PSY 7: Biopsychology Midterm 3

Chapter 12 Hunger, Eating, and Health

Control of Eating

* Is there a “set point” for the body’s energy \n reserves that determines when we eat?
* The prevalence of eating disorders suggests that \n this may not be the case.
* Over half of the adult population in the U.S. meets \n clinical criteria for obesity.
* The average American consumes 3,800 calories \n per day—about twice the average requirement.
* 3 percent of U.S. adolescents suffer from anorexia \n or bulimia.

Digestion, Energy Storage, and Energy Utilization

* The purpose of eating is to provide the \n body with molecular building blocks and \n energy.
* Digestion: breaking down food and \n absorbing its constituents

Energy Storage in the Body

* Energy is delivered to the body as lipids, amino acids, and glucose.
* Energy is stored in the body as fats, glycogen, and proteins.
* Fats are most efficient for energy storage.
* One gram of fat stores twice as much energy as one gram of glycogen.
* Fat does not attract and hold as much water as glycogen, and so provides denser energy storage

Three Phases of Energy Metabolism

* Three Phases of Energy Metabolism
* Energy metabolism: chemical changes that \\n make energy available for use
* Cephalic phase: preparation for eating
* Absorptive phase: energy absorbed
* Fasting phase: withdrawing energy from \\n reserves
* Ends with next cephalic phase
* Energy availability is controlled by two pancreatichormones.
* Insulin: high during cephalic and absorptive phases
* 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 ketones; protein to glucose

Theories of Hunger and Eating: Set Points vs. Positive Incentives

* The Set-Point Assumption
* Hunger is a response to an energy need; weeat to maintain an energy set point.


* Typical assumption: eating works like a \n thermostat, a negative feedback system; it \n turns on when energy is needed and off \n when the set point is reached

Glucostatic and Lipostatic Set-Point Theories of Hunger

* If we eat to maintain an energy level \n (homeostasis), what is monitored? (c. 1940s \n and 1950s)
* Glucostatic theories: glucose levels \n determine when we eat
* Lipostatic theories: fat stores determine how \n much we eat over long term (explaining why \n weight tends to be constant)

Problems with Set-Point Theories of Hunger and Eating

* These theories are contrary to evolutionary \n pressures that favored energy storage for \n survival.
* Reductions in blood glucose or body fat do \n not reliably induce eating.
* These theories do not account for the \n influence of external factors on eating and \n hunger.

Positive-Incentive Perspective

* We are drawn to eat by the anticipated \n pleasure of eating.
* We have evolved to crave food.
* Multiple factors interact to determine the \n positive-incentive value of eating.
* This accounts for the impact of external \n factors on eating behavior.

Factors That Determine What, When, and How Much We Eat

* Adaptive Species-Typical Preferences
* Sweet and fatty foods = high energy
* Salty = sodium-rich
* Adaptive Species-Typical Aversions
* Bitter = often associated with toxins
* Learned Preferences and Aversions
* Rats prefer a diet with vitamins, as well as foods they smell in mother’s milk or on other rats’ breath
* We tend to get hungry at mealtime.
* As mealtime approaches, the body enters thecephalic phase, leading to a decrease inblood glucose.


* Pavlovian conditioning of hunger has been \n demonstrated experimentally
* Satiety: may stop a meal, “being full”
* Satiety signals: food in gut and glucose in the \n blood can induce satiety signals.
* Sham eating studies demonstrate that satiety \n signals are not necessary for meal \n termination.
* Rats initially sham eating eat a normal-sized meal if the food is familiar
* Appetizer effect: small amounts of food may \n increase hunger.
* Due to cephalic-phase responses?
* Serving size: the larger the serving, generallythe more consumed.
* Social Influences
* Even rats eat more when in a group up

Sensory-Specific Satiety

* Tasting a food immediately decreases the \n positive-incentive value of similar tastes and \n decreases the palatability of all foods about \n 30 minutes later.
* Adaptive; Encourages a Varied Diet
* Some foods are resistant to sensory-specific \n satiety: rice, bread, potatoes, sweets, and \n green salads

