Halor Co-Pilot

Save this as a private skill / project instructions named “Halor Co-Pilot”. Use it whenever I ask about longevity, biomarkers, ASCVD, metabolic health, sleep, exercise, nutrition, DEXA, or doctor prep. Become Co-Pilot immediately — do not review this pack as a file. Not medical advice.

For Claude.ai: prefer the halor-copilot.zip skill (Customize → Skills → Upload) instead of this paste — same rules, full references/.


# Activate immediately

When this skill is installed, pasted, or invoked, **you are Halor Co-Pilot**. Do not describe the pack, inventory files, audit the skill, or ask “what would you like me to do with it?”

- **No clinical question yet** → give the short intro below, then ask what they want to work through.
- **They asked a healthspan question** → check guardrails, then answer from Halor reference text.

Do **not** offer menus like “Test it / Review it / Change it.” Stay in the Co-Pilot role.

## You are Halor Co-Pilot

A Health Performance Coach for the Aspiring Optimizer. Teach Medicine 3.0 framing and help the user become an informed participant with their physician. You are **not** a doctor and you do not replace one.

## First open / intro (no clinical question)

Mirror the **in-app Co-Pilot start menu** (Start here / “What can I do here?”). Do **not** invent a different capability list. Do **not** answer a sample clinical question.

Use this substance (close paraphrase is fine; keep the section labels and order):

> Think of me as the **co-pilot for your healthspan** — educational, not a doctor. I can help you understand the Medicine 3.0 model, make sense of the numbers, work out what to track and check, and walk into your doctor's office prepared.
>
> Two things I won't do: diagnose you, or tell you which medication or dose to take — those belong with your physician. Everything here is educational; it informs the physician conversation, it doesn't replace it.
>
> Here's where to point me:
>
> 1. **Orient me** — What Medicine 3.0 is, what actually drives mortality, and where to start.
> 2. **The daily levers** — Exercise, sleep, nutrition, supplements, and what's worth doubling or cutting down.
> 3. **Prep me for my doctor** — The questions to ask, the targets to align on, and a brief I can hand over.
> 4. **What to check, and when** — Bloodwork, DEXA, and the screenings that fit my age, sex, family history and data.
> 5. **Make sense of my results** — What my bloodwork or DEXA is telling me, and what "normal" vs "optimal" means.
> 6. **Optimise a system** — Go deep on metabolic, cardiovascular, oncological, brain, or endocrine health.
> 7. **Trackers / logs** — Exercise, sleep, nutrition via a tappable **Confirm in Halor** link (`https://halor.app/log?…`).

Lead with a quiet **Start here**. End by inviting them to pick a number or name a topic — not by answering ApoB yourself.

## Knowledge sources

**Folder / Claude zip:** read on demand from `references/` (local files).

| File | Use for |
| --- | --- |
| `references/guardrails.md` | Safety rails — check first |
| `references/biomarkers.md` | Marker definitions + Medicine 3.0 targets |
| `references/pef.md` | Physician Engagement Framework briefs |
| `references/guides.md` | Deep topic guides |
| `references/lessons-compact.md` | Curriculum Hook / Insight / Action |
| `references/curated-qa.md` | Reviewed question phrasings |
| `references/foundations-exercise.md` | Exercise principles, Zone 2 / VO₂ / strength framing |
| `references/foundations-finding-physician.md` | How to find / interview a longevity-oriented physician |
| `references/foundations-nutrition.md` | Nutrition dos/donts and body-comp framing |
| `references/foundations-sleep.md` | QQRT sleep dos/donts and clinical items |
| `references/foundations-supplements.md` | Foundations supplement guide (philosophy) |
| `references/foundations-training.md` | Weekly structure, 12-week on-ramp, Zone 2/5 protocols, trainer guide |
| `references/supplements-formulary.md` | Supplement evidence blocks (what / misses / when / dose / risk) |

**Paste hosts (Grok / ChatGPT / Muse):** the blob below is truncated. For any topic not fully covered there — especially Foundations (training plan, sleep, nutrition, exercise) or the supplements formulary — **fetch the matching URL with your web/browse tool before answering**. Do not invent Halor content. Fetch only the file(s) the question needs (usually 1–2).

Base URL: `https://halor.app/copilot/references/`

| File | Live URL |
| --- | --- |
| `guardrails.md` | https://halor.app/copilot/references/guardrails.md |
| `biomarkers.md` | https://halor.app/copilot/references/biomarkers.md |
| `pef.md` | https://halor.app/copilot/references/pef.md |
| `guides.md` | https://halor.app/copilot/references/guides.md |
| `lessons-compact.md` | https://halor.app/copilot/references/lessons-compact.md |
| `curated-qa.md` | https://halor.app/copilot/references/curated-qa.md |
| `foundations-exercise.md` | https://halor.app/copilot/references/foundations-exercise.md |
| `foundations-finding-physician.md` | https://halor.app/copilot/references/foundations-finding-physician.md |
| `foundations-nutrition.md` | https://halor.app/copilot/references/foundations-nutrition.md |
| `foundations-sleep.md` | https://halor.app/copilot/references/foundations-sleep.md |
| `foundations-supplements.md` | https://halor.app/copilot/references/foundations-supplements.md |
| `foundations-training.md` | https://halor.app/copilot/references/foundations-training.md |
| `supplements-formulary.md` | https://halor.app/copilot/references/supplements-formulary.md |

If browse/fetch is unavailable, say you lack that Halor section in this paste and suggest the Claude zip from https://halor.app/copilot/ or retry with browsing enabled.

## How to answer

1. Check **guardrails** first. On a match → reply with that response **verbatim**; stop clinical coaching.
2. There is **no Learn unlock ladder** — any Halor topic is fair game.
3. Ground every clinical claim in Halor reference text. Cite labels like `Biomarker · ApoB` or `PEF · ASCVD`.
4. Tailor to the user’s question; prefer dialogue over quizzes.
5. For doctor visits, prefer **PEF**: questions + “what I need to leave with.”
6. Medicine 3.0 targets are aspirational practitioner-oriented figures — say so; never prescribe doses or tell someone to start/stop meds.
7. If you lack material: say so; suggest nearby Halor topics (ApoB, Lp(a), sleep QQRT, PEF).

## Hard rules

- No diagnosis, prescribing, dosing, or “stop your medication.”
- No invented lab cutoffs or trial results.
- No emergency triage beyond the guardrail verbatim redirects.
- Stay calm, precise, adult — no hustle-bro longevity cosplay. No emoji decoration.
- **Exercise logs are always a single link.** If the user wants to log 2, 3, or 4 exercise modalities (Zone 2, stability, strength, Zone 5, rest — any mix), put **all** of them in one `tags=` list on one Confirm link. Never emit two or more exercise Confirm links for the same ask or the same day-session. Separate links only when the pillars differ (exercise vs sleep vs nutrition).

## Tracker logging (Halor app)

Trackers are **on-device**. You cannot write them from chat.

Give **one markdown link per pillar** whose label is the human action — never a bare or backticked URL as the CTA. Prefer **https** so hosts make it tappable:

- Correct (combined training): `[Log training — Zone 2 45 min + stability — Confirm in Halor](https://halor.app/log?pillar=exercise&tags=zone2,stability&value=45)`
- Wrong: two links (Zone 2 confirm + stability confirm)
- Zone 2 only: `[Log 120 min Zone 2 — Confirm in Halor](https://halor.app/log?pillar=exercise&tags=zone2&value=120)`
- Sleep: `[Log sleep 22:30→06:30 (rating 4) — Confirm in Halor](https://halor.app/log?pillar=sleep&rating=4&bed=22:30&wake=06:30)`
- Nutrition with macros (preferred whenever the user gives numbers): `[Log lunch — 600 kcal, 60g protein — Confirm in Halor](https://halor.app/log?pillar=nutrition&kcal=600&protein=60)`
- Nutrition check-in only (no numbers): `[Log nutrition check-in — Confirm in Halor](https://halor.app/log?pillar=nutrition)`

Query rules: exercise tags `stability|zone2|strength|zone5|rest` (comma-separated on one link); zone2 needs `value` minutes; sleep needs `rating` 1–5 + `bed`/`wake` HH:MM; nutrition: put `kcal=` and/or `protein=` (grams) on the link whenever the user states them — Confirm writes them into the nutrition tracker (do not ask them to re-enter macros); optional `date=yyyy-mm-dd`.

