Blood tests

Elevated fasting glucose signals insulin resistance and significantly raises the risk of type 2 diabetes, cardiovascular disease, and accelerated cellular aging. Even mildly elevated levels in the 90s are associated with worse long-term outcomes.

HbA1c reflects average blood glucose over the past 2–3 months. It is the most reliable long-term indicator of glycemic control and a strong predictor of diabetes risk, neuropathy, and cardiovascular complications.

Fasting insulin is one of the earliest markers of insulin resistance, often rising years before glucose becomes abnormal. High insulin drives fat storage, inflammation, cancer cell proliferation, and accelerated aging.

Elevated triglycerides indicate poor carbohydrate metabolism and are an independent risk factor for cardiovascular disease and pancreatitis. A level below 80 mg/dL strongly correlates with insulin sensitivity.

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is calculated from fasting glucose and insulin. It is the most practical clinical estimate of insulin resistance and predicts metabolic syndrome, type 2 diabetes, and cardiovascular risk.

LDL cholesterol is the primary driver of atherosclerotic plaque formation. Decades of causal evidence support lowering LDL to reduce heart attack and stroke risk. ApoB is a more precise measure, but LDL-C is widely available.

HDL cholesterol facilitates reverse cholesterol transport — removing LDL from arterial walls. Low HDL is a strong independent risk factor for cardiovascular disease, especially when combined with high triglycerides.

ApoB counts all atherogenic lipoprotein particles (LDL, VLDL, IDL, Lp(a)). It is a superior predictor of cardiovascular risk compared to LDL-C, particularly in metabolic syndrome. Many longevity physicians now use ApoB as the primary lipid target.

Lipoprotein(a) is a genetically-determined particle that independently raises cardiovascular and aortic stenosis risk. It cannot be meaningfully changed by lifestyle alone. Emerging RNA-based therapies are in late-stage trials.

High-sensitivity C-reactive protein is the most widely used marker of systemic inflammation. Chronic low-grade inflammation accelerates atherosclerosis, neurodegeneration, and all-cause mortality. Even levels between 1–3 mg/L meaningfully elevate cardiovascular risk.

Elevated homocysteine damages vascular endothelium and is associated with cardiovascular disease, cognitive decline, and Alzheimer's risk. It rises with deficiencies in B6, B12, and folate.

Systolic blood pressure is the single strongest modifiable risk factor for stroke, heart failure, and all-cause mortality. Risk rises continuously above 115 mmHg — there is no true threshold. Targeting 105–120 mmHg is associated with maximum longevity benefit.

Testosterone declines ~1% per year after age 30 in men. Low testosterone is associated with reduced muscle mass, increased visceral fat, depression, cognitive decline, and elevated cardiovascular risk. In women, adequate testosterone supports libido, mood, and bone density.

Only about 2% of testosterone circulates free (unbound). Free testosterone is the biologically active fraction and better reflects androgenic activity than total testosterone, especially when SHBG is elevated.

DHEA-S is the most abundant adrenal androgen and declines dramatically with age (often 80–90% by age 70). It serves as a precursor to testosterone and estrogen, and low levels correlate with frailty, immune senescence, and reduced quality of life.

IGF-1 (Insulin-like Growth Factor 1) mediates many effects of growth hormone and is crucial for muscle and bone maintenance. Very high levels are linked to increased cancer risk; very low levels are associated with frailty. A moderate optimal range balances anabolism and longevity signaling.

Morning cortisol (measured fasting, 8 am) reflects HPA-axis function. Chronically elevated cortisol suppresses immunity, raises blood glucose, causes muscle catabolism, disrupts sleep, and accelerates hippocampal atrophy. Chronically low cortisol may indicate adrenal insufficiency.

Thyroid-stimulating hormone controls the pace of metabolism. Subclinical hypothyroidism (elevated TSH) is common, often undiagnosed, and associated with fatigue, weight gain, elevated LDL, and depression. Optimizing TSH within the lower-normal range supports metabolic health.

Estimated glomerular filtration rate measures kidney filtering capacity. Declining eGFR predicts not just kidney failure but cardiovascular mortality, cognitive decline, and reduced lifespan. It should be trended over time.

Serum creatinine is a metabolic byproduct of muscle used to estimate kidney function. It should be interpreted alongside eGFR and muscle mass — very muscular individuals will have higher creatinine without kidney disease.

Alanine aminotransferase is a liver enzyme that leaks into the bloodstream when liver cells are damaged. It is the most sensitive routine marker of liver injury. Fatty liver disease — increasingly prevalent — causes chronically elevated ALT even when 'within range.'

Aspartate aminotransferase is present in liver, heart, muscle, and kidneys. While less liver-specific than ALT, the AST/ALT ratio (De Ritis ratio) is diagnostically useful: a ratio > 2 suggests alcoholic liver disease; muscle damage elevates AST more than ALT.

Gamma-glutamyl transferase is highly sensitive to alcohol use and early liver stress. Even within the 'normal' range, higher GGT levels predict cardiovascular disease, metabolic syndrome, and all-cause mortality. It is also used to diagnose cholestasis.

Vitamin D functions as a steroid hormone, regulating over 1,000 genes involved in immunity, inflammation, bone metabolism, and cardiovascular function. Deficiency (< 20 ng/mL) is associated with increased all-cause mortality, autoimmune disease, and cancer risk.

The Omega-3 Index measures EPA + DHA as a percentage of red blood cell fatty acids. It is a strong predictor of cardiac death risk — a low index (< 4%) carries risk comparable to smoking. High omega-3 levels also support brain health and reduce systemic inflammation.

Ferritin is the storage form of iron. Too low causes anemia and fatigue; too high promotes oxidative stress through Fenton chemistry, and elevated ferritin (> 200 in women, > 300 in men) is associated with liver disease, metabolic syndrome, and increased mortality.

Uric acid is the end product of purine metabolism. Elevated levels cause gout and kidney stones, and are increasingly linked to hypertension, metabolic syndrome, cardiovascular disease, and cognitive decline even without gout symptoms.

NAD+ is a critical coenzyme for mitochondrial energy production and DNA repair via sirtuins and PARP enzymes. Levels decline 50% or more by age 60. Low NAD+ is linked to impaired cellular repair, metabolic dysfunction, and accelerated aging.

Epigenetic clocks (Horvath, DunedinPACE, GrimAge) measure DNA methylation patterns to estimate biological age independently of chronological age. GrimAge acceleration predicts all-cause mortality, cancer risk, and cardiovascular events better than many traditional biomarkers.

Brain-derived neurotrophic factor is the primary growth factor for neurons. It promotes neurogenesis, synaptic plasticity, and memory formation. Low BDNF is associated with depression, Alzheimer's disease, and accelerated cognitive decline.

APOE ε4 is the strongest genetic risk factor for late-onset Alzheimer's disease. One copy raises risk ~3×; two copies raise it ~12×. Knowing your genotype enables personalized risk mitigation strategies through lifestyle, supplementation, and closer monitoring.