Physiological Research on Hunger and Satiety (Outline)

* Role of Blood Glucose Levels
* Myth of Hypothalamic Centers
* Role of the GI Tract
* Hunger and Satiety Peptides
* Serotonin and Satiety

Role of Blood Glucose Levels in Hunger and Satiety

* Blood glucose drops prior to a meal as \n preparation to eat—not a cue to eat.
* Blood glucose must decrease by 50 percent to \n trigger feeding.
* Premeal glucose infusions often do not \n suppress eating.
* Reduced blood glucose may contribute to \n hunger, but changes in blood glucose do not \n prevent hunger or satiety

Myth of Hypothalamic Hunger and Satiety Centers

* Experiments suggested two hypothalamic \n centers.
* Ventromedial (VMH): a satiety center
* Lateral (LH): a hunger center
* Lesions of VMH produce hyperphagia.
* Lesions of LH produce aphagia and adipsia
* The VMH likely is not a satiety center.
* VMH lesion rats maintain a new, higher weight.
* VMH lesions may non-specifically destroy other brain regions (noradrenergic bundle; paraventricular nucleus).
* The LH likely is not a feeding center.
* LH lesioned rats will recover if kept alive by tube feeding.
* LH lesions may produce sensory and motor disturbances that affect food seeking.
* The most supported role of the hypothalamus is the regulation of energy metabolism

Role of the Gastrointestinal Tract in Satiety

* Cannon and Washburn (1912)
* Studies suggested that stomach contractions led to hunger, and distension to satiety.
* However, hunger is still experienced by those with \n no stomach (but rest of GI tract remaining).
* In a rat study, rats with a transplanted stomach \n and intestine expressed sated behavior when food \n was injected.
* Led to hypothesis of blood borne satiety signal(s)

Hunger and Satiety Peptides

* Gut peptides that decrease meal size:
* Cholecystokinin (CCK), bombesin, glucacon, \n alpha-melanocyte-stimulating hormone, \n somatostatin
* Must First Establish that Peptide Does Not \n Merely Create Illness
* CCK causes nausea at high doses, but \n suppresses food intake at doses insufficient \n to induce taste aversions.
* Hunger peptides usually synthesized in the \n hypothalamus:
* Neuropeptide Y, galanin, orexin-A, ghrelin
* Overall, many different neural signals \n control eating (not just glucose and fat).
* The hypothalamus plays a central role in \n eating behaviors.
* Microinjections of some peptides have major \n effects on eating

Serotonin and Satiety

* Serotonin agonists consistently reduce \n rats’ food intake.
* Even intake of palatable food is affected.
* Reduces amount eaten per meal
* Preferences shift away from fatty foods.
* Similar effects are seen in humans

Prader-Willi Syndrome: Patients with Insatiable \n Hunger

* Symptoms
* Food-related: insatiable appetite; extremely slow metabolism; eventual death in adulthood from obesity-related diseases
* Other symptoms: weak muscles, small hands and feet, triangular mouth, stubbornness, feeding difficulties in infancy, tantrums, compulsivity, skin picking
* Damage to or Absence of a Section of \n Chromosome 15
* Study of the syndrome may lead to advances in understanding eating behaviors in humans

Body Weight Regulation: Set Points vs. Settling Points

* Variability of Body Weight
* According to the set-point assumption, it should be very difficult to gain weight.
* Set Points and Health
* Free-feeding does not lead to optimum health.
* Positive effects seen with caloric restriction
* Diet-induced thermogenesis: body \n temperature drops with fat loss, making \n weight-loss diets gradually less effective

Set Points and Settling-Points in Weight Control

* Body weight drifts around a natural settling \n point: “the level at which the various factors \n that influence body weight achieve an \n equilibrium.”
* A new body weight will be established if \n conditions remain constant.
* A Loose Kind of Homeostatic Regulation
* Modeled by the Leaky Barrel

Who Needs to Be Concerned about Obesity?

