HORMONES AND SEXUAL BEHAVIOR



The human body contains 2 general types of secretory glands:



Exocrine glands secrete chemical through ducts to some specific area of the body. These include for ex. tear glands that secrete tears through tear ducts; sebaceous glands that secrete oils through pores in the skin; mammary glands that secrete milk; etc.



Endocrine glands secrete chemical messengers called hormones into the bloodstream, where they are then carried throughout the body. Hormones usually produce widespread changes in many different organ systems. They are similar to neurotransmitters in some respects, except: 1) most hormones are released by non-neural cells; 2) hormones often travel a long distance in the body before binding to their receptors, whereas neurotransmitters travel only across the tiny synaptic cleft; 3) hormones usually produce long-lasting changes in their target cells, whereas neurotransmitters cause electrical changes that usually last less than a second.



Despite these differences, a few chemicals in the body act as both hormones and neurotransmitters. For ex., CCK acts as a hormone when released by the duodenum, but acts as a neurotransmitter when released by certain neurons in the PVN of the hypothalamus.



There are 2 main types of hormones. 1) Protein or peptide hormones consist of chains of amino acids (short chains are called peptides; long chains are called proteins). These hormones bind to receptors on the cell membrane of the target cell, where they activate the second messenger cyclic AMP which then catalyzes many chemical reactions inside the cell to alter the cell’s functions in various ways, depending on the cell. 2) Steroid hormones all have a common basic structure that includes 4 carbon rings. These highly fat-soluble hormones penetrate the cell membrane of target cells and bind to receptors in the cytoplasm of the cell. The hormone-receptor complex then attaches to the chromosomes inside the nucleus of the cell, where it directly alters gene expression. This of course alters the functional activity of the cell, since the genes ultimately determine what a cell does.



There are also 3) other hormones that do not fit into these 2 main categories. The catecholamine hormone Epinephrine (or adrenaline) is one example of those; it is neither a steroid nor a peptide.



SOME GLANDS AND THE HORMONES THEY RELEASE



The adrenal glands sit atop the kidneys and release over 50 different hormones. The inner part is called the adrenal medulla, and it releases the hormones epinephrine and norepinephrine which stimulate the target organs of the sympathetic nervous system, contributing to the fight-flight reaction. The outer part is called the adrenal cortex. It releases many different steroid hormones, including corticosteroids such as cortisone. Corticosteroids produce many effects in the body including an anti-inflammatory effect, the breakdown of proteins for energy, etc. Cortisone and its relative prednisone are widely used to reduce inflammation in diseases such as arthritis, allergies and chronic muscle pain.



The gonads or sex glands are another example. They release steroid hormones called sex hormones. The ovaries release estrogen and progesterone at different phases of the menstrual cycle, whereas testes release androgens such as testosterone. As we’ll see, the sex hormones have both physical and behavioral effects.



The thyroid gland in the throat secretes thyroxine, which incorporates iodine as part of its molecular structure. The level of thyroxine controls the metabolic rate of cells throughout the body. Too much thyroxine produces nervousness and weight loss due to an excessively high metabolic rate, while too little produces obesity and, in children, a form of mental retardation called cretinism. A lack of thyroxine can result from a lack of iodine in the diet.



Some other endocrine glands were already discussed: the pancreas, which secretes insulin and glucagon; the duodenum, which secretes CCK; the kidneys secrete renin; the pineal gland secretes melatonin, etc.



The so-called master gland that controls many other glands of the endocrine system is in the brain: the pituitary gland (or hypophysis), which sits just below the hypothalamus. The pituitary consists of 2 distinct parts, both of which are controlled by the hypothalamus.



The anterior pituitary is controlled by the hypothalamus via a group of blood vessels called the hypothalamic-hypophyseal portal system. These blood vessels carry releasing hormones secreted by the hypothalamus to the anterior pituitary to trigger release of pituitary hormones. Thus the hypothalamus itself acts as an endocrine gland, and can be regarded as the master of the master gland.



