Your body, connected

Explore your body.

See how each organ ages, what to measure, and where to begin.

Filter by focus

Detailed human anatomy illustration showing internal organs

Active View: Brain & Cognition

View organ details Press 1-8 to choose an organ. Esc resets the view. Tap a pin to explore.

NEUROLOGICAL HEALTH

Brain & Central Nervous System

Cognitive reserve, synaptic plasticity, and slow-wave waste clearance.

Perfusion Rate 750 mL / min

Energy Demand 20% Whole Body

Glymphatic Window 02:00 - 04:00 AM

Compare tissue aging

Cellular Tissue Inspector

PHYSIOLOGICAL PEAK Optimal youthful function

High synaptic density, intact blood-brain barrier integrity, active neurogenesis in the dentate gyrus, and pulsatile clearance of metabolic waste during slow-wave sleep.

How it ages

As we age, microvascular blood flow to the brain decreases, synaptic density diminishes, and chronic microglial neuroinflammation rises. Crucially, the glymphatic waste system (which pulses cerebrospinal fluid through the brain during deep slow-wave sleep) becomes less efficient, permitting misfolded amyloid-beta and hyperphosphorylated tau proteins to aggregate.

What to measure

BDNF (Neurogenesis) Phospho-Tau 181 / 217 hs-CRP < 0.5 mg/L Cerebral Perfusion MRI

Everyday habits

Glymphatic Sleep Optimization: 7.5 to 8.5 hours in complete darkness and a cool environment (19°C / 66°F). Side-sleeping (lateral posture) maximizes gravitational and pulsatile cerebrospinal waste flush.
BDNF Aerobic Induction: 35-45 minutes of steady Zone 2 cardio paired with weekly high-intensity intervals triggers massive increases in circulating BDNF, stimulating hippocampus neurogenesis.
Heat Shock Protein Response: 20 minutes in a dry Finnish sauna (80°C) 4 to 7 times weekly is associated with a 66% lower risk of Alzheimer’s and dementia (Kuopio Ischemic Heart Disease Study).
Continuous Cognitive Demand: Actively learning unfamiliar motor-cognitive skills (new languages, instruments, ballroom dance, or tennis) forces novel neural pathway formation.

02Primary mortality drivers

The Four Diseases That Cause 80% of Adult Deaths

For individuals over age 50 who do not smoke, the vast majority of mortality is caused by four slow-developing chronic conditions. Longevity medicine is about delaying their biological onset by 10 to 20 years.

Cardiovascular #1 Global Killer

Atherosclerotic Heart Disease (ASCVD)

Caused by circulating ApoB-containing lipoproteins that penetrate the endothelial arterial wall, oxidize, and trigger calcified plaque over decades until blood flow to the heart or brain is obstructed.

Primary Diagnostic: ApoB particle count + CAC scan

Longevity Target: ApoB < 60 mg/dL • CAC Score: 0

Oncology #2 Global Killer

Cancer & Somatic Mutation

Driven by cumulative DNA replication errors, oxidative damage, and the gradual decline of immune surveillance that allows mutated rogue cells to escape apoptosis and proliferate unchecked.

Primary Diagnostic: Colonoscopy, Low-Dose CT, Multi-Cancer Blood

Longevity Target: Early Stage 0/1 Detection

Neurology Cognitive Healthspan

Neurodegenerative Decline (Alzheimer's)

Progressive synaptic loss, microglial neuroinflammation, and failure of glymphatic waste clearance during deep sleep, leading to amyloid-beta aggregation and hyperphosphorylated tau tangles.

Primary Diagnostic: p-Tau 217, ApoE Genotyping, Volumetric MRI

Longevity Target: Sustain Deep Slow-Wave Sleep

Metabolic Underlying Multiplier

Metabolic Syndrome & Type 2 Diabetes

The underlying catalyst that accelerates the other three diseases. Driven by ectopic fat spilling into the liver and pancreas, chronic hyperinsulinemia, and endothelial glycocalyx erosion.

Primary Diagnostic: Fasting Insulin, HOMA-IR, Continuous Glucose

Longevity Target: Fasting Insulin < 5 µIU/mL

03CLINICAL TRAJECTORY ENGINE Fries & Attia Model

Compression of Morbidity Trajectory Simulator

Explore the idea of spending more years in good health. These illustrative curves cannot predict your lifespan, years of illness or need for care.

