Health Glossary

ApoB (Apolipoprotein B) is a protein that forms the structural backbone of all potentially atherogenic lipoprotein particles — including LDL, VLDL, IDL, and Lp(a). Because each of these particles carries exactly one ApoB molecule, measuring ApoB gives a direct count of the total number of atherogenic particles in circulation.

Many experts — including Peter Attia, MD — consider ApoB a more accurate cardiovascular risk marker than LDL cholesterol, because it measures particle number rather than cholesterol content. A person can have high LDL cholesterol but low ApoB (large, buoyant particles) or normal LDL cholesterol but high ApoB (many small, dense particles). Particle number is what drives arterial wall penetration and plaque formation.

Optimal ApoB is generally considered below 80 mg/dL for most adults, and below 60 mg/dL for those at elevated cardiovascular risk.

Autophagy (from the Greek "self-eating") is the cellular process by which damaged proteins, dysfunctional organelles, and other cellular debris are broken down and recycled. It is the body's primary quality-control mechanism at the cellular level.

Autophagy is activated by cellular stress — particularly nutrient deprivation (fasting), exercise, and heat stress. It declines with age, and reduced autophagy is associated with the accumulation of cellular damage that drives aging and chronic disease.

The 2016 Nobel Prize in Physiology or Medicine was awarded to Yoshinori Ohsumi for his work on the mechanisms of autophagy. Researchers including David Sinclair, PhD and Peter Attia, MD discuss autophagy extensively in the context of longevity medicine.

A Coronary Artery Calcium (CAC) score is derived from a low-dose CT scan that measures the amount of calcified plaque in the coronary arteries. Calcium deposits in arterial walls are a marker of atherosclerosis — the buildup of plaque that can lead to heart attack and stroke.

A CAC score of 0 is highly reassuring and associated with very low near-term cardiovascular risk. Scores above 100 significantly change risk stratification and often influence treatment decisions. The test involves a small amount of radiation (roughly equivalent to a mammogram) and typically requires a physician order.

The CAC scan is considered one of the most powerful tools for cardiovascular risk reclassification — it can identify high-risk individuals who appear low-risk on standard lipid panels, and low-risk individuals who might otherwise be over-treated.

Carotid Intima-Media Thickness (CIMT) is a non-invasive ultrasound measurement of the thickness of the inner two layers of the carotid artery wall. Increased thickness indicates early atherosclerosis — arterial wall changes that precede plaque formation and cardiovascular events.

Unlike the CAC scan, CIMT involves no radiation and can detect early arterial changes before calcification occurs. It is particularly useful for younger individuals or those with a family history of cardiovascular disease who may have soft (non-calcified) plaque not visible on a CAC scan.

CIMT is also used to track the progression or regression of atherosclerosis over time in response to lifestyle or therapeutic interventions.

Dual-Energy X-ray Absorptiometry (DEXA) is an imaging technique that uses two low-dose X-ray beams to measure bone mineral density, lean muscle mass, and body fat — including visceral fat (fat surrounding internal organs).

DEXA provides a far more detailed body composition picture than BMI or standard weight measurements. Visceral fat — which DEXA can quantify — is metabolically active and strongly associated with insulin resistance, cardiovascular disease, and metabolic syndrome, even in individuals with a normal BMI.

DEXA is also used to diagnose osteopenia and osteoporosis, and to track changes in muscle mass over time — particularly relevant for assessing sarcopenia risk in aging adults.

Fasting insulin is a blood test that measures the level of insulin in the bloodstream after an overnight fast. It is one of the earliest and most sensitive markers of insulin resistance — the condition in which cells become less responsive to insulin's signal to absorb glucose.

Standard metabolic panels typically include fasting glucose and HbA1c, but not fasting insulin. This is a significant gap: a person can have normal fasting glucose but markedly elevated fasting insulin — indicating that the pancreas is working much harder than normal to maintain blood sugar. This compensatory hyperinsulinemia is the earliest stage of metabolic dysfunction.

Optimal fasting insulin is generally considered below 7 µIU/mL. Levels above 10 µIU/mL suggest meaningful insulin resistance even when glucose and HbA1c appear normal. Researcher Benjamin Bikman, PhD considers fasting insulin the most important metabolic marker routinely omitted from standard care.

FibroScan (transient elastography) is a non-invasive ultrasound-based device that measures liver stiffness and fat content. It is used to assess the degree of liver fibrosis (scarring) and steatosis (fat accumulation) without a liver biopsy.

Non-alcoholic fatty liver disease (NAFLD) — now increasingly called metabolic-associated steatotic liver disease (MASLD) — is strongly linked to insulin resistance and metabolic syndrome. FibroScan can detect liver fat accumulation early, before it progresses to fibrosis or cirrhosis.

