Comprehensive Hormone Testing — Male & Female Panels

Hormones are the body’s signaling language. They do not operate in isolation — they exist in webs of feedback, conversion, clearance, and receptor sensitivity. A testosterone level without SHBG, estradiol, LH, and free testosterone tells you almost nothing. An estradiol without knowing progesterone, SHBG, and estrogen metabolites is a single data point floating in clinical darkness.

This guide covers the complete hormone evaluation for both women and men — when to test, what to order, optimal ranges, clinical patterns, and intervention strategies.

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Female Hormone Panel

When to Test

Timing is everything in female hormone assessment. Hormones fluctuate dramatically across the menstrual cycle, and a random draw is often uninterpretable.

Day 3 of cycle (early follicular phase): Baseline hormones — FSH, LH, estradiol. This is when the system is at its quietest. FSH and LH should be low-normal. If FSH is already elevated on Day 3, ovarian reserve is declining.

Day 19–22 of cycle (mid-luteal phase): Peak progesterone assessment. Progesterone should be at its highest 5–7 days after ovulation. This is the window that confirms ovulation quality and corpus luteum function. If the cycle is 28 days, Day 21 is ideal. If the cycle is 32 days, test Day 25. Adjust: test 7 days before expected period.

DUTCH test: Collected during the luteal phase for the most clinically useful data — it captures progesterone metabolites, estrogen metabolites, and cortisol simultaneously.

Perimenopause/menopause: Timing becomes less relevant as cycling becomes irregular or ceases. Test any time. Serial testing (every 3–6 months) tracks the trajectory.

The Complete Female Panel

Estradiol (E2)

• Follicular (Day 3): 30–100 pg/mL
• Ovulatory peak: 200–500 pg/mL
• Luteal: 100–300 pg/mL
• Optimal mid-luteal: 100–250 pg/mL
• Postmenopausal: <30 pg/mL (without HRT)

Estradiol drives follicular development, endometrial growth, bone density, cognitive function, cardiovascular protection, and skin elasticity. Low estradiol in premenopausal women: investigate hypothalamic amenorrhea (stress, undereating, overexercising), premature ovarian insufficiency, or hyperprolactinemia. Elevated estradiol outside of expected peaks: consider estrogen dominance, obesity (adipose tissue produces estrone → estradiol via aromatase), or exogenous exposure (xenoestrogens, HRT, OCP).

Progesterone

• Follicular: <1.0 ng/mL
• Mid-luteal peak (Day 19–22): 10–25 ng/mL
• Optimal luteal: >12 ng/mL (confirms ovulation)
• Postmenopausal: <0.5 ng/mL

Progesterone below 10 in the luteal phase suggests anovulation or luteal phase defect — even if a period occurs. Low progesterone is the most common hormonal imbalance in premenopausal women and drives many symptoms attributed to “estrogen dominance” (which is often actually progesterone deficiency creating a relative estrogen excess).

Progesterone-to-Estradiol (Pg/E2) Ratio

• Optimal: 100:1 to 500:1 (when both measured in same units: pg/mL progesterone x1000 / pg/mL estradiol)
• Estrogen dominance: <100:1

This ratio is more clinically useful than either value alone. A woman with estradiol of 150 pg/mL and progesterone of 8 ng/mL (= 8000 pg/mL) has a Pg/E2 ratio of 53:1 — estrogen dominant despite individually “normal” values.

Testosterone (Total)

• Optimal: 20–50 ng/dL
• Low testosterone in women: decreased libido, fatigue, reduced muscle mass, depression, thinning hair. Commonly seen with oral contraceptive use (OCP dramatically increases SHBG, binding free testosterone).
• High testosterone: PCOS (check DHEA-S, fasting insulin, and androstenedione to identify the source — ovarian vs adrenal), congenital adrenal hyperplasia, insulin resistance (insulin stimulates ovarian testosterone production).