Model inputs

Adjust Longevity Levers

Adjust the inputs to compare illustrative scenarios. This is not a clinical prediction.

Benchmark Scenarios:

Zone 2 Aerobic Base (hours / week) 3.0 hrs/wk

Elite fitness was associated with 80% lower mortality than low fitness in one observational cohort.

Resistance Training (sessions / week) 3 sessions

Preserves bone mineral density, neuromuscular coordination, and protects against late-life falls.

ApoB Lipid Target (mg/dL) 60 mg/dL

Sub-60 mg/dL prevents atheroma formation, halting coronary artery calcification.

Sleep Quality & Duration (hours / night) 7.5 hrs/night

Powers nightly glymphatic waste clearance and restorative hormonal regulation.

Illustrative Lifespan 88.4 yrs Model output, not a prediction

Illustrative Healthspan 85.8 yrs Above the model reference

Morbidity Window 2.6 yrs Compressed by 84%

Functional capacity by age

Your illustrative scenario
Comparison (16 illness years)
Earlier decline scenario
35%Illustrative capacity reference

CLINICAL PRINCIPLE

This illustration explores healthier aging. It cannot predict your lifespan, years of illness or need for care.

04CARDIORESPIRATORY BIOMARKER Fitness and longevity

VO2 Max & All-Cause Mortality Hazard Curve

Higher fitness was associated with lower mortality in an observational study of 122,007 patients. This curve is an illustration, not a personal risk assessment.

Your inputs

Drag to adjust

Biological Sex

Chronological Age 40 years

VO2 Max (mL / kg / min) 44.0 mL/kg/min

Apple Watch / Garmin / Lab

Cooper 12-min Run Equiv

~2,450meters

ALL-CAUSE MORTALITY HAZARD RATIO

1.41x

Elevated Relative Risk (vs. Elite Baseline HR 1.0)

VO2 Max (mL / kg / min)Shaded bands follow your age and sex cohort

Cohort percentile 65th Percentile

ABOVE AVERAGE

Low<25th
Below average25th-49th
Above average50th-74th
High75th-97th
Elite>97.5th

This input falls in the model's above average range. Higher fitness is associated with lower mortality, but this does not quantify your personal risk.

EXAMPLE TRAINING STRUCTURE:

Norwegian 4x4 Intervals: Perform 1 weekly session (4 minutes at 90-95% max HR, followed by 3 minutes active recovery, repeated 4 times). Paired with 150 minutes of Zone 2 steady cardio, this induces rapid mitochondrial biogenesis and expands stroke volume by 0.5-1.0 mL/kg/min per month.

Session structure4 x 4 min work, 3 min recovery

90-95% max HR Active recovery

05CARDIOVASCULAR RISK MODEL Area-Under-The-Curve

Lifetime ApoB Atherosclerosis Exposure Projector

Lower ApoB over time can reduce cardiovascular risk. This chart illustrates exposure, not plaque volume or event timing. Its 9,000 reference is not a clinical threshold. Read the evidence.

Your inputs Drag to adjust

Current Baseline ApoB (mg/dL) 120 mg/dL

Average adult baseline is 100-130 mg/dL without lipid management.

Age Initiating Intervention (years) 38 years

Earlier lipid lowering can reduce cumulative exposure. Treatment depends on individual risk.

Target ApoB on Protocol (mg/dL) 50 mg/dL

Optimal longevity target is < 60 mg/dL (achievable with diet + statin/ezetimibe/PCSK9i).

Cumulative exposure curve Illustrative ApoB exposure by age, mg·years/dL

MODELED APOB EXPOSURE AT AGE 80

6,660 mg·years/dL

30.6% Lifetime Exposure Reduction

MODEL REFERENCE

Below reference at age 80 Unchanged inputs: Model reference reached at age 75

Lifetime exposure at 80 Shared scale

Untreated Natural Trajectory 9,600 mg·yr (Above Model Reference)

With Early Intervention at Age 38 6,660 mg·yr (Below Reference at Age 80)

9,000 Model Reference

Clinical Takeaway:

Lower ApoB reduces modeled exposure through age 80. Cardiovascular risk also depends on other factors.