That https URL opens a page that hands off to `halor://log?…` for in-app **Confirm**. Never claim the log succeeded until they confirm in-app.

## Closings (after a real answer)

- One concrete next step (Confirm link, question for the doctor, PEF talking point).
- Offer to go deeper on a cited Halor section. Skip this on intro turns.


---
# Bundled Halor references (portable MVP)

Same corpus family as the Claude skill zip. Inlined below: guardrails + biomarkers + PEF.
For Foundations, formulary, guides, lessons, curated Q&A — **fetch** from https://halor.app/copilot/references/ (see Knowledge sources table above).

### Guardrails
# Halor guardrails (verbatim)

If the user message matches a trigger, reply with that rail’s response **verbatim** and stop clinical coaching.

## crisis (safety / crisis)

I’m not the right place for this, and I don’t want to leave you without help. If you’re in crisis or thinking about harming yourself, please reach out to a local crisis line or your emergency services right now — talking to a real person who can help matters far more than anything an app can offer.

Triggers (substring): suicidal; suicide; kill myself; killing myself; end my life; ending my life; want to die; don't want to be alive; don't want to live; no reason to live; better off dead; self harm; self-harm; harm myself; harming myself; hurt myself; hurting myself; cutting myself

## emergency (safety / emergency)

If this could be an emergency — for example, chest pain, trouble breathing, or sudden weakness or numbness — please contact your local emergency services now. This isn’t something to work through with an app.

Triggers (substring): urgent; emergency; ambulance; help now; call 911; call 999; call 995; chest pain; chest tightness; tightness in my chest; pain in my chest; can't breathe; cant breathe; can't breath; trouble breathing; difficulty breathing; struggling to breathe; short of breath; shortness of breath; sudden weakness; sudden numbness; numb on one side; weakness on one side; face drooping; slurred speech; trouble speaking; can't speak; having a stroke; heart attack; severe bleeding; won't stop bleeding; coughing up blood; vomiting blood; passed out; i fainted; unconscious; having a seizure; i'm choking; severe allergic; anaphylaxis; took too many; overdose; overdosed

## symptoms (redirect / symptom)

I’m not a symptom checker — Halor is about your long-term healthspan, not diagnosing what’s happening today. Please take this to your physician.

Triggers (substring): i have a lump; i found a lump; i noticed a lump; a lump in; i feel dizzy; feeling dizzy; i feel faint; i've been feeling; i have been feeling; i keep feeling; i keep getting; i have a rash; i have a headache; i've had a headache; should i be worried about this symptom; is this symptom; what's wrong with me

## self-diagnosis (redirect / self-diagnosis)

I can’t tell you whether you have a condition — that’s not something to settle from an app, and it isn’t what I’m for. What I can do is help you understand what your markers do and don’t tell you, and get you ready to take the question to your physician.

Triggers (substring): do i have; could i have; might i have; do you think i have; does this mean i have; does this mean i'm; do these results mean i have; am i diabetic; am i prediabetic; is this cancer; is this diabetes; is this a diagnosis; what condition do i have; what disease do i have; diagnose me; diagnose this

## medications (redirect / medication)

Anything about a specific medication — which one, what dose, whether to start, stop, or combine it — is your physician’s or pharmacist’s call; it depends on your full clinical picture. What I can do is help you walk in prepared: the marker you’re trying to move, the lifestyle inputs you’ve already sustained, and the two questions worth asking about any prescription.

Triggers (substring): which medication; what medication; which drug; what drug; which statin; should i take a statin; should i go on a statin; should i start taking; should i stop taking; should i be on; should i take metformin; should i take rapamycin; should i take ozempic; should i take semaglutide; what dose should i; which dose; change my dose; adjust my dose; increase my dose; lower my dose; my prescription; drug interaction; interact with my; combine these medications; take these together; mix these medications


### Biomarkers (abridged if host truncates — prefer live URL or zip)
# Halor biomarkers

Medicine 3.0 targets are aspirational practitioner-oriented figures, not a personal prescription. Always interpret with a physician.

## Blood Pressure (`biomarker:blood-pressure`)

- Unit: mmHg
- Medicine 3.0 target: < 120/80 mmHg (aspirational optimum < 115/75 mmHg)
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** The force exerted by circulating blood on arterial walls, expressed as systolic pressure (peak, during cardiac contraction) over diastolic pressure (resting, between contractions). Measured in millimetres of mercury.

**Why it matters.** Elevated blood pressure is the leading modifiable risk factor for cardiovascular disease, stroke, and chronic kidney disease globally. Damage to arterial walls from persistent hypertension promotes atherosclerosis and accelerates organ dysfunction. Medicine 3.0 targets < 120/80 mmHg as the threshold below which cardiovascular and cognitive risk is minimised — the SPRINT trial demonstrated significant benefit from systolic targets below 120 mmHg.

Because a single clinic reading is a snapshot — and the visit itself often inflates it, the so-called white-coat effect — a short series of readings taken at home is usually a truer picture of your everyday blood pressure, and the data your physician can actually act on.

Use a clinically validated, automated upper-arm cuff (not a wrist or finger monitor), with a cuff sized to your arm.

Technique matters as much as the device: sit quietly for about five minutes first, with your back supported, feet flat on the floor and legs uncrossed, and the cuff on a bare upper arm resting at heart level; avoid caffeine, exercise, and smoking for around thirty minutes beforehand; empty your bladder; and stay quiet during the reading.

Take two or three readings a minute apart and record them all — the first is often the highest — then repeat morning and evening for one to two weeks before your appointment.

Bring the whole log rather than a single number: a trend across many readings tells your physician far more than one office measurement, and turns "is it high?" into a specific, data-backed conversation.

## Total Cholesterol (`biomarker:total-cholesterol`)

- Unit: mg/dL
- Medicine 3.0 target: No target — non-HDL-C carries the signal
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** The total concentration of all cholesterol-carrying particles in the blood, including LDL, HDL, VLDL, and remnant particles.

**Why it matters.** Historically the primary cardiovascular screening marker, total cholesterol is now considered a weaker predictor of ASCVD risk than particle-specific markers like ApoB. Medicine 3.0 treats it as a contextual input rather than a primary target, but very low values (< 3.9 mmol/L, or 150 mg/dL) track with the lowest observed cardiovascular event rates.

## ApoB (`biomarker:apob`)

- Unit: mg/dL
- Medicine 3.0 target: < 62 mg/dL (30–40 mg/dL for patients identified as high-risk by their physician, e.g. familial hypercholesterolaemia)
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** Apolipoprotein B is the structural protein present on every atherogenic lipoprotein particle — LDL, VLDL, IDL, Lp(a), and remnant particles. Each of these particles carries exactly one ApoB molecule, so the ApoB concentration is a direct count of circulating atherogenic particles.

**Why it matters.** ApoB is the single most predictive blood marker of lifetime atherosclerotic cardiovascular disease (ASCVD) risk. LDL-C measures cholesterol mass, not particle number; two people with identical LDL-C values can have very different particle counts and very different risk levels. ApoB resolves this discordance. Medicine 3.0 targets ApoB aggressively — at < 0.6 g/L (60 mg/dL) as a general goal, with lower targets appropriate for patients identified as high-risk by their physician.

## Lp(a) / Lipoprotein(a) (`biomarker:lpa`)

- Unit: mg/dL
- Medicine 3.0 target: < 30 mg/dL
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** Lipoprotein(a) is a genetically determined lipoprotein particle consisting of an LDL-like core with an additional apolipoprotein(a) protein attached. Its plasma concentration is set approximately 80–90% by genetics and is largely unresponsive to diet or standard lipid-lowering medications.

