Complete Hormone Panel: Male & Female

Why Hormones Cannot Be Measured by Symptoms Alone

Every hormone in the body speaks through symptoms, but none of them speaks uniquely. Fatigue is low thyroid, low testosterone, low cortisol, low iron, and high estrogen. Weight gain is insulin resistance, hypothyroid, high cortisol, low testosterone, and estrogen dominance. Low libido is low testosterone in both sexes, high prolactin, low DHEA, adrenal dysfunction, and depression. Trying to diagnose hormonal imbalance by symptoms alone is like trying to identify an instrument in an orchestra by listening to the full ensemble. You need the sheet music — the lab panel.

But not just any lab panel. The timing of the blood draw, the type of test (serum vs. urine vs. saliva), and the reference ranges applied all determine whether the results are clinically meaningful or medically useless.

The DUTCH Test: The Gold Standard for Hormone Assessment

The Dried Urine Test for Comprehensive Hormones (DUTCH) is the most sophisticated hormone assessment available. Unlike serum (a single snapshot), DUTCH collects four to five dried urine samples over 24 hours, capturing the full diurnal pattern of cortisol and the complete picture of hormone metabolites.

Why metabolites matter: serum estradiol tells you how much estrogen is circulating. The DUTCH test tells you how that estrogen is being processed — and estrogen metabolism is where the cancer risk lives.

Estrogen Metabolites

Estrogen is metabolized through three primary pathways:

2-OH estrone (2-hydroxyestrone): The protective pathway. 2-OH metabolites have weak estrogenic activity and may even be anti-estrogenic. Higher 2-OH production is associated with lower breast cancer risk.

4-OH estrone (4-hydroxyestrone): The genotoxic pathway. 4-OH metabolites can form quinone intermediates that directly damage DNA by creating depurinating adducts. If 4-OH metabolites are not rapidly methylated (via COMT enzyme using SAMe as methyl donor), they become mutagenic. This pathway is a direct link between estrogen metabolism and estrogen-sensitive cancers.

16-OH estrone (16-alpha-hydroxyestrone): The proliferative pathway. 16-OH metabolites are strongly estrogenic — they bind estrogen receptors with high affinity and promote cell proliferation. Elevated 16-OH is associated with increased breast cancer risk and estrogen-driven conditions (fibroids, endometriosis, fibrocystic breasts).

2-OH:16-OH ratio: >2.0 desired. This ratio reflects the balance between the protective and proliferative pathways. A ratio below 2.0 indicates estrogen is being shunted toward proliferative metabolism. Interventions to shift the ratio: DIM (diindolylmethane, 100-200 mg/day), I3C (indole-3-carbinol, 200-400 mg/day), cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, kale), flaxseed (lignans modulate estrogen metabolism).

4-OH methylation percentage: The DUTCH test shows what percentage of 4-OH estrone is being methylated to the safer 4-methoxy metabolite. Low methylation indicates COMT enzyme insufficiency (COMT Val158Met polymorphism — the “worrier” variant has lower COMT activity), SAMe depletion, magnesium deficiency (COMT cofactor), or general methylation impairment. Support: magnesium, SAMe, methylated B vitamins, and limit catechol competition (dopamine and norepinephrine are also COMT substrates).

Female Hormone Panel

When to Test

Timing is everything in female hormone testing. The menstrual cycle creates a hormonal symphony with distinct movements:

• Day 3 (early follicular): FSH, LH, estradiol — baseline ovarian function assessment
• Day 19-21 (mid-luteal, approximately 7 days post-ovulation): Progesterone peak — confirms ovulation and luteal adequacy
• DUTCH test: Collected during the mid-luteal phase (days 19-22 of a 28-day cycle)

Testing at the wrong time produces uninterpretable results. A progesterone drawn on Day 8 will always be low — that is physiology, not pathology.

