Hormone replacement therapy supplies reproductive hormones after menopause to reduce symptoms linked to falling estrogen and progesterone concentrations in body tissues.
Evidence about hormone replacement therapy (HRT) and coronary heart disease (CHD) changed when randomized controlled trials tested a correlation reported by observational studies.
| Evidence source | Finding | Best interpretation |
|---|---|---|
| Early epidemiological studies | HRT users had lower CHD incidence | Association only; users differed from non-users in other ways |
| Later randomized controlled trials | HRT caused a small increase in CHD risk | Random assignment better isolates the causal effect of HRT |
HRT users in the observational studies tended to have higher socioeconomic status. Socioeconomic status itself is causally associated with lower CHD risk, so it confounded the apparent protective association.
If lower CHD is caused by healthcare access, diet or other factors linked to socioeconomic status, comparing self-selected HRT users with non-users can wrongly attribute that difference to HRT.
A strong correlation can still be non-causal. The syllabus conclusion is not that HRT prevents CHD: randomized trials found a small increase in risk.
HL D3.1 is about ordered mechanisms and evidence judgment: endocrine control, gametogenesis contrast, one-sperm fertilization, early embryo stages, hCG detection, placental exchange, birth feedback, and HRT evaluation.
HL D3.1 moves from reproductive events into control and evidence. The strongest answers keep sequences in order: endocrine axis at puberty, gametogenesis outcomes, fertilization blocks, blastocyst implantation, hCG testing, placental exchange, childbirth feedback, and HRT evaluation.