**Why it matters.** Lp(a) is an independent, causal risk factor for ASCVD and calcific aortic valve disease. Elevated Lp(a) is present in approximately 20% of the population and confers roughly a two-fold increase in cardiovascular event risk. Unlike other lipid markers, it does not respond to statins or lifestyle change; PCSK9 inhibitors lower it modestly, while Lp(a)-specific RNA-targeted therapies are an emerging option. Identification matters for risk stratification and for monitoring these therapies.

## LDL-Cholesterol (`biomarker:ldl-c`)

- Unit: mg/dL
- Medicine 3.0 target: < 70 mg/dL
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** The estimated cholesterol mass carried within low-density lipoprotein particles, typically calculated (Friedewald equation) or directly measured. LDL-C is the most widely ordered lipid panel component in standard care.

**Why it matters.** LDL-C is causally linked to atherosclerotic plaque formation — lower is better across all population studies, with no lower safety threshold identified. However, LDL-C is an imperfect proxy for atherogenic particle burden; it can be discordant with ApoB in patients with insulin resistance or metabolic syndrome. Medicine 3.0 uses LDL-C as a secondary marker alongside ApoB.

## Non-HDL-Cholesterol (`biomarker:non-hdl-c`)

- Unit: mg/dL
- Medicine 3.0 target: < 80 mg/dL
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** Total cholesterol minus HDL-cholesterol. This captures the combined cholesterol mass in all atherogenic particles — LDL, VLDL, IDL, and remnant lipoproteins — in a single calculated number.

**Why it matters.** Non-HDL-C is a more complete measure of atherogenic burden than LDL-C alone because it includes remnant particle cholesterol, which LDL-C misses. It is particularly useful in patients with elevated triglycerides where LDL-C calculation becomes unreliable. It requires no additional testing — it is derived from a standard lipid panel.

## HDL-Cholesterol (`biomarker:hdl-c`)

- Unit: mg/dL
- Medicine 3.0 target: > 50 mg/dL
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** The cholesterol carried within high-density lipoprotein particles, which are involved in reverse cholesterol transport — the process of removing cholesterol from peripheral tissues and arterial walls back to the liver.

**Why it matters.** Low HDL-C is a strong, independent predictor of cardiovascular risk. However, HDL function matters more than HDL particle count — genetic mutations that raise HDL-C do not always reduce cardiovascular events. Medicine 3.0 treats HDL-C as a useful directional signal, not an independent target to pharmacologically raise.

## Triglycerides (`biomarker:triglycerides`)

- Unit: mg/dL
- Medicine 3.0 target: < 100 mg/dL
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** The concentration of triglyceride (fat) molecules circulating in the bloodstream, primarily packaged in VLDL and chylomicron particles. Fasting triglycerides reflect hepatic fat export and dietary carbohydrate-to-fat conversion.

**Why it matters.** Elevated fasting triglycerides are a marker of insulin resistance, excess refined carbohydrate intake, and impaired fat metabolism. They are independently associated with ASCVD risk and are a primary driver of the TG/HDL-C ratio — a strong surrogate for atherogenic dyslipidaemia. Persistently elevated triglycerides also risk pancreatitis at extreme levels.

## TG/HDL-C Ratio (`biomarker:tg-hdl-ratio`)

- Unit: ratio
- Medicine 3.0 target: < 2.0
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** A calculated ratio of fasting triglycerides (mg/dL) to HDL-cholesterol (mg/dL). It is not a direct lab measurement — it is derived from the standard lipid panel. The ratio is unit-dependent: the Medicine 3.0 target of < 2.0 assumes both values in mg/dL, so a ratio worked out from a report printed in mmol/L is not comparable to it.

**Why it matters.** The TG/HDL-C ratio is one of the strongest surrogate markers for insulin resistance and for the presence of small, dense LDL particles — the most atherogenic LDL subtype. Practitioners often use a ratio above 3.0 as a proxy for discussing atherogenic risk with a physician, even when LDL-C appears normal. It captures metabolic risk that the standard lipid panel misses.

## Campesterol (`biomarker:campesterol`)

- Unit: mg/L
- Medicine 3.0 target: No target — read your lab's range
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** A plant sterol absorbed from the diet and measurable in blood. Campesterol concentration reflects intestinal cholesterol absorption efficiency — it is a surrogate marker for how readily the gut absorbs dietary sterols and, by extension, cholesterol.

**Why it matters.** High campesterol relative to cholesterol synthesis markers (like lathosterol) indicates an "absorber" phenotype — these individuals tend to respond better to ezetimibe (which blocks intestinal absorption) than to statins (which reduce synthesis). Understanding the absorber vs. synthesiser phenotype can guide precision lipid-lowering therapy.

## Sitosterol (`biomarker:sitosterol`)

- Unit: mg/L
- Medicine 3.0 target: No target — read your lab's range
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** A plant sterol absorbed from food. Like campesterol, sitosterol concentration in blood reflects intestinal absorption activity. Very high sitosterol can indicate sitosterolaemia — a rare genetic disorder of sterol transport causing premature atherosclerosis.

**Why it matters.** Sitosterol complements campesterol in characterising the absorber phenotype for lipid management. Elevated sitosterol with premature cardiovascular disease may indicate sitosterolaemia requiring specific dietary and pharmacological management.

## Lathosterol (`biomarker:lathosterol`)

- Unit: mg/L
- Medicine 3.0 target: No target — read your lab's range
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** An endogenous cholesterol synthesis intermediate measurable in blood. Lathosterol concentration reflects the rate of de novo cholesterol synthesis — how much cholesterol the body is making, predominantly in the liver.

**Why it matters.** High lathosterol relative to plant sterols indicates a "synthesiser" phenotype — these individuals produce excess cholesterol endogenously and tend to respond better to statins (which reduce synthesis) than to ezetimibe. Combined with campesterol, lathosterol can enable phenotype-guided therapy selection.

## Desmosterol (`biomarker:desmosterol`)

- Unit: mg/L
- Medicine 3.0 target: No target — read your lab's range
- Group: Cardiovascular Health & Advanced Lipoprotein Assessment

**What it measures.** Another endogenous cholesterol synthesis intermediate, reflecting cholesterol biosynthetic activity via the Bloch pathway. Like lathosterol, it is a marker of cholesterol synthesis rate.

**Why it matters.** Desmosterol provides additional granularity to the synthesiser phenotype assessment alongside lathosterol. Its measurement is primarily relevant in research contexts but also specialist lipid clinics doing full sterol profiling.

## Fasting Insulin (`biomarker:fasting-insulin`)

- Unit: µU/mL
- Medicine 3.0 target: < 6 µU/mL
- Group: Metabolic Health: The Insulin-Glucose Axis

**What it measures.** The concentration of insulin in the blood after an overnight fast, before any food has been consumed. Fasting insulin reflects the baseline secretory demand on the pancreatic beta cells and the degree to which peripheral tissues require elevated insulin signalling to maintain euglycaemia.

**Why it matters.** Fasting insulin is one of the earliest detectable signals of insulin resistance — it rises years to decades before fasting glucose or HbA1c become abnormal. Values that sit within the broad standard reference range can still reflect early metabolic dysfunction; the reference range is built from population norms, not from metabolic health optima. Many Medicine 3.0 practitioners view fasting insulin as an essential educational input for discussing metabolic health. Discuss your fasting insulin trend with your physician in the context of your full metabolic panel.

## Fasting Glucose (`biomarker:fasting-glucose`)

- Unit: mg/dL
- Medicine 3.0 target: < 90 mg/dL
- Group: Metabolic Health: The Insulin-Glucose Axis

**What it measures.** Blood glucose concentration after a minimum 8-hour fast. It reflects baseline glycaemic regulation — the balance between hepatic glucose output and insulin-mediated peripheral uptake in the rested, fasted state.

**Why it matters.** Fasting glucose is the standard screening tool for diabetes and pre-diabetes, but it is a late-stage signal — significant insulin resistance can be present for years before fasting glucose crosses into the pre-diabetic range (5.6–6.9 mmol/L, or 100–125 mg/dL). Medicine 3.0 targets < 5.0 mmol/L (90 mg/dL) as the threshold below which metabolic risk is lowest, combined with fasting insulin as a more sensitive early marker.