Serum Optimal Ranges

Estradiol (E2):

• Follicular phase: 30-100 pg/mL
• Ovulatory peak: 100-400 pg/mL
• Luteal phase: 100-300 pg/mL
• Menopause: <30 pg/mL (symptoms usually emerge below 50)

Estradiol is the primary estrogen during reproductive years. It maintains bone density, cardiovascular protection, brain function (memory, mood, neuroprotection), skin elasticity, vaginal and urethral mucosal health, and cholesterol metabolism. The precipitous decline at menopause drives the cascade of symptoms and disease risk.

Progesterone:

• Follicular phase: <1 ng/mL
• Luteal phase (Day 21): 15-25 ng/mL optimal (standard “adequate” is >5, which is barely sufficient)
• Menopause: <0.5 ng/mL

Progesterone is the calming counterbalance to estrogen. It is anxiolytic (metabolized to allopregnanolone, which activates GABA-A receptors), promotes sleep, builds bone (stimulates osteoblasts), protects the uterine lining against estrogen-driven proliferation, and is essential for pregnancy maintenance. A luteal progesterone of 8 ng/mL is “normal” by standard criteria but represents suboptimal ovulation and inadequate luteal support.

Progesterone:Estradiol Ratio (P:E2): 100-500:1 in the luteal phase (using progesterone in pg/mL / estradiol in pg/mL, where 1 ng/mL progesterone = 1000 pg/mL). This ratio is more clinically meaningful than either hormone alone. A woman with estradiol of 150 pg/mL needs luteal progesterone of at least 15,000 pg/mL (15 ng/mL) for balance.

Testosterone (total): 40-70 ng/dL in women Free testosterone: 1-3 pg/mL

Testosterone in women drives libido, motivation, muscle maintenance, bone density, and cognitive sharpness. Levels decline approximately 50% between ages 20 and 40, well before menopause. Low testosterone in women is associated with low libido, fatigue, depression, sarcopenia, and osteoporosis. Testosterone is rarely tested in women and even more rarely treated.

DHEA-S: 150-350 mcg/dL (age-dependent — peaks in mid-20s, declines steadily)

DHEA-S is the most abundant steroid hormone in the body and the primary adrenal androgen precursor. It is a reservoir — convertible to both testosterone and estrogen peripherally. Low DHEA-S reflects adrenal depletion (chronic stress), aging, or autoimmune adrenal insufficiency. Supplementation: 5-25 mg/day in women (start low — excessive doses cause acne, oily skin, hair loss from androgenic conversion).

FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone):

• Follicular: FSH 3-10 mIU/mL, LH 2-8 mIU/mL
• Ovulatory surge: LH 20-100 mIU/mL (triggers ovulation)
• Perimenopause: FSH >25 mIU/mL (rising FSH = ovarian decline, the pituitary screams louder as the ovary becomes deaf)
• Menopause: FSH >40 mIU/mL

SHBG (Sex Hormone Binding Globulin): 40-80 nmol/L in women

SHBG is the protein that binds and inactivates sex hormones. Only unbound (free) hormones are biologically active. Low SHBG means more free androgens — seen in insulin resistance, PCOS, hypothyroidism, and obesity. High SHBG means less free hormone available — seen with oral contraceptives (estrogen increases hepatic SHBG production), hyperthyroidism, anorexia, and aging. Oral contraceptives can raise SHBG 3-4x, dramatically reducing free testosterone and contributing to persistent low libido even after discontinuation.

Prolactin: <20 ng/mL

Elevated prolactin (hyperprolactinemia) suppresses GnRH, causing anovulation, amenorrhea, and galactorrhea. Causes: prolactinoma (pituitary adenoma — get MRI), medications (antipsychotics, SSRIs, metoclopramide, opioids), hypothyroidism (TRH stimulates prolactin), chronic stress, chest wall irritation. Mild elevations (20-40) can be stress-related; levels >100 strongly suggest prolactinoma.

AMH (Anti-Mullerian Hormone): Produced by granulosa cells of small antral follicles. AMH reflects ovarian reserve — the remaining egg supply. It does not fluctuate with the menstrual cycle, so it can be tested any day. AMH declines with age, rapidly after 35. AMH <1.0 ng/mL suggests diminished ovarian reserve. Used in fertility planning and IVF response prediction. AMH cannot assess egg quality — only quantity.

