Female CardioMetabolic & Hormone Profile | Specialist Doctor Report Included

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Test ID: SB-645 | Saliva 4-Point Cortisol + Blood Spot LCMS Hormones 7 with SHBG & CardioMetabolic Panel

The Female CardioMetabolic & Hormone Profile is an advanced at-home health assessment for women measuring 18 key hormones and markers across three interconnected systems: the full daily cortisol stress rhythm, a complete blood spot LCMS sex hormone panel including SHBG, and a six-marker blood spot cardiometabolic panel. Using saliva 4-point cortisol assessment combined with blood spot LCMS sex hormones, SHBG, and a full cardiometabolic panel, this test reveals how female hormones, cortisol, SHBG, and metabolic health interact to drive the symptoms that standard NHS blood panels consistently miss in women.

In women, these three systems are mechanistically inseparable. Cortisol is the primary driver of both hormonal imbalance and cardiometabolic deterioration — suppressing progesterone via pregnenolone steal, driving oestrogen dominance, elevating SHBG (which inactivates oestradiol and testosterone regardless of their production levels), and causing insulin resistance, visceral fat, and hsCRP elevation — all simultaneously. SHBG determines what fraction of every sex hormone actually reaches tissue — and is altered by cortisol, oestrogen, insulin, and body weight in ways that make hormone measurement without SHBG clinically incomplete. Oestrogen decline in perimenopause withdraws insulin sensitisation, HDL support, and SHBG modulation at the same time. This test maps all three systems together across the full daily cortisol rhythm — providing the mechanistic insight that single-point or single-system tests cannot achieve.

Test from home with confidence — no clinic visit required. Results within 3–5 working days.


Why Cortisol Rhythm, SHBG, and Cardiometabolic Health Must Be Assessed Together in Women

  • The 4-point cortisol rhythm determines both what hormones are available and how the metabolic system responds across the entire day in women — the morning cortisol awakening response sets oestrogen receptor sensitivity, SHBG hepatic synthesis rate, and insulin sensitivity before any other system operates; elevated cortisol at any time point suppresses progesterone, elevates SHBG to inactivate oestradiol and testosterone, drives visceral fat and insulin resistance, raises triglycerides, suppresses HDL, and elevates hsCRP; only four-time-point measurement identifies the specific phase of cortisol dysregulation — a single cortisol value cannot distinguish morning-blunted from evening-elevated patterns, each of which produces distinct hormonal, SHBG, and metabolic consequences
  • SHBG is the bioavailability gatekeeper for every sex hormone in women — and is altered by every factor this panel measures — SHBG binds and inactivates oestradiol and testosterone regardless of their total production levels; elevated SHBG from cortisol excess, oestrogen, low insulin, or HRT/pill use produces full hormonal deficiency symptoms in women with normal total hormone values; low SHBG from insulin resistance, visceral fat, and hypothyroidism increases free oestrogen and testosterone, driving oestrogen dominance and PCOS symptoms; SHBG cannot be meaningfully interpreted without the cortisol rhythm and cardiometabolic markers that determine it
  • Insulin resistance in women is hormonally driven and SHBG-mediated in ways standard metabolic tests cannot reveal — cortisol at any time point impairs hepatic insulin receptor sensitivity; low progesterone and oestrogen decline remove insulin-sensitising effects; PCOS creates insulin resistance even in lean women through androgen-driven mechanisms that simultaneously suppress SHBG; elevated insulin lowers SHBG, increasing free testosterone and driving the androgenic PCOS cycle; fasting insulin is the earliest detectable marker of this process — elevated years before HbA1c becomes abnormal — and its interpretation requires SHBG and cortisol context to be clinically actionable
  • hsCRP in women is the convergence marker of all three systems assessed here — elevated simultaneously by cortisol dysregulation at any time point, progesterone deficiency and oestrogen imbalance, low SHBG-mediated free androgen excess, insulin resistance, and visceral fat; a stronger independent predictor of cardiovascular disease in women than LDL cholesterol; and a direct measure of the integrated inflammatory load that only a combined cortisol rhythm, SHBG, and cardiometabolic assessment can fully attribute and target
  • Oestrogen and SHBG interact to determine cardiovascular risk in perimenopausal women independently of standard lipid testing — oestradiol supports HDL cholesterol and suppresses LDL oxidation; its decline in perimenopause simultaneously reduces SHBG’s protective oestrogen modulation, raises triglycerides, and elevates hsCRP in a directly hormonal pattern; SHBG measurement alongside oestradiol, cortisol, and cardiometabolic markers reveals whether cardiovascular risk changes are hormonally driven — the insight that cholesterol testing alone cannot provide

