Australian Biomarker Optimal-Range Reference 2026
Comprehensive Australian SI-unit reference: lab vs functional optimal ranges for 60+ biomarkers across metabolic, lipid, hormone, thyroid, iron, nutrient, and adrenal panels.
Disclaimer: This reference is for educational and research purposes only. It does not constitute medical advice. All results must be interpreted by a qualified medical practitioner in the context of your full clinical picture, symptoms, history, and other investigations.
This page provides a single citable reference for Australian clinicians, biohackers, and health researchers who want to compare standard Australian laboratory reference ranges against evidence-informed functional optimal ranges for major blood biomarkers, all expressed in Australian SI units.
For each marker the table shows: the conventional AU lab reference range (as used by major Australian pathology providers including Sonic Healthcare subsidiaries, Australian Clinical Labs, and QML Pathology), the functional optimal range drawn from peer-reviewed literature, the unit in SI notation, and a primary source. A brief clinical context note follows each section.
A note on units: Australian pathology reports use SI units throughout. Common US sources express many of the same markers in mg/dL (glucose, cholesterol, triglycerides) or ng/dL (testosterone, cortisol). Values in this reference have been converted to Australian SI equivalents. Always confirm the unit column before applying a value.
For a primer on how reference ranges are established and why "normal" does not mean optimal, see the Australian blood test interpretation guide.
1. Metabolic Panel
Metabolic markers reflect insulin sensitivity, glucose regulation, and the downstream consequences of hyperinsulinaemia. The conventional diabetic threshold captures late-stage dysregulation; functional targets aim to identify risk at the inflection point where intervention is most effective.
Medicare / MBS coverage notes: Fasting glucose (MBS 66500) and HbA1c (MBS 66551) are rebated when ordered by a GP for monitoring or diagnosis. Fasting insulin is not currently covered by MBS and must be ordered privately. OGTT (MBS 66512) requires a clinical indication.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| HbA1c | <48 mmol/mol (non-diabetic) | 28–36 mmol/mol | mmol/mol | ADA Standards of Care 2024; RACGP Red Book |
| Fasting glucose | 3.9–5.5 mmol/L | 4.0–5.0 mmol/L | mmol/L | RACGP Diabetes Guidelines 2024 |
| Fasting insulin | 2–25 mIU/L (lab-dependent) | 3–8 mIU/L | mIU/L | Kraft DR, AACE 2022 consensus |
| HOMA-IR | Not routinely reported | <1.5 (optimal); <2.0 (acceptable) | ratio | Matthews DR et al., Diabetologia 1985; PMID 3899825 |
| OGTT 1-hour glucose | Not flagged below 11.1 mmol/L | <8.6 mmol/L | mmol/L | Ahuja V et al., Diabetes Care 2021; PMID 33741697 |
| OGTT 2-hour glucose | <7.8 mmol/L (non-diabetic) | <6.7 mmol/L | mmol/L | RACGP Diabetes Guidelines 2024 |
| Uric acid (male) | 200–430 µmol/L | 250–350 µmol/L | µmol/L | Fang J & Alderman MH, JAMA 2000; PMID 10815083 |
| Uric acid (female) | 140–360 µmol/L | 180–300 µmol/L | µmol/L | Fang J & Alderman MH, JAMA 2000; PMID 10815083 |
Clinical context: HOMA-IR is calculated as (fasting insulin mIU/L × fasting glucose mmol/L) ÷ 22.5. A result above 1.5 suggests early insulin resistance well before glucose rises above the pre-diabetic threshold. The 1-hour OGTT glucose is increasingly recognised as the most sensitive single OGTT timepoint for identifying future type 2 diabetes risk; values above 8.6 mmol/L at 1 hour carry risk even when the 2-hour result is normal. For a dedicated deep-dive on HbA1c functional targets, see HbA1c optimal ranges and what they mean beyond diabetes.
2. Comprehensive Lipid Panel
Standard lipid panels in Australia report total cholesterol, LDL-C (usually calculated via Friedewald equation), HDL-C, and triglycerides. ApoB and Lp(a) require specific requesting and are not currently MBS-rebated for primary prevention, though this is under review. Particle size and number (LDL-P) is available through a small number of specialist labs.
