycerol molecule, stored in adipose tissues.
Released when energy levels are low, breaking down into fatty acids usable by most cells.
Brain's Energy Source: The brain exclusively utilizes glucose and does not utilize fatty acids as an energy source.
Illustration: Refer to Figure 6-4 for visual aid on long-term energy storage.
Theories of Hunger and Homeostasis
Glucostatic Theory:
Suggests that hunger is driven by the need to restore normal blood glucose levels.
Lipostatic Theory:
Proposes that hunger is related to maintaining fat levels within a stable range.
Detection Mechanisms:
The body can sense drops in glucose and fat levels, signaling the brain to produce the sensation of hunger and motivate eating.
Glucose-sensitive neurons located in the hypothalamus play a key role in energy level detection.
Limitations of Homeostasis:
Homeostasis cannot fully explain all aspects of eating behaviors, such as:
Eating dessert when already satiated
Eating driven by pleasure, habit, or social influences.
Signals of Hunger and Satiety
Ghrelin:
A peptide hormone released to signal hunger when the stomach is empty.
Vagus Nerve:
Activates in response to stomach stretching when full, contributing to sensations of satiety.
Cholecystokinin (CCK):
Another signal for satiety, released as food enters the small intestine.
Leptin:
A long-term satiety hormone, released in response to the accumulation of adipose (fat) cells.
Illustration: Refer to Figure 6-5 for a chart outlining hunger and satiety signals.
Genetic Influence on Hunger Signals
Genetic Example:
Discussion of a mouse genetically modified to lack the leptin gene. This mouse exhibits increased food consumption and fat accumulation due to the absence of the satiety signal.
Illustration: Refer to Figure 6-6 for visual representation of this genetic study.
Emotional and Cognitive Factors in Eating
Cognitive Control:
Individuals often use cognitive control to manage eating habits, particularly in dieting.
Behavioral Observations:
"Restrained eaters" may consume more food during emotional situations.
Cues Triggering Cravings:
Certain social contexts can trigger specific food cravings, resulting in impulsive eating.
The Hypothalamus: Control Center for Hunger and Satiety
Neuronal Mechanisms:
Neurons in the arcuate nucleus of the lateral hypothalamus (LH) detect ghrelin and activate to signal hunger.
The vagus nerve detects sensory information related to satiety and activates the solitary nucleus.
Neuron Activation:
After food intake, a separate set of arcuate neurons activate the paraventricular nucleus (PVN), signaling satiety.
Illustration: Refer to Figure 6-7 for a visual schematic of hypothalamic circuits.
Neuronal Interactions in Hunger and Satiety
Arcuate Hunger Neurons:
Release neuropeptide Y (NPY) to excite LH neurons, which promotes hunger.
NPY inhibits the activity of the PVN (satiety).
Arcuate Satiety Neurons:
Release alpha melanocyte-stimulating hormone (⍺-MSH), stimulating the PVN and inhibiting LH neurons, reducing hunger signals.
Orexin:
Another appetite-stimulating peptide produced in the lateral hypothalamus.
Illustration: Refer to Figure 6-8 for a depiction of neuronal interactions in hunger and satiety control.
Other Influencing Factors on Eating Habits
Body Weight Influences:
Body weight can fluctuate due to various factors, including:
Pregnancy
Physical illnesses
Sedentary lifestyles (e.g., prolonged sitting)
Social and cultural influences
Disordered eating patterns
Eating Disorders:
Overview of three primary eating disorders:
Anorexia
Bulimia
Binge-eating disorder
Illustration: Refer to Figure 6-12 for an overview of these disorders and their characteristics.