The test is quick (approximately 10 minutes), painless, and involves no radiation. It is particularly relevant for individuals with elevated liver enzymes (ALT, AST, GGT), metabolic syndrome, or type 2 diabetes.

GHK-Cu (Glycyl-L-Histidyl-L-Lysine copper complex) is a naturally occurring copper peptide found in human plasma, saliva, and urine. It was first identified in the 1970s and has since been studied extensively for its roles in wound healing, skin regeneration, and anti-aging.

GHK-Cu stimulates collagen and elastin synthesis, promotes angiogenesis (new blood vessel formation), and activates genes associated with tissue remodeling. It also has antioxidant and anti-inflammatory properties. Topical GHK-Cu is widely used in cosmetic formulations for its skin-tightening and regenerative effects.

Beyond topical applications, systemic research suggests GHK-Cu may reset the expression of a large number of human genes toward a younger, healthier state. It is also studied in the context of hair follicle stimulation.

HbA1c (Hemoglobin A1c, or glycated hemoglobin) is a blood test that reflects average blood glucose levels over the preceding 2–3 months. It measures the percentage of hemoglobin molecules that have glucose attached to them — a process called glycation.

HbA1c is the standard diagnostic test for type 2 diabetes (≥6.5%) and prediabetes (5.7–6.4%). However, it has significant limitations as a standalone metabolic health marker: it can appear normal while fasting insulin is already significantly elevated, and it can be falsely low in individuals with certain anemias or high red blood cell turnover.

Optimal HbA1c for metabolic health is generally considered below 5.4%. Levels in the 5.5–5.9% range, while technically "normal," may indicate early metabolic dysfunction when combined with elevated fasting insulin or other markers.

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is a calculated index derived from fasting glucose and fasting insulin levels. It provides a quantitative estimate of insulin resistance and beta-cell function.

The formula is: HOMA-IR = (Fasting Insulin [µIU/mL] × Fasting Glucose [mg/dL]) ÷ 405. A HOMA-IR below 1.0 is generally considered optimal. Values above 2.0 suggest meaningful insulin resistance; values above 3.0 indicate significant insulin resistance.

HOMA-IR is a useful clinical tool because it combines two markers to give a more complete picture than either alone. It requires both fasting insulin and fasting glucose — neither of which is included in most standard metabolic panels without a specific request.

hs-CRP (high-sensitivity C-reactive protein) is a marker of systemic inflammation produced by the liver in response to inflammatory signals. The "high-sensitivity" version of the test can detect low levels of inflammation that the standard CRP test misses.

Elevated hs-CRP is associated with increased cardiovascular risk, metabolic dysfunction, insulin resistance, and a range of chronic diseases. It is a useful complement to standard lipid testing — two individuals with identical LDL cholesterol levels may have very different cardiovascular risk profiles based on their hs-CRP.

Optimal hs-CRP is generally considered below 1.0 mg/L. Levels above 3.0 mg/L indicate high cardiovascular risk. Levels above 10 mg/L typically suggest acute infection or injury rather than chronic inflammation.

Humanin is a mitochondria-derived peptide (mitokine) encoded within the 16S rRNA region of mitochondrial DNA. It was originally identified for its neuroprotective properties — specifically its ability to protect neurons from amyloid-beta toxicity, a hallmark of Alzheimer's disease.

Subsequent research has expanded the understanding of Humanin's role to include cytoprotection (protecting cells from stress-induced death), anti-inflammatory signaling, and metabolic regulation. Humanin levels decline with age and are lower in individuals with age-related diseases.

Humanin can cross the blood-brain barrier, giving it potential relevance in both peripheral and central nervous system health. It is considered one of the most promising mitokines in longevity research, alongside MOTS-c.

Inflammation is the immune system's response to injury, infection, or perceived threat. Acute inflammation — the redness, swelling, and heat that follows a cut or infection — is a healthy, protective response. Chronic low-grade inflammation is a different phenomenon: a persistent, low-level activation of the immune system that drives tissue damage over time.

Chronic inflammation is now recognized as a central mechanism in virtually every major chronic disease — cardiovascular disease, type 2 diabetes, cancer, Alzheimer's disease, and autoimmune conditions. It is both a cause and a consequence of metabolic dysfunction: insulin resistance promotes inflammation, and inflammation worsens insulin resistance.

Key drivers of chronic inflammation include ultra-processed food, excess body fat (particularly visceral fat), poor sleep, chronic stress, environmental toxin exposure, and sedentary behavior. Markers of systemic inflammation include hs-CRP, IL-6, TNF-alpha, and fibrinogen.

