Biomarker Glossary

Each LDL, VLDL, and Lp(a) particle carries exactly one ApoB protein. ApoB counts total atherogenic particle number, which predicts plaque formation far better than LDL-C alone. High LDL-C with low ApoB = relatively safe. Normal LDL-C with high ApoB = dangerous.

Lp(a) is largely genetic — you can't diet or exercise it away. It accelerates atherosclerosis and is found in ~20% of the population at elevated levels. Test once — it barely changes. High Lp(a) requires more aggressive LDL lowering as compensation.

Elevated homocysteine damages arterial walls and is an independent cardiovascular risk factor. It is elevated by B12, B6, and folate deficiency. Easily corrected with B-complex supplementation. Often overlooked on standard panels.

HRV measures the variation in time between heartbeats. Higher HRV = more adaptive ANS. It reflects recovery status, stress load, sleep quality, and training readiness. Declining HRV trend over weeks indicates cumulative stress or illness. Single values are less useful than 7-day rolling average.

VO2 max measures how efficiently your cardiorespiratory system delivers and uses oxygen. Each 1 MET increase in VO2 max reduces all-cause mortality by ~13%. Moving from "low" to "above average" VO2 max reduces mortality risk more than quitting smoking.

NAD+ is required for mitochondrial energy production (ATP synthesis), DNA repair (via PARP), and sirtuin activation (longevity proteins). Levels decline ~50% by age 50. Supplementation with NMN or NR can restore levels.

Autophagy is the process by which cells break down and recycle intracellular junk — damaged proteins, dysfunctional mitochondria, protein aggregates linked to neurodegeneration. It is activated by fasting, exercise, and caloric restriction. Declining autophagy with age is thought to contribute to neurodegenerative diseases.

Senescent cells secrete inflammatory cytokines (SASP — senescence-associated secretory phenotype) that damage surrounding tissue. They accumulate with age. Senolytics (quercetin, fisetin, dasatinib) selectively kill them. Clearance of senescent cells extends healthspan in mouse models dramatically.

Telomeres are repeated DNA sequences at chromosome ends that protect against degradation. They shorten with each cell division and with oxidative stress, chronic inflammation, and poor lifestyle. Short telomeres = accelerated cellular aging. Exercise, sleep, and stress management preserve telomere length.

mTOR activation = growth mode (build muscle, grow cells). mTOR inhibition = repair mode (autophagy, cellular maintenance). Rapamycin inhibits mTOR. Fasting inhibits mTOR. Caloric restriction inhibits mTOR. The longevity implication: chronic mTOR activation (excess calories, constant protein intake) may accelerate aging.

AMPK activates when energy is low (fasting, exercise). It inhibits mTOR, triggers autophagy, and improves insulin sensitivity. Metformin and berberine activate AMPK pharmacologically — it is one reason both are studied for longevity.

Insulin resistance develops when cells stop responding normally to insulin, requiring ever-higher insulin levels to manage blood glucose. It underlies type 2 diabetes, cardiovascular disease, NAFLD, and is increasingly linked to Alzheimer's (sometimes called "type 3 diabetes").

Fasting insulin is the most sensitive early marker of insulin resistance — often elevated for decades before fasting glucose rises. Most standard panels don't include it. Chronically elevated insulin drives fat storage, inflammation, and metabolic disease.

CRP is produced by the liver in response to inflammation. Chronic low-grade elevation — even within "normal" ranges — predicts cardiovascular events, cancer, and cognitive decline. Diet (Mediterranean pattern), exercise, and sleep are the strongest reducers.

Zone 2 training (conversational pace, fat-burning zone) maximises mitochondrial biogenesis, builds the aerobic base, and improves metabolic flexibility. 3–4 hours/week is the target. It is the training zone most associated with longevity benefits in elite athletes and general populations.

BDNF promotes neuroplasticity, protects neurons from death, and is essential for learning and memory. Exercise (especially aerobic) is the most potent BDNF stimulator known. Low BDNF is associated with depression and neurodegeneration. Sauna and cold exposure also increase BDNF.