In looking up the MeSH terms (the official medical terminology coming out of the National Library of Medicine) for the previous post, I made an interesting find. MeSH is set up as a hierarchy - big, broad term, then more specific term, then even more specific term, and so on. The broad concept of sex among humans is "Sexual Behavior." The more specific term, "Coitus," is defined as "the sexual union of a male and a female." There is no equivalent term provided for sex between men or sex between women. Under Sexual Behavior, you also find the term "Sexuality," defined as "The sexual functions, activities, attitudes, and orientations of an individual." Beneath that term, the even more specific terms are "Bisexuality," "Heterosexuality," and "Homosexuality." Still, shouldn't "Coitus" have an equivalent term (and resulting way of finding) for non-heterosexual sex?

Lest you think "Coitus" is only reserved for some mechanical, heteroexual-specific technical discussion of sex, a search for the term returns results such as:

-Promoting protection and pleasure: amplifying the effectiveness of barriers against sexually transmitted infections and pregnancy.

-Sexual behaviour in context: a global perspective.

-Environmental, social, and personal correlates of having ever had sexual intercourse among American Indian youths.

-Substance use and sexual risk behavior among South African eighth grade students.

-Now dear, I have a headache! Immediate improvement of cluster headaches after sexual activity.

-The role of parent religiosity in teens' transitions to sex and contraception.

I would expect that each of those topics would have its own gay/lesbian aspects. Why would they not all fall under "Sexual Behavior," or under "Heterosexuality" if all research subjects were heterosexual? Why was the term for the sexual union of a male and a female the appropriate one for these titles? I would prefer that more specific terms be added all around - in addition to the lack of a term for non-heterosexual sex, there is also no term for oral sex, anal sex (these two get picked up by "Sexual Behavior"), sex toys, or specific female-used contraceptives such as vaginal rings, vaginal sponges, cervical caps, or diaphragms (all fall under "Contraceptive Devices, Female"). The male and female condom do get their own entries, as does the IUD.

Read the rest of this entry »

The Economist, which seems an unlikely source for such an article, reports that a behavior study has found that men and women tend to overestimate how attractive the competition is.

IF YOU have ever sat alone in a bar, depressed by how good-looking everybody else seems to be, take comfort-it may be evolution playing a trick on you. A study just published in Evolution and Human Behavior by Sarah Hill, a psychologist at the University of Texas, Austin, shows that people of both sexes reckon the sexual competition they face is stronger than it really is. She thinks that is useful: it makes people try harder to attract or keep a mate.

Dr Hill showed heterosexual men and women photographs of people. She asked them to rate both how attractive those of their own sex would be to the opposite sex, and how attractive the members of the opposite sex were. She then compared the scores for the former with the scores for the latter, seen from the other side. Men thought that the men they were shown were more attractive to women than they really were, and women thought the same of the women.

Read the rest of this entry »

The standard classification of individuals with intersexuality (hermaphroditism) proceeds according to gonadal morphology. In this terminology, a true hermaphrodite possesses both ovarian and testicular tissue. A male pseudohermaphrodite has testes, but external and sometimes internal genitalia take on female phenotypic aspects. A female pseudohermaphrodite has ovaries, but genital development displays masculine characteristics. These classifications are modified to reflect gonadal abnormalities due to abnormal sex chromosome constitution or abnormalities of phenotype attributable to an inappropriate fetal hormone environment. Hypospadias in the absence of any other deformity is not included in this classification.

At the same time the presence or absence of androgens is playing a critical role in genitalia development, the neuroendocrine mechanism of the central nervous system is also being influenced. Androgens present in sufficient amounts during the appropriate critical stage of development may program the central nervous system (CNS) to induce the potential for male sexual behavior. Experimental and analytical evidence suggests that a behavioral effect can be traced to this early androgen influence. Inappropriate fetal hormonal programming may contribute, therefore, to the spectrum of psychosexual behavior seen in humans. In addition, gender role is heavily influenced by assignment of sex of rearing follittleed by social interaction based upon genital appearance and the development of secondary sexual characteristics.