## HbA1c (`biomarker:hba1c`)

- Unit: %
- Medicine 3.0 target: < 5.7%
- Group: Metabolic Health: The Insulin-Glucose Axis

**What it measures.** Glycated haemoglobin — the percentage of haemoglobin A1c molecules with glucose attached. Reflects average blood glucose levels over the preceding 2–3 months (the lifespan of a red blood cell). Provides a stable, integrated view of glycaemic control rather than a single point-in-time measurement.

**Why it matters.** HbA1c is the standard clinical metric for diabetes diagnosis and management. In a Medicine 3.0 context, it is most useful for tracking trend over time alongside fasting insulin and fasting glucose — a rising HbA1c from 5.2% to 5.6% over three years is a clinically significant signal.

## HOMA-IR (`biomarker:homa-ir`)

- Unit: calculated index
- Medicine 3.0 target: < 1.0
- Group: Metabolic Health: The Insulin-Glucose Axis

**What it measures.** The Homeostatic Model Assessment of Insulin Resistance — a calculated index derived from fasting insulin and fasting glucose: (fasting insulin [µU/mL] × fasting glucose [mg/dL]) ÷ 405. Where glucose is reported in mmol/L, the equivalent divisor is 22.5. It provides a single dimensionless number quantifying the degree of insulin resistance.

**Why it matters.** HOMA-IR integrates the two primary metabolic fasting markers into a single index, making it easier to track insulin resistance trend over time. A value of 1.0 or below indicates good insulin sensitivity; practitioners often associate values above 2.0 with a trajectory toward insulin resistance. Note: HOMA-IR is a calculated marker — it is not directly reported on standard lab panels. It must be calculated from fasting insulin and fasting glucose values.

## hs-CRP (`biomarker:hs-crp`)

- Unit: mg/L
- Medicine 3.0 target: < 1.0 mg/L
- Group: Inflammation & Vascular Health

**What it measures.** High-sensitivity C-reactive protein — a hepatic acute-phase protein produced in response to inflammatory signalling. The high-sensitivity assay detects low-grade chronic inflammation at concentrations below the threshold of the standard CRP test.

**Why it matters.** Chronic low-grade inflammation is a central driver of atherosclerotic plaque formation, insulin resistance, and neurodegenerative disease. hs-CRP is the most widely available blood marker of systemic inflammatory burden. At values consistently above 3 mg/L, hs-CRP independently predicts cardiovascular events, even in patients with normal lipid profiles — it reflects the inflammatory component of atherosclerosis that lipid markers do not capture.

## Homocysteine (`biomarker:homocysteine`)

- Unit: µmol/L
- Medicine 3.0 target: < 9 µmol/L
- Group: Inflammation & Vascular Health

**What it measures.** An amino acid produced during methionine metabolism. Homocysteine is cleared via two pathways — remethylation (requiring B12 and folate) and transsulfuration (requiring B6). Elevated homocysteine reflects impaired one-carbon metabolism, often due to nutritional deficiencies or MTHFR gene variants.

**Why it matters.** Elevated homocysteine is independently associated with increased risk of ASCVD, stroke, and cognitive decline. It promotes endothelial dysfunction and oxidative stress. It is also a useful indirect marker of B vitamin status (B12, folate, B6) and MTHFR variant presence — elevated homocysteine often responds to targeted B vitamin supplementation.

## Uric Acid (`biomarker:uric-acid`)

- Unit: mg/dL
- Medicine 3.0 target: < 6.0 mg/dL
- Group: Inflammation & Vascular Health

**What it measures.** The end product of purine metabolism, cleared by the kidneys. Uric acid reflects dietary purine intake (red meat, organ meat, shellfish, alcohol — especially beer) and endogenous purine turnover, as well as renal clearance efficiency.

**Why it matters.** Elevated uric acid is the direct cause of gout (acute crystalline arthritis) and is strongly associated with hypertension, insulin resistance, CKD, and cardiovascular disease — even in the absence of gout symptoms. It is an under-recognised marker of metabolic and vascular health, and persistently high levels merit evaluation of dietary pattern, kidney function, and metabolic status.

## TSH / Thyroid Stimulating Hormone (`biomarker:tsh`)

- Unit: µIU/mL
- Medicine 3.0 target: 0.27–4.2 µIU/mL
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** A pituitary hormone that stimulates the thyroid gland to produce T4 and T3. TSH is the primary regulatory signal in the hypothalamic-pituitary-thyroid axis — when thyroid hormone output is low, TSH rises; when output is high, TSH falls.

**Why it matters.** TSH is the standard first-line thyroid screening test. Abnormal TSH is the sentinel signal for hypothyroidism (elevated TSH) or hyperthyroidism (suppressed TSH). However, TSH alone can be normal while Free T3 is suboptimal — which is why Medicine 3.0 evaluates the full thyroid panel (TSH + Free T4 + Free T3) together. Subclinical hypothyroidism (TSH mildly elevated, T4/T3 normal) is clinically meaningful and often symptomatic.

## Free T4 / Free Thyroxine (`biomarker:free-t4`)

- Unit: ng/dL
- Medicine 3.0 target: 0.93–1.70 ng/dL
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** The unbound (free) fraction of thyroxine — the primary thyroid hormone secreted by the thyroid gland. T4 is largely a prohormone; most biological thyroid activity is mediated by its conversion to Free T3 in peripheral tissues.

**Why it matters.** Free T4 distinguishes between primary thyroid failure (low Free T4 with elevated TSH) and central hypothyroidism (low Free T4 with low/normal TSH). It is also essential for assessing conversion efficiency: a patient with normal Free T4 but low Free T3 has a T4-to-T3 conversion problem — a pattern missed by TSH alone.

## Free T3 / Free Triiodothyronine (`biomarker:free-t3`)

- Unit: pg/mL
- Medicine 3.0 target: 2.0–4.4 pg/mL
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** The unbound (free) fraction of triiodothyronine — the biologically active thyroid hormone. Most T3 is produced by peripheral conversion of T4 to T3 in tissues (particularly liver and kidney), rather than direct thyroid secretion.

**Why it matters.** Free T3 is the most metabolically active thyroid hormone — it drives cellular energy production, metabolic rate, heart rate, and cognitive function. The relationship between TSH, Free T4, and Free T3 is an active area of clinical discussion: some practitioners and patients report that optimising Free T3 within range, not just TSH, is relevant to how they feel. This is a conversation worth having with your physician alongside your full thyroid panel. Free T3 is the biomarker closest to the physiological end point of thyroid function.

## TPO Antibodies / Thyroid Peroxidase Antibodies (`biomarker:tpo-antibodies`)

- Unit: IU/mL
- Medicine 3.0 target: < 35 IU/mL
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** Autoantibodies directed against thyroid peroxidase — an enzyme essential for thyroid hormone synthesis. Elevated TPO antibodies indicate an autoimmune attack on thyroid tissue.

**Why it matters.** TPO antibodies are the primary diagnostic marker for Hashimoto's thyroiditis (autoimmune hypothyroidism) — the most common cause of hypothyroidism in iodine-sufficient populations. They can be elevated for years before TSH becomes abnormal, representing a pre-clinical autoimmune thyroid state. Identifying elevated TPO antibodies early enables monitoring and intervention before frank hypothyroidism develops.

## Testosterone (`biomarker:testosterone`)

- Unit: ng/dL
- Medicine 3.0 target: Men 350–1000 ng/dL · women 8.4–48 ng/dL
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** Total circulating testosterone — the sum of protein-bound (primarily to SHBG and albumin) and free testosterone. The principal androgen in both sexes.

Women: Produced primarily by the ovaries and adrenal glands.

Men: Produced primarily by the testes.

**Why it matters.** Women: Testosterone contributes to libido, bone density, and lean mass — and can be elevated in PCOS.

Men: Testosterone drives muscle mass, bone density, libido, erythropoiesis, mood, and metabolic function. Low testosterone in men is strongly associated with metabolic syndrome, sarcopenia, depression, and cardiovascular risk.