Medicare / MBS coverage notes: Standard fasting lipid panel (MBS 66503) is rebated. ApoB (MBS 66716) is rebated in specific clinical contexts. Lp(a) is not currently MBS-rebated for routine screening.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| Total cholesterol | <5.5 mmol/L (general); <4.0 mmol/L (high CVD risk) | 4.0–5.2 mmol/L | mmol/L | NHF Australia Lipid Guidelines 2022 |
| LDL-C | <3.0 mmol/L (general); <1.8 mmol/L (high risk) | <2.0 mmol/L | mmol/L | NHF Australia Lipid Guidelines 2022 |
| HDL-C (male) | >1.0 mmol/L | >1.3 mmol/L | mmol/L | NHF Australia Lipid Guidelines 2022 |
| HDL-C (female) | >1.2 mmol/L | >1.5 mmol/L | mmol/L | NHF Australia Lipid Guidelines 2022 |
| Triglycerides (fasting) | <2.0 mmol/L | <1.0 mmol/L | mmol/L | NHF Australia Lipid Guidelines 2022 |
| ApoB | <1.0 g/L (general); <0.8 g/L (high risk) | <0.7 g/L | g/L | Sniderman AD et al., JAMA Cardiol 2019; PMID 31642874 |
| Lp(a) | <75 nmol/L (risk threshold) | <50 nmol/L | nmol/L | Kronenberg F et al., Atherosclerosis 2023 (EAS Lp(a) 2022 consensus); PMID 37188555 |
| TG:HDL ratio | Not routinely reported | <1.0 | ratio | McLaughlin T et al., Am J Cardiol 2005; PMID 16054467 |
Clinical context: ApoB is now considered by many cardiovascular researchers to be the superior primary treatment target compared with LDL-C, because it counts every atherogenic particle (LDL, VLDL, IDL, Lp(a)) regardless of size. Discordance between LDL-C and ApoB (high ApoB with apparently normal LDL-C) is common in metabolic syndrome and identifies a cohort at substantially elevated risk. The TG:HDL ratio (in mmol/L units, not mg/dL) is a validated surrogate marker of insulin resistance and LDL particle size. For full ApoB interpretation see ApoB: the cardiovascular marker your doctor may not be ordering.
3. Inflammation and Liver Function
Chronic low-grade inflammation is the common thread linking metabolic disease, cardiovascular risk, and accelerated biological ageing. Liver function markers double as inflammation signals, particularly GGT, which rises early in response to oxidative stress, alcohol, NAFLD, and medication burden before formal "elevation" is reached.
Medicare / MBS coverage notes: hs-CRP (MBS 66500 group, varies by context), LFTs (MBS 66500), eGFR and creatinine (MBS 66500), cystatin C is not MBS-rebated and is available through select private pathology providers.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| hs-CRP | <5 mg/L (standard); <10 mg/L (infection threshold) | <0.7 mg/L | mg/L | Ridker PM et al., NEJM 2002; PMID 12432042 |
| Ferritin (male) | 30–500 µg/L | 70–150 µg/L | µg/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
| Ferritin (female, pre-menopause) | 10–200 µg/L | 50–100 µg/L | µg/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
| GGT (male) | <65 U/L | <25 U/L | U/L | Lee DH et al., Atherosclerosis 2005; PMID 15694941 |
| GGT (female) | <45 U/L | <18 U/L | U/L | Lee DH et al., Atherosclerosis 2005; PMID 15694941 |
| ALT (male) | <45 U/L | <25 U/L | U/L | Prati D et al., Ann Intern Med 2002; PMID 12093239 |
| ALT (female) | <35 U/L | <19 U/L | U/L | Prati D et al., Ann Intern Med 2002; PMID 12093239 |
| AST | <40 U/L | <22 U/L | U/L | Prati D et al., Ann Intern Med 2002; PMID 12093239 |
| eGFR | >90 mL/min/1.73m² (optimal); >60 reported as normal | >90 mL/min/1.73m² | mL/min/1.73m² | KDIGO CKD Guidelines 2024 |
| Creatinine (male) | 60–110 µmol/L | 70–95 µmol/L | µmol/L | KDIGO CKD Guidelines 2024 |
| Creatinine (female) | 45–90 µmol/L | 55–80 µmol/L | µmol/L | KDIGO CKD Guidelines 2024 |
| Cystatin C | 0.52–0.98 mg/L (age-dependent) | <0.85 mg/L | mg/L | Stevens LA et al., Am J Kidney Dis 2008; PMID 18295055 |
Clinical context: hs-CRP below 0.7 mg/L is associated with lowest cardiovascular event rates in the JUPITER and PROVE-IT trials. The conventional "normal" cut-off of <5 mg/L encompasses a range across which risk differs by a factor of three or more. GGT, even within formal reference range, rises in proportion to oxidative stress and serves as one of the earliest detectable signals of non-alcoholic fatty liver disease. ALT reformulation in 2002 (Prati criteria) lowered the clinical upper limit of normal to 30 U/L for males and 19 U/L for females. Cystatin C, unlike creatinine, is not influenced by muscle mass and provides a more reliable eGFR estimate in lean individuals and older adults.
