Hormonal balance is a cornerstone of health at every stage of life, yet the specific hormones that matter most, the optimal timing for testing, and the interpretation of results shift dramatically as we age. Unlike static panels such as basic metabolic or lipid screens, hormone panels must be tailored to the physiological milestones that define each decade—from the rapid growth of early childhood to the subtle endocrine changes of late adulthood. This article walks through the age‑specific hormone panels that clinicians and health‑conscious individuals can use as part of a comprehensive preventive‑screening strategy, highlighting why each test matters, what typical reference ranges look like, and how results should be integrated into broader health‑maintenance plans.
Infancy and Early Childhood (0–5 Years)
Key Hormonal Axes
- Growth Hormone (GH) / Insulin‑Like Growth Factor‑1 (IGF‑1)
- Adrenocorticotropic Hormone (ACTH) and Cortisol
- Sex Steroids (Estradiol, Testosterone) – low baseline
- Dehydroepiandrosterone Sulfate (DHEA‑S)
Why Test?
During the first five years, the endocrine system orchestrates linear growth, brain development, and the establishment of the hypothalamic‑pituitary‑adrenal (HPA) axis. Abnormalities in GH/IGF‑1 can signal growth hormone deficiency, while dysregulated cortisol may point to congenital adrenal hyperplasia (CAH) or early‑onset adrenal insufficiency. Although sex steroids are present at low levels, markedly elevated values can indicate precocious puberty.
Typical Panel
| Analyte | Typical Reference (age‑adjusted) | Clinical Triggers |
|---|---|---|
| GH (random) | < 5 ng/mL (stimulated > 10 ng/mL) | Short stature, growth velocity < ‑2 SD |
| IGF‑1 | 50–250 ng/mL (varies with age) | Same as GH, also screening for GH excess |
| Morning Cortisol | 5–25 µg/dL | Suspected adrenal insufficiency, CAH |
| ACTH | 10–60 pg/mL | Paired with cortisol for adrenal axis |
| DHEA‑S | 20–150 µg/dL | Early signs of adrenal hyperplasia |
| Estradiol / Testosterone (sensitive assays) | < 10 pg/mL (E2), < 5 ng/dL (T) | Precocious puberty, adrenal tumors |
Interpretation Tips
- Dynamic testing (e.g., GH stimulation with arginine or clonidine) is often required because random GH levels are pulsatile.
- IGF‑1 provides a more stable surrogate for GH secretion and is less affected by acute stress.
- Cortisol should be drawn before 9 am; a low morning value warrants an ACTH stimulation test.
- Sex steroids in this age group are best interpreted in the context of bone age and clinical signs.
Pre‑Pubertal Years (6–12 Years)
Key Hormonal Axes
- Thyroid‑stimulating hormone (TSH) and Free T4 – *briefly mentioned for completeness; detailed thyroid work‑up is covered elsewhere*
- GH/IGF‑1 (continued growth monitoring)
- Leptin and Ghrelin (energy balance)
- Insulin‑like Growth Factor‑Binding Protein‑3 (IGFBP‑3)
Why Test?
The pre‑pubertal window is marked by steady linear growth and the gradual accumulation of adipose tissue, which influences leptin signaling and sets the stage for puberty. Hormone panels at this stage help differentiate constitutional growth delay from endocrine pathology and can uncover early insulin resistance that may precede type 2 diabetes.
Typical Panel
| Analyte | Typical Reference (age‑adjusted) | Clinical Triggers |
|---|---|---|
| IGF‑1 | 150–350 ng/mL | Persistent growth lag |
| IGFBP‑3 | 2.5–5.0 µg/mL | Low IGF‑1 with normal GH |
| Leptin | 1–10 ng/mL (girls higher) | Obesity, early puberty |
| Ghrelin (fasting) | 300–800 pg/mL | Appetite disorders |
| Fasting Insulin | 2–12 µIU/mL | BMI > 95th percentile, acanthosis nigricans |
Interpretation Tips
- IGF‑1/IGFBP‑3 together improve diagnostic accuracy for GH axis disorders.
- Leptin rises with increasing adiposity; markedly high levels in a child with normal BMI may suggest leptin resistance.
