IB DP Biology: Human reproduction in detail: puberty, gametogenesis, pregnancy and HRT (HL) (DP Biology)

This study guide is aligned to the IB Biology guide, first assessment 2025, and covers the second part of sub-topic D3.1 (Reproduction): statements D3.1.13 to D3.1.20. All of it is Additional higher level, so it is HL only. If you take SL, you do not need it. The first part of D3.1 (sexual and asexual reproduction, the male and female systems, the ovarian and uterine cycles, fertilization, IVF and flowering plants) is taught elsewhere and is not repeated here.

Related pages: revision notes, practice questions, the IB DP Biology syllabus guide, the course hub, the printable checklist and all free 10-minute diagnostics.

What this unit covers

Guide statement	What you must be able to do	Tier
D3.1.13	Explain how rising GnRH release from the hypothalamus raises LH and FSH and so sex hormone output, producing the changes of puberty	HL only
D3.1.14	Outline spermatogenesis and oogenesis (mitosis, growth, two meiotic divisions, differentiation) and compare the numbers and cytoplasm of the cells produced	HL only
D3.1.15	Explain the acrosome reaction and the cortical reaction as mechanisms that prevent polyspermy	HL only
D3.1.16	Describe blastocyst development and implantation in the endometrium	HL only
D3.1.17	Explain pregnancy testing by detecting hCG with monoclonal antibodies	HL only
D3.1.18	Explain the placenta’s exchange roles and how it allows later foetal development in the uterus	HL only
D3.1.19	Explain the hormonal control of pregnancy (progesterone) and childbirth (oxytocin, positive feedback)	HL only
D3.1.20	Evaluate evidence on HRT and coronary heart disease (CHD), including correlation versus causation	HL only

Puberty and GnRH (D3.1.13)

Puberty is the period when the reproductive system matures. The guide limits the control story to one chain of events.

1. In childhood the hypothalamus increases its release of gonadotropin-releasing hormone (GnRH).
2. GnRH reaches the anterior pituitary, which then releases more luteinizing hormone (LH) as well as more follicle-stimulating hormone (FSH).
3. LH and FSH act on the gonads. Output of the steroid sex hormones rises: testosterone from the testes, oestradiol and progesterone from the ovaries.
4. The sex hormones bring about the developmental changes of puberty.

In typical male bodies these changes include testis enlargement, sperm production, deeper voice and body and facial hair. In typical female bodies they include breast development, widening of the hips, the start of the ovarian and uterine cycles and body hair. Both sexes have a growth spurt.

Points to be precise about: the hypothalamus makes GnRH, the pituitary makes LH and FSH, and the gonads make the steroids. Do not say that the pituitary releases testosterone. GnRH, LH and FSH are peptide or protein hormones. Testosterone and oestradiol are steroids.

Worked example. A boy aged 8 has an LH concentration of 0.8 IU/L. At age 14 it is 4.2 IU/L. Percentage increase = (4.2 − 0.8) / 0.8 × 100 = 425%. The rise in LH acts on the testes, so testosterone concentration also rises, here from 0.3 to 15 nmol/L, which is a 50-fold increase. The question to ask of any such data is “which gland, which hormone, which target?”

Gametogenesis (D3.1.14)

Both processes pass through the same four phases: mitosis to multiply germ cells, cell growth, meiosis (two successive divisions) and differentiation into specialised gametes. The outcomes differ.

Spermatogenesis

This takes place in the seminiferous tubules of the testes.

• Germ cells divide by mitosis to make many diploid cells. This keeps up a supply.
• Some of these grow into primary spermatocytes (46 chromosomes).
• Meiosis I produces two secondary spermatocytes (23 chromosomes, each still made of two chromatids).
• Meiosis II produces four haploid spermatids.
• Spermatids differentiate into sperm. They lose most cytoplasm and gain a tail (flagellum), a mid-piece packed with mitochondria and an acrosome containing digestive enzymes.