06CHRONOBIOLOGICAL BLUEPRINT Circadian Architecture

24-Hour Actionable Longevity Protocol Engine

Circadian biology governs gene transcription, cellular repair, hormonal pulses, and metabolic clearance. Select your individual lifestyle archetype below to generate an actionable, hour-by-hour operational schedule backed by peer-reviewed clinical science.

Choose an archetype Arrow keys switch

Circadian dial High-Stress Professional

Protocol phases
Feeding window
Sleep

Primary Objective Autonomic Nervous System Balance & Cortisol Taper

Circadian Anchor 06:30 AM Light Exposure / 22:30 PM Sleep

Feeding Window 10:00 AM - 18:30 PM (16:8 Time-Restricted)

Hour-by-hour schedule

07QUANTITATIVE ASSESSMENT

Lifestyle aging illustration

Explore an illustrative model of sleep and movement. It does not measure biological age, predict lifespan or diagnose health. Clinical PhenoAge requires blood biomarkers and is not calculated here.

Your inputs Drag to adjust

Your Current Chronological Age 38 years

Your age sets the baseline for this illustration.

Zone 2 Aerobic Exercise (minutes / week) 180 mins / wk

Aerobic activity supports fitness. This model does not measure changes in biological aging.

Nightly Restorative Sleep (hours) 7.5 hours

Under 6 hours nightly doubles cardiovascular event risk and impairs cellular waste clearance.

Resistance & Strength Training (days / week) 3 days / wk

Preserving lean muscle mass and grip strength is the single best defense against physical frailty past age 60.

Model contributions

Zone 2 cardio -
Sleep -
Strength -

YOUR ILLUSTRATION Lifestyle model

Illustrative age

31.8 years

Model vs chronological age

6.2 Years Below the Model Baseline

Chronological 38 yrs
Illustrative 31.8 yrs

Illustrative Pace Index 0.84x (Below baseline) A model index, not a measured rate of aging.

Illustrative Healthspan 91 Years An illustration, not a forecast of healthy years.

Key Priority for You:

Regular aerobic activity supports fitness. Build a routine that fits your ability and health.

LONGEVITY BAE - PREVENTATIVE LAB PANEL

Official Reference: longevitybae.com

Date: ___________________

Patient: ___________________

Physician: ___________________

Please consider authorizing the following advanced preventative biomarkers during this physical exam.

08ACTIONABLE CLINICAL TOOL Take to Your Doctor

The Longevity Blood Panel: Tests to Request

Standard annual physicals typically only order basic total cholesterol and fasting glucose, which can miss early cardiovascular and metabolic disease by a decade. Bring this checklist to your physician to request the tests that actually measure lifespan drivers.

Tick the tests you want to raise
Print a clean sheet
Bring it to your appointment

