Mitochondria and the modifiable biology

Mitochondrial function is the cellular engine of metabolic health. Its decline tracks with most of the chronic disease picture in the second half of life. The underlying biology is genuinely modifiable.

Every cell in the body that does substantial work has mitochondria. The energy currency the body runs on, ATP, is produced inside them. Their number per cell, their size, their membrane integrity and the efficiency with which they produce ATP are all measurable, all reflect underlying biology health, and all change with what we eat, how we sleep and how we move.

The story of mitochondrial decline through mid-life is one of the cleanest mechanistic accounts of why chronic disease compounds the way it does. Less efficient mitochondria produce more reactive oxygen species. More reactive oxygen species drive smouldering chronic inflammation. Smouldering chronic inflammation drives the late expression of cardiovascular, metabolic, neurological and autoimmune disease.

What moves the mitochondrial biology

Aerobic exercise of sufficient duration and intensity to drive mitochondrial biogenesis. Strength training to maintain the muscle mass that hosts the largest fraction of body mitochondria. Adequate sleep, particularly slow-wave sleep, for mitochondrial recovery. Nutritional inputs that support mitochondrial membrane integrity and function, including omega-3 fatty acids and the B-vitamin cofactors. Time-restricted eating windows that allow mitochondrial autophagy. The preventive work that EPOCH delivers across the five pillars is, in cellular terms, mitochondrial work.

The long arc consequence

The mitochondrial biology at fifty determines the cardiovascular biology at sixty, the cognitive biology at seventy and the frailty underlying biology at eighty. Modifiable now. Less modifiable later. The case for engaging the preventive work in mid-life rests substantially on what mitochondrial biology tells us about how the second half of life unfolds.