Common Female Hormone Patterns

Estrogen Dominance: The most common hormonal imbalance in reproductive-age women. This is not necessarily high absolute estrogen — it is estrogen that is high relative to progesterone. Symptoms: PMS (especially breast tenderness, mood swings, bloating), heavy or prolonged periods, fibroids, endometriosis, fibrocystic breasts, weight gain in hips and thighs, anxiety, and insomnia in the luteal phase. Drivers: anovulatory cycles (no corpus luteum = no progesterone), chronic stress (cortisol steal — pregnenolone diverted from progesterone to cortisol), xenoestrogens (BPA, phthalates, parabens, pesticides), poor estrogen metabolism (sluggish liver detoxification, constipation preventing estrogen excretion, low fiber intake, dysbiosis — beta-glucuronidase-producing bacteria deconjugate excreted estrogen, recirculating it).

Low Progesterone / Luteal Phase Defect: Progesterone <10 ng/mL on Day 21. Luteal phase shorter than 12 days. Causes: anovulation, poor corpus luteum function, excessive exercise, caloric restriction, hypothyroidism, hyperprolactinemia. Consequences: infertility, recurrent early miscarriage, PMS, anxiety, insomnia. Support: vitex (chasteberry — 20-40 mg standardized extract, raises LH and supports corpus luteum), bioidentical progesterone (oral micronized progesterone 100-200 mg at bedtime during luteal phase), vitamin B6 (P5P 50-100 mg — supports corpus luteum function), vitamin C (750 mg/day — shown to raise progesterone).

PCOS (Polycystic Ovary Syndrome): The most common endocrine disorder in women of reproductive age (10-15%). Hallmarks: hyperandrogenism (high total and/or free testosterone, acne, hirsutism, hair thinning), oligo/anovulation (irregular or absent periods), polycystic ovarian morphology (12+ antral follicles on ultrasound). Lab pattern: elevated LH:FSH ratio (>2:1, sometimes >3:1), high testosterone, low SHBG, high insulin (the root driver in most cases), often high DHEA-S. The insulin connection: hyperinsulinemia stimulates ovarian theca cells to produce excess androgens and suppresses SHBG, creating a vicious cycle. Treatment must address insulin resistance first — metformin or inositol (myo-inositol 4g + D-chiro-inositol 100mg daily), low-glycemic diet, resistance training, weight loss.

Perimenopause: The 2-10 year transition before menopause (average onset age 47). Pattern: erratic, often high estrogen (the ovary sputters — some cycles produce excessive estrogen, others insufficient), declining progesterone (early and consistent), rising FSH (gradual), worsening PMS, heavier periods, new onset anxiety or insomnia, vasomotor symptoms (hot flashes, night sweats). This is the most volatile hormonal phase in a woman’s life, and it is routinely dismissed as “stress” or “depression.”

Male Hormone Panel

Optimal Ranges

Total Testosterone: 700-1000 ng/dL (Standard “normal” 264-916 ng/dL — this range allows a 35-year-old man with a total T of 280 to be called “normal”)

The standard lower limit of 264 ng/dL was derived from population data that includes elderly, obese, and chronically ill men. It does not represent health. Symptoms of testosterone deficiency — fatigue, low libido, erectile dysfunction, depression, brain fog, loss of muscle mass, increased body fat, poor recovery from exercise — commonly emerge below 500 ng/dL and are nearly universal below 400.

Male testosterone has declined approximately 1% per year since the 1980s across all age groups (Travison et al., 2007, Journal of Clinical Endocrinology & Metabolism). A 60-year-old man today has significantly lower testosterone than a 60-year-old man in 1988. This population-wide decline is driven by obesity, endocrine disruptors, sleep deprivation, chronic stress, and sedentary lifestyles.

Free Testosterone: 15-25 pg/mL

This is the biologically active fraction — only 1-3% of total testosterone circulates unbound. The rest is bound to SHBG (tightly, inactive) or albumin (loosely, partially available). A man can have a total testosterone of 600 ng/dL and still be symptomatic if his SHBG is 70 nmol/L, leaving his free testosterone at 8 pg/mL.