One primary spermatocyte gives four functional sperm of equal size. Production continues from puberty, in huge numbers.

Oogenesis

• Mitosis of germ cells in the ovary of the foetus makes the cells that become primary oocytes. These start meiosis I before birth and pause.
• At puberty, in each cycle, one primary oocyte usually finishes meiosis I. Cell growth gives it a very large store of cytoplasm.
• Meiosis I divides the cytoplasm unequally: one large secondary oocyte and one tiny first polar body.
• Meiosis II of the secondary oocyte happens only if a sperm enters. It again divides unequally, giving a large ovum and a second polar body.
• Polar bodies contain a nucleus but almost no cytoplasm. They do not function as gametes and degenerate.

One primary oocyte gives one functional egg. Over the reproductive years only a few hundred are ovulated.

Comparison

Feature	Spermatogenesis	Oogenesis
Gametes per starting cell	4	1 (plus polar bodies)
Cytoplasm division	Equal	Unequal, egg keeps nearly all
Timing	Continuous from puberty	Starts in foetus, pauses, completes after fertilization
Cell size	Small, motile	Large, with food reserves

The cytoplasm difference links to D3.1.3: the egg carries the food reserves, while the sperm travels to the egg.

Worked example. A study follows 120 primary spermatocytes and 120 primary oocytes. Sperm made = 120 × 4 = 480. Eggs made = 120 × 1 = 120. Polar bodies = two or three per oocyte, so 240 to 360 (the first polar body may or may not divide).

Worked example (magnification). A photomicrograph shows an egg 36 mm across. Its actual diameter is 0.12 mm. Magnification = image size / actual size = 36 / 0.12 = ×300.

Preventing polyspermy (D3.1.15)

Polyspermy is entry of more than one sperm into an egg. In humans two sperm would give 23 × 3 = 69 chromosomes, a triploid zygote that cannot develop normally. Two events prevent it.

Acrosome reaction. A sperm binds to the zona pellucida, the glycoprotein layer round the egg. This triggers exocytosis of the acrosome. Released enzymes digest a path through the zona pellucida, and the sperm head reaches the egg membrane. The membranes fuse and the sperm nucleus enters.

Cortical reaction. Fusion triggers exocytosis of cortical granules, vesicles lying just under the egg’s membrane. Their contents alter the zona pellucida so other sperm cannot bind to it or pass through. This is why the egg is penetrated only once.

Common error: swapping the two. The acrosome reaction belongs to the sperm and lets it in. The cortical reaction belongs to the egg and keeps the rest out.

Blastocyst and implantation (D3.1.16)

After fertilization the zygote divides by mitosis as it travels down the oviduct (fallopian tube). The result is a hollow ball of cells, the blastocyst. It has an outer layer of cells (the trophoblast), an inner cell mass that goes on to form the embryo, and a fluid-filled cavity. You do not need the names of other embryo stages.

About a week after fertilization the blastocyst reaches the uterus. Its outer cells attach to the endometrium and release enzymes that digest some of the lining. The blastocyst sinks in. This is implantation. The endometrium is thick and rich in blood vessels because of progesterone from the corpus luteum. The embryo and the developing placenta begin to secrete hCG.

Pregnancy testing and hCG (D3.1.17)

Human chorionic gonadotropin (hCG) is produced by the embryo and then the developing placenta. It appears in the mother’s blood and passes into her urine. Home tests use monoclonal antibodies: all identical, all binding one site on the hCG molecule.

How a typical strip works:

1. Urine moves along the strip by capillary action.
2. Mobile antibodies, labelled with a coloured marker, bind to any hCG and travel on with it.
3. A fixed line of further anti-hCG antibodies traps the hCG-antibody complex, so a coloured line appears.
4. A control line shows that the test has worked.

Monoclonal antibodies are specific, so the test seldom responds to other hormones such as LH.