- Ghrelin inversely correlates with body weight; low fasting ghrelin can be a red flag for hyperphagia.
Adolescence and Puberty (13–19 Years)
Key Hormonal Axes
- Sex Steroids (Estradiol, Testosterone, Progesterone)
- Luteinizing Hormone (LH) & Follicle‑Stimulating Hormone (FSH)
- Androstenedione & DHEA‑S
- Prolactin
- Cortisol (diurnal pattern)
Why Test?
Adolescence is the period of maximal endocrine flux. Hormone panels help confirm normal pubertal progression, diagnose disorders such as polycystic ovary syndrome (PCOS), primary ovarian or testicular failure, and assess for hyperandrogenism or hypogonadism. Prolactin evaluation is essential when menstrual irregularities or galactorrhea are present.
Typical Panel
| Analyte | Typical Reference (age‑adjusted) | Clinical Triggers |
|---|---|---|
| Estradiol (females) | 20–400 pg/mL (varies with cycle) | Amenorrhea, delayed puberty |
| Testosterone (males) | 300–1,200 ng/dL | Delayed puberty, gynecomastia |
| LH | 0.5–15 IU/L (pubertal surge) | Delayed/precocious puberty |
| FSH | 0.5–12 IU/L (pubertal surge) | Same as LH |
| DHEA‑S | 150–500 µg/dL | Hyperandrogenic symptoms |
| Androstenedione | 0.5–3.0 ng/mL | PCOS, adrenal tumors |
| Prolactin | 5–20 ng/mL (women), 3–15 ng/mL (men) | Menstrual disturbances, galactorrhea |
| Midnight Cortisol (saliva) | < 0.1 µg/dL | Suspected Cushing’s syndrome |
Interpretation Tips
- Timing matters: LH/FSH should be drawn in the early morning; for females, estradiol interpretation depends on cycle day.
- Free vs. total testosterone: In obese adolescents, SHBG is often low, making free testosterone a more reliable marker of androgen excess.
- Prolactin: Macroprolactin can cause false‑positive elevations; a polyethylene glycol (PEG) precipitation test can differentiate.
Reproductive Years (20–39 Years)
Key Hormonal Axes
- Reproductive Hormones (Estradiol, Progesterone, Testosterone, LH, FSH, Inhibin B)
- Anti‑Müllerian Hormone (AMH) – ovarian reserve
- Sex Hormone‑Binding Globulin (SHBG)
- DHEA‑S & Androstenedione (adrenal contribution)
- Cortisol (diurnal rhythm)
- Prolactin (infertility work‑up)
Why Test?
In the prime reproductive window, hormone panels serve three major purposes: (1) evaluating fertility potential, (2) diagnosing endocrine contributors to menstrual irregularities or subfertility, and (3) monitoring conditions such as PCOS, premature ovarian insufficiency (POI), or hypogonadism. AMH and inhibin B have become standard markers for ovarian reserve, while SHBG helps contextualize free testosterone levels.
Typical Panel
| Analyte | Typical Reference (age‑adjusted) | Clinical Triggers |
|---|---|---|
| AMH | 1.0–4.0 ng/mL (declines after 30 y) | Infertility evaluation, POI risk |
| Inhibin B | 80–250 pg/mL (women) | Ovarian reserve, PCOS |
| Estradiol (mid‑cycle) | 150–500 pg/mL | Ovulation assessment |
| Progesterone (luteal phase) | > 3 ng/mL (adequate luteal) | Luteal phase defect |
| Total Testosterone | 30–90 ng/dL (women), 300–1,000 ng/dL (men) | Hyperandrogenism, hypogonadism |
| Free Testosterone | 0.3–1.5 pg/mL (women) | More accurate for androgen excess |
| SHBG | 20–120 nmol/L (women), 10–57 nmol/L (men) | Interpreting free T |
| DHEA‑S | 80–350 µg/dL (women), 150–620 µg/dL (men) | Adrenal source of androgens |
| Prolactin | 5–20 ng/mL | Infertility, galactorrhea |
| Midnight Salivary Cortisol | < 0.1 µg/dL | Suspected Cushing’s, stress‑related infertility |
Interpretation Tips
- AMH is relatively cycle‑independent; a single measurement suffices for reserve assessment.