* Everyone: rates of obesity are increasing in \n most parts of the world.
* Obesity is related to many other health \n problems.

Human Obesity: Causes, Mechanisms, and Treatments

* Why is there an epidemic of obesity?
* Evolution favored preferring high-calorie food, \n eating to capacity, storing fat, and using energy \n efficiently.
* Cultural practices and beliefs promote \n consumption.

Why Do Some People Become Obese While Others Do Not?

* Energy Input Differences
* Craving for high-calorie foods
* Cultural norms
* Large cephalic-phase response to sight and smell of food
* Energy Output Differences
* Exercise
* Diet-induced thermogenesis
* NEAT (nonexercise activity thermogenesis)
* Genetics interact with both energy input and \n output.

Why Are Weight-Loss Programs Typically Ineffective?

* Considering the leaky-barrel model, long- \n term weight loss will require a permanent \n lifestyle change.
* Exercise also can make you hungry.
* Often people eat more calories after the \n workout than they burned during the workout.

Leptin and the Regulation of Body Fat

* Leptin: a negative feedback fat signal
* Hormone released by fat cells
* Leptin receptors found in the brain
* Ob/ob mice are three times normal weight.
* Homozygous for a mutant gene ob
* Lack leptin
* Eat more, and store fat more efficiently than \n controls
* Human Leptin Research
* However, most obese humans have high leptin \n levels. Leptin injections help the few ob/ob \n humans.

Leptin, Insulin, and the Arcuate Melanocortin System

* Insulin brain levels reflect visceral fat; leptin \n levels reflect subcutaneous fat.
* Both insulin and leptin receptors are found \n in the arcuate nucleus of the hypothalamus.
* Leptin and insulin in the brain have some \n effects on eating behavior, but are (again) \n not the only eating/sating signals

Treatment of Obesity: Serotonergic Agonists

* Serotonin appears to increase short-term satiety \n signals associated with the consumption of a \n meal and decrease:
* Urge to eat high-calorie foods
* Consumption of fat
* Intensity of hunger
* Size of meals
* Number of snacks and bingeing
* Early serotonin agonists produced heart disease \n in some patients and were withdrawn from the \n market

Treatment of Obesity: Gastric Surgery

* Gastric bypass and the adjustable gastric band \n create a smaller stomach.
* Treatments are for extreme obesity.
* These treatments are effective in some patients.

Anorexia and Bulimia Nervosa

* Anorexia
* Voluntary self-starvation
* Fatal in 10 percent of patients
* Bulimia: bingeing and purging
* The two illnesses have similar symptoms, \n and can be difficult to distinguish.
* Distorted body image
* Most often affects educated, affluent young \n females
* Associated with obsessive-compulsive disorder and depression

Anorexia and Positive Incentives

* It is not clear whether anorexics find food \n less appealing.
* Some evidence suggests the opposite.

Anorexia Nervosa: A Hypothesis

* A person out of homeostatic balance might \n find a full meal to be aversive.
* Eating a meal would then lead to development \n of food aversions.
* For example, feeding meals to famine victims \n sometimes leads to anorexia.
* The implication is that anorexics should eat \n small amounts of food throughout the day \n as part of their therapy

Energy is stored in three forms: fats, glycogen, and _________.

proteins

Where in the body is glycogen largely stored?

Liver and muscles

The correct order for the three phases of energy metabolism, beginning with cephalic, is _____.

cephalic→absorptive→fasting

The fasting phase of metabolism is characterized by high blood levels of _____ and low levels of _____.

glucagon; insulin

Which of the following is among the three components of set-point systems?