Six hormones are released by the anterior pituitary in response to the appropriate releasing factor from the hypothalamus:



Two gonadotrophic hormones: follicle-stimulating hormone (FSH) promotes growth of the gonads and release of sex hormones from them; and luteinizing hormone (LH) triggers ovulation in females and release of androgens in males. FSH and LH are released in response to gonadotropin releasing hormone (GRH) secreted by the hypothalamus (in the video, the man who lost his sex drive and beard had suffered a head injury that shut down his hypothalamus’s production of GRH).



Adrenocorticotrophic hormone (ACTH) - secreted in response to stress or injury; stimulates the adrenal cortex to secrete corticosteroids.



Thyroid-stimulating hormone (TSH) - stimulates growth of the thyroid gland and release of thyroxine. Normally, if thyroxine levels in the blood are low, the hypothalamus tells the pituitary to secrete more TSH to cause the thyroid to release more thyroxine. On the other hand, if thyroxine levels are high, the hypothalamus tells the pituitary to reduce its TSH secretion, which in turn causes reduction of thyroxine secretion. This is called negative feedback and it is the basic mechanism by which hormone levels are regulated by the brain. If the blood levels of thyroxine remain chronically low, TSH will be secreted at a very high level, stimulating the thyroid gland so much that it swells up to the point where it protrudes from the neck. This disease is called goiter and it can result from iodine deficiency.



Prolactin stimulates production of milk by the mammary glands, which are exocrine glands.



Growth hormone acts directly on bones and muscles to promote growth. It is mainly secreted during childhood, when we are actively growing. Too little growth hormone during childhood produces dwarfism, while too much produces giantism.



The posterior pituitary consists of the axon terminals of certain hypothalamic neurons. The axons of these hypothalamic neurons make up the hypothalamic-hypophyseal tract. Action potentials in these axons triggers release of hormones from the axon terminals. The process is like neurotransmitter release except the chemicals that are released go directly into the bloodstream. The 2 main hormones released by the posterior pituitary are: vasopressin (antidiuretic hormone) which is released during states of dehydration; it tells the kidneys to reabsorb water; and oxytocin, which promotes milk release by the mammary glands, and stimulates the contractions of labor. In female rats, high levels of oxytocin in the mother at birth promote maternal bonding of the mother rat to her offspring. In humans, oxytocin is also released during sexual excitement and is present in the blood in especially high concentrations during orgasm, so it may promote emotional bonding between sexual partners as well.



HORMONES AND GENDER


Humans have 23 pairs of chromosomes (46 in all); one chromosome of each pair is from the father, and the other is from the mother. These pairs include a pair of sex chromosomes. There are 2 types of sex chromosomes, X and Y. The mother contributes only an X chromosome to the offspring, while the father can contribute either an X or a Y. If the combination of sex chromosomes is XX, a female normally develops. If the combination of sex chromosomes is XY, a male usually develops. So the father’s genetic contribution determines the gender of the child.



The XX combination causes development of ovaries in the fetus, which secrete the female sex hormones or estrogens. The XY combination causes development of testes in the fetus. The testes begin to secrete the male sex hormones called androgens (most importantly testosterone) during the first few months of pregnancy. It is this prenatal secretion of androgens that causes development of male genitalia. By contrast, no hormone is needed to produce female genitalia; female genitalia result even when no hormones are present in the developing fetus.



The proof of this is that if a genetic male or XY fetus has testes that produce androgens, but the body lacks receptors for androgens, then the individual will develop like a female even though the person is genetically male! This is called androgen insensitivity syndrome. These individuals generally look and act like normal females. The condition usually comes to light only at puberty, when the individual raised as a girl fails to menstruate. Surprisingly, estrogens from the internal testes and adrenals trigger development of secondary sexual characteristics such as breasts and feminine hips at puberty.