Calculated free testosterone (using the Vermeulen equation from total T, SHBG, and albumin) is more reliable than direct free testosterone assays (analog methods are notoriously inaccurate). Equilibrium dialysis is the gold standard but expensive and rarely available.

SHBG: 25-45 nmol/L in men

Low SHBG (<25): insulin resistance, obesity, hypothyroidism, nephrotic syndrome. Low SHBG means more free testosterone initially, but the excess is rapidly metabolized, creating a boom-bust pattern with net lower testosterone effect.

High SHBG (>45): aging, liver disease (cirrhosis increases SHBG), hyperthyroidism, anticonvulsants, excessive alcohol, HIV. High SHBG traps testosterone, lowering the free fraction despite “normal” total T.

Estradiol (E2) in men: 20-35 pg/mL

Men need estrogen. It protects bones (estrogen deficiency in men causes osteoporosis), maintains joint health (too-low E2 causes joint pain and stiffness), supports cognitive function, and modulates libido (both too-low and too-high E2 impair libido and erectile function).

Too high (>35-40): gynecomastia (breast tissue growth), water retention, emotional lability, erectile dysfunction, increased clotting risk. Driven by aromatase overactivity — the enzyme that converts testosterone to estradiol. Aromatase is concentrated in adipose tissue (especially visceral fat), making obesity the primary driver of high male estradiol.

Too low (<20): bone loss, joint pain, dry skin, low mood, poor libido. Can occur with excessive aromatase inhibitor use (anastrozole) or very low body fat.

DHT (Dihydrotestosterone): The most potent androgen — 3-10x more androgenic than testosterone. Produced by 5-alpha reductase from testosterone. DHT drives male pattern baldness, prostate growth, body hair, and acne. 5-alpha reductase inhibitors (finasteride, dutasteride) block DHT but can cause persistent sexual side effects (post-finasteride syndrome).

DHEA-S: 250-500 mcg/dL in men

LH (Luteinizing Hormone) and FSH: In men, LH stimulates Leydig cells to produce testosterone; FSH stimulates Sertoli cells for spermatogenesis. Testing LH distinguishes primary from secondary hypogonadism:

• Low T + low LH = secondary (pituitary/hypothalamic problem — the brain is not sending the signal)
• Low T + high LH = primary (testicular problem — the testes cannot respond to the signal)

Prolactin: <15 ng/mL in men. Elevated prolactin suppresses GnRH, causing hypogonadism. In men, always rule out prolactinoma (pituitary MRI) when prolactin is significantly elevated, especially >50 ng/mL.

PSA (Prostate Specific Antigen): Baseline measurement for prostate cancer screening. Age-adjusted thresholds are debated. PSA velocity (rate of change over time) may be more informative than a single value. PSA also rises with BPH, prostatitis, ejaculation (within 48 hours), and vigorous cycling.

Common Male Hormone Patterns

Low T + High SHBG: Total testosterone may look adequate, but free testosterone is low because SHBG is binding it. Investigate: liver function (cirrhosis, fatty liver), thyroid status (hyperthyroidism raises SHBG), alcohol intake, and aging.

Low T + Low LH (Secondary Hypogonadism): The pituitary is not sending the signal. Causes: obesity (adipose tissue estrogen suppresses GnRH via negative feedback), chronic opioid use (potent GnRH suppressor), obstructive sleep apnea (hypoxia suppresses GnRH), chronic stress (cortisol suppresses GnRH), pituitary adenoma (prolactinoma or non-functioning), anabolic steroid use (exogenous testosterone suppresses LH/FSH — testicular atrophy), head trauma. This is the most common pattern in clinical practice — and it is potentially reversible by addressing the root cause.

Low T + High LH (Primary Hypogonadism): The testes are failing despite adequate pituitary drive. Causes: Klinefelter syndrome (47,XXY — most common genetic cause), varicocele, orchitis (mumps), testicular torsion/trauma, chemotherapy/radiation, and age-related Leydig cell decline.

