Blood Spot Thyroids + Dried Urine GCMS Hormone Metabolites

Thyroid-stimulating hormone is the anterior pituitary glycoprotein that drives thyroid follicular cell synthesis and release of thyroid hormones. Measurement from dried blood spot correlates well with serum TSH but requires method-specific validation for each assay platform.

TSH is the single most sensitive screening test for primary thyroid dysfunction — suppressed in hyperthyroidism, elevated in hypothyroidism. Dried blood spot collection offers convenience for home sampling and paediatric or needle-averse populations.

Free thyroxine represents the unbound, biologically active fraction of T4 and is the predominant secretory product of the thyroid gland. Dried blood spot free T4 measurement bypasses binding-protein interference but requires calibration against serum immunoassays.

Free T4 confirms the metabolic state when TSH is abnormal and monitors levothyroxine replacement. Low free T4 with elevated TSH defines overt primary hypothyroidism; high free T4 with suppressed TSH defines hyperthyroidism.

Free triiodothyronine is the unbound, metabolically active thyroid hormone generated predominantly by peripheral deiodination of T4. Measurement from dried blood spot captures the circulating active hormone pool without the confounders of serum binding proteins.

Free T3 is disproportionately elevated in T3 thyrotoxicosis and may remain low despite adequate T4 replacement in patients with impaired peripheral conversion, a pattern explored in functional-medicine practice.

Thyroid peroxidase antibodies are the hallmark autoantibody of Hashimoto thyroiditis, directed against the thyroid enzyme that catalyses iodination and coupling of tyrosyl residues to form T3 and T4.

Elevated TPO antibodies confirm autoimmune thyroid disease, predict progression of subclinical hypothyroidism to overt disease, and are associated with increased risk of miscarriage and postpartum thyroiditis.

Oestrone is the predominant oestrogen after menopause, formed by peripheral aromatisation of androstenedione in adipose tissue and by direct ovarian secretion during reproductive years. Dried urine GCMS measures the parent hormone and, in extended panels, its oxidative metabolites.

Urinary E1 reflects overall oestrogenic load and, when combined with metabolite ratios, is used in functional assessments of oestrogen metabolism and potential breast-cancer risk stratification.

Oestradiol is the most potent endogenous oestrogen, secreted primarily by ovarian granulosa cells in premenopausal women and by peripheral conversion in postmenopausal women and men. Dried urine GCMS captures the urinary excretion rate normalised to creatinine.

Urinary E2 assessment complements serum levels in evaluating ovarian reserve, menopausal transition, and hormone-replacement dosing, and forms part of the functional evaluation of oestrogen metabolism.

Oestriol is a weaker oestrogen, formed by 16α-hydroxylation of oestrone and oestradiol. In non-pregnant adults it is a minor metabolite; in pregnancy the foetoplacental unit produces large amounts. Urinary E3 is often measured as part of functional oestrogen metabolism panels.

E3 is sometimes characterised as a less proliferative oestrogen with potential protective effects, though this remains debated. Its ratio to the other oestrogens is explored in functional risk assessments.

Progesterone is the principal progestogen secreted by the corpus luteum after ovulation and by the placenta during pregnancy. Dried urine measurement captures total daily excretion, smoothing the pulsatile variation seen in serum.

Urinary progesterone confirms ovulation, monitors luteal adequacy, and assesses exogenous progesterone dosing in hormone-replacement regimens.

Testosterone is synthesised primarily in the testes in men, in the ovaries and adrenal glands in women. Urinary measurement via GCMS reflects the sum of free and conjugated metabolites excreted over the collection window.

Urinary testosterone complements serum assessment, particularly when evaluating androgen-replacement dosing, hyperandrogenism in women, and androgen-metabolite patterns in functional endocrine work-ups.

Dehydroepiandrosterone is the principal C19 steroid secreted by the adrenal zona reticularis and a precursor to androgens and oestrogens. Urinary DHEA, measured by GCMS, reflects adrenal androgen output.

DHEA serves as a marker of adrenal reserve and is often measured in functional adrenal and stress assessments, though its physiological role and the clinical benefit of supplementation remain contested.

Cortisol is the principal glucocorticoid secreted by the adrenal zona fasciculata in a diurnal rhythm, with peak morning levels and a nadir at night. Dried urine captures free cortisol excretion at the time of collection, bypassing the effect of cortisol-binding globulin.

Urinary cortisol is used to assess the diurnal cortisol rhythm, screen for Cushing syndrome when very elevated, and evaluate functional adrenal 'stress' patterns in integrative medicine.

Cortisone is the inactive metabolite of cortisol, interconverted by 11β-hydroxysteroid dehydrogenase isoenzymes. The cortisol:cortisone ratio in urine reflects tissue-level glucocorticoid activation and inactivation.

The cortisol:cortisone ratio is explored in functional adrenal panels as a marker of 11β-HSD activity, with shifts hypothesised to influence local glucocorticoid availability.

Oestrogens are metabolised via cytochrome P450 and catechol-O-methyltransferase pathways to 2-hydroxy (less proliferative), 4-hydroxy (potentially genotoxic), and 16α-hydroxy (more proliferative) metabolites. The distribution is measured by GCMS in dried urine.

Metabolite ratios are used in functional and integrative medicine to stratify theoretical breast-cancer and hormone-responsive-tumour risk, though prospective intervention trials demonstrating clinical benefit are lacking.