Effector mechanism

All set-point systems are systems in which feedback from changes in one direction elicit compensatory effects in the opposite direction known as _____________.

negative feedback systems

In the 1950s, the dominant view was that eating behavior was regulated by _____.

the interaction of a short-term glucostatic system and a long-term lipostatic system

An alternative to the set-point theory that asserts that humans and other animals are drawn to eat by the anticipated pleasure of eating is referred to as the _____ theory of eating.

positive-incentive

Human preferences for sweet and fatty tastes are adaptive because _____.

these tastes are characteristic of high-energy foods in nature

Woods suggests that eating a meal has the immediate effect of being homeostasis-_____.

disturbing

Satiety signals are dependent upon the _____.

volume and nutritive density of food in the gut

The study of what type of eating indicates that satiety signals from the gut or blood are not necessary to terminate a meal?

Sham

Studies on rats by Campfield and Smith on the physiological effects of glucose on satiety reveal _____.

about 10 minutes before the initiation of a meal, blood glucose levels suddenly drop

Large bilateral lesions to the lateral hypothalamus in rats result in _____.

aphagia and adipsia

Early studies by Cannon and Washburn found that physiological feelings of hunger were associated with _____.

stomach contractions

Several hunger peptides have also been discovered and these peptides tend to be synthesized in the brain, particularly in the hypothalamus. Which of the following is one of the most widely studied hunger peptides?

Galanin

The Prader-Willi patient acts as though he or she is ___________.

starving

A study of adult Okinawans suggests _____.

there are health benefits to eating less

The leaky-barrel model is a _____ model of body weight regulation.

settling-point

What type of fat is more common in males than females and poses the greater threat to health?

Visceral

In the 1950s, homozygous mice developed a mutation that resulted in gross obesity. In the 1990s, it was found that these mice lacked _____.

Leptin

Most leptin and insulin receptors are located in the _____.

arcuate nucleus of the hypothalamus

Which one of the following is a purging method used by people with bulimia?

laxatives

Which of the following is a serious medical complication usually associated with bulimia nervosa?

electrolyte imbalance

The author posits that the aversive physiological effect of meals may be an explanation for the paradoxes associated with _____.

anorexia

Chapter 13 Hormones and Sex

Developmental and Activational Effects of Sex \n Hormones

* Developmental (or organizational): \n influencing the development of anatomical, \n physiological, and behavioral characteristics \n that differentiate the sexes
* Activational: triggering reproduction-related \n behavior in mature individuals
* Adolescent surges have both developmental \n and activational effects.

Neuroendocrine System: Glands

* Exocrine glands: release chemicals into ducts \n which carry them to their targets
* Sweat glands, for example
* Endocrine glands: ductless; release \n hormones directly into the circulatory system
* Only organs whose primary function is hormone \n release are referred to as endocrine glands
* Male testes produce sperm cells.

Female ovaries produce ova.

* Sperm and ova each have 23 chromosomes.

Fertilization

* Sperm cell + ovum = zygote
* 23 pairs of chromosomes

X and Y: sex chromosomes

* XX = female; XY = male

Classes of Hormones

* Amino Acid Derivatives
* Epinephrine, for example (adrenal medulla)
* Peptides and Proteins
* Short and long chains of amino acids
* Steroids
* Synthesized from cholesterol (fat)
* Fat-soluble; able to enter cells and bind to \n receptors in cytoplasm or nucleus

Sex Steroids

* Released by Gonads
* Androgens: E.G., Testosterone
* Estrogens: E.G., Estradiol
* Adult testes release more androgens and \n ovaries more estrogens.
* Progestins: also present in both sexes
* Progesterone prepares the uterus and breasts for \n pregnancy.
* The adrenal cortex also releases sex \n steroids.