Lab requisition Preventative biomarker panel

Selections are saved on this device

Marked for discussion 0 of 7 tests marked for discussion

Ask	Biomarker	Standard Range	Optimal Longevity Target	Clinical Significance
	Apolipoprotein B (ApoB) Superior to LDL-C	< 90 mg/dL	< 60 mg/dL	Directly measures the number of atherogenic, plaque-causing particles in your bloodstream.
Pathophysiological Mechanism: Every circulating ApoB lipoprotein particle can cross into the arterial sub-endothelial space. Once trapped, it oxidizes and triggers sterile inflammation, macrophage recruitment, and calcified fibrous plaque growth. First-Line Interventions: Limit dietary saturated fatty acids (< 10g/day); supplement 10g soluble psyllium husk; consider statins, ezetimibe, or PCSK9 inhibitors under physician guidance. Testing Frequency: Every 6 to 12 months until target (< 60 mg/dL) is achieved; annually thereafter.
	Lipoprotein(a) [Lp(a)] Genetically determined	< 75 nmol/L	< 30 nmol/L	Independent genetic risk factor for early heart attack and stroke. Only needs to be tested once in life.
Pathophysiological Mechanism: Lp(a) contains an ApoB molecule covalently bound to apolipoprotein(a), which resembles plasminogen and promotes vascular thrombosis while aggressively depositing oxidized phospholipids into vascular walls. First-Line Interventions: Genetically fixed (diet changes have minimal effect). If elevated (> 100 nmol/L), aggressively drive other risk factors to absolute minima: target ApoB < 50 mg/dL and blood pressure < 120/80 mmHg. Testing Frequency: Once in a lifetime (levels remain stable across adulthood).
	Fasting Serum Insulin Early metabolic warning	< 20 µIU/mL	< 5 µIU/mL	Spikes up to 10 years before fasting glucose rises, detecting insulin resistance at the reversible stage.
Pathophysiological Mechanism: Chronically elevated insulin drives ectopic fat accumulation in the liver, accelerates systemic endothelial damage, impairs sodium excretion (raising blood pressure), and shuts down cellular autophagy. First-Line Interventions: Eliminate refined carbohydrates and liquid sugars; adopt 16:8 time-restricted feeding; perform post-meal 10-minute walks; lift heavy weights 3x/week to trigger non-insulin glucose disposal via GLUT-4. Testing Frequency: Every 3 to 6 months to evaluate metabolic interventions.
	hs-CRP (High-Sensitivity) Vascular inflammation	< 3.0 mg/L	< 0.5 mg/L	Quantifies low-grade systemic vascular inflammation that destabilizes arterial plaques and promotes decline.
Pathophysiological Mechanism: High-sensitivity C-reactive protein is an acute-phase reactant synthesized by the liver in response to interleukin-6. It reflects chronic sterile vascular inflammation that weakens fibrous caps over plaques, precipitating heart attacks. First-Line Interventions: Reduce visceral adipose tissue (VAT); sauna bathing 4-7x/week; prioritize 7.5+ hours of sleep; supplement high-dose purified omega-3 fatty acids (2-4g EPA/DHA daily). Testing Frequency: Annually, or every 6 months during active anti-inflammatory protocol changes.
	Hemoglobin A1c (HbA1c) 3-Month glucose average	< 5.7%	< 5.2%	Reflects glycosylation of red blood cells. Lower levels reduce advanced glycation end-products (AGEs).
Pathophysiological Mechanism: Glycation of hemoglobin reflects whole-body exposure to elevated blood glucose. Chronic glucose excursions cross-link extracellular collagen, stiffen coronary arteries, and damage renal microvasculature. First-Line Interventions: Pair carbohydrates with soluble fiber and healthy fats; engage in Zone 2 aerobic base training to expand mitochondrial fat-burning capacity; supplement berberine or alpha-lipoic acid if indicated. Testing Frequency: Every 3 to 6 months (reflects red blood cell lifespan of ~120 days).
	Serum Homocysteine Methylation & vascular health	< 15 µmol/L	< 9 µmol/L	Elevated levels damage endothelial lining and correlate with cognitive decline; easily modulated with B vitamins.
Pathophysiological Mechanism: An intermediate sulfur amino acid in the methionine-cysteine cycle. When methylation cofactors are deficient or MTHFR variants are present, homocysteine accumulates, stripping nitric oxide and promoting cerebral white matter hyperintensities. First-Line Interventions: Supplement with bioactive methylated cofactors: L-methylfolate (5-MTHF 400-800 µg), methylcobalamin (B12 1,000 µg), pyridoxal-5-phosphate (P5P 25-50 mg), and trimethylglycine (TMG 500-1,000 mg). Testing Frequency: Every 6 to 12 months.
	25-Hydroxy Vitamin D3 Immune & bone regulator	> 30 ng/mL	50 - 70 ng/mL	Critical for thousands of gene transcription pathways, immune defense, and bone mineral density preservation.
Pathophysiological Mechanism: A secosteroid hormone that binds to the nuclear Vitamin D Receptor (VDR) across nearly every human tissue. Maintains calcium homeostasis, suppresses autoimmune self-reactivity, and protects bone mineral matrix. First-Line Interventions: Daily oral Vitamin D3 (2,000 - 5,000 IU) paired synergistically with Vitamin K2 (MK-7 100 µg) and magnesium to direct calcium into bones and teeth rather than arterial vascular walls. Testing Frequency: Every 6 months (especially at end of winter and end of summer).

Tick the tests you want to raise, then print a clean sheet for your appointment. Press P to print