Free Testosterone

• Optimal: 1.0–5.0 pg/mL
• Free testosterone reflects what is biologically active. If total T is normal but SHBG is very high, free T will be low — and she will be symptomatic.

DHEA-S (Dehydroepiandrosterone Sulfate)

• Optimal: 150–350 mcg/dL (premenopausal)
• DHEA-S is the adrenal androgen reservoir. Low DHEA-S = adrenal depletion, chronic stress, aging. High DHEA-S = adrenal-driven androgen excess (differentiate from ovarian source in PCOS).
• DHEA-S declines with age — by menopause, levels are often 50–70% lower than peak values in the 20s.

FSH (Follicle-Stimulating Hormone)

• Day 3: 3–8 mIU/mL (optimal)
• Day 3 FSH >10: diminished ovarian reserve. The pituitary is working harder to stimulate follicles.
• Menopausal: >25–40 mIU/mL

LH (Luteinizing Hormone)

• Day 3: 2–6 mIU/mL
• LH/FSH ratio >2:1 on Day 3 strongly suggests PCOS (excess LH drives androgen production from theca cells).
• LH surge at ovulation: 20–100 mIU/mL (detected by ovulation prediction kits).

SHBG (Sex Hormone-Binding Globulin)

• Optimal: 40–120 nmol/L
• Low SHBG (<40): Insulin resistance, metabolic syndrome, PCOS, hypothyroidism. Low SHBG means more free hormones — but in the case of androgens, more free testosterone drives acne, hirsutism, and hair loss.
• High SHBG (>120): Oral contraceptive use, hyperthyroidism, liver disease, anorexia. High SHBG binds too much testosterone — she has no libido despite “normal” total testosterone.

Prolactin

• Optimal: 5–20 ng/mL
• Elevated prolactin: pituitary adenoma (prolactinoma — get MRI), medications (SSRIs, antipsychotics, metoclopramide), hypothyroidism (TRH stimulates prolactin), chronic stress.
• Prolactin suppresses GnRH → suppresses FSH/LH → causes anovulation, amenorrhea, and galactorrhea.

Estrogen Dominance — The Full Clinical Picture

Estrogen dominance is not simply “too much estrogen.” It is estrogen excess relative to progesterone, combined with impaired estrogen clearance.

Causes:

• Anovulatory cycles (no corpus luteum = no progesterone production)
• Excess body fat (adipose tissue contains aromatase, converting androgens to estrone)
• Xenoestrogens: BPA, phthalates, parabens, pesticides, plastics — environmental chemicals that mimic estrogen at receptor sites
• Poor liver clearance: Phase I and Phase II detoxification impairment (check DUTCH estrogen metabolites)
• Constipation: estrogen conjugated by the liver for excretion gets deconjugated by beta-glucuronidase (produced by dysbiotic gut bacteria) and reabsorbed through enterohepatic recirculation
• Low progesterone: the most common driver — perimenopause begins with progesterone decline years before estrogen declines
• Oral contraceptives: paradoxically, OCPs can mask estrogen dominance by suppressing the HPO axis while providing synthetic estrogen/progestin

Symptoms: Heavy periods, breast tenderness, fibrocystic breasts, fibroids, endometriosis, PMS, mood swings, bloating, weight gain (especially hips/thighs), headaches (menstrual migraines), anxiety.

Treatment Protocol:

1. DIM (Diindolylmethane): 100–200 mg/day. Shifts estrogen metabolism toward the protective 2-OH pathway and away from the proliferative 16-OH and genotoxic 4-OH pathways. Derived from cruciferous vegetable metabolism (I3C → DIM in the stomach).
2. Calcium-D-Glucarate: 500 mg 2x/day. Inhibits beta-glucuronidase, preventing estrogen reabsorption from the gut. Supports Phase II glucuronidation.
3. Sulforaphane: From broccoli sprouts or supplement (50–100 mg/day). Potent Phase II inducer (Nrf2 pathway activation). Upregulates glutathione conjugation and other detox pathways.
4. Fiber: 30–40 g/day. Binds estrogen in the gut and promotes excretion. Ground flaxseed (2 tbsp/day) contains lignans that modulate estrogen receptor activity.
5. Liver support: Milk thistle (silymarin 200–400 mg/day), NAC (600 mg/day), B vitamins for methylation (methyl donors needed for COMT-mediated estrogen clearance).
6. Progesterone support — Vitex/Chasteberry: 400 mg standardized extract daily, taken in the morning. Vitex acts on the pituitary to increase LH relative to FSH, promoting ovulation and progesterone production. Takes 3–6 cycles to reach full effect. Not appropriate during pregnancy or with dopamine agonist medications.
7. Reduce xenoestrogen exposure: Switch to glass food containers, clean beauty products, filtered water, organic produce (especially the Dirty Dozen).

Perimenopause and Menopause

Perimenopause begins 5–10 years before the final period. The hallmark is progesterone decline with erratic estrogen fluctuations — cycles become irregular, shorter or longer, heavier or lighter. Estrogen does not simply decline in a straight line; it swings wildly before finally dropping.

HRT vs Bioidentical Hormone Therapy (BHRT):

• Conventional HRT uses conjugated equine estrogens (Premarin — from pregnant mare urine) and synthetic progestins (medroxyprogesterone acetate). The Women’s Health Initiative (WHI) trial in 2002 showed increased breast cancer, stroke, and clot risk with this specific combination.
• BHRT uses bio-identical hormones: estradiol (transdermal patch or cream, 0.025–0.1 mg/day), micronized progesterone (Prometrium 100–200 mg at bedtime — also improves sleep via GABA-A modulation), and testosterone cream if needed.
• Transdermal estradiol avoids first-pass liver metabolism — lower clot risk than oral forms.
• The timing hypothesis: HRT initiated within 10 years of menopause (or before age 60) shows cardiovascular benefit. Starting after 60 or more than 10 years post-menopause increases cardiovascular risk.
• Estrogen metabolite safety: Monitor DUTCH test estrogen metabolites during BHRT. Ensure 2-OH pathway is favored. Support methylation of 4-OH metabolites.
• Progesterone for bone and sleep: Micronized progesterone stimulates osteoblasts (bone building) and modulates GABA-A receptors (sedating, anxiolytic). It should be prescribed for any woman with an intact uterus receiving estrogen (to prevent endometrial hyperplasia) and can be used alone for sleep and anxiety.

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Male Hormone Panel

When to Test

Testosterone follows a diurnal rhythm — it peaks between 7–10 AM and declines through the day, reaching its nadir in the evening. Always draw male hormones fasting, in the morning (before 10 AM) for accurate results. Two measurements on separate days should confirm low testosterone before initiating treatment.

The Complete Male Panel

Total Testosterone

• Standard range: 300–1000 ng/dL (varies by lab)
• Optimal functional range: 600–900 ng/dL
• Symptomatic threshold: Most men become symptomatic below 500 ng/dL — fatigue, low libido, erectile dysfunction, depressed mood, poor concentration, reduced muscle mass, increased body fat, poor recovery from exercise.
• “Normal” total testosterone of 350 ng/dL in a 35-year-old man is not normal — it is the level typically seen in men in their 70s. The standard range is built from a sick population.

Free Testosterone

• Standard range: 5–25 pg/mL
• Optimal: 15–25 pg/mL
• Free testosterone is the unbound, biologically active fraction — only 1–3% of total testosterone. If total T is 600 ng/dL but SHBG is 60 nmol/L, free T may be low and the man will be symptomatic despite “normal” total T.
• Calculated free T (using total T, SHBG, and albumin) is more reliable than direct free T assays in many labs.