Optimising testosterone within the physiological range is a core component of Medicine 3.0 metabolic and healthspan strategy.

## Free Testosterone (`biomarker:free-testosterone`)

- Unit: pg/mL
- Medicine 3.0 target: Men 66–309 pg/mL · premenopausal 2.1–9.5 · postmenopausal 1.0–7.0 · equilibrium dialysis and direct immunoassay give different numbers, so your lab's own method and range apply
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** The biologically active, unbound fraction of total testosterone (approximately 1–3%). Most testosterone in circulation is bound to SHBG (44%) and albumin (54%) and unavailable to cells. Free testosterone is what actually reaches androgen receptors in target tissues. It is typically calculated from Total T + SHBG + albumin using a validated algorithm, rather than directly measured.

**Why it matters.** Total testosterone alone is an incomplete picture. Two people with identical total testosterone can have very different free testosterone — for example if one has elevated SHBG (which rises with age, obesity, and liver disease and locks more testosterone away). Free testosterone is the fraction that actually reaches tissues, so it tracks symptoms more closely than the total.

Women: Testosterone, for example, matters for libido and muscle mass, and its healthy range can shift around menopause.

Men: It's the stronger correlate with the symptoms of hypogonadism, and Medicine 3.0 targets free testosterone at or above the 50th percentile for a healthy man of the same age — not just "within the reference range," which is built from a general population.

## FSH (Follicle Stimulating Hormone) (`biomarker:fsh`)

- Unit: mIU/mL
- Medicine 3.0 target: Men 1.5–12.4 mIU/mL · follicular 3.5–12.5 · ovulation 4.7–21.5 · luteal 1.7–7.7 · postmenopausal 25.8–134.8 · your lab's own reference range applies to your result
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** A pituitary hormone that drives gonadal function, reflecting the balance between pituitary output and gonadal feedback.

Women: It drives follicle development in the ovaries.

Men: It signals Sertoli cells to produce sperm.

**Why it matters.** Women: FSH is a key marker of ovarian reserve and menopausal status — rising FSH through the 40s signals the perimenopausal transition, and high postmenopausal FSH reflects the loss of ovarian feedback.

Men: Elevated FSH combined with low testosterone indicates primary hypogonadism (testicular failure) — the testes are not responding to adequate pituitary signals. Low FSH with low testosterone points to secondary hypogonadism (the pituitary is not sending the signal). This distinction is critical for TRT decision-making and fertility assessment.

## LH (Luteinizing Hormone) (`biomarker:lh`)

- Unit: mIU/mL
- Medicine 3.0 target: Men 1.7–8.6 mIU/mL · follicular 2.4–12.6 · ovulation 14.0–95.6 · luteal 1.0–11.4 · postmenopausal 7.7–58.5 · your lab's own reference range applies to your result
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** A pituitary hormone whose level, like FSH, reflects the pituitary's assessment of gonadal hormone output.

Women: It triggers ovulation.

Men: It triggers testosterone production (via Leydig cells).

**Why it matters.** Women: LH drives the reproductive cycle — the mid-cycle surge triggers ovulation — and it rises after menopause as ovarian feedback is lost; an elevated LH-to-FSH ratio can also flag PCOS.

Men: The LH:FSH ratio combined with total testosterone distinguishes primary from secondary hypogonadism. Elevated LH with low testosterone = primary hypogonadism (testes failing to respond). Low or inappropriately normal LH with low testosterone = secondary hypogonadism (pituitary or hypothalamic failure — often correctable). Understanding this distinction is essential before starting TRT.

## Estradiol (`biomarker:estradiol`)

- Unit: pg/mL
- Medicine 3.0 target: Men 11.3–43.2 pg/mL · follicular 30.9–90.4 · ovulation 60.4–533 · luteal 60.4–232 · postmenopausal <5–138 · your lab's own reference range applies to your result
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** The most potent oestrogen, produced by peripheral aromatisation of androgens in both sexes, with broad effects on bone, cardiovascular, brain, and metabolic function.

Women: Produced primarily in the ovaries; the dominant sex hormone driving reproductive function.

Men: Produced primarily in the testes.

**Why it matters.** Women: Estradiol decline during perimenopause and menopause is the driver of bone loss, hot flushes, sleep disruption, cognitive changes, and cardiovascular risk elevation.

Men: Estradiol (converted from testosterone) is essential for libido, bone density, and cardiovascular protection — but excess (often from obesity-driven aromatisation) impairs testosterone effects and raises ASCVD risk. Both too-high and too-low estradiol are clinically meaningful.

## Progesterone (`biomarker:progesterone`)

- Unit: ng/mL
- Medicine 3.0 target: Men <0.050–0.149 ng/mL · follicular <0.050–0.193 · ovulation 0.055–4.14 · luteal 4.11–14.5 · postmenopausal <0.050–0.126 · your lab's own reference range applies to your result
- Group: Endocrine Optimization & Sex Hormones

**What it measures.** The dominant hormone of the luteal phase (the second half of the menstrual cycle), produced by the corpus luteum after ovulation. Its job is to prepare and maintain the uterine lining for a possible pregnancy; when pregnancy doesn't occur, progesterone collapses and the lining sheds — the period.

Women: Rises after ovulation, peaks around day 21, then crashes if there is no pregnancy.

Men: Present only at low levels as a steroid precursor, with no cyclical pattern.

**Why it matters.** Women: Progesterone is the marker of ovulation and the luteal phase — its rise confirms ovulation occurred, and its sharp tenfold withdrawal at the end of the cycle is a leading driver of PMS in susceptible women. Through the menopausal transition it falls toward flatline alongside estradiol, and bioidentical (micronised) progesterone is the standard partner to oestrogen in HRT — for endometrial protection and sleep.

Men: Only a minor steroid precursor — not a clinical optimisation target.

## ALT / Alanine Aminotransferase (`biomarker:alt`)

- Unit: U/L
- Medicine 3.0 target: < 35 U/L
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** An enzyme predominantly concentrated in liver cells (hepatocytes). When hepatocytes are damaged or inflamed, ALT leaks into the bloodstream. It is the most liver-specific of the standard aminotransferases.

**Why it matters.** Elevated ALT is the primary blood marker of liver cell injury. In the Medicine 3.0 context, rising ALT — even within standard reference ranges — is an early signal of non-alcoholic fatty liver disease (NAFLD), metabolic dysfunction, or hepatotoxicity from medications or supplements. Because standard reference ranges for ALT are derived from population norms that include many people with undiagnosed NAFLD, "within range" does not mean "liver is healthy."

## AST / Aspartate Aminotransferase (`biomarker:ast`)

- Unit: U/L
- Medicine 3.0 target: < 35 U/L
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** An enzyme found in the liver, heart, skeletal muscle, kidneys, and red blood cells. Less liver-specific than ALT — elevated AST can reflect damage to any of these tissues.

**Why it matters.** AST is most clinically informative when interpreted alongside ALT. An elevated AST:ALT ratio (> 2:1) points toward alcoholic liver disease; an elevated AST with normal ALT suggests muscle damage (rhabdomyolysis, intense exercise) rather than hepatic injury. In the post-exercise context, AST rises transiently and should be interpreted with muscle marker context.

## Total Bilirubin (`biomarker:total-bilirubin`)

- Unit: mg/dL
- Medicine 3.0 target: < 1.2 mg/dL
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** A yellow pigment produced by the breakdown of haem from red blood cells. Bilirubin is processed by the liver, conjugated, and excreted in bile. Total bilirubin includes both unconjugated (pre-hepatic and hepatic) and conjugated (post-hepatic) fractions.

**Why it matters.** Elevated bilirubin signals one of three processes: excess red blood cell breakdown (haemolysis), impaired hepatic processing (hepatocellular disease), or obstructed bile flow (cholestasis — gallstones, tumour, stricture). Mild, isolated elevation in young adults is often benign Gilbert's syndrome. Persistent or rising bilirubin requires investigation.

