Fractal mechanism of aging

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Fractal mechanism of aging

Fractal forms are composed of subunits (and sub-sub-units, etc.) that resemble the structure of the overall object. In an idealized model, this property holds on all scales. The real world, however, necessarily imposes upper and lower bounds over which such scale-invariant behavior applies.

A hallmark of physiologic systems is their extraordinary complexity. Healthy systems are self-regulated to reduce variability and maintain physiologic constancy. The nonstationarity and nonlinearity of signals generated by living organisms defy traditional mechanistic approaches based on homeostasis and conventional biostatistical methodologies.

A variety of other organ systems contain fractal-like structures that facilitate information dissemination (nervous system), nutrient absorption (bowel), as well as distribution, collection, and transport (biliary ducts, renal calyces, choroidal plexus, and placental chorionic villae). With aging and disease, fractal anatomic structures may show degradation in their structural complexity. Examples include loss of dendritic arbor in aging cortical neurons and vascular ‘‘pruning’’ in primary pulmonary hypertension. The fractal concept can be applied not just to irregular geometric forms that lack a characteristic (single) scale of length, but also to certain complex processes that lack a single scale of time. Fractal processes generate irregular fluctuations across multiple time scales, analogous to scale-invariant objects that have a branching or wrinkly structure across multiple length scales.

A defining feature of healthy function is adaptability, the capacity to respond to unpredictable stimuli and stresses. Functional plasticity requires a broad range of integrated outputs. Physiologic aging is associated with a generalized loss of complexity in the dynamics of healthy organ system function and such loss of complexity leads to an impaired ability to adapt to physiologic stress. The breakdown of fractal physiologic complexity may be associated with excessive order (pathologic periodicity), on the one hand, or uncorrelated randomness, on the other. A unifying theme underlying both routes to pathology is the degradation of correlated, multiscale dynamics. Transitions to strongly periodic dynamics are observed in many pathologies