4. Hormones: Male and Female
Sex hormone reference ranges are among the widest and most clinically contentious in pathology. A male with total testosterone of 8.0 nmol/L sits within the Australian lab reference range yet may be symptomatic. Functional medicine targets use narrower windows derived from symptom threshold and outcomes research.
Medicare / MBS coverage notes: Total testosterone (MBS 66695) is rebated for males with clinical symptoms consistent with hypogonadism. SHBG (MBS 66719), estradiol (MBS 66718), and progesterone (MBS 66722) are rebated in specific clinical contexts. DHEA-S, free testosterone (calculated), and prolactin are rebated under appropriate clinical indications.
Male Hormones
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| Total testosterone | 10–35 nmol/L | 20–30 nmol/L | nmol/L | Bhasin S et al., J Clin Endocrinol Metab 2010; PMID 20525905 |
| Free testosterone (calculated) | 170–670 pmol/L | 350–600 pmol/L | pmol/L | Bhasin S et al., JCEM 2010; PMID 20525905 |
| SHBG (male) | 10–70 nmol/L | 20–40 nmol/L | nmol/L | Vermeulen A et al., JCEM 1999; PMID 10523012 |
| Estradiol (male) | 40–160 pmol/L | 70–110 pmol/L | pmol/L | Finkelstein JS et al., NEJM 2013; PMID 24350954 |
| DHEA-S (male, 20–40y) | 2.0–13.0 µmol/L | 7.0–12.0 µmol/L | µmol/L | Endocrine Society Clinical Practice Guideline 2019 |
| Prolactin (male) | <400 mIU/L | <200 mIU/L | mIU/L | Melmed S et al., JCEM 2011; PMID 21296991 |
Female Hormones
| Marker | AU Lab Reference | Functional Optimal (follicular) | Unit | Primary Source |
|---|---|---|---|---|
| Total testosterone (female) | 0.4–2.7 nmol/L | 1.0–2.0 nmol/L | nmol/L | Davis SR et al., J Clin Endocrinol Metab 2019; PMID 31498871 |
| SHBG (female) | 20–160 nmol/L | 40–80 nmol/L | nmol/L | Vermeulen A et al., JCEM 1999; PMID 10523012 |
| Estradiol (female, follicular) | 95–730 pmol/L | 200–400 pmol/L | pmol/L | Speroff L & Fritz MA, Clinical Gynecologic Endocrinology (8th ed) |
| Progesterone (mid-luteal) | >25 nmol/L (ovulation confirmation) | 35–80 nmol/L | nmol/L | Prior JC, Climacteric 2018; PMID 29962257 |
| DHEA-S (female, 20–40y) | 1.0–9.0 µmol/L | 4.0–8.0 µmol/L | µmol/L | Endocrine Society Clinical Practice Guideline 2019 |
| Prolactin (female, non-pregnant) | <700 mIU/L | <400 mIU/L | mIU/L | Melmed S et al., JCEM 2011; PMID 21296991 |
| AMH | Age-dependent (varies lab to lab) | 10–35 pmol/L (25–35y) | pmol/L | Broer SL et al., Hum Reprod Update 2014; PMID 24821925 |
Clinical context: Free testosterone is not reliably measured directly by most Australian pathology labs and is most accurately calculated from total testosterone, SHBG, and albumin using the Vermeulen equation. In males, SHBG above 45 nmol/L in the context of low-normal total testosterone may produce significant free testosterone deficiency. In females, SHBG above 100 nmol/L is associated with symptomatic androgen insufficiency even when total testosterone sits in the middle of the reference range. Mid-luteal progesterone should be collected day 19–22 of a 28-day cycle (or 7 days before the next expected period) to capture the luteal peak, timing errors are the most common cause of falsely low results.