- Inhibin B adds nuance, especially in women with borderline AMH.
- SHBG is influenced by estrogen, thyroid status, and insulin resistance; low SHBG often accompanies PCOS.
- Free testosterone can be calculated using Vermeulen’s equation or measured directly via equilibrium dialysis.
Perimenopause and Menopause (40–55 Years)
Key Hormonal Axes
- Estradiol, Estrone, and Estriol (estrogen decline)
- FSH & LH (elevated)
- Progesterone (low/absent)
- Testosterone (gradual decline in women)
- DHEA‑S (declining)
- Sex Hormone‑Binding Globulin (SHBG) – rises
- Cortisol (possible dysregulation)
Why Test?
The transition to menopause is marked by a steep fall in ovarian estrogen production, leading to a cascade of metabolic and symptomatic changes. Hormone panels help differentiate natural menopause from premature ovarian insufficiency, guide hormone‑replacement therapy (HRT) decisions, and identify lingering androgen excess that may contribute to cardiovascular risk or mood disorders.
Typical Panel
| Analyte | Typical Reference (perimenopause) | Clinical Triggers |
|---|---|---|
| Estradiol (early follicular) | 20–80 pg/mL (declining) | Hot flashes, bone loss |
| Estrone | 30–120 pg/mL (dominant post‑menopause) | Hormone balance assessment |
| FSH | 30–120 IU/L (rising) | Confirmation of menopause |
| LH | 15–70 IU/L (rising) | Same as FSH |
| Progesterone (luteal) | < 1 ng/mL (absent) | Amenorrhea, HRT planning |
| Total Testosterone | 10–40 ng/dL (women) | New‑onset hirsutism, libido changes |
| DHEA‑S | 30–150 µg/dL (declining) | Adrenal contribution to androgens |
| SHBG | 30–150 nmol/L (increasing) | Interpreting free testosterone |
| Cortisol (morning) | 5–20 µg/dL (may be elevated) | Stress‑related symptoms |
Interpretation Tips
- FSH > 30 IU/L on two separate occasions, combined with amenorrhea for 12 months, is a reliable marker of menopause.
- Estrone becomes the predominant estrogen after ovarian failure; its measurement can guide low‑dose HRT formulations.
- Free testosterone often rises relative to total testosterone because SHBG increases; calculate free values for accurate assessment.
Post‑Menopausal and Later Life (56+ Years)
Key Hormonal Axes
- Residual Estrogen (Estrone) & Androgens
- DHEA‑S (low)
- Cortisol (possible flattening of diurnal curve)
- Growth Hormone/IGF‑1 (decline)
- Prolactin (often stable)
Why Test?
Even after menopause, low‑level estrogen and androgen activity influence bone health, cognition, and cardiovascular risk. In older adults, a modest decline in GH/IGF‑1 contributes to sarcopenia, while altered cortisol rhythms can exacerbate frailty and metabolic syndrome. Targeted hormone panels can therefore inform interventions such as selective estrogen receptor modulators (SERMs), low‑dose testosterone, or GH‑releasing agents.
Typical Panel
| Analyte | Typical Reference (older adults) | Clinical Triggers |
|---|---|---|
| Estrone | 10–30 pg/mL (women) | Osteoporosis risk, mood changes |
| Total Testosterone | 5–30 ng/dL (women), 200–600 ng/dL (men) | Low libido, muscle loss |
| Free Testosterone | 0.1–0.5 pg/mL (women), 0.5–2.0 pg/mL (men) | Same as total, adjusted for SHBG |
| DHEA‑S | 10–80 µg/dL | General vitality, adrenal insufficiency |
| IGF‑1 | 80–150 ng/mL (decline with age) | Sarcopenia, frailty assessment |
| Morning Cortisol | 5–20 µg/dL (flattened rhythm) | Cognitive decline, metabolic syndrome |
| Prolactin | 5–20 ng/mL | Persistent galactorrhea, pituitary lesions |
Interpretation Tips
- IGF‑1 declines ~1% per year after age 30; values < 80 ng/mL in a frail individual may justify a GH‑secretagogue trial.