The effect of prenatal androgens on genital development is an example of an organizing effect of a hormone, which means a hormonal effect on physical structure. Prenatal androgens also have an organizing effect on brain development. At birth, there are distinct differences in brain structure between males and females. For ex., the medial preoptic nucleus of the hypothalamus is 3 times larger in males than in females - which is not surprising since it controls male sexual behaviour (another nucleus nearby is called the sexually dimorphic nucleus because it is also much larger in males). Also, in females, the left cerebral cortex is thicker than the right, while in males, the right cerebral cortex is thicker than the left. A third structural difference is that the anterior commissure is larger in females than in males. The anterior commissure is a small tract between the 2 hemispheres in the frontal part of the brain; it is much smaller than the corpus callosum, which is the main tract connecting the 2 hemispheres. Recent evidence indicates that the corpus callosum itself is also proportionally larger in females.



Studies have shown that these and other differences between the brains of men and women largely depend on exposure to prenatal androgens during a critical period of fetal development. This critical period is during the 3rd and 4th months of pregnancy. If a female fetus is exposed to high levels of androgens during this critical period, the result will be masculinization of the brain. The degree of masculinization depends on the level and timing of androgen exposure.



How might a female fetus be exposed to androgens? This has happened in several ways. The adrenal gland produces small amounts of androgens in both males and females, so if the pregnant woman has a hyperactive adrenal gland (called congenital adrenal hyperplasia) it could produce enough androgen to masculinize the female fetus. Also, in the 1950s and 1960s, a number of pregnant women took the synthetic estrogen DES to prevent miscarriage. Though an estrogen, high levels of DES have a masculinizing effect on fetal development (ie, it acts like testosterone in this respect). When a female fetus is exposed to high levels of androgens or androgen-like chemicals from an early stage of development, the result at birth will usually be an intersex, which means that the genitals are intermediate in structure between male and female (in contrast note that a true hermaphrodite has both ovaries and testes, which is a very rare genetic defect). In many intersex cases the doctors can’t tell whether the infant is a boy or a girl! This happens in about 1/2000 births. The interesting thing that can happen from a psychological point of view is that in some cases of prenatal androgen exposure in female fetuses, the brain was masculinized but the genitals were not. This can occur because the critical period for masculinization of the brain is slightly later than the critical period for masculinization of the genitals. So if the androgen exposure occurs after the genitals have already developed as a female, the brain can still be masculinized. These cases shed light on the role of prenatal hormones on brain development and gender identity.



Females exposed to prenatal androgens showed some interesting behavioral differences from normal little girls. As children, they were more aggressive than normal girls of their age. They enjoyed more sports and rough and tumble play compared to normal girls, and were more physically active in general. They were usually regarded as tomboys. They also preferred to play with boy’s toys, such as toy soldiers and trucks, instead of girl’s toys like dolls and houses. And as adults, these women showed a much higher rate of lesbianism than normal women: nearly a quarter of them became lesbians versus only a 1-2% rate of lesbianism in the general female population. So the effect of prenatal androgens on brain development seems to predispose people to physical aggressiveness, male sexual behavior, and a generally high activity level.



In rats, exposure to prenatal androgens will make a female rat behave just like a male. As an adult, she will fight with males and mount other females. Studies have also shown that if a pregnant rat is subjected to stressful experiences during pregnancy, this causes release of stress hormones into the blood which can block the effects of testosterone in the developing male rat’s brain. The result is that the male rat is physically a normal male, but exhibits homosexual behavior as an adult. He is attracted to other males, and assumes the female position in the presence of other male rats.



Can this also happen in humans? Intriguing evidence comes from a study of men born in Germany during the highly stressful period of WWII compared to men born either before or after WWII. The study found a much higher rate of homosexuality among men born during WWII than in men born either before or after the war, supporting this idea. However, this cannot explain all instances of male homosexuality, because most mothers of homosexuals did not experience unusual stress during pregnancy. So other factors must be involved too.



One such factor is genetics. The concordance rate for homosexuality is higher in identical twins than in fraternal twins. Concordance rate means the frequency at which both twins exhibit the behavior in question. The concordance rate for homosexuality in identicals is around 50%, while the rate for fraternals is around 20%. Since identicals share 100% of genes that vary in the human population, while fraternals share only 50% of those genes, a higher concordance in identicals implies a genetic contribution to homosexual behavior. But genes obviously aren’t the whole story, otherwise the concordance rate for identicals would be 100% instead of 50%. So there must be more to homosexuality than genes alone.