Ketosis is a metabolic state in which the liver produces ketone bodies — primarily beta-hydroxybutyrate (BHB), acetoacetate, and acetone — from fatty acids, in response to low carbohydrate availability. This occurs during fasting, prolonged exercise, or adherence to a ketogenic diet.

Ketones serve as an alternative fuel source to glucose, particularly for the brain and heart. Beyond their role as fuel, ketones function as signaling molecules. Research — including work by Dominic D'Agostino, PhD — suggests ketones influence gene expression, reduce oxidative stress, modulate inflammation, and support mitochondrial function. BHB in particular has been identified as a histone deacetylase (HDAC) inhibitor.

Nutritional ketosis (blood BHB approximately 0.5–3.0 mmol/L) is distinct from diabetic ketoacidosis (DKA), a dangerous condition in type 1 diabetes where ketones reach 10–25 mmol/L due to absent insulin. In metabolically healthy individuals, the body tightly regulates ketone levels.

Lp(a) (Lipoprotein(a)) is a lipoprotein particle structurally similar to LDL but with an additional protein called apolipoprotein(a) attached. It is largely determined by genetics — approximately 90% of an individual's Lp(a) level is inherited — and does not change significantly with diet or lifestyle.

Elevated Lp(a) is an independent risk factor for cardiovascular disease, aortic stenosis, and stroke. It is not included in standard lipid panels and must be specifically requested. The American Heart Association and European Society of Cardiology recommend that every adult have their Lp(a) measured at least once.

Because Lp(a) is genetically determined, knowing your level allows for appropriate risk stratification and more aggressive management of modifiable risk factors. Optimal Lp(a) is generally considered below 30 mg/dL (or below 75 nmol/L, depending on the assay used).

Metabolic flexibility is the ability of the body to efficiently switch between fuel sources — primarily glucose and fatty acids — depending on availability and demand. A metabolically flexible individual can burn fat effectively during fasting or low-intensity activity, and switch to glucose during high-intensity exercise or after a carbohydrate-containing meal.

Metabolic inflexibility — the inability to efficiently switch fuel sources — is a hallmark of insulin resistance and metabolic syndrome. Metabolically inflexible individuals tend to rely heavily on glucose even during fasting, experience energy crashes between meals, and have difficulty burning stored body fat.

Metabolic flexibility is improved by regular Zone 2 aerobic exercise, fasting, reducing refined carbohydrate intake, and improving sleep quality. It is considered one of the most meaningful indicators of overall metabolic health.

Mitochondria are membrane-bound organelles found in nearly every cell of the body. Often described as the "powerhouses of the cell," they produce the majority of cellular energy in the form of ATP (adenosine triphosphate) through a process called oxidative phosphorylation.

Beyond energy production, mitochondria regulate apoptosis (programmed cell death), calcium signaling, reactive oxygen species (ROS) production, and the production of mitochondria-derived peptides (mitokines) including MOTS-c and Humanin. They also play a central role in cellular stress responses.

Mitochondrial dysfunction — reduced number, impaired function, or increased ROS production — is now recognized as a central mechanism in aging and chronic disease. Mitochondrial health is supported by Zone 2 aerobic exercise (the most potent stimulus for mitochondrial biogenesis), fasting, heat stress (sauna), and adequate sleep.

MOTS-c (Mitochondrial Open Reading Frame of the 12S rRNA-c) is a mitochondria-derived peptide encoded within mitochondrial DNA — a discovery that challenged the long-held assumption that mitochondria do not produce functional peptides.

Research suggests MOTS-c acts as a metabolic regulator, improving insulin sensitivity, activating AMPK (a key energy-sensing enzyme), and enhancing mitochondrial function. Animal studies have shown that MOTS-c administration can reverse age-related metabolic decline and improve physical performance in older subjects.

MOTS-c levels decline with age, and this decline is associated with reduced metabolic flexibility and increased insulin resistance. It represents a novel class of mitochondria-derived signaling molecules — called mitokines — that communicate metabolic status throughout the body.

The Omega-3 Index measures the percentage of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) in red blood cell membranes. Because red blood cells turn over approximately every 120 days, the Omega-3 Index reflects average omega-3 status over the preceding 3–4 months — similar to how HbA1c reflects average blood glucose.

An Omega-3 Index below 4% is associated with significantly elevated cardiovascular risk. An index of 8% or above is considered optimal. Most adults in Western countries have an Omega-3 Index in the 4–6% range — below the optimal threshold.

EPA and DHA have distinct roles: EPA is primarily anti-inflammatory and cardiovascular-protective; DHA is the dominant structural omega-3 in the brain and retina. Both are found in fatty fish and high-quality fish oil supplements. Testing the Omega-3 Index is the only reliable way to know whether supplementation is achieving its intended effect.