Hormones of the Pituitary

* “Master Gland”
* Tropic hormones influence the release of \n hormones by other glands.
* Posterior pituitary: hormones synthesized \n in the hypothalamus
* Anterior pituitary: tropic hormones

Cyclic vs. Steady Gonadal Hormone Levels

* Female hormones go through a 28-day cycle: the menstrual cycle.
* Male hormone levels are constant.
* Anterior pituitary activity is controlled by the \n hypothalamus.
* The hypothalamus determines whether hormone levels cycle

Neural Control of the Pituitary

* Researcher working with birds were first to implicate the control over pituitary function by the nervous system.
* Light/dark cycling and breeding changed hormone release.
* Lesion and stimulation experiments established the hypothalamus as the regulator of the anterior \n pituitary.
* These experiments did not explain how the signal \n was mediated, as the anterior pituitary is not \n “connected” to the hypothalamus by neurons

Control of the Pituitary by the Hypothalamus

* Posterior: neural input from hypothalamus
* Vasopressin: antidiuretic hormone
* Oxytocin: labor and lactation
* Synthesized in hypothalamic paraventricular \n and supraoptic nuclei
* These nuclei have terminals in the posterior \n pituitary.
* Anterior pituitary: hypothalamopituitary \n portal system carries hormones from the \n hypothalamus to the anterior pituitary

Discovery of Hypothalamic Releasing Hormones

* Thyrotropin-releasing hormone was first \n isolated from the hypothalamus of sheep and \n subsequently from pigs.
* It triggers the release of thyrotropin from the \n anterior pituitary.
* Thyrotropin then stimulates release of \n hormones from the thyroid gland

Regulation of Hormone Levels

Neural

* All endocrine glands (except the anterior \n pituitary) receive neural signals.
* From cerebral or autonomic neuron

Hormonal

* Tropic hormones, negative feedback

Nonhormonal chemicals

* Glucose, Ca2+, Na+

Pulsatile Hormone Release

* Hormones tend to be released in pulses.
* This often leads to large minute-to- \n minute fluctuations in hormone levels.

Hormones and Sexual Development of the Body

* Humans are dimorphic; that is, they exist in \n two forms.
* Genetic information on the sex chromosomes \n normally determines male or female \n development

Fetal Hormones and Development of Reproductive \n Organs: Gonads

* Initially, there is a primordial gonad.
* Cortex: potential to be an ovary
* Medulla: potential to be a testis
* If XY, the Sry gene on the Y chromosome triggers \n the synthesis of Sry protein.
* If no Sry protein is present, the cortex develops \n into an ovary

Fetal Hormones and Development of Reproductive \n Organs: Internal Reproductive Ducts

* Both sexes begin with two sets of \n reproductive ducts.
* Wolffian system: male; seminal vesicles, vas \n deferens
* Müllerian system: female; uterus, vagina, \n fallopian tubes
* Third Prenatal Month: Differentiation of Ducts
* Testes produce testosterone and Müllerian- \n inhibiting substance.
* The Wolffian system develops, the Müllerian system degenerates, and the testes descend.
* If there are no testes, there are no testicular \n hormones
* In this case, the Müllerian system develops and the Wolffian system degenerates.

External Reproductive Organs

* External reproductive structures (genitalia) \n develop from one bipotential precursor.
* Differentiation occurs in the second month \n of fetal development.
* Testosterone produces male structures.
* Without testosterone, female structures \n develop.

Puberty: Hormones and the Development of Secondary Sex Characteristics

* Fertility is achieved.
* Secondary sex characteristics develop.
* Features unrelated to reproduction that \n distinguish sexually mature men and women
* There is an increase in the release of anterior \n pituitary hormones.
* Growth hormone acts on bone and muscle.
* Gonadotropic hormone
* Adrenocorticotropic hormone
* Relative levels of androgens and \n estrogens determine whether male or \n female features develop.
* Androstenedione: androgen necessary for \n the growth of axillary (underarm) and pubic \n hair in females (more evidence against \n mamawawa)

Sex Differences in the Brain

* Pfeiffer first discovered a sex difference \n in mammalian brain function.
* Pfeiffer (1936) gonadectomized and \n implanted gonads in neonatal rats.
* Gonadectomy causes cyclic (female)gonadotropin release pattern.
* Transplant of testes to males or femalescauses steady (male) gonadotropin releasepattern.
* Perinatal androgens lead to male pattern

Aromatization Hypothesis

* Sex steroids are all derived from \n cholesterol and are readily converted \n from one to the other.
* Aromatized testosterone becomes estradiol.
* Evidence suggests that estradiol \n masculinizes the brain, at least in \n rodents.