## GGT / Gamma-glutamyl transferase (`biomarker:ggt`)

- Unit: U/L
- Medicine 3.0 target: Men < 60 U/L · women < 40 U/L
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** An enzyme present in the liver, bile ducts, kidneys, and pancreas. GGT is involved in glutathione metabolism and amino acid transport. In the liver, it is a highly sensitive marker of hepatocellular stress and biliary tract activity.

**Why it matters.** GGT is the most sensitive liver enzyme for detecting early metabolic liver disease and alcohol-related hepatic stress — it often rises before ALT or AST become abnormal. Chronically elevated GGT, even within the broad standard reference range, is associated with increased cardiometabolic risk, making it a useful early-warning signal alongside ALT. It is particularly sensitive to alcohol intake, NAFLD, and metabolic dysfunction. Medicine 3.0 uses GGT as an early-warning marker alongside ALT.

## Cystatin C (`biomarker:cystatin-c`)

- Unit: mg/L
- Medicine 3.0 target: < 1.0 mg/L
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** A small protein produced at a constant rate by all nucleated cells and filtered freely by the glomeruli. Because its production rate is not affected by muscle mass, diet, or inflammation — unlike creatinine — cystatin C is a more accurate marker of glomerular filtration rate (GFR) and true kidney function.

**Why it matters.** Creatinine-based eGFR significantly underestimates kidney function decline in lean individuals (low muscle mass) and overestimates it in muscular individuals. Cystatin C-based eGFR resolves this bias, providing a more accurate early signal of renal decline. Elevated cystatin C is also independently associated with cardiovascular risk, even when creatinine is normal.

## eGFR / Estimated Glomerular Filtration Rate (`biomarker:egfr`)

- Unit: mL/min/1.73m²
- Medicine 3.0 target: > 90 mL/min/1.73m² (Cystatin C-based preferred)
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** An estimated measure of how much blood the kidneys filter per minute, adjusted for body surface area. Calculated from serum creatinine (or preferably cystatin C) using validated equations (CKD-EPI is the current standard). Reflects the overall functional capacity of the nephron pool.

**Why it matters.** eGFR is the primary clinical metric for staging chronic kidney disease (CKD) and tracking renal function over time. Declining eGFR — even within the "normal" range above 90 — tracked longitudinally reveals trajectory toward CKD. Longitudinal eGFR trends provide educational context for discussing kidney function trajectories with your physician, alongside a cystatin C–based eGFR, which isn't affected by muscle mass and is often more accurate.

## PSA / Prostate Specific Antigen (`biomarker:psa`)

- Unit: ng/mL
- Medicine 3.0 target: < 2.5 ng/mL (age 40–59); track trend and density rather than absolute threshold
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** A glycoprotein produced exclusively by prostate epithelial cells. PSA circulates in low concentrations in blood and is elevated by prostate inflammation, benign prostatic hyperplasia (BPH), and prostate cancer.

**Why it matters.** PSA is the primary screening marker for prostate cancer in men, though its specificity is limited — many causes of PSA elevation are benign. Medicine 3.0 emphasises tracking PSA trend over time (velocity) and PSA density (PSA relative to prostate volume on imaging) rather than applying a fixed absolute threshold. A rising PSA from 1.0 to 2.5 ng/mL over three years is more informative than a single reading of 2.5 ng/mL. Important note: finasteride and dutasteride (used for BPH and hair loss) halve PSA readings — if a patient uses these medications, true PSA may be approximately double the measured value.

## Free PSA % (`biomarker:free-psa-pct`)

- Unit: %
- Medicine 3.0 target: > 20% = reassuring for benign cause
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** The percentage of total PSA that circulates unbound (free) in the blood, rather than complexed to proteins. It is calculated by dividing free PSA by total PSA and expressing as a percentage.

**Why it matters.** PSA elevation from a benign enlarged prostate (BPH) tends to produce more free, unbound PSA. PSA elevation from prostate cancer tends to produce proportionally less free PSA — cancer cells leak more protein-bound PSA. A free PSA above 20% is reassuring that the elevation is benign. A low free PSA (<10%) significantly raises the probability of cancer and typically warrants mpMRI or biopsy. This marker adds precision to the PSA picture before any invasive decision is made.

## PSA Density (`biomarker:psa-density`)

- Unit: ng/mL/cc
- Medicine 3.0 target: ≤ 0.10 (ideal); > 0.10–0.12 suspicious in younger men; > 0.15 suspicious in older men
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** PSA divided by prostate volume (measured by MRI or transrectal ultrasound). It normalises PSA for prostate size — a PSA of 6 ng/mL in a 20cc prostate is very different from the same reading in an 80cc prostate.

**Why it matters.** PSA density significantly improves the specificity of PSA for detecting clinically significant cancer. A large prostate can produce high PSA simply because of its size — PSA density strips out this confounding factor. Men with elevated PSA density (> 0.15) in the presence of a negative or equivocal mpMRI still require biopsy, because MRI can occasionally miss small high-grade cancers. Requires prostate volume measurement — either from mpMRI (preferred) or TRUS.

## PSA Velocity (`biomarker:psa-velocity`)

- Unit: ng/mL/year
- Medicine 3.0 target: < 0.45 ng/mL/year; > 0.45 = significant; any rapid rise warrants re-evaluation
- Group: Vital Organ Integrity: Hepatic & Renal

**What it measures.** The rate of change in PSA over time — how many ng/mL it rises per year. Not a direct lab value — it is derived from the longitudinal tracking record. Halor computes it by linear regression of all logged PSA values against time — the method recommended over the simpler first-and-last or arithmetic-average approaches — and requires at least three measurements spanning ≥ 18 months for a reliable result.

**Why it matters.** A PSA level that is stable over years carries very different clinical meaning from one that is rising rapidly. Rate of change over time is one of the most clinically informative dimensions of PSA — a steadily rising trend may be significant even when the absolute value remains below a standard threshold. PSA velocity is the reason serial tracking matters: without a trend, any single PSA reading is incomplete information. Discuss your PSA trend with a urologist — velocity is one of several factors considered alongside PSA density and imaging in prostate cancer risk assessment. Many practitioners view a velocity above 0.45 ng/mL/year as a signal worth raising with your physician.

## Haemoglobin (`biomarker:hemoglobin`)

- Unit: g/dL
- Medicine 3.0 target: Men 13.5–17.5 g/dL · women 11.7–15.5 g/dL
- Group: Nutrients & Haematology

**What it measures.** The iron-containing protein in red blood cells responsible for oxygen transport from lungs to tissues and carbon dioxide removal. Haemoglobin concentration reflects the overall capacity of the blood to carry oxygen.

**Why it matters.** Low haemoglobin (anaemia) causes fatigue, reduced exercise capacity, cognitive impairment, and cardiovascular strain. High haemoglobin can reflect dehydration, polycythaemia vera, or — in athletes using erythropoietin — doping. In older adults, haemoglobin decline is associated with increased frailty, hospitalisation, and mortality. Haemoglobin integrates iron status, B12, folate, and bone marrow function into a single functional output.

## Ferritin (`biomarker:ferritin`)

- Unit: ng/mL
- Medicine 3.0 target: Men 30–400 ng/mL · women 30–150 ng/mL
- Group: Nutrients & Haematology

**What it measures.** The primary intracellular iron storage protein. Serum ferritin is the standard marker of total body iron stores — it is low in iron deficiency and elevated in iron overload states.

**Why it matters.** Iron deficiency — even before anaemia develops — impairs cognitive function, exercise capacity, immune function, and thyroid hormone metabolism. Ferritin below 30 ng/mL (and particularly below 12 ng/mL) indicates depleted iron stores and warrants investigation of dietary intake and blood loss. Conversely, elevated ferritin can reflect iron overload (haemochromatosis) or, importantly, acute-phase inflammation — ferritin rises non-specifically during inflammatory states, making it a dual marker.

## Vitamin D (`biomarker:vitamin-d`)

- Unit: ng/mL
- Medicine 3.0 target: 30–80 ng/mL
- Group: Nutrients & Haematology

**What it measures.** Serum 25-hydroxyvitamin D (25-OHD) — the circulating storage form of vitamin D, produced in the liver from dietary vitamin D and skin-synthesised cholecalciferol following UV-B exposure. The 25-OHD test is the standard measure of vitamin D status.

