Replacing estrogen lost in midlife reliably suppresses hot flushes and night sweats, reduces broken bones, and, as low-dose vaginal preparations, reverses the tissue thinning behind repeated bladder infections. Against this sit clots, stroke, gallbladder disease, worsened bladder leakage, and more breast cancer when a second hormone protects the womb lining. Most clotting harm tracks oral dosing, not the hormone. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Estradiol | 50–100 pg/mL on systemic therapy | Confirms absorption and guides dose |
| Follicle-stimulating hormone | <30 mIU/mL | Cross-checks estradiol at baseline |
| Triglycerides | <100 mg/dL | Detects the oral first-pass rise |
| LDL cholesterol | <100 mg/dL, lower with vascular disease | Tracks the lipid shift oral estrogen produces |
| Lipoprotein(a) | <30 mg/dL | Oral estrogen lowers it, unlike most agents |
| Sex hormone-binding globulin | 40–80 nmol/L | Flags excessive hepatic estrogen effect |
| Alanine aminotransferase | <25 U/L in women | Detects hepatic strain |
| Thyroid-stimulating hormone | 0.5–2.0 mIU/L | Oral estrogen raises thyroid hormone requirement |
| Endometrial thickness | <5 mm on continuous combined therapy | Detects hyperplasia before it progresses |
| Bone mineral density, T-score | Above −1.0, or improving from own baseline | Confirms the skeletal benefit is materialising |
| High-sensitivity C-reactive protein | <1.0 mg/L | Oral estrogen raises it; transdermal does not |
| Blood pressure | <120/80 mmHg | Guards against the vascular risks |
Cadence: Symptom and blood pressure review at 6–8 weeks; lipids, liver enzymes and estradiol at 12 weeks, then every 6–12 months once stable; mammography annually; bone densitometry every two years; endometrial imaging whenever unscheduled bleeding occurs.