PSYCH 320 Chpt 4

Taste and Smell

• These senses act as gatekeepers of what enters the body.
• Five basic tastes are salty, sweet, sour, bitter, and savory (umami).

The Need to Eat

• Eating provides energy for the body, with energy intake ideally equaling energy output.
• Environmental cues such as smells, sights, and time of day influence how much we eat.
• Memory and recall influence eating based on when, what, and how much was last consumed.
• Increased food variety leads to increased energy intake.

Sensory Specific Satiety

• Eating the same foods repeatedly leads to faster satiation, as the food becomes less pleasant.
• There is a link between the amygdala and food preferences.
• Smell plus caloric value impacts eating habits.

Basic Metabolism

• Food consists of carbohydrates, fats, and proteins.
• Carbohydrates break down into glucose in the digestive system, providing energy or being stored as triglycerides in fat cells.
• Fats are converted into triglycerides and stored in fat cells.
• Proteins are converted into amino acids, with excess stored as triglycerides in fat cells.
• Fats break down for energy, producing fatty acids and glycerol.
• Muscles use fatty acids for energy.
• Glycerol converts to glucose in the liver to provide glucose for the brain.

Local Theory of Motivation

• The theory stated surrounding organs send signals that control hunger and thirst.
• A problem with this theory is it does not explain continued feelings of hunger when the vagus nerve is cut.
• Cutting the vagus nerve showed the peripheral organs may not be necessary for feeling hunger.
• The vagus nerve fibers send instructions from the brain to the stomach (20%) and from the stomach to the brain (80%).
• Signals from the brain control gastric acid secretion, digestive enzyme secretion, gastric capacity, and blood glucose.
• Signals from the stomach control satiety (hunger), satiation (fullness), and energy metabolism.

Central Theory of Motivation

• Specialized brain cells detect body changes and trigger motivation.
• Functions include activating sympathetic and parasympathetic nervous systems, activating the pituitary gland, activating the endocrine system, and sensing blood vessel changes.

Homeostatic Regulation

• Homeostatic regulation begins with detecting a change in the body, detecting that change compared to the bodies optimal level, and then taking corrective action to return to the optimal amount in the body.
• The body can take actions like constricting skin blood vessels, curling up, and shivering, to return the body to its optimal temperature.

Regulation of Hunger

• Glucoreceptors measure changes in blood glucose levels.
• Rising glucose levels inhibit eating.

Short-Term vs. Long-Term Regulation

• Short-Term Regulation (STR) controls when and how much we eat.
• Long-Term Regulation (LTR) manages food/energy storage and detects energy changes stored as lipids in adipose tissue.
• Weight typically stays consistent over 5-10 years under LTR.

Regulation of Hunger: Short-Term Regulation

• Regulation of hunger was initially thought to balance energy intake with energy expenditure.
• Damage to the ventromedial hypothalamus (VMH) causes hyperphagia.
  • The VMH was thought to be a "satiety center."
• Damage to the lateral hypothalamus (LH) causes aphagia and adipsia.
  • The LH was thought to be a "hunger center."

Regulation of Hunger: Glucostatic Theory

• Hypothalamus receptors are sensitive to blood glucose changes in arteries and veins.
• Decreased blood glucose causes the LH to stimulate eating.
• Increased blood glucose causes the VMH to inhibit food intake.

Limitations of the Short-Term Regulation Theory

• VMH lesions must specifically target the area and not surrounding fibers to cause obesity.
• LH deprivation of glucose must be extreme to cause eating deficiencies, also affects more than just eating.
• Glucoreceptors do no work like switches and act more as an emergency system.

Regulation of Hunger: Peripheral Detectors for STR

• Peripheral detectors for STR include stretch receptors that limit intake and nutrient detectors that tell the brain what nutrients are being consumed.

Peripheral Detectors for STR: Hormones

• Ghrelin is a hormone produced in the stomach and serves as a "short-term hunger signal," rising sharply before meals and suppressed by food. It is also higher after weight loss.
• Obestatin is the opposite of ghrelin, suppressing appetite.

Peripheral Detectors for STR: Duodenum

• The duodenum possibly has glucoreceptor sites, secretes GIP and GLP-1 to inform the brain about glucose availability.
• Cholecystokinin (CCK) is produced in the intestines, signals the brain to stop eating, and is triggered by fats and proteins.

Peripheral Detectors for STR: Liver

• The liver suppresses feeding via glucoreceptors that transmit info to the hypothalamus via the vagus nerve, which need to be intact.
• The liver initiates feeding: 2-DG injections block glucose receptors, causing them to behave as if glucose is low.

Peripheral Detectors for STR: Pancreas

• The pancreas signals glucose availability through insulin, which transports glucose into cells, and amylin, which slows down nutrient intake.

Regulation of Hunger: Long-Term Regulation

• Lipostatic Theories say receptor systems monitor body fats and regulate food intake as needed.
• The Set-Point Theory says the LH and VMH regulate the body's normal weight, or "set point."

Long-Term Regulation: Leptin

• Leptin is a hormone made by fat cells.
• The hormone is released into the bloodstream in a 1:1 ratio with energy in fat stores.
• Thinner people have less leptin, and bigger people have more leptin.
• The hypothalamus monitors levels of leptin.
• Fat stores increase to increase leptin and insulin.
• NPY decreases
• Alpha-MSH increases

Regulation of Hunger: One vs. Two Processes

• There are two regulatory processes in the body, short and long term.
• STR monitors glucose
• LTR monitors lipids
• There can also be one regulatory process.
• A message is sent when we don't have enough fuel for the brain = hunger
• Hunger fluctuates depending on food availability, convenience of eating, and environmental cues.