What This Test Measures — 18 Markers Across Three Systems

Saliva — 4-Point Cortisol Profile (4 markers)

  • Morning Cortisol (Cortisol Awakening Response): Sets oestrogen receptor sensitivity, SHBG hepatic synthesis rate, and insulin sensitivity for the entire day. An exaggerated morning response drives progesterone suppression, SHBG elevation, and morning insulin resistance; a blunted awakening response signals HPA burnout, reduced oestrogen responsiveness, and impaired insulin sensitivity that persists through the day.
  • Noon Cortisol: Elevated noon cortisol drives visceral fat deposition, promotes aromatase-driven oestrogen excess, elevates SHBG, raises triglycerides via hepatic lipid dysregulation, and suppresses HDL — the direct mechanism by which chronic midday stress accelerates hormonal imbalance and cardiometabolic deterioration in women during the working day.
  • Evening Cortisol: Should decline significantly to allow oestrogen, progesterone, and growth hormone to rise during early sleep cycles. Elevated evening cortisol suppresses overnight sex hormone production, elevates SHBG, maintains insulin resistance into the night, and drives hsCRP elevation — producing next-day fatigue, mood instability, and worsening hormonal and metabolic function regardless of the morning value.
  • Night Cortisol: Drives sleep-phase suppression of oestrogen and progesterone synthesis, promotes overnight visceral fat accumulation and fasting insulin elevation, maintains elevated SHBG into the morning, and raises hsCRP overnight — the mechanism by which poor sleep quality is both a symptom and a driver of progressive hormonal and cardiometabolic deterioration in women.

Blood Spot LCMS — Sex Hormones & SHBG (8 markers)

  • Oestradiol (E2): The primary premenopausal oestrogen — protecting cardiovascular health, bone density, insulin sensitivity, and mood stability. Declining E2 in perimenopause simultaneously triggers hormonal symptoms and the cardiometabolic risk shift that characterises the menopausal transition. Measured by blood spot LCMS for accuracy across the full hormonal range. Interpreted alongside SHBG to determine free, bioavailable oestradiol — the clinically relevant fraction.
  • Oestriol (E3): Reflects oestrogen conversion and metabolic activity. The E3-to-E2 and E3-to-E1 ratios reveal how oestrogen is being metabolised — relevant for cardiovascular and hormonal risk assessment in women.
  • Oestrone (E1): The dominant postmenopausal oestrogen, produced by adipose conversion of androgens. Elevated E1 in women with higher body fat drives oestrogenic load and metabolic inflammation; low SHBG in these women compounds the free oestrogen excess that drives oestrogen dominance symptoms and cardiovascular inflammation.
  • Progesterone (Pg): The essential counterbalance to oestrogen — anti-inflammatory, cardioprotective, sleep-promoting, and insulin-sensitising. Low progesterone from anovulation, chronic stress, luteal phase deficiency, or perimenopause drives oestrogen dominance, worsens insulin resistance, elevates hsCRP, and allows cortisol-driven SHBG elevation to go unopposed — the hormonal pattern underlying the majority of perimenopausal cardiometabolic deterioration.
  • Testosterone (T): Essential in women for energy, libido, muscle mass, and metabolic rate. Low free testosterone from elevated SHBG reduces lean mass and worsens insulin resistance; elevated free testosterone in PCOS from low SHBG drives insulin resistance, visceral fat, and cardiometabolic risk directly. The combination of testosterone + SHBG provides the definitive free androgenic status assessment for women.
  • DHEAS (DS): The primary adrenal androgen precursor in women, declining from the mid-30s and depleted under chronic cortisol elevation. Low DHEAS reduces oestrogen and testosterone precursor availability and has direct anti-inflammatory and insulin-sensitising effects. The 4-point cortisol rhythm directly reveals the HPA dysregulation mechanism driving DHEAS depletion alongside the SHBG and metabolic consequences.
  • Cortisol (C) — Blood Spot LCMS: The single blood spot cortisol measurement by LCMS provides a direct comparator to the 4-point saliva cortisol rhythm, enabling cross-matrix cortisol validation. Confirms the diurnal pattern identified by the saliva rhythm with blood spot LCMS precision and links directly to the SHBG and cardiometabolic markers measured in the same blood spot sample.
  • Sex Hormone Binding Globulin (SHBG): The bioavailability gatekeeper for all sex hormones in women. Elevated SHBG — driven by cortisol, oestrogen, HRT, and the contraceptive pill — binds and inactivates oestradiol and testosterone regardless of their production, causing full hormonal deficiency symptoms with normal total hormone values. Low SHBG — driven by insulin resistance, visceral fat, and low oestrogen — increases free oestrogen and testosterone, driving oestrogen dominance and PCOS symptoms. SHBG cannot be meaningfully interpreted without the cortisol rhythm and cardiometabolic markers this panel provides.