5. Thyroid Panel
The TSH reference range used by most Australian laboratories (approximately 0.4–4.0 mIU/L) spans a tenfold difference in pituitary output. The clinical and research literature on thyroid optimal targets has evolved substantially over the past two decades, with growing consensus that the upper half of the conventional range (TSH 2.5–4.0 mIU/L) carries meaningful symptom burden and metabolic consequence in susceptible individuals.
Medicare / MBS coverage notes: TSH (MBS 66716) is rebated annually for diagnosed hypothyroidism. Free T4 (MBS 66716) and free T3 (MBS 66720) are rebated when TSH is abnormal. Reverse T3 and thyroid antibodies (MBS 66722) are rebated under specific clinical indications.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| TSH | 0.4–4.0 mIU/L | 1.0–2.0 mIU/L | mIU/L | Wartofsky L & Dickey RA, JCEM 2005; PMID 16148345 |
| Free T4 (fT4) | 10–20 pmol/L | 14–18 pmol/L | pmol/L | Jonklaas J et al., Thyroid 2014; PMID 25266247 |
| Free T3 (fT3) | 3.5–6.5 pmol/L | 4.5–6.0 pmol/L | pmol/L | Jonklaas J et al., Thyroid 2014; PMID 25266247 |
| fT3:fT4 ratio | Not routinely reported | >0.30 | ratio | Hoermann R et al., Eur J Clin Invest 2018; PMID 30022470 |
| Reverse T3 (rT3) | <0.54 nmol/L (lab-dependent) | <0.30 nmol/L | nmol/L | Hoermann R et al., Eur J Clin Invest 2018; PMID 30022470 |
| TPO antibodies | <35 IU/mL (varies by lab) | <10 IU/mL (lowest risk) | IU/mL | Vanderpump MPJ, Br Med Bull 2011; PMID 21893493 |
| Thyroglobulin antibodies (TgAb) | <115 IU/mL (varies) | Undetectable (<10 IU/mL) | IU/mL | Vanderpump MPJ, Br Med Bull 2011; PMID 21893493 |
Clinical context: The fT3:fT4 ratio reflects peripheral conversion efficiency, the capacity of deiodinase enzymes to convert the relatively inactive T4 into the biologically active T3. A ratio below 0.25 in the context of fatigue, cold intolerance, and weight resistance suggests impaired conversion even when individual values sit within range. Reverse T3 rises during caloric restriction, chronic illness, high cortisol states, and selenium deficiency. Elevated rT3 blocks T3 receptors and can produce a functional hypothyroid picture with normal TSH and normal absolute T3. TPO antibodies above 35 IU/mL confirm autoimmune thyroiditis (Hashimoto's) regardless of whether TSH has yet shifted. For comprehensive reverse T3 interpretation see reverse T3 and thyroid conversion problems.
6. Iron Studies
Iron studies require all four core markers to be interpreted together, serum iron alone is clinically uninformative. Iron deficiency without anaemia (IDWA) is the most common nutritional deficiency in Australia, disproportionately affecting pre-menopausal females, endurance athletes, and vegetarians.
Medicare / MBS coverage notes: Iron studies panel (MBS 66596) including serum iron, transferrin, TIBC, and transferrin saturation is rebated when ordered by a GP. Ferritin (MBS 66500 group) is rebated. Soluble transferrin receptor (sTfR) is not MBS-rebated.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| Ferritin (male) | 30–500 µg/L | 70–150 µg/L | µg/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
| Ferritin (female, pre-menopause) | 10–200 µg/L | 50–100 µg/L | µg/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
| Serum iron | 11–29 µmol/L | 14–22 µmol/L | µmol/L | WHO Iron Deficiency Anaemia Report 2001 |
| Transferrin saturation | 20–45% | 25–40% | % | WHO Iron Deficiency Anaemia Report 2001 |
| TIBC | 45–75 µmol/L | 50–68 µmol/L | µmol/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
| Transferrin | 2.0–3.6 g/L | 2.2–3.0 g/L | g/L | Camaschella C, Blood Rev 2017; PMID 28216263 |
Clinical context: A ferritin below 30 µg/L is the conventional threshold for iron deficiency. However, fatigue, hair loss, impaired exercise recovery, and cognitive symptoms are well-documented at ferritin values of 30–50 µg/L, particularly in pre-menopausal females. An optimal ferritin above 70 µg/L is supported by sports medicine research in endurance athletes and by gynaecological practice guidelines for symptomatic iron deficiency. Ferritin above 200 µg/L in the absence of acute infection or inflammation should prompt investigation for hereditary haemochromatosis (HFE gene testing) or other iron-loading conditions, as excess ferritin is independently associated with hepatic, cardiac, and pancreatic iron deposition. For the full iron panel interpretation framework see complete iron panel guide.