Intriguingly, recent evidence indicates there are signs of feminization of the brain in gay men, suggesting an influence of prenatal hormones. For ex., the anterior commissure is not only larger in heterosexual women than in heterosexual men; it is also larger in homosexual men than in heterosexual men. So there is abundant evidence that homosexuality probably has a biological basis, although the exact mechanism is not fully understood at present.



Homosexuality appears to be fairly common in the animal kingdom. For example, a recent study found that about 8% of rams are gay, and the gay rams show signs of feminization of the hypothalamus.



Sociologists used to argue that sexual preference and gender-typed behaviors are entirely determined by sociocultural factors and not biology. The famous case that was once cited to support this view involved an infant boy whose penis was accidentally destroyed during circumcision. Based on the notion that gender is entirely a product of upbringing, the parents were advised by the doctors to raise the child as a girl named Brenda. Prior to puberty, the child was reported by the doctors to display gender-typed behaviors that were appropriate for a little girl. This was later exposed as a lie, however. It turned out that Brenda continually rebelled against the female gender role. At puberty, Brenda started openly acting like a man despite not knowing about the sex reassignment surgery that took place in childhood. Brenda also refused further hormone treatments and surgery that would produce a more feminine appearance. As a result of all this conflict, the parents finally told Brenda what had happened in infancy. As an adult, Brenda first became a lesbian and then had another sex-change operation to allow a fully male identity. He is now named David and is happily married to a woman. So this case that was so often cited in support of a sociocultural explanation of gender identity turned out not to support that view, and in fact very strongly supports the biological perspective.



Androgens have organizing effects on the genitals and the brain during critical periods of prenatal development. Sex hormones also have organizing effects during a specific postnatal stage of development: puberty. Puberty is triggered when the hypothalamus starts releasing gonadotropin releasing hormone (GRH), which causes the pituitary to secrete gonadotrophic hormones (LH and FSH). In females, gonadotropins stimulate the release of estrogens by the ovaries; this initiates the menstrual cycle and causes growth of breasts, widening of the hips, and deposition of body fat. In males, gonadotropins stimulate release of androgens by the testes, which triggers growth of body hair, muscular development, deepening of the voice, and sperm production. Secretion of GRH by the hypothalamus is responsive to the level of leptin in the blood, which indicates fat levels in the body; thus caloric restriction or intense exercise regimens can delay puberty by preventing fat storage.



Sex hormones also have activating effects from puberty onward. Activating effects refer to behavioral changes triggered by hormones. Sexual interest and behavior are obviously triggered during and following puberty. In addition, males become more aggressive. Violent crime rates are highest in the male age group that has the highest blood testosterone level - which is between 15 and 25 years of age. We can see the effect of testosterone on behavior by observing what happens when the main source of testosterone is removed – the testes.



Castration has 2 effects on behavior of male mammals: one is a loss of sex drive; the other is a loss of aggressiveness. A normal bull is a very aggressive and dangerous animal, but a steer or castrated bull is not dangerous. These kinds of effects occur in human males as well. Rapists and pedophiles have been treated with androgen-blocking drugs such as Depo-provera, which inhibits release of GRH by the hypothalamus. This powerfully reduces the recidivism rate for sexual offenses. This effect only works as long as the criminal takes the drug, however. If they stop taking it, their sexual and aggressive impulses will likely trigger more crimes. Side effects of these drugs include feminization of the body.