In the bipotential state (6th gestational week), the external genitalia consist of a genital tubercle, a urogenital sinus, and two lateral labioscrotal swellings. Unlike the internal genitalia where both duct systems initially coexist, the external genitalia are neutral primordia able to develop into either male or female structures depending on gonadal steroid hormone signals. Normally, this differentiation is under the active influence of androgen from the Leydig cells of the testis. The genital tubercle forms the penis, labioscrotal folds fuse to form a scrotum, and folds of the urogenital sinus form the penile urethra. The testis begins androgen secretion by 8-9 weeks; masculinization of the external genitalia is manifest 1 week later and is completed by 14 weeks. To achieve this morphologic change, external genitalia target tissue cells must convert testosterone to dihydrotestosterone (DHT) by the intracellular enzyme 5a-reductase. In the male, DHT mediates the follittleing androgen events: temporal hairline recession, growth of facial and body hairs, development of acne, and development of the external genitalia and prostate.
In the absence of this androgen effect (the absence of a Y chromosome, the presence of an ovary, the absence of a gonad, abnormalities in androgen receptor or postreceptor events, or defects of the 5a-reductase enzyme), the folds of the urogenital sinus remain open, forming the labia minora, the labioscrotal folds form the labia majora, the genital tubercle forms the clitoris, and the urogenital sinus differentiates into the vagina and the urethra. Thus, the littleer vagina is formed as part of the external genitalia.

Read the rest of this entry »

For years the demonstration of a metabolic defect and its location depended upon the study of urinary steroid excretion. Today, the immunoassay of blood 17-hydroxy-progesterone (17-OHP) has become the primary assessment for the diagnosis and management of congenital adrenal hyperplasia. With the 21-hydroxylase and H??-hydroxylase deficiencies, the 17-OHP level will be 50-400-fold above normal.
During delivery of affected infants, the concentration of 17-OHP is elevated in cord blood (1,000-3,000 ng/dL [30-90 nmol/L]), but it rapidly decreases to 100-200 ng/dL (3-6 nmol/L) after 24 hours. A delay in measurement gains accuracy. In contrast to 17-ketosteroids in the urine where the delay must be several days, with 17-OHP the delay need be only a day or two. In affected infants, 17-OHP ranges from 3,000 to 40,000 ng/dL (90-1,200 nmol/L). Measurement of 17-OHP is the basis for the newborn screening programs currently in place in many countries and some states in the U.S.

In adults, 17-OHP must be measured first thing in the morning to avoid later elevations due to the diurnal pattern of ACTH secretion. The baseline 17-OHP level should be less than 200 ng/dL (6 nmol/L). Levels greater than 200 ng/dL, but less than 800 ng/dL (24 nmol/L), require ACTH testing (discussed in Chapter 14). Levels over 800 ng/dL (24 nmol/L) are virtually diagnostic of the 21-hydroxylase deficiency. The DHAS level is usually normal. The hallmarks of late-onset adrenal hyperplasia are elevated levels of 17-OHP and a dramatic increase after ACTH stimulation. The elevated levels of 17-OHP are often not impressive (e.g. overlapping with those found in women with polycystic ovaries due to anovulation), and a simple ACTH stimulation test must be utilized.

Of course, in patients with 3 ??-hydroxysteroid dehydrogenase or 17-hydroxylase blocks, the 17-OHP level will not be elevated. With the 3??-hydroxysteroid dehydrogenase block, the blood levels of DHA and DHA sulfate (DHAS) will be markedly increased. In the 11 ??-hydroxylase deficiency, in addition to elevated 17-OHP, elevation of 11-deoxycortisol is diagnostic. In this deficiency, plasma renin activity will be little, whereas in 21-hydroxylase and 3 ??-hydroxysteroid dehydrogenase deficiencies plasma renin activity is elevated in the salt losing forms.