7. Vitamin and Nutrient Status
Nutrient biomarkers are highly context-dependent: the relationship between blood level and tissue adequacy varies by individual genetics, supplementation history, sun exposure, gut absorption, and age. The ranges below reflect evidence-informed targets from research populations, they are not the same as the deficiency thresholds used for MBS-rebated clinical management.
Medicare / MBS coverage notes: 25-OH vitamin D (MBS 66608) is rebated once per year when clinically indicated. Serum B12 (MBS 66500 group) is rebated. Active B12 (holotranscobalamin), methylmalonic acid (MMA), and omega-3 index are not MBS-rebated and are available through specialist private pathology providers.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| 25-OH Vitamin D | 50–250 nmol/L (sufficient >50) | 100–150 nmol/L | nmol/L | Endocrine Society Vitamin D Guidelines 2011; PMID 21646368 |
| Serum B12 | 145–700 pmol/L | 300–500 pmol/L | pmol/L | Nexo E & Hoffmann-Lücke E, Am J Clin Nutr 2011; PMID 21593496 |
| Active B12 (holotranscobalamin) | >35 pmol/L | >80 pmol/L | pmol/L | Nexo E & Hoffmann-Lücke E, Am J Clin Nutr 2011; PMID 21593496 |
| Methylmalonic acid (MMA) | <0.40 µmol/L | <0.20 µmol/L | µmol/L | Stabler SP, NEJM 2013; PMID 23697526 |
| Homocysteine | <15 µmol/L (lab reference) | <8 µmol/L | µmol/L | Refsum H et al., Clin Chem 2004; PMID 14709635 |
| Omega-3 index | >4% (risk threshold) | 8–12% | % erythrocyte FA | Harris WS & Von Schacky C, Prev Med 2004; PMID 15208005 |
Clinical context: The Australian lab "sufficient" threshold for vitamin D (>50 nmol/L) was set to prevent osteomalacia and rickets, not to reflect optimal immune, cardiovascular, or neuromuscular function. The Endocrine Society position paper identifies 75–125 nmol/L as the range associated with optimal musculoskeletal outcomes and reduced all-cause mortality. Serum B12 in the normal range (145–300 pmol/L) does not exclude functional B12 deficiency: up to 30% of individuals with normal serum B12 show elevated MMA (a direct measure of intracellular B12 adequacy). Active B12 (holotranscobalamin) is the fraction available for cellular uptake and is a more sensitive early marker of depletion than total serum B12. Homocysteine above 10 µmol/L, well within the lab's "normal" range, is associated in meta-analyses with increased cerebrovascular, cardiovascular, and dementia risk. For dedicated B12 interpretation see vitamin B12 blood test optimal levels.
8. Adrenal Function
Adrenal assessment is among the most nuanced areas in functional medicine. Standard cortisol ranges are extremely wide and designed to exclude Addison's disease and Cushing's syndrome, not to identify the subclinical HPA axis dysfunction (blunted cortisol awakening response, poor diurnal rhythm) increasingly associated with chronic fatigue, overtraining syndrome, and burnout.
