Your entire health picture. One number.

ApoB measures the actual number of atherogenic particles in circulation, which is often more predictive of vascular risk than LDL alone.

Lp(a) is a genetically determined risk factor most clinicians never test. You cannot fully lifestyle your way out of elevated Lp(a), but it changes how aggressively other risks should be managed.

AIP (Atherogenic Index of Plasma) predicts atherosclerosis better than standard cholesterol snapshots. Foundation optimal is under 0.11; risk rises significantly above 0.24.

Homocysteine reflects methylation stress and metabolic disruption. Every 5 umol/L elevation above optimal is linked to ~40% higher heart disease and Alzheimer's risk.

Fasting insulin is often the earliest metabolic warning signal. Over half of people with elevated insulin still look 'normal' on glucose and A1c.

Glucose above ~85 mg/dL can create daily endothelial irritation long before diabetes thresholds are crossed.

HbA1c reflects ~120 days of glucose exposure and helps expose silent glycemic drift.

ESR reflects red-cell electrostatic behavior and inflammatory burden. The 'normal' 10-15 band has been linked to 136% higher all-cause mortality in apparently healthy people.

hsCRP is often dismissed as non-specific, but that broad responsiveness is exactly what makes it clinically powerful.

NLR amplifies hidden immune patterns by combining bacterial-leaning and viral/cancer-leaning directions into one prognostic signal.

WBC trend and level are deeply prognostic; chronic mild elevation is not benign.

Chlamydia pneumoniae (not the STI) is a respiratory intracellular pathogen linked in research to atherosclerosis and potentially neurodegenerative progression.

H. pylori can persist for years with minimal symptoms while driving gut barrier dysfunction, nutrient disruption, and chronic inflammatory cascades.

Foundation explicitly models chronic infection as a core mechanism in long-horizon disease risk-this is a major differentiator vs standard DTC panels.

TSH is a central pituitary-thyroid communication signal and often widens before overt thyroid disease is diagnosed.

TPO and Thyroglobulin antibodies expose autoimmune thyroid patterns that routine panels frequently miss.

Reverse T3 can rise under chronic stress states, functionally suppressing metabolic output despite 'normal' thyroid labs.

Vitamin D functions hormonally across immune, oncologic, and metabolic systems; bone-only thresholds understate its broader role.

Ferritin is bidirectional risk intelligence: deficiency and overload are both clinically meaningful.

Iron physiology requires panel-level interpretation; single-marker review is frequently misleading.

GGT is frequently an earlier liver stress signal than ALT/AST and can reflect oxidative and toxic burden.

Alkaline phosphatase provides hepatobiliary patterning that helps separate liver, bile, and bone-linked processes.

eGFR catches decline earlier than creatinine because kidneys have substantial reserve capacity.

BUN/Creatinine ratio offers strong hemodynamic and catabolic context often missed in single-marker review.

RDW is among the strongest vascular risk correlates and can surface endothelial stress long before overt disease events.

Hemoglobin reflects oxygen delivery capacity and iron biology simultaneously; both low and high states carry risk.

Cortisol AM anchors circadian stress axis function; chronic dysregulation cascades into sleep, glucose, immunity, and cognition.

BDNF is a central neuroplasticity and neuroprotection signal linked to learning and cognitive resilience.