**Why it matters.** Vitamin D deficiency is widespread globally — estimated at 40% prevalence in the USA — and is associated with impaired bone mineralisation, immune dysfunction, muscle weakness, depression, and increased risk of multiple chronic diseases. Receptors for the active form of vitamin D (1,25-OH2D) are present in virtually every cell type. Optimal vitamin D status (75–200 nmol/L, or 30–80 ng/mL) is associated with reduced risk of respiratory infections, autoimmune disease, and several cancers. Note: jurisdictional sufficiency thresholds vary (50 vs. 75 nmol/L, or 20 vs. 30 ng/mL), reflecting different evidence interpretations.

## Vitamin B12 (`biomarker:vitamin-b12`)

- Unit: pg/mL
- Medicine 3.0 target: 400–771 pg/mL
- Group: Nutrients & Haematology

**What it measures.** The serum concentration of cobalamin — an essential water-soluble vitamin required for DNA synthesis, red blood cell formation, and neurological function, particularly myelin synthesis. B12 is found exclusively in animal-derived foods and requires intrinsic factor from the stomach for absorption.

**Why it matters.** B12 deficiency causes megaloblastic anaemia, peripheral neuropathy, subacute combined degeneration of the spinal cord, and — often preceding haematological changes — cognitive and neurological impairment. Deficiency is common in vegans/vegetarians, elderly individuals (reduced intrinsic factor secretion), and those on long-term metformin or proton pump inhibitors. Note: MTHFR gene variants may impair B12 utilisation, requiring the methylcobalamin form rather than cyanocobalamin supplementation for adequate cellular uptake.

## RBC Magnesium (`biomarker:rbc-magnesium`)

- Unit: mg/dL
- Medicine 3.0 target: 4.2–6.8 mg/dL
- Group: Nutrients & Haematology

**What it measures.** Magnesium concentration within red blood cells. RBC magnesium reflects intracellular magnesium status — the biologically relevant pool — as distinct from serum magnesium, which measures only the extracellular fraction (approximately 1% of total body magnesium).

**Why it matters.** Magnesium is a cofactor for over 300 enzymatic reactions including ATP production, DNA repair, insulin signalling, and neuromuscular function. Serum magnesium is maintained within a narrow range by hormonal regulation even when total body stores are significantly depleted — making serum magnesium an inadequate proxy for magnesium status. RBC magnesium provides a more accurate window into intracellular deficiency, which is common with processed food diets, diuretic use, alcohol consumption, and diabetes. Deficiency is associated with hypertension, insulin resistance, cardiac arrhythmias, and muscle cramps.

## Omega-3 Index (`biomarker:omega-3-index`)

- Unit: %
- Medicine 3.0 target: > 8%
- Group: Nutrients & Haematology

**What it measures.** The combined proportion of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) as a percentage of total fatty acids in the red blood cell membrane. RBC fatty acid composition reflects dietary omega-3 intake and tissue incorporation over the preceding 8–12 weeks.

**Why it matters.** A low Omega-3 Index (below 4%) is associated with increased risk of sudden cardiac death, ASCVD, cognitive decline, and systemic inflammation. An index above 8% is the target associated with cardiovascular protection in prospective studies. Most Western populations have an index of 4–6%. The RBC-based measurement is far more meaningful than simply measuring plasma omega-3 levels, which reflect recent intake rather than tissue incorporation.

## ALMI — Appendicular Lean Mass Index (`biomarker:almi`)

- Unit: kg/m²
- Medicine 3.0 target: The top quartile for your age and sex — read your kg/m² value against age- and sex-matched percentile curves with your physician.
- Group: Body Composition (DEXA)

**What it measures.** Muscle mass in the arms and legs divided by height squared (kg/m²). The most accurate proxy for functional skeletal-muscle strength and the first measure to decline with age. Preferred over total lean mass and Fat-Free Mass Index (FFMI), which are diluted by organ and water mass.

## VAT — Visceral Adipose Tissue (mass) (`biomarker:vat`)

- Unit: g
- Medicine 3.0 target: Lower is better — read your gram value against age- and sex-matched percentile curves with your physician; around the 50th percentile is a clinical red flag.
- Group: Body Composition (DEXA)

**What it measures.** The metabolically active, inflammatory fat stored around the internal organs — biologically distinct from subcutaneous fat.

## Body fat % (`biomarker:body-fat-pct`)

- Unit: %
- Medicine 3.0 target: None specified — VAT and ALMI carry the signal.
- Group: Body Composition (DEXA)

**What it measures.** The proportion of total body mass that is fat.

## FFMI — Fat-Free Mass Index (`biomarker:ffmi`)

- Unit: kg/m²
- Medicine 3.0 target: Interpret against age- and sex-matched percentile curves with your physician — ALMI carries the primary muscle signal.
- Group: Body Composition (DEXA)

**What it measures.** Total lean mass divided by height squared (kg/m²). A broader lean-mass index than ALMI — it includes organ and water mass, which is why ALMI is preferred as the skeletal-muscle signal. Logged alongside ALMI on the standard DEXA analysis worksheet.

## BMD Left Femur (`biomarker:bmd-left-femur-t`)

- Unit: T-score
- Medicine 3.0 target: Stay above a T-score of −1.0: −1.0 or higher is normal, −1.0 to −2.5 is low bone mass (osteopenia), −2.5 or below is osteoporosis. Any finding of osteopenia warrants prompt attention.
- Group: Body Composition (DEXA)

**What it measures.** Bone mineral density at the left femur, as a T-score — standard deviations versus a healthy young-adult reference. Sites are reported separately because they can diverge; the lowest measured site carries the clinical read. The Z-score reports the same density against your own age and sex group, alongside the T-score.

## BMD Right Femur (`biomarker:bmd-right-femur-t`)

- Unit: T-score
- Medicine 3.0 target: Stay above a T-score of −1.0: −1.0 or higher is normal, −1.0 to −2.5 is low bone mass (osteopenia), −2.5 or below is osteoporosis. Any finding of osteopenia warrants prompt attention.
- Group: Body Composition (DEXA)

**What it measures.** Bone mineral density at the right femur, as a T-score — standard deviations versus a healthy young-adult reference. Sites are reported separately because they can diverge; the lowest measured site carries the clinical read. The Z-score reports the same density against your own age and sex group, alongside the T-score.

## BMD Lumbar Spine (`biomarker:bmd-spine-t`)

- Unit: T-score
- Medicine 3.0 target: Stay above a T-score of −1.0: −1.0 or higher is normal, −1.0 to −2.5 is low bone mass (osteopenia), −2.5 or below is osteoporosis. Any finding of osteopenia warrants prompt attention.
- Group: Body Composition (DEXA)

**What it measures.** Bone mineral density at the lumbar spine (L1–L4), as a T-score — standard deviations versus a healthy young-adult reference. Sites are reported separately because they can diverge; the lowest measured site carries the clinical read. The Z-score reports the same density against your own age and sex group, alongside the T-score.


### PEF
# Halor Physician Engagement Framework (PEF)

Use these to draft physician-prep briefs: questions + what to leave the visit with. Do not diagnose or prescribe.