- Cortisol flattening (elevated evening levels) is a red flag for chronic stress or subclinical Cushing’s; consider a 24‑hour urinary free cortisol if suspicion persists.
- Free testosterone is especially informative in men, as SHBG rises with age, masking true androgen deficiency.
Special Considerations: Pregnancy and Hormone‑Related Conditions
Pregnancy‑Specific Hormones
- Human Chorionic Gonadotropin (hCG) – early pregnancy detection, trophoblastic disease monitoring.
- Progesterone (luteal phase & placental) – supports uterine quiescence; low levels may signal miscarriage risk.
- Estradiol & Estriol – rise dramatically; estriol is a marker of fetal well‑being.
- Placental Lactogen (hPL) – modulates maternal metabolism.
When to Test
- First‑trimester bleeding or suspected ectopic pregnancy: quantitative hCG and progesterone.
- Recurrent miscarriage: serial progesterone and hCG curves.
- Gestational diabetes risk: while not a hormone panel per se, measuring prolactin and cortisol can provide insight into stress‑related glucose dysregulation.
Hormone‑Related Pathologies Across Ages
- Polycystic Ovary Syndrome (PCOS): elevated total/free testosterone, DHEA‑S, LH/FSH ratio > 2, low SHBG.
- Premature Ovarian Insufficiency (POI): high FSH (> 40 IU/L) before age 40, low estradiol, low AMH.
- Hypogonadotropic Hypogonadism: low LH/FSH with low sex steroids; often requires MRI of the pituitary.
- Cushing’s Syndrome: elevated midnight salivary cortisol, loss of diurnal variation, high ACTH (if ACTH‑dependent).
Practical Tips for Interpreting Hormone Panels Across Ages
- Chronobiology Matters – Many hormones (cortisol, GH, LH) have diurnal peaks. Always note the collection time and, when possible, standardize to a morning draw (e.g., 7–9 am).
- Use Age‑Adjusted Reference Ranges – Laboratories often provide adult ranges that are too broad for pediatric or geriatric patients. Cross‑reference with pediatric endocrinology guidelines or geriatric endocrine societies.
- Consider Binding Proteins – SHBG, albumin, and corticosteroid‑binding globulin (CBG) can dramatically alter free hormone concentrations. When binding protein levels are abnormal (e.g., low albumin in liver disease), calculate free fractions or order direct free assays.
- Dynamic Testing Over Static Levels – For GH, ACTH, and the gonadotropins, stimulation or suppression tests (e.g., insulin tolerance test, dexamethasone suppression) provide more diagnostic clarity than basal values alone.
- Integrate Clinical Context – Hormone values must be interpreted alongside symptoms, physical findings, and imaging. A “normal” testosterone in a 70‑year‑old man may be relatively high for his age and warrant evaluation for polycythemia or prostate issues.
- Serial Monitoring – Hormonal transitions (puberty, menopause) are best captured by trends rather than a single snapshot. Repeat testing every 6–12 months during rapid change phases.
Integrating Hormone Testing into Preventive Care
- Annual Wellness Visits – Include a baseline hormone panel appropriate for the patient’s age group, especially for those with risk factors (obesity, family history of endocrine disease, menstrual irregularities).
- Electronic Health Record (EHR) Alerts – Set age‑specific reminders (e.g., “Consider AMH and FSH at age 35 for fertility counseling”).
- Lifestyle Counseling Coupled with Labs – Nutrition, sleep hygiene, stress reduction, and resistance training can favorably modulate cortisol, IGF‑1, and sex hormone balance; discuss these interventions when abnormal results arise.
- Referral Pathways – Establish clear criteria for endocrinology referral (e.g., persistent GH deficiency, unexplained hyperandrogenism, refractory menopausal symptoms).
By aligning hormone panels with the physiological milestones of each life stage, clinicians can detect subtle endocrine shifts before they manifest as overt disease. This proactive, age‑specific approach not only supports reproductive health and metabolic stability but also contributes to long‑term quality of life across the entire lifespan.