SHBG (Sex Hormone-Binding Globulin)

• Optimal: 20–40 nmol/L
• Low SHBG (<20): Insulin resistance, obesity, metabolic syndrome, type 2 diabetes, hypothyroidism. Low SHBG means more free testosterone and free estradiol — but it reflects underlying metabolic disease.
• High SHBG (>50): Aging, hyperthyroidism, liver disease, low caloric intake, excessive endurance exercise. High SHBG binds testosterone — total T can be “normal” while free T is deficient.

Estradiol (Sensitive Assay)

• Optimal: 20–35 pg/mL
• Use the sensitive assay (LC-MS/MS) — the standard estradiol assay (immunoassay) was designed for female ranges and is inaccurate in the male range.
• Too high (>35 pg/mL): Gynecomastia (breast tissue growth), water retention, emotional lability, erectile dysfunction, increased cardiovascular risk. Usually from excess aromatase activity — adipose tissue converts testosterone to estradiol.
• Too low (<15 pg/mL): Joint pain, bone loss (estradiol is critical for male bone density), low libido (paradoxically — men need some estradiol for libido), dry skin, cognitive impairment.
• The goal is balance: enough estradiol for bones, brain, and cardiovascular protection, not so much that it causes estrogenic symptoms.

DHT (Dihydrotestosterone)

• Standard: 30–85 ng/dL
• Optimal: 30–50 ng/dL
• DHT is produced from testosterone by 5-alpha-reductase. It is the most potent androgen — 3–5x stronger than testosterone at the androgen receptor.
• High DHT: Drives male pattern baldness, prostate growth (BPH), acne, oily skin. 5-alpha-reductase inhibitors (finasteride, dutasteride) reduce DHT but can cause sexual side effects. Natural alternatives: saw palmetto (320 mg/day), pygeum (100 mg/day), zinc (competes with 5-AR), nettle root (binds SHBG, indirectly modulating DHT).
• Low DHT: Can cause reduced body hair, reduced penile sensitivity, and diminished sense of masculinity/drive.

LH (Luteinizing Hormone)

• Standard: 1.5–9.0 mIU/mL
• Optimal: 3–6 mIU/mL

FSH (Follicle-Stimulating Hormone)

• Standard: 1.5–12.0 mIU/mL
• Optimal: 2–6 mIU/mL

LH and FSH distinguish primary from secondary hypogonadism:

• Primary (testicular failure): Low testosterone, HIGH LH and FSH. The pituitary is screaming at the testes to produce more. Causes: Klinefelter syndrome, testicular injury, orchitis, varicocele, age-related testicular decline.
• Secondary (pituitary/hypothalamic): Low testosterone, LOW or normal LH and FSH. The pituitary is not sending the signal. Causes: pituitary tumor, head trauma, chronic opioid use (opioid-induced hypogonadism — extremely common and underdiagnosed), obesity (excess estradiol suppresses GnRH), chronic stress (cortisol suppresses GnRH), sleep deprivation, overtraining.

This distinction determines treatment: primary hypogonadism may require TRT. Secondary hypogonadism often responds to addressing the underlying cause (weight loss, opioid cessation, sleep optimization) or clomiphene citrate (stimulates endogenous production).

Prolactin

• Optimal: 4–15 ng/mL
• Elevated prolactin in men: pituitary adenoma, medications, hypothyroidism. Prolactin suppresses GnRH, reducing testosterone production. Elevated prolactin can cause erectile dysfunction, low libido, and galactorrhea (even in men).
• Always check prolactin in men with secondary hypogonadism. If elevated, get pituitary MRI.

DHEA-S

• Optimal: 200–400 mcg/dL (age-dependent — declines ~2% per year after age 25)
• Low DHEA-S = adrenal depletion. DHEA is the most abundant steroid hormone in the body and a precursor to both testosterone and estrogen. Supplementation (25–50 mg/day for men) can improve androgen status, mood, and immune function.