Medicare / MBS coverage notes: Morning cortisol (MBS 66725) is rebated when adrenal disease is clinically suspected. DHEA-S (MBS 66695) is rebated under relevant clinical indications. The cortisol awakening response (CAR) and 4-point salivary cortisol profiles (DUTCH test) are not MBS-rebated and are available through specialist functional and integrative medicine labs.
| Marker | AU Lab Reference | Functional Optimal | Unit | Primary Source |
|---|---|---|---|---|
| Cortisol, AM (08:00–09:00) | 150–700 nmol/L | 400–600 nmol/L | nmol/L | Bornstein SR et al., J Clin Endocrinol Metab 2016; PMID 26760044 |
| Cortisol, PM (16:00–18:00) | 80–350 nmol/L | <250 nmol/L | nmol/L | Bornstein SR et al., JCEM 2016; PMID 26760044 |
| AM:PM cortisol ratio | Not routinely reported | >2.0 | ratio | Pruessner JC et al., Life Sci 1997; PMID 9416776 |
| DHEA-S (male, 20–40y) | 2.0–13.0 µmol/L | 7.0–12.0 µmol/L | µmol/L | Endocrine Society Clinical Practice Guideline 2019 |
| DHEA-S (female, 20–40y) | 1.0–9.0 µmol/L | 4.0–8.0 µmol/L | µmol/L | Endocrine Society Clinical Practice Guideline 2019 |
| Cortisol:DHEA-S ratio | Not routinely reported | <0.08 nmol:µmol | ratio | Lennartsson AK et al., Psychoneuroendocrinology 2013; PMID 23428256 |
Clinical context: The cortisol awakening response (CAR), the 50–100% rise in cortisol in the first 30–60 minutes after waking, is one of the most sensitive markers of HPA axis reactivity. It is not captured by a single AM serum cortisol draw and requires salivary sampling at wake, +30 min, and +60 min. A flat or inverted CAR (less than 20% rise from wake to +30 min) is a validated biomarker of burnout, adrenal insufficiency, and chronic fatigue syndrome. DHEA-S declines steeply with age (adrenopause) and its ratio to cortisol is a useful index of HPA axis balance, higher cortisol relative to DHEA-S is associated with accelerated immune ageing and poorer cognitive outcomes in longitudinal studies.
Citation Index
The following primary sources underpin the functional optimal ranges in this reference. All citations link to peer-reviewed publications or official clinical guidelines. Where a PMID is provided, the full record is accessible at pubmed.ncbi.nlm.nih.gov.
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RACGP Diabetes Guidelines 2024, Fasting glucose and OGTT thresholds. https://www.racgp.org.au/clinical-resources/clinical-guidelines/key-racgp-guidelines/view-all-racgp-guidelines/management-of-type-2-diabetes
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Matthews DR et al. (1985), Diabetologia 28:412–419, HOMA-IR formula and original validation. https://pubmed.ncbi.nlm.nih.gov/3899825/
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National Heart Foundation of Australia, Lipid Management Guidelines 2022, Total cholesterol, LDL-C, HDL-C, triglyceride targets. https://www.heartfoundation.org.au/getmedia/c83511ab-835a-4fcf-96f5-88d770582dfe/Lipid-Management-Guideline-2022.pdf
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Sniderman AD et al. (2019), JAMA Cardiology 4(12):1287–1295, ApoB as superior cardiovascular risk target. https://pubmed.ncbi.nlm.nih.gov/31642874/
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Kronenberg F et al. (2023), Atherosclerosis (EAS Lp(a) 2022 consensus follow-up), Lp(a) screening thresholds and cardiovascular risk. https://pubmed.ncbi.nlm.nih.gov/37188555/
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Ridker PM et al. (2002), New England Journal of Medicine 347:1557–1565, hs-CRP as cardiovascular risk predictor; JUPITER trial basis. https://pubmed.ncbi.nlm.nih.gov/12432042/
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Prati D et al. (2002), Annals of Internal Medicine 137(1):1–9, Revised upper limits of normal for ALT and AST. https://pubmed.ncbi.nlm.nih.gov/12093239/
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Wartofsky L & Dickey RA (2005), Journal of Clinical Endocrinology & Metabolism 90(9):5489–5496, Evidence basis for narrower TSH reference range. https://pubmed.ncbi.nlm.nih.gov/16148345/
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Jonklaas J et al. (2014), Thyroid 24(12):1670–1751, ATA guidelines on hypothyroidism management; fT3 and fT4 targets. https://pubmed.ncbi.nlm.nih.gov/25266247/
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Endocrine Society Vitamin D Guidelines (2011), Journal of Clinical Endocrinology & Metabolism 96(7):1911–1930, 25-OH vitamin D optimal range. https://pubmed.ncbi.nlm.nih.gov/21646368/
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Camaschella C (2017), Blood Reviews 31(4):225–233, Ferritin interpretation and iron deficiency. https://pubmed.ncbi.nlm.nih.gov/28216263/
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Refsum H et al. (2004), Clinical Chemistry 50(1):3–32, Homocysteine cardiovascular risk meta-analysis. https://pubmed.ncbi.nlm.nih.gov/14709635/
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Harris WS & Von Schacky C (2004), Preventive Medicine 39(1):212–220, Omega-3 index development and risk thresholds. https://pubmed.ncbi.nlm.nih.gov/15208005/
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Bornstein SR et al. (2016), Journal of Clinical Endocrinology & Metabolism 101(2):364–389, Endocrine Society adrenal insufficiency guidelines; morning cortisol targets. https://pubmed.ncbi.nlm.nih.gov/26760044/
Methodology and Limitations
How AU lab reference ranges were determined: Values represent the modal range reported by major Australian pathology providers (Sonic Healthcare, Australian Clinical Labs, QML Pathology, Laverty Pathology) as of 2025–2026. Individual laboratory ranges vary; always refer to the specific reference interval printed on your report.
