The Role of Chromosomes & Hormones (AQA A Level Psychology): Flashcards

False.

Males and females produce the same hormones but in different concentrations.

False.

Although women are typically said to release more, both sexes release oxytocin in equal quantities during some behaviours, e.g. amorous activity.

XY individuals in the Dominican Republic with 5-alpha-reductase deficiency (5-ARD) appeared female at birth and were raised as girls, but became masculinised at puberty when testosterone surged, with the large majority adopting a male identity, showing the strong influence of androgens.

Female guinea pigs exposed to testosterone in the womb developed masculinised genitals and male-typical mating behaviour in adulthood, demonstrating the organisational effect of prenatal androgens on the developing brain.

Giving testosterone therapy to hypogonadal men, whose bodies produce very little testosterone, improved muscle strength, body shape and libido, demonstrating the role of testosterone in male secondary sexual characteristics.

Individuals with CAIS have XY chromosomes but develop female external anatomy due to androgen receptor dysfunction, showing that hormones, not just chromosomes, are essential to sex development.

Of 16 genetic males born without a functional penis, 14 were raised as female, but 8 of these reassigned themselves as male by the age of 16, showing that biological factors can override socialisation.

XX mice implanted with the SRY gene developed as male mice, supporting the claim that the SRY gene initiates male development.

It is unethical to manipulate prenatal hormones or chromosomes in humans, so most evidence comes from naturally occurring DSD cases, where genes, hormones and socialisation interact, making the relationship complex.

Publication bias has inflated apparent sex differences, and most brain features show extensive overlap between males and females, weakening the claim that prenatal hormones produce distinctly 'male' or 'female' brains.

It supports the nature side, as chromosomes and hormones determine sex, though critics argue environmental factors such as upbringing and social expectations also shape sex-related behaviour and identity.

Focusing solely on SRY gene activation or hormone levels reduces complex development to simple biological causes; a holistic view would also consider psychological, cognitive and social influences.

DSD is the modern term for congenital variations in chromosomal, hormonal or anatomical sex characteristics that mean development differs from the typical XX or XY pattern; it replaces older labels such as 'disorders of sex development', 'intersex' and 'atypical sex chromosome patterns'.

AIS is a genetic condition in XY individuals in which androgen receptor dysfunction means the body cannot respond fully or partially to androgens, affecting the development of the genitals and reproductive organs; it affects about 1 in 20,000 people.

A penis does not form or is underdeveloped, so the child's genitals may develop as female or as underdeveloped male.

In complete AIS the genitals appear female, so it is usually diagnosed at puberty when menstruation does not start; in partial AIS the genitals may appear female or male, so it is usually discovered at birth.

False.

The genetic alteration is passed along the female line; carrier women do not have AIS themselves, but each child has a 1 in 4 chance of being born with it.

A person with AIS has no uterus or ovaries, as their genotype is male (XY), but has internal, usually undescended, testes.

All babies have an X chromosome, but XXY, XYY and XO (where the second X is missing) are possible; these patterns may be inherited, occur at conception or arise from the division of reproductive cells.

Klinefelter's syndrome involves an extra X chromosome, giving the atypical pattern XXY and resulting in underdeveloped testes and reduced testosterone; it affects about 1 in 600 males.

KS is due to an error in the egg cell as it develops, or to the father's sperm carrying an extra X chromosome.

Mosaic KS is the more common and milder form in which only some of the boy's cells have the XXY pattern, so it may not be discovered until puberty.

Physical characteristics include:

• small testes producing low testosterone, and a small penis

• no facial hair and limited body hair

• broader hips, long limbs and breast tissue

• delayed or incomplete puberty and likely infertility

These include:

• poor language skills affecting reading and writing

• poor mathematical skills

• a quiet, shy temperament with attention difficulties

• increased risk of anxiety and/or depression

False.

KS is incurable; additional testosterone can increase muscle and bone development but cannot reverse infertility.

Turner's syndrome involves having all or part of an X chromosome missing, giving the atypical pattern XO; it affects about 1 in 2,000 live female births.

The second sex chromosome is missing or partially missing, so development cannot follow the typical XX pattern, but with no Y chromosome to direct the foetal gonads to develop male characteristics, the baby develops as female.

TS occurs at conception; the cause is not precisely known but is thought to be an error in the division of a parent's reproductive cells, and it also has a mosaic form.

Physical characteristics include:

• delayed puberty and underdeveloped ovaries, leading to menstruation problems and infertility

• short height, a webbed neck, narrow hips and a broad 'shield' chest

• heart and kidney abnormalities

These include:

• average or above-average ability with high verbal skill

• social immaturity and difficulty relating to peers, often being treated as younger than their age

• impaired visuospatial skills

Hormone replacement therapy is needed to develop breasts, normal female body contours and proper bone growth.

Of 14 individuals with CAIS, the majority identified as female and reported satisfactory psychological adjustment, supporting the role of androgens rather than chromosomes alone in shaping gender identity.

Using clinical interviews, cognitive tests and MRI, 10 of 11 KS participants had mental health and cognitive issues and smaller frontal lobes, temporal lobes and superior temporal gyrus, suggesting a biological basis for their language deficits.

Oestrogen replacement therapy given before puberty produced a greater increase in breast tissue in females with TS, suggesting early diagnosis and treatment are vital.

DSD research has enabled early hormone treatment and, in some cases, sperm or egg preservation to counteract infertility.

It has supported the growth of online support communities, reducing isolation and stigma and giving individuals a platform to advocate for their needs and share lived experience.

Those diagnosed tend to have the most severe symptoms, while milder mosaic cases go undiagnosed, so findings are based on an unrepresentative sample.

It ignores individual differences in symptoms and their progression, which vary widely, limiting generalised diagnosis and treatment recommendations.

They strongly support the nature side, arising from genetic and hormonal variations present from conception, though nurture shapes how individuals experience their identity, especially under rigid gender norms.

It raises ethical concerns such as informed consent for early hormone treatment and the risk of medicalising natural variation, alongside issues of labelling, stigma and assumptions about 'normality'.

Early diagnosis enables treatment and support, but labelling may create stigma and self-fulfilling expectations about cognitive or social difficulties.