High E2:T Ratio (Aromatase Overactivity): Excess conversion of testosterone to estradiol. Symptoms: gynecomastia, water retention, mood instability, erectile dysfunction. Root cause is almost always visceral adiposity — lose the belly fat and aromatase activity normalizes. Zinc deficiency also increases aromatase activity. Interventions: weight loss (primary), zinc 30 mg/day (natural aromatase inhibitor), DIM 100-200 mg/day (promotes 2-OH estrogen metabolism), limit alcohol (directly increases aromatase expression), address liver function (the liver clears estrogen — fatty liver impairs clearance).

Natural Hormone Optimization Protocol (Both Sexes)

Sleep: 7-9 hours in a dark, cool room. Testosterone production peaks during deep sleep. One week of 5-hour sleep nights reduces testosterone by 10-15% (Leproult & Van Cauter, 2011, JAMA). Growth hormone — critical for tissue repair and body composition — is released primarily during slow-wave sleep. Cortisol, melatonin, and sex hormones all depend on circadian rhythm integrity.

Resistance training: 2-4x/week with compound movements. Squats, deadlifts, bench press, rows — large muscle group engagement acutely raises testosterone and growth hormone. The effect is dose-dependent: heavier loads (70-85% of 1RM), shorter rest periods (60-90 seconds), and higher volume amplify the hormonal response.

Reduce visceral fat. Adipose tissue is an endocrine organ. It produces aromatase (converting T to E2), inflammatory cytokines (IL-6, TNF-alpha — suppress GnRH), and adipokines (leptin resistance impairs reproductive hormones). Every 10% reduction in body fat can raise testosterone 50-100 ng/dL.

Manage insulin. Hyperinsulinemia suppresses SHBG (increasing free estrogen and androgen clearance), drives ovarian androgen production in women (PCOS), and promotes visceral fat accumulation. Low-glycemic diet, time-restricted eating, berberine, inositol, and chromium all improve insulin sensitivity.

Key supplements:

• Zinc (30 mg/day as picolinate or bisglycinate): Required for testosterone synthesis, sperm production, and aromatase inhibition. Zinc deficiency is rampant — depleted by stress, sweat, alcohol, and medications.
• Vitamin D (5000 IU/day, target 50-70 ng/mL): Vitamin D receptors exist on Leydig cells, ovarian tissue, and the pituitary. Supplementation raises testosterone in deficient men (Pilz et al., 2011).
• Magnesium (400-600 mg/day as glycinate or threonate): Increases free testosterone by reducing SHBG binding. Also supports sleep, stress resilience, and over 300 enzymatic reactions.
• Boron (6-9 mg/day): Reduces SHBG, increases free testosterone, supports estrogen metabolism. One of the most underappreciated minerals for hormonal health (Naghii et al., 2011).
• DIM/I3C: Diindolylmethane (100-200 mg/day) promotes the 2-OH estrogen detoxification pathway over the 4-OH and 16-OH pathways. Protective for both sexes.
• Ashwagandha (KSM-66, 600 mg/day): Reduces cortisol 25-30%, raises testosterone in stressed men (Lopresti et al., 2019), improves thyroid function, enhances sleep quality, and supports fertility (increases sperm count and motility).

Reduce xenoestrogen exposure: BPA (plastic containers, receipts, can linings), phthalates (fragrances, soft plastics, vinyl), parabens (cosmetics, lotions), pesticides (atrazine — turns male frogs female, Syngenta’s own data), and dioxins. Use glass containers, eat organic when possible, avoid heating food in plastic, filter water (reverse osmosis or solid carbon block), and choose fragrance-free personal care products.

Limit alcohol. Alcohol directly increases aromatase activity, impairs hepatic estrogen clearance, damages Leydig cells, and suppresses GnRH. Even moderate consumption (2 drinks/day) measurably lowers testosterone.

Hormones are not isolated molecules floating in the blood. They are signals in a conversation — between the brain, the gonads, the adrenals, the thyroid, the liver, the gut, and the adipose tissue. Testing the full panel, at the right time, with functional optimal ranges, reveals not just where the imbalance lives but what is driving it. And when you know the driver, you know the intervention. The body wants to be in balance. Remove the obstacles, provide the raw materials, and the orchestra tunes itself.