PSA (Prostate-Specific Antigen)

• Normal: <2.5 ng/mL (men under 50), <4.0 ng/mL (over 50)
• Baseline PSA should be established before any testosterone therapy. Monitor every 6–12 months on TRT.
• Rapid PSA rise (>1.4 ng/mL increase per year) is more concerning than absolute value.
• PSA is organ-specific but not cancer-specific — prostatitis, BPH, and recent ejaculation can elevate it.

Natural Testosterone Optimization

Before considering TRT, address the foundations. Many men with testosterone in the 400–550 range can reach 600–800 with lifestyle intervention alone.

Sleep: 7–9 hours of quality sleep. Testosterone is produced during deep sleep (stages 3–4 NREM). One week of 5-hour sleep reduces testosterone by 10–15%. Sleep apnea devastates testosterone — screen with home sleep study if BMI >30 or snoring is reported.

Resistance training: Compound movements (squat, deadlift, bench press, overhead press, row) with heavy loads (70–85% 1RM) for 3–4 sets of 5–8 reps. This stimulus drives the highest acute testosterone response. Avoid chronic excessive endurance training (marathon training, 2+ hours of cardio daily) — this elevates cortisol and suppresses testosterone.

Body fat reduction: Every 1% decrease in body fat percentage increases testosterone. Adipose tissue contains aromatase — the enzyme converting testosterone to estradiol. Visceral fat is the worst offender. Target body fat: 12–18% for optimal testosterone.

Targeted supplementation:

• Zinc: 30 mg/day (zinc picolinate or zinc bisglycinate). Zinc inhibits aromatase and is required for testosterone synthesis. Zinc deficiency is common — check RBC zinc levels. Do not exceed 50 mg/day long-term without balancing copper (2 mg copper per 30 mg zinc).
• Magnesium: 400 mg/day (glycinate, threonate, or malate). Magnesium increases free testosterone by reducing SHBG binding. Also supports sleep quality, which indirectly supports testosterone.
• Vitamin D: 5000 IU/day (with K2). Testosterone levels correlate directly with vitamin D status. Men with 25-OH-D above 50 ng/mL have significantly higher testosterone than those below 30. Target: 50–70 ng/mL.
• Boron: 6–10 mg/day. Reduces SHBG (increasing free testosterone), reduces estradiol, supports vitamin D metabolism. One of the most evidence-backed yet underused testosterone support minerals.
• Ashwagandha KSM-66: 600 mg/day. Randomized controlled trials show ~15% increase in testosterone, improved sperm quality, and significant cortisol reduction (~30%). The cortisol-lowering effect is likely the primary mechanism — reduced cortisol allows the HPG axis to function without suppression.
• Tongkat ali (Eurycoma longifolia): 200–400 mg/day (standardized extract). Evidence for stress hormone modulation and modest testosterone increase, particularly in stressed men and late hypogonadal men. Mechanism includes competitive inhibition of SHBG binding and possible direct Leydig cell stimulation.
• Fadogia agrestis: 600–1200 mg/day. Emerging evidence from animal studies showing increased testosterone, but human clinical trial data is limited. The safety profile is not yet well-established — possible testicular toxicity at high doses in rodent studies. Use cautiously, cycle on/off (5 days on, 2 off), and monitor labs.
• DIM or Calcium-D-Glucarate: If estradiol is elevated (>35 pg/mL), use DIM 100–200 mg or calcium-d-glucarate 500 mg 2x/day to support estrogen metabolism and clearance.