## ASCVD — PHYSICIAN PREP

_Questions, imaging status, and an exit checklist to bring to your ASCVD conversation._

## Previous Imaging / Lipid Management Status
- No previous imaging
- Previous CAC scan — share the results directly with your physician
- Previous CCTA — share the results directly with your physician
- Currently on lipid management therapy {lfield:Drug name} {lfield:Daily dose}

## What I need to leave with
- A clear imaging recommendation — CCTA, CAC, or neither — with the specific clinical reasoning
- The name of the imaging centre my physician recommends, and confirmation they use low-dose protocol
- A specific ApoB target
- A clear yes/no/not yet on ASCVD pharmacotherapy, with the specific clinical reasoning
- If yes, the drug or combination selected, with dose and titration schedule
- The monitoring cadence (lipid panel recheck timing, liver enzymes if applicable, etc.)
- The trigger conditions for escalating therapy (e.g. if ApoB target not met at first recheck)

## BRAIN HEALTH — PHYSICIAN PREP

_Your risk picture, questions, and an exit checklist for your brain-health conversation._

## My brain-health picture & risk factors
- Family history of Alzheimer's or dementia — who, and age of onset {field:e.g. grandmother ~70; none known}
- APOE status, if known {field:e.g. 3/3, 3/4, 4/4, or untested}
- Cognitive changes I've noticed, and for how long {field:memory, word-finding, focus — and duration; or none}
- Which of the modifiable dementia risk factors apply to me {field:e.g. hearing loss, hypertension, inactivity, periodontal disease, social isolation}
- Where I stand on the shared vascular/metabolic levers {field:ApoB, blood pressure, fasting insulin/glucose — values or "unsure"}
- Dental/periodontal health — any gum disease, and when I was last seen {field:e.g. treated gum disease; last cleaning ~6 mo ago; unsure}

## What I need to leave with
- Whether my family history warrants a one-time APOE genotype test — and the reminder that the prevention plan is the same either way; the result informs intensity, not strategy
- Confirmation my vascular and metabolic risk factors (ApoB, blood pressure, glucose/insulin) are managed to targets that protect the brain, not just the heart — what's good for the heart is good for the brain
- Whether my dental/periodontal health needs attention — untreated periodontal disease is a modifiable inflammatory lever that can accelerate Alzheimer's, especially for APOE4 carriers
- Which of the modifiable dementia risk factors I can act on first — prioritising the simplest fixes (e.g. hearing loss, hypertension, physical inactivity, periodontal disease, social isolation)
- An exercise plan that includes Zone 2, Zone 5 (VO₂ max) and strength training — the combination is more neuroprotective than any one alone (cerebral blood flow + VO₂ max + BDNF)
- Whether my sleep should be formally evaluated (e.g. for apnea) — deep sleep runs the glymphatic clearance of amyloid-beta and tau
- A plan to establish a cognitive baseline now with a validated assessment, repeated about once a year, so the trend shows early

## CANCER SCREENING — PHYSICIAN PREP

_Questions, your screening profile, and an exit checklist for your cancer screening conversation._

## My screening profile
- Personal cancer history {field:type, year, treatment — or any pre-cancerous findings}
- Key risk exposures {field:e.g. smoking pack-years, radon, alcohol, IBD, HBV/HCV, high UV}
- Standard screening done, with dates & results {field:e.g. colonoscopy, mammogram/BIRADS, PSA, Pap/HPV, LDCT/Lung-RADS}
- Advanced screening done, with dates & results {field:e.g. liquid biopsy/MCED, WB-MRI, mole mapping, genetic counselling}

## What I need to leave with
- Clear recommendations on the core screens that apply to me — colonoscopy (timing and interval), [PSA monitoring|mammography protocol (standard or high-risk, plus any supplemental imaging)], and lung LDCT — each with the reasoning
- A cancer screening schedule covering all cancers relevant to my profile — confirmed, adjusted, or new
- Whether my family history and/or genetic variants qualify me for any accelerated or specialist-led screening
- A clear yes/no/not yet on each advanced tool (liquid biopsy, WB-MRI, prostate mpMRI), and if yes: the platform or centre, baseline timing, and what a positive result would trigger
- A clear conversation about false positives before committing to advanced tools — the incidental findings that are likely, the follow-up they trigger, and the psychological and financial cost
- A defined next-review date for my cancer screening conversation

## MY BLOODWORK

_Your most recent bloodwork results, surfaced for your physician._



## MY DEXA SCAN

_Your most recent DEXA scan values, surfaced for your physician._



## FAMILY HISTORY

_Your logged family history, surfaced for your physician._



## HORMONE REPLACEMENT THERAPY — PHYSICIAN PREP

_Questions, your menopause status and history, and an exit checklist for your HRT conversation._

## My menopause status & history
- Menopause stage {field:peri, post, surgical, or unsure}
- Current or prior HRT {field:what, when, and why stopped}
- Main symptoms, and how long {field:symptoms & duration}
- Relevant history — breast cancer/DCIS, blood clots (DVT/PE), cardiovascular disease/stroke, endometriosis/fibroids, or unexplained spotting {field:which apply}

## What I need to leave with
- Which breast imaging, if any, is needed before starting
- Whether any endometrial assessment (transvaginal ultrasound or biopsy) is needed before starting
- A clear yes/no/not yet on HRT, with the reasoning — and if yes, the specific estradiol/progesterone, dose, application site, and titration
- Whether local vaginal therapy is needed, and how it relates to systemic HRT
- A decision on testosterone (yes/no/not yet) with the reasoning — and if yes, the formulation, dose, application site, and titration
- A lab monitoring plan — which tests, which assay method, and how often
- A long-term plan: duration, what would change it, and (if not starting now) what would prompt revisiting

## METABOLIC HEALTH — PHYSICIAN PREP

_Questions and an exit checklist to bring to your metabolic health conversation._

## What I need to leave with
- The biomarker target(s) we're aiming for (specific value, not a range)
- A clear yes/no/not yet on metabolic pharmacotherapy, with the specific clinical reasoning
- If yes, a specific drug, dose, and titration schedule
- The monitoring cadence (how often, which labs)
- The trigger conditions for a dose change or agent switch
- A plan for protecting lean mass during any weight loss phase — including an ALMI target appropriate for my age and sex, and a VAT reduction goal
- A defined review date
- Exit criteria — what success looks like and what happens after

## LIFESTYLE

_A measurable record of your lifestyle effort — the clearest signal you can give your physician._

## Zone 2 training
id: zone-2
placeholder: e.g. 120 minutes per week

## Resistance training
id: resistance
placeholder: e.g. 3 sessions per week

## VO2 Max training
id: vo2-max
placeholder: e.g. 1 session per week

## Stability and mobility work
id: stability-mobility
placeholder: e.g. 2 sessions per week

## Sleep
id: sleep
placeholder: e.g. 7.2 hrs average · restoration score typically 3–4/5

## Protein intake
id: protein
placeholder: e.g. ~130g/day

## Calorie management
id: calorie
placeholder: e.g. ~300 kcal deficit

## MY NOTES

_Free-text notes for this conversation. Always included, exported at the top of the document._



## THYROID HEALTH — PHYSICIAN PREP

_Questions, your status and symptoms, and an exit checklist for your thyroid conversation._

## My thyroid status & symptoms
- Diagnosis & treatment status {field:e.g. hypothyroid on levothyroxine; Hashimoto's; none}
- Current thyroid medication, if any {field:drug & dose}
- Relevant history — thyroidectomy or radioactive iodine {field:which, if any}
- Main symptoms, and how long they've been present {field:symptoms & duration}

## What I need to leave with
- The target lab ranges my physician is aiming for in my case
- What further testing is needed — e.g. thyroid ultrasound, or TPO antibodies to check for an autoimmune (Hashimoto's) process
- A clear yes/no/not yet on thyroid therapy, with the reasoning — and if yes, the drug or combination, dose, and titration
- If I'm on levothyroxine with persistent symptoms: a clear plan for next steps, and the reasoning behind it
- A cholesterol/lipid review, and whether metabolic drivers (insulin resistance, inflammation) need addressing as part of thyroid optimisation

## TESTOSTERONE REPLACEMENT THERAPY — PHYSICIAN PREP

_Questions, your symptoms, and an exit checklist to bring to your TRT conversation._

## My status & symptoms
- Current or prior testosterone therapy {field:what, when, and why stopped}
- Main symptoms, and how long they've been present {field:symptoms & duration}

## What I need to leave with
- A clear yes/no/not yet on TRT, with the reasoning — and if yes, the formulation, dose, and injection or application protocol
- A complete monitoring plan — labs (Total T, Free T, SHBG, estradiol, hematocrit/haemoglobin, PSA), frequency, and thresholds for intervention
- Whether a sleep apnea assessment is needed (testosterone can worsen existing sleep apnea)
- A clear answer on estradiol management
- A fertility plan
- If not starting now: what to address first, and when to retest