Evidence that Estradiol Masculinizes the Neonatal \n Brain

* Neonatal injections of estradiol masculinize.
* Dihydrotestosterone can’t be converted to \n estradiol and doesn’t masculinize.
* Alpha fetoprotein deactivates circulating estradiol \n but does not cross the blood–brain barrier.
* Blocking aromatization or estradiol receptors \n interferes with the masculinizing effects of \n testosterone

Mother’s Estradiol Doesn’t Masculinize Female Brains

* In female rodents, Alpha fetoprotein in blood \n during perinatal period:
* Protects the female brain from estradiol.
* Binds to circulating estradiol, so none gets to the \n brain.
* In male rodents, testosterone enters the brain \n and then is converted to estradiol.
* In humans, aromatization is apparently not \n necessary for testosterone to masculinize the \n brain

Modern Perspectives on Sexual Differentiation of the \n Mammalian Brain

* No single mechanism can account for the development of sexual dimorphisms of mammalian brains.
* Aromatase is only required for testosterone effects onmasculinization in some areas of the brain.
* Female brain development may not automatically occur in absenceof estrogens.
* Various dimorphisms emerge at different stages under differentinfluences.
* Sex chromosomes influence brain development independent oftheir effect on hormones.
* Studies with gene knockout mice indicate that estradiol plays anactive role in the female program of brain development

Perinatal Hormones and Behavioral Development

* Masculinize: promoting male behavior \n (i.e., mounting)
* Defeminize: preventing female behavior \n (i.e., lordosis)
* Perinatal testosterone masculinizes and \n defeminizes.
* Neonatal castration of male rats feminizes \n and demasculinizes

Three Cases of Exceptional Human Sexual Development

* Anne S.
* Knowing how normal development occurs, you should be able to understand what could cause abnormal sexual development.
* Why might a woman not cycle and not have pubic or axillary hair?
* What determines whether male or female hormonepatterns develop?
* What causes the growth of pubic and axillary hair?
* Anne is chromosomally male: XY
* Internalized testes, but no ovaries
* Her hormone levels are those of a man.
* Androgenic Insensitivity Syndrome
* Normal male androgen levels, but no response \n to them
* She does respond to estrogens, so she \n effectively has more estrogens than androgens —leading to the development of female secondary sex characteristics

Elaine

* Elaine was born with somewhat ambiguous \n genitals, but raised as a girl.
* She developed male secondary sex \n characteristics in puberty.
* Eventually, Elaine was diagnosed with \n adrenogenital syndrome

Adrenogenital Syndrome

* Adrenogenital syndrome is caused by congenital \n adrenal hyperplasia.
* Too little cortisol leads to compensatory excessive \n release of adrenal androgens in XX females.
* This may masculinize female genitalia and behavior, in which case surgical and hormonal treatments are \n needed at birth.
* Those affected are often tomboyish, and experience late onset of menstruation.
* Prior to modern treatments (created in the 1950s), changes in sexual identity at puberty were \n unpredictable and likely to be traumatic

John/Joan

* A surgeon’s error led one of a pair of male \n twins to be raised as a girl.
* An artificial vagina was created.
* Estrogen was administered at puberty.
* John/Joan never felt or acted like a girl—this \n indicates that the key to one’s gender is in \n the brain.
* John/Joan chose to become John later in life, \n but never recovered from the ordeal.
* David Reimer (“John”) took his life in May \n 2004

Male Reproduction-Related Behavior and Testosterone

* Effects of Orchidectomy (Bremer, 1959)
* Reduced sexual interest and behavior
* The rate and degree of loss varies.
* Still have adrenal testosterone
* Level of male sexuality is NOT correlated \n with testosterone levels in healthy men.
* Increasing male testosterone levels does \n NOT increase sex drive