Worked example. hCG concentration in a woman’s blood rises from 6 mIU/mL on day 9 after ovulation to 120 mIU/mL on day 17. Rise = 114, so the fold change is 120 / 6 = 20-fold in 8 days. Between day 11 (13) and day 13 (27) the percentage change is (27 − 13) / 13 × 100 = 108%, close to doubling every two days. A test that needs 25 mIU/mL first turns positive on day 13. (These are illustrative values written for practice.)

The placenta (D3.1.18)

The placenta forms from embryonic tissue and maternal endometrium. You need only one structural fact: the villi give a large surface area for exchange. Maternal and foetal blood stay separate, so exchange crosses thin barriers.

Moves to foetus	Moves to mother
Oxygen, glucose, amino acids, water, minerals, vitamins	Carbon dioxide, urea and other wastes
Antibodies (IgG) for passive immunity	Heat

Processes include simple diffusion (oxygen, carbon dioxide), facilitated diffusion and active transport (nutrients) and endocytosis (antibodies). The placenta also secretes hormones, and it can let through harmful substances such as alcohol and some viruses and drugs.

The placenta lets the foetus stay in the uterus until a later stage than in mammals without one. Marsupials, for example, give birth to very undeveloped young which then develop in a pouch. Placental mammals supply the foetus from the mother’s blood over a long period.

Hormones of pregnancy and childbirth (D3.1.19)

Pregnancy. The corpus luteum secretes progesterone, stimulated by hCG, so the endometrium is maintained and menstruation does not occur. The placenta then takes over progesterone secretion. Progesterone also inhibits uterine muscle contraction.

Childbirth.

1. Near the end of pregnancy, progesterone level falls.
2. The uterus becomes sensitive to oxytocin and contractions start.
3. Contractions push the baby’s head against the cervix. Stretch receptors send impulses to the hypothalamus.
4. The posterior pituitary releases oxytocin, which stimulates stronger contractions.
5. Stronger contractions press more on the cervix, so more oxytocin is released.

This is positive feedback: the output increases the stimulus. It ends when the baby is born and the pressure on the cervix stops. Contrast this with the negative feedback of the ovarian cycle.

HRT and coronary heart disease (D3.1.20)

After the menopause, the ovaries secrete much less oestrogen. Hormone replacement therapy (HRT) gives hormones to replace some of it. The guide treats this as a Nature of Science case about evidence.

• Early epidemiological studies compared women who chose HRT with women who did not, and found less CHD in the HRT group. This was taken to mean HRT caused the reduction.
• Later randomized controlled trials gave HRT or a placebo to randomly assigned women. They found a small increase in CHD risk with HRT.
• Explanation. The early link was a correlation, not cause and effect. Women taking HRT tended to have higher socioeconomic status, which itself lowers CHD risk. This is a confounding variable. Randomization shares such variables evenly between groups.

Worked example. In an observational study, 36 of 2400 HRT users (1.5%) and 150 of 6000 non-users (2.5%) developed CHD. Relative risk = 1.5 / 2.5 = 0.6. In a randomized trial, 104 of 8000 (1.3%) on HRT and 88 of 8000 (1.1%) on placebo developed CHD. Relative risk = 1.3 / 1.1 = 1.18, an absolute difference of 2 per 1000 women. (These numbers were made up for practice.)

Common errors

• Writing “LH is made by the ovary”. LH and FSH come from the anterior pituitary.
• Saying a primary oocyte gives four eggs.
• Saying the zona pellucida is the egg membrane.
• Saying the placenta mixes maternal and foetal blood.
• Saying oxytocin acts by negative feedback.
• Saying a correlation proves HRT protects the heart.

Use the practice questions next, then test yourself with the revision notes.

Official syllabus

Source: Biology guide, first assessment 2025, International Baccalaureate Organization (Diploma Programme), sub-topic D3.1, statements D3.1.13 to D3.1.20 (Additional higher level).