In females of many mammalian species, sexual receptivity is limited to around the time of ovulation, when estrogen levels are highest. This is when the female is said to be “in heat.” In primates, however, this is not the case. Female monkeys are most interested at ovulation, but they can also be receptive to the right male at any time of the menstrual cycle. In humans, this desynchronization of sexual interest from the menstrual cycle is most evident. Studies have found only a very small average increase in women’s sexual interest at the time of ovulation. This is because the sex drive of human females is not highly dependent on estrogen, unlike dogs and cats. In dogs and cats, removal of the ovaries completely eliminates female sex drive, but this does not happen following removal of the ovaries in humans. However, if the adrenal cortex is damaged, there is a profound loss of female sex drive in humans. This is because androgens are necessary for female sex drive in humans as they are for male sex drive, and in females, the main source of androgens is the adrenal cortex. So androgens stimulate sex drive in both men and women - a very different situation from that seen in most other species of mammals.



Neural control of sexual behavior includes the spinal sexual reflexes: the spinal cord contains motor programs for sexual responses. In males who’ve suffered high-level spinal cord damage such that they can experience no sensations from the body, the spinal cord alone can still mediate erection, pelvic thrusting and ejaculation in response to genital stimulation. They can ejaculate, but of course they do not experience any pleasure - and no orgasm - from this because no signals can reach the brain. Nevertheless, even many quadriplegics can still father children.



The role of the brain appears to be to inhibit the spinal sexual reflexes under normal circumstances, and then disinhibit them when a receptive partner is present. The part of the brain that seems to contribute the most to male sexual behavior is the medial preoptic area of the hypothalamus. In animals, male sexual behavior is completely eliminated if this part of the hypothalamus is damaged, while administration of androgens directly to the medial preoptic area stimulates male sexual activity by promoting release of dopamine. Dopamine is the neurotransmitter that most directly stimulates sexual arousal and orgasm. Thus drugs that increase dopamine activity have well-documented aphrodisiac effects, such as cocaine and amphetamines as well as some of the drugs used to treat Parkinson's disease. Serotonin however antagonizes dopamine release, hence many antidepressants that promote serotonin activity (such as SSRIs) induce loss of libido as a side effect.



Damaging the medial preoptic area has no effect on female sexual activity; however, damage to the ventromedial nucleus of the hypothalamus does abolish female sexual behavior in animals. In female rats, direct administration of estrogens here stimulates female sexual activity. So the hypothalamus appears to be where the sex hormones have their activating effects.



A recent discovery is that melanocyte stimulating hormone, which is produced by skin cells in response to sun exposure to trigger tanning, also acts on the sex centers of the hypothalamus to increase sex drive. Thus a drug called melanotan, which was developed as an analogue of this hormone to promote a natural tan as protection against skin cancer, was found to have the side effect of dramatically increasing libido in men and women during clinical trials. Female rats increased their rate of copulation by 300% after a dose of melanotan, and 80% men suffering from impotence reported getting normal erections after taking this drug. Melanotan also inhibits appetite by suppressing the action of the hunger center of the hypothalamus. So it makes you tanned, thin and horny - which is why it is sometimes called the "Ken and Barbie drug."



Another brain region involved in sexual behavior is the amygdala, part of the limbic system located within the temporal lobe. In animals or humans, damage to the amygdala often produces hypersexuality - a dramatic increase in sex drive. If the overlying temporal cortex is damaged along with the amygdala (which usually is the case in naturally occurring lesions), there is often an increase in indiscriminate sexual behavior and bisexual activity as well. This is known as the Kluver-Bucy syndrome. Monkeys with lesions of the temporal cortex and amygdala will attempt to mate with virtually any object in the environment. One conclusion is that the amygdala is involved in the inhibition of sex drive, while the temporal cortex is important for choosing an appropriate sexual object.




http://www.hss.bond.edu.a...9notes.htm




Personally, I believe that homosexuality is biological. There are MANY reported incidences of homosexual animals, even. (I mean like penguins and stuff...not Supa ) P.S. I disagree with the use of the word "normal" in this article simply because what is normal is relative.
[Edited 1/25/05 7:26am]

AsianBomb777 said:

Yup. That is so straight.

not to be redundant...

BIOLOGICAL

I totally missed this thread.....

bananacologne said:

Good answer!

Fauxie said:

say what?

AsianBomb777 said:

quote of the week...

charlottegelin said:

interesting
[Edited 1/28/05 6:20am]