Blood Spot — CardioMetabolic Panel (6 markers)

  • Fasting Insulin: The earliest detectable marker of insulin resistance in women — elevated years before HbA1c becomes abnormal. Directly driven by cortisol at any time point, low progesterone, oestrogen decline, and PCOS. Elevated fasting insulin lowers SHBG, raising free testosterone and perpetuating the PCOS hormonal cycle; promotes visceral fat; raises triglycerides; suppresses HDL; and elevates hsCRP. The most actionable early metabolic marker for women with hormonal and cardiometabolic symptoms.
  • HbA1c: Reflects average blood sugar regulation over 8–12 weeks. Women’s risk of pre-diabetes and type 2 diabetes rises markedly in perimenopause and postmenopause as oestrogen’s insulin-sensitising effects are lost; HbA1c contextualises the fasting insulin result with medium-term blood sugar trajectory and anchors the cortisol-SHBG-insulin interaction assessment.
  • HDL Cholesterol: The protective cardiovascular fraction supported by oestradiol and suppressed by cortisol elevation, insulin resistance, and oestrogen decline simultaneously. HDL fall in perimenopausal women is a directly hormonal event measurable alongside oestradiol, SHBG, and cortisol in this single panel.
  • Triglycerides: Elevated by cortisol at any of the four time points, insulin resistance, and oestrogen decline simultaneously. Often rise before LDL changes and are a primary cardiometabolic risk marker particularly relevant for perimenopausal, postmenopausal, and PCOS women with cortisol dysregulation and low SHBG.
  • Total Cholesterol: Provides overall lipid context. Rising cholesterol in perimenopausal and postmenopausal women is frequently a direct consequence of declining oestradiol and elevated SHBG — a hormonal event best assessed alongside the hormone levels and SHBG this panel measures directly.
  • hsCRP (High-Sensitivity C-Reactive Protein): A stronger independent predictor of cardiovascular disease in women than LDL cholesterol. Elevated simultaneously by cortisol dysregulation at any time point, progesterone deficiency, oestrogen imbalance, low SHBG-mediated free androgen excess, and insulin resistance — all five pathways directly assessed by this panel. The convergence biomarker of the female hormonal-metabolic system.

Who Should Consider This Test?

This test is particularly relevant for women who:

  • Have persistent fatigue, low energy, or exhaustion not explained by sleep alone
  • Experience unexplained weight gain or difficulty losing weight, particularly around the abdomen
  • Have sugar cravings, energy crashes, or afternoon slumps
  • Have elevated cholesterol or triglycerides on previous testing
  • Experience PMS, heavy, irregular, or absent periods, or breast tenderness
  • Are experiencing perimenopausal symptoms: hot flushes, night sweats, low mood, brain fog
  • Have low libido, reduced sexual interest, or lack of motivation
  • Experience anxiety, irritability, or emotional volatility especially in the second half of the cycle
  • Struggle with insomnia, night waking, or unrefreshing sleep
  • Are under chronic stress or experiencing burnout
  • Have diagnosed or suspected PCOS or oestrogen dominance
  • Are currently on HRT or the contraceptive pill (where SHBG assessment is essential for accurate hormone interpretation)
  • Have had previous hormone testing with normal results that do not match their symptoms
  • Want a comprehensive hormonal and cardiometabolic baseline without the thyroid panel (covered in the Female Advanced or Comprehensive Hormone, Thyroid & CardioMetabolic tests)
  • Have a family history of heart disease, diabetes, or metabolic syndrome
  • Are women over 35 seeking a comprehensive hormonal, SHBG, and cardiometabolic health assessment

Key Features

  • 18-marker tri-system panel: 4-point saliva cortisol rhythm, blood spot LCMS sex hormones + SHBG, and full cardiometabolic panel
  • 4-point cortisol profile — morning, noon, evening, and night — the only method that reveals the full daily cortisol rhythm and its effects on SHBG, sex hormones, and metabolic function
  • Blood spot LCMS sex hormones — gold standard accuracy across the full female hormonal range
  • SHBG included — essential for interpreting free oestradiol and testosterone in women on HRT, the pill, or with PCOS, insulin resistance, or cortisol dysregulation
  • All three oestrogens (E1, E2, E3) for complete oestrogen metabolism and dominance assessment
  • Six cardiometabolic markers — fasting insulin, HbA1c, HDL, triglycerides, total cholesterol, hsCRP
  • Results within 3–5 working days after lab receipt
  • Expert analysis by a Hormone Specialist PhD Doctor
  • Clear graphical and numerical results with personalised commentary
  • All-inclusive price — laboratory fees included, no hidden costs
  • Valid for 12 months from purchase