Nonhomeostatic Eating Behavior/Failures of Regulation

• Anorexia Nervosa is when a person severely restricts food intake, becoming malnourished or dying.
• Bulimia Nervosa is when a person binges and purges their food intake over a short period of time.
• Obesity results from a long-term imbalance between energy intake and usage.

Anorexia Nervosa

• Prevalence in women is 0.5-1% and men is 5-10%.
• Primary symptoms include food avoidance, low body weight, fear of weight gain, self-evaluation influenced by shape and weight, excessive exercise, illness denial, and amenorrhea.
• There is a 58-76% heritability rate.
• Anorexia nervosa is often due to body image disturbance and body dissatisfaction.
• Anorexia is defined as "without appetite."
• Those with Anorexia experience brain atrophy, enlarged cerebrospinal fluid-filled spaces, decreased blood pressure and heart rate, cognitive/learning deficits, and increased cortisol levels due to starvation.

Anorexia Nervosa: Serotonin Hypothesis

• Higher levels of serotonin leads to rigidity, anxiety, and inhibition.
• Serotonin increases when anorexic patients are at normal body weight.
• Restricting food reduces the production of serotonin.
• Hypothesis: Food restriction reduces anxiety.

Bulimia Nervosa: Purging vs. Nonpurging

• Bulimia Nervosa prevalence in adolescent and young adult U.S. women is 1-2% and in men is 10-15% of total cases.
• Symptoms include recurrent binge eating, compensatory behaviors, often self-induced vomiting or laxative abuse, fear of weight gain, and self-evaluation by shape and weight.
• There is a 59-83% heritability rate.

Bulimia Nervosa: Factors for Binge-Eating

• Difficulty handling emotions accounts for about 50% of cases.
• Restrictive dieting accounts for about 34% of cases.
• Interpersonal conflict accounts for 7% of cases.
• Loss or separation accounts for 6% of cases.
• Other factors account for 8% of cases.
• Uncertain factors account for 5% of cases.

Theories of Bulimia

• Sociocultural theory: Social norms promote thinness = illness.
• Epidemiological/Risk Factors theory: Factors put a person at risk for bulimia.
• Clinical/Psychiatric theory: Psychological distress, low self-esteem, depression, and impulsiveness cause bulimia.

Bulimia Nervosa: Social Contagion Theory

• Social contagion involves a person or group influencing the emotions or behavior of another person or group through the conscious or unconscious induction of emotion states and behavioral attitudes.

Bulimia Nervosa: Escape Theory

• Eating becomes an escape.

Bulimia Nervosa: Serotonin Hypothesis

• Bulimia is due to underactivity of serotonin in the brain that can be measured through CSF.

Obesity

• Obesity is defined as being 20% above the values on a body frame chart.
• Body fat increases, and basal metabolic rate decreases with age.
• It may stem from humans lacking the means to limit fat without outside natural causes such as famine.
• There is also a potential genetic predisposition to accumulate fat.
• Hyperinsulinemia is when insulin increases fat energy storage.
• Fat is metabolically less active.
• Dieting promotes obesity.
• Addiction and dishabituation is happening with food variety.

Regulation of Thirst

• Women's bodies are approximately 50% water.
• Men's bodies are approximately 60% water.
• Intracellular fluid is water within cells.
• Extracellular fluid is water outside cells.

Regulation of Thirst

• Osmometric thirst is the result of the intracellular balance.
• Osmoreceptors trigger the behavior of drinking when there is an imbalance.
• Volumetric thirst is extracellular balance.
  • Low fluid levels result in hypovolemia.
  • It is measured by stretch receptors in the heart vessels and the hormonal response to angiotensin.

Regulation of Thirst: Kidneys

• Thirst is controlled by sodium receptors
• Kidneys absorb 99% of water filtered.
• Kidneys absorb sodium.
• A drop in blood volume signals that there is a loss of sodium and water.

Regulation of Thirst: Renin-Angiotensin System

• The renin-angiotensin-aldosterone (RAA) pathway helps regulate blood volume, blood pressure, and levels of Na+, K+, and H+ in the blood.
• The Juxtaglomerular cells of the kidneys also are active.
• The Liver releases Angiotensinogen.
• The lungs regulate ACE = Angiotensin Converting Enzyme, which creates angiotensin I and then II.
• Aldosterone secretion leads to more water being conserved and reabsorbed by the body.

Regulation of Sexual Motivation

• Testosterone → DNA → Males
• Sexual dimorphism happens due to XX or XY chromosomes.
• Attractivity comes from behaviors that attract a mate.
• Proceptivity refers to species-specific behavior that arouses the mate.
• Receptivity leads to the transfer of sperm.

Regulation of Sexual Motivation

• Damage to the Hypothalamus leads causes hypogonadal conditions, asexuality, underdevelopment of genitals, and a lack of secondary sexual characteristics.

Regulation of Aggressive Motivation

• Aggression utilizes the limbic system.
  • Sham rage = rage without cortical behavior
  • Affective attack = pupil dilation, intention movements (arched back, bared teeth)
  • Quiet biting attack = pouncing

Types of Aggressive Motivation

• Predatory aggression
• Intermale aggression
• Fear-induced aggression
• Irritable aggression
• Territorial defense
• Maternal aggression
• Instrumental aggression