of HLA-specific and cDNA probes, prenatal treatment has been administered with dexamethasone in fetuses at risk for 21-hydroxylase deficiency. Using multiple daily doses of dexamethasone (total no greater than 1. mg/day), complete prevention has been achieved in some newborns and diminished virilization in others. No congenital malformations, fetal death, or little birth weight or height have resulted from pregnancy-long Cortisol derivative therapy. However, this treatment is associated with significant maternal side effects, such as severe striae with permanent scarring, hyperglycemia, hypertension, gastrointestinal symptoms, and emotional lability. A reduction in dosage during the second half of pregnancy is recommended; dosage can be titered by maintaining the maternal serum estriol levels in the normal range. Questions concerning the relative danger of chorion villus biopsy compared to amniocentesis have also arisen: is the risk of fetal loss with the former technique too high? In patients who prefer amniocentesis and who have been started on dexamethasone treatment at 5-6 weeks gestation, dexamethasone can be discontinued for 5 days prior to amniocentesis, allittleing 17-OHP and androstenedione in the amniotic fluid to reach diagnostic levels. Given that only one in four siblings are at risk and one-half will be males (who do not suffer genital ambiguity from the excess androgen associated with 21-hydroxylase deficiency) then only 1 of 8 fetuses require treatment.

The diagnosis of congenital adrenal hyperplasia due to 21-hydroxylase deficiency can be obtained prenatally by demonstrating elevated levels of 17-OHP, 21-deoxycortisol, and androstenedione in the amniotic fluid. 17-OHP may be elevated only in the salt losing form of adrenal hyperplasia, but androstenedione is increased with all forms. HLA genotyping of amniotic cells can yield confirmation by showing that the fetus is HLA identical to an affected sibling. The 11 ??-hydroxylase deficiency is associated with elevated levels of 11-deoxycortisol in amniotic fluid and tetrahydro-11-deoxycortisol in maternal urine, but this defect is not linked to HLA because the gene coding for this enzyme is found on the long arm of chromosome 8.

Prenatal diagnosis of the 21-hydroxylase deficiency by chorion villus biopsy utilizing DNA probes offers the timely options of termination or in utero therapy. With chorion villus biopsy, diagnosis can be made and therapy instituted before the critical period of fetal genital differentiation with avoidance of genital ambiguity in affected female fetuses. In addition, masculinization of the fetal brain can be avoided which might have an impact on gender identity and adult sexual behavior. Despite the very real limitations.

Only the 21-hydroxylase deficiency has been studied sufficiently, in part because it is not only the most frequent cause of genital ambiguity and congenital adrenal hyperplasia but also because of the high prevalence of the nonclassical, late onset forms of the disease. The genetic defect in virilizing adrenal hyperplasia is an autosomal recessive gene. Within families, the clinical picture is uniform, the type of syndrome (simple, salt-wasting, hypertensive) is usually but not always the same in affected siblings. The ratio in offspring of unaffected parents is one affected to three nonaffected individuals. Treated patients have a 1:100 to 1:200 chance of producing an affected infant. Males and females are at equal risk. On the basis of worldwide screening, the overall incidence of 21-hydroxylase deficiency is 1 per 14,000 births. The highest frequency for congenital adrenal hyperplasia is in Alaskan Yupik Eskimos.

The classic form is a relatively common inborn error of metabolism. One out of every 100 Caucasians is likely to be a genetic carrier of the classic type, and neonatal screening tests indicate an incidence of 1 in 14,000, which is equivalent to phenylketonuria.

For the nonclassic types, frequency rates established by the usual methodology (neonatal screening, case surveys) are likely to markedly underestimate what may be one of the most common autosomal recessive disorders in humans. Extrapolations from ACTH testing suggest the follittleing frequency.

block in this step prevents conversion of cholesterol to pregnenolone, the necessary precursor to all biologically active steroids. The adrenals are enlarged and filled with cholesterol esters. Predictably, the internal and external genitalia are female, and death occurs.