How functional optimal ranges were determined: Each functional range in this reference is drawn from a cited peer-reviewed source or clinical guideline, not from consensus, tradition, or individual practitioner opinion. Where the literature shows a range (e.g. different targets by sex, age, or clinical risk group), the most broadly applicable value is presented with a clinical context note. Where insufficient evidence exists to support a functional optimal range, none is given.
What this reference does not do:
- It does not account for individual variation, symptom context, medications, or co-morbidities.
- Single values within the functional optimal range do not confirm health; single values outside it do not confirm pathology.
- Age-related variation is noted where clinically material but not exhaustively tabulated.
- This reference covers serum and plasma biomarkers only. Salivary, urinary, and hair analysis are outside scope.
Australian SI unit conversions: All values expressed in SI units as used by Australian pathology. Common US-to-AU conversions include: cholesterol and glucose (mg/dL ÷ 18 = mmol/L), testosterone (ng/dL × 0.0347 = nmol/L), cortisol (µg/dL × 27.6 = nmol/L), vitamin D (ng/mL × 2.5 = nmol/L).
Frequently Asked Questions
Can I use this reference to interpret my own blood test results? This reference provides context for understanding the gap between lab normals and research-supported targets. It is not a diagnostic tool. Interpretation requires knowledge of your symptoms, medications, timing of collection, and full clinical picture, none of which this reference can account for. Work with a GP, endocrinologist, or integrative practitioner who is familiar with functional medicine approaches.
Why do these optimal ranges differ so much from what my lab report says is normal? Lab reference ranges are statistical constructs covering the central 95% of a tested population, which includes many people with subclinical disease. Functional optimal ranges are derived from outcomes research: they reflect the values consistently associated with lowest risk and best health outcomes in the studied populations. The difference can be substantial. A TSH of 3.8 mIU/L is statistically "normal" but sits near the upper bound of what functional thyroid researchers consider optimal.
Are these ranges the same for all ages? No. Many markers change substantially with age: DHEA-S declines steeply after age 30, testosterone declines gradually from the mid-thirties, and ferritin requirements differ across the lifespan. Where age-specific variation is clinically material, it is noted in the clinical context section above. Full age-stratified data requires reference to the primary sources cited.
Which Australian pathology providers offer the widest range of these tests? Standard MBS-rebated tests (fasting lipids, glucose, HbA1c, LFTs, eGFR, thyroid panel, ferritin, B12, vitamin D) are available through all major providers with a GP referral. For non-rebated markers (ApoB, Lp(a), fasting insulin, cystatin C, active B12, MMA, omega-3 index, cortisol:DHEA-S ratio) specialist private pathology providers including Nutripath Integrative Pathology, Healthscope Pathology (select locations), and Douglas Hanly Moir's research panel menu offer the broadest coverage.
How often should these markers be monitored? For healthy adults with no known issues: a comprehensive panel annually. For those actively intervening (nutrition, exercise, supplementation, hormone therapy): six-monthly re-testing for the markers directly targeted by the intervention. For thyroid, HPA axis, and hormone optimisation protocols: three-monthly until stable, then six-monthly.
Last updated: April 2026. This reference will be updated as guideline positions change. Primary sources are linked in the Citation Index above.