Member story
My periods came back after 4 months. Insulin was the problem all along.
1 in 5 Indian women have PCOS. Only 30% are tested correctly. Your gynaecologist reads insulin, androgens, AMH, and thyroid against South Asian ranges — then builds the protocol around what is actually driving your cycle.
Every panel includes a 15–20 minute video consult with a specialist — read against South Asian-calibrated ranges. The AI works invisibly. The doctor does the medicine.
Irregular periods. Cystic acne. Hair loss. weight gain despite diet and exercise. Exhaustion. These are signs your hormones are dysregulated — but standard bloodwork misses it. Most women are dismissed as "normal" when actually their insulin is spiking, androgens are elevated, or thyroid function is suppressed.
PCOS affects 1 in 5 Indian women but most get diagnosed by ultrasound alone. Proper diagnosis requires bloodwork: testosterone, DHEA-S, insulin, SHBG, AMH, thyroid panel, and cortisol. Treatment depends on your PCOS phenotype — there are 4 distinct types, each needing a different approach.
These biomarkers reveal the root causes — and what actually works to fix them.
Complete biomarker reference for PCOS diagnosis and treatment monitoring
| Biomarker | What It Tests | Why It Matters for PCOS | Optimal Range |
|---|---|---|---|
| Total Testosterone | Ovarian androgen production | Elevated in 70% of PCOS cases; drives acne, hair loss, ovulation issues | <0.7 ng/mL women |
| Free Testosterone | Unbound, active androgen | Better indicator of symptomatic hyperandrogenism than total testosterone alone | 0.0–4.2 pg/mL |
| DHEA-S | Adrenal androgen reserve | Elevated in non-classic PCOS; identifies adrenal dysfunction; affects acne severity | 35–430 µg/dL (age-dependent) |
| Fasting Insulin | Basal insulin levels at rest | Insulin resistance drives 70% of PCOS; >12 mIU/L indicates problem; key for treatment | 2–12 mIU/L |
| HOMA-IR | Insulin resistance index (glucose × insulin) | Better than fasting insulin alone; HOMA-IR >2.0 = insulin resistance confirmed | <2.0 |
| SHBG | Sex hormone binding globulin | Insulin suppresses SHBG; low SHBG = more free (active) testosterone; drives symptoms | 30–100 nmol/L |
| AMH | Anti-müllerian hormone (ovarian reserve) | Elevated in PCOS; indicates higher cyst burden; predictor of fertility outcomes | 1.0–3.0 ng/mL (PCOS typically >3.0) |
| LH:FSH Ratio | Luteinizing hormone to follicle-stimulating hormone ratio | Elevated ratio (>3:1) = dysfunctional GnRH pulsatility; impairs follicle development | (Day 3) LH/FSH <3:1 |
| TSH + Free T4 | Thyroid function (stimulating hormone + free thyroxine) | Hypothyroidism worsens insulin resistance and PCOS symptoms; must be ruled out | TSH: 0.4–2.0 mIU/L; Free T4: 1.0–1.7 ng/dL |
| Fasting Glucose | Baseline blood sugar at rest | 40% of PCOS women develop diabetes by age 40; early detection critical | <100 mg/dL (fasting) |
| HbA1c | 3-month average glucose control | Shows long-term metabolic risk; >5.7% indicates prediabetes; requires intervention | |
| Cortisol (morning) | Adrenal stress hormone baseline | Chronic stress elevates androgens; elevated morning cortisol worsens metabolic dysfunction | 10–20 µg/dL (8am) |
Three steps. Your data. Your physician. Your protocol.
100+ biomarkers drawn at your door in 10 minutes. NABL-accredited labs. Results in 5 days. No clinic visit, no waiting rooms — just data.
Your physician reviews every marker — insulin, androgens, AMH, thyroid — and explains what's driving your PCOS. Root cause identified. Questions answered.
Hormonal regulation, insulin sensitisation, lifestyle changes, and prescriptions if needed — every recommendation built on your markers. Delivered in 48h. Adjusted quarterly.
Not all PCOS is created equal. Your phenotype determines your root cause and treatment approach.
| Phenotype | Key Features | Prevalence | Metabolic Risk | Key Biomarkers | Treatment Focus |
|---|---|---|---|---|---|
| Type A (Classic) | Hyperandrogenism + Ovulatory Dysfunction + Polycystic Ovaries | ~40% | Highest insulin resistance risk; 70% metabolic syndrome | ↑Testosterone, ↑Insulin, ↓SHBG, ↑AMH | Insulin sensitization (Metformin/inositol), androgen suppression, lifestyle |
| Type B (Classic) | Hyperandrogenism + Ovulatory Dysfunction (no polycystic ovaries) | ~20% | Moderate; often adrenal-dominant; 50% metabolic syndrome | ↑DHEA-S, ↑LH/FSH, ↑Testosterone, Normal AMH | Androgen suppression (OCP or spironolactone), stress reduction, cortisol management |
| Type C (Ovulatory) | Hyperandrogenism + Polycystic Ovaries (regular cycles) | ~20% | Lower insulin resistance; primarily ovarian androgen excess | ↑Testosterone, Normal Insulin, ↑AMH, Normal LH/FSH | Androgen suppression (OCP preferred), cosmetic symptom management (hair, acne) |
| Type D (Non-HA) | Ovulatory Dysfunction + Polycystic Ovaries (normal androgens) | ~20% | High insulin resistance despite normal androgens; metabolic dysfunction masked | ↑Insulin, ↑LH/FSH, Normal Testosterone, ↑AMH | Intensive insulin management (Metformin, GLP-1), weight loss, metabolic intervention |
Why phenotyping matters: Type A requires insulin management; Type B requires androgen suppression and stress control; Type C responds well to birth control; Type D is the most metabolically dangerous and often missed. Your arq. physician identifies your phenotype and personalizes treatment accordingly.
No AI chat. No templates. No copy-paste PDFs. A specialist reads your panel against South Asian-calibrated ranges and writes the protocol on a 15–20 minute video consult — inside 7 days of your home draw.