How It Works

  1. Order the kit online — delivered directly to your door.
  2. Collect your saliva samples at four time points (morning, noon, evening, night) for the cortisol rhythm panel, and your blood spot sample via a simple finger-prick for the LCMS hormone, SHBG, and cardiometabolic panels, following the detailed instructions. Guidance on optimal cycle timing and morning collection for cortisol accuracy is included.
  3. Post your samples to the lab using the return instructions in your kit.
  4. Receive your results within 3–5 working days with specialist commentary and clear next-step guidance.

What Your Report Includes

  • All 18 marker results with female-specific reference ranges
  • Visual cortisol rhythm chart showing your full four-point daily curve
  • Visual charts for all six sex hormones, SHBG, and all six cardiometabolic markers
  • Integrated clinical interpretation of how your cortisol rhythm, sex hormones, SHBG, and cardiometabolic results interact as a single female hormonal-metabolic system
  • SHBG-adjusted free hormone bioavailability assessment for oestradiol and testosterone
  • Oestrogen-progesterone dominance ratio analysis in cortisol and SHBG context
  • Cortisol-SHBG interaction assessment — identifying how each cortisol time point is affecting hormone bioavailability
  • Insulin resistance pattern assessment (fasting insulin + HbA1c) in SHBG and PCOS context
  • Cardiovascular risk profile in full female hormonal and SHBG context (HDL, triglycerides, cholesterol, hsCRP)
  • Specialist commentary by a Hormone Specialist PhD Doctor
  • Personalised next-step recommendations

Frequently Asked Questions

What does this test measure?

4-point saliva cortisol (morning, noon, evening, night) + Oestradiol (E2), Oestriol (E3), Oestrone (E1), Progesterone, Testosterone, DHEAS, Cortisol, SHBG (blood spot LCMS) + Fasting Insulin, HbA1c, HDL Cholesterol, Triglycerides, Total Cholesterol, hsCRP (blood spot) — 18 markers in total.

How does this test differ from the Female Advanced and Female Comprehensive Hormone, Thyroid & CardioMetabolic tests?

The Female CardioMetabolic & Hormone Profile (SB-645F) does not include the thyroid panel (TSH, FT3, FT4, TT4, TPO antibodies, Tg antibodies). It is the optimal choice for women whose thyroid function has been recently assessed or excluded as a factor, and who want the most comprehensive hormonal, SHBG, cortisol rhythm, and cardiometabolic assessment available. Women who have thyroid symptoms, a family history of thyroid disease, Hashimoto’s, or unexplained weight gain and cold sensitivity alongside their hormonal symptoms should consider the Female Advanced Hormone, Thyroid & CardioMetabolic Test (SB-649F) or the Female Comprehensive Hormone, Thyroid & CardioMetabolic Profile (SB-646F).

Why do I need SHBG tested alongside my hormones?

SHBG binds and inactivates sex hormones in the bloodstream. A woman with normal total oestradiol and testosterone but elevated SHBG — caused by cortisol excess, HRT, or the contraceptive pill — may have full symptoms of hormonal deficiency despite normal-range total hormone values. Conversely, low SHBG from insulin resistance or visceral fat elevates free testosterone and drives oestrogen dominance and PCOS symptoms in women with normal-range total hormone values. Without SHBG, hormone results in women cannot be accurately interpreted.

Why is a 4-point cortisol rhythm more informative than a single cortisol measurement for women?

A single cortisol measurement cannot identify the pattern of dysregulation — whether the morning awakening response is blunted or exaggerated, whether cortisol elevates at midday or evening, or whether night cortisol is suppressing overnight oestrogen and progesterone production. Each pattern produces distinct effects on SHBG, insulin, triglycerides, and hsCRP. The four-point rhythm identifies exactly which phase of the day is driving the SHBG elevation, insulin resistance, or cardiometabolic deterioration visible in the blood spot results.

Is this test suitable for women on HRT or the contraceptive pill?

Yes — and it is particularly valuable for these women. HRT and the pill significantly elevate SHBG, which alters the bioavailability of all sex hormones. Without SHBG measurement, hormone results in women on HRT or the pill cannot be accurately interpreted. This test provides SHBG al