Avoid:

• Excess alcohol (2+ drinks/day directly suppresses testosterone and increases aromatase activity)
• Chronic psychological stress (cortisol and testosterone are inversely related — the pregnenolone steal concept)
• BPA, phthalates (endocrine disruptors — switch to glass containers, avoid plastic water bottles, receipt paper)
• Excess soy (phytoestrogens — moderate consumption is fine, but large daily intake of processed soy products may suppress testosterone in susceptible individuals)
• Sleep deprivation (the single most destructive factor for testosterone)
• Chronic caloric restriction (prolonged severe dieting drops testosterone dramatically)

TRT (Testosterone Replacement Therapy)

When to consider TRT:

• Confirmed low testosterone (<300 ng/dL on two morning draws) with symptoms, after lifestyle optimization has been attempted for 3–6 months
• Primary hypogonadism (elevated LH/FSH) with symptomatic low T
• Secondary hypogonadism that does not respond to treating the underlying cause

Delivery methods:

• Intramuscular injection (testosterone cypionate or enanthate): 100–200 mg/week (or 50–100 mg twice weekly for more stable levels). Most cost-effective. Peak and trough levels can cause mood and energy fluctuations — twice-weekly dosing smooths this curve.
• Subcutaneous injection: Same esters, same doses. Shallower injection (insulin needle, 27–29 gauge). More stable absorption curve than IM. Increasingly preferred.
• Transdermal (gel/cream): 50–100 mg applied daily. Steady levels, no injections. Risk of transference to partners/children through skin contact. Higher DHT conversion than injectable (skin has high 5-alpha-reductase activity).
• Pellets (subcutaneous implant): 600–1200 mg inserted every 3–6 months. Very stable levels. Requires minor in-office procedure. Difficult to adjust dose once implanted.

Monitoring on TRT (every 3–6 months):

• Total and free testosterone (target mid-upper optimal range)
• Estradiol sensitive (target 20–35 pg/mL — add aromatase management if elevated)
• Hematocrit/hemoglobin (testosterone stimulates erythropoiesis — hematocrit above 52–54% increases blood viscosity and clot risk. Donate blood if hematocrit rises above 52%)
• PSA (monitor trend)
• Lipid panel (testosterone can improve or worsen lipid profile depending on dose and route)
• Liver function (rare hepatotoxicity, mainly with oral forms — avoid oral methyltestosterone)

Fertility implications: Exogenous testosterone shuts down the HPG axis via negative feedback — LH and FSH plummet to near zero. Without LH stimulating Leydig cells and FSH stimulating Sertoli cells, intratesticular testosterone drops and spermatogenesis stops. Testicular atrophy follows. TRT is a male contraceptive — not reliably enough for birth control, but significantly enough to cause infertility.

Fertility preservation strategies:

• hCG (human chorionic gonadotropin): 500–1000 IU subcutaneous 2–3x/week. hCG mimics LH, maintaining intratesticular testosterone and Leydig cell function. Co-prescribed with TRT to maintain testicular size and spermatogenesis. Essential for any man on TRT who may want future fertility.
• Clomiphene citrate (Clomid): 25–50 mg every other day. Selective estrogen receptor modulator (SERM) that blocks estrogen feedback at the hypothalamus/pituitary, causing increased GnRH → LH/FSH release → increased endogenous testosterone production. Preserves fertility. Used as TRT alternative in younger men. Off-label use. Side effects: visual changes (rare), mood changes. Can raise testosterone 200–400 ng/dL in secondary hypogonadism.
• Enclomiphene: The active trans-isomer of clomiphene. Fewer estrogenic side effects than clomiphene. Similar mechanism. Increasingly available through compounding pharmacies and specialty clinics.
• hMG (human menopausal gonadotropin): Contains FSH and LH. Used to restore spermatogenesis in men who have been on TRT long-term. Often combined with hCG.

Coming off TRT: Abrupt cessation leads to a hormonal crash — the HPG axis takes weeks to months to recover (and may not fully recover after years of suppression). Taper protocols: reduce TRT dose gradually over 4–8 weeks while introducing hCG and/or clomiphene to stimulate endogenous recovery. Monitor LH, FSH, and testosterone every 4 weeks during recovery.

The decision to start TRT is not trivial. It is potentially a lifelong commitment. Exhaust natural optimization first. Test thoroughly. Understand the implications for fertility. And if TRT is initiated, monitor closely, consistently, and comprehensively.