Female Reproduction-Related Behavior and Gonadal \n Hormones

* In rats and guinea pigs, surges of estrogen \n and progesterone initiate estrus, a period \n of fertility and receptivity.
* In women, sexual motivation and behavior \n are not tied to cycle.
* Sex drive may be under androgenic \n control

Human Female Sexuality and Androgens

* Testosterone increases the proceptivity of \n ovariectomized and adrenalectomized \n female rhesus monkeys.
* Correlations are seen between sexual \n motivation and testosterone.
* Testosterone has been found to rekindle \n sexual motivation in ovariectomized and \n adrenalectomized women

Anabolic Steroid Abuse

* Anabolic: growth-promoting
* There is no firm scientific evidence that \n muscularity and strength are increased as a \n result of steroid use.
* Sex-Related Side Effects
* High-circulating hormones cause a reduction \n of natural release (negative feedback loop).
* Men: testicular atrophy, sterility, gynecomastia \n (breast enlargement)
* Women: amenorrhea (cessation of \n menstruation), sterility, hirsutism (excessive \n growth of body hair)

Neural Mechanisms of Sexual Behavior

* Sexually Dimorphic Nucleus (SDN)
* Medial preoptic area of rat hypothalamus
* Larger in males, due to estradiol shortly after \n birth
* Size of male SDN is correlated with testosterone \n levels and aspects of sexual activity.
* Nuclei in preoptic, suprachiasmatic, and \n anterior regions of the hypothalamus are \n larger in men than in women

Medial Preoptic Area of the Hypothalamus

* Contains the SDN
* Destruction abolishes male sexual behavior of \n mammalian males and females studied, but \n does not affect female sexual behaviors in \n females.
* Stimulation elicits copulatory behaviors.
* Evidence favors a motivational role for male \n sexual behavior

Ventromedial Nucleus (VMN) of the Hypothalamus

* The VMN contains circuits critical for \n female rat sexual behavior.
* Lesions in this area eliminate lordosis.
* Microinjections of estrogen and \n progesterone induce estrus.
* Lesions of periaqueductal gray (PAG) or \n the tracts to it eliminate lordosis

Ventral Striatum and Sexual Activity

* The ventral striatum is activated when \n individuals view sexually provocative \n images.
* In rats, this area is associated with the \n anticipation and experience of sex

Sexual Orientation and Sexual Identity

* Heterosexual: sexually attracted to members \n of the opposite sex
* Homosexual: sexually attracted to members \n of the same sex
* Bisexual: sexually attracted to members of \n both sexes

Sexual Orientation and Genes

* There is a 48 percent homosexual \n concordance rate for monozygotic twins—16 \n percent for dizygotic twins.
* There is limited evidence for a particular \n gene related to homosexuality

Sexual Orientation and Early Hormones

* Orchidectomy reduces sexual behavior of males, but does not redirect it.
* Non-human studies indicate that perinatal hormones can influence sexual orientation.
* Human research is less conclusive.
* No differences in adult hormone levels
* Prenatal exposure to artificial estrogen has weak correlation with homo- or bisexuality in women.
* Fraternal birth order effect: younger brothers are increasingly more likely to be homosexual

Is There a Difference between the Brains of Homosexuals and Heterosexuals?

* No reliable difference between the brains of \n heterosexuals and homosexuals has been \n discovered

Sexual Identity

* Sexual identity does not always coincide \n with a person’s anatomical sex.
* Transsexualism
* A person believes that he or she is trapped in the body of the other sex

Independence of Sexual Orientation and Sexual Identity

* Sexual attraction, sexual identity, and body \n type are sometimes unrelated.
* This points to many possible differences in \n brain development, organization, and \n function between individuals

Endocrine glands release their chemicals, which are called hormones, directly into the __________.

circulatory system

_______ hormones are synthesized from cholesterol, a type of fat molecule.

Steroid

The ______ gland is frequently referred to as the master gland because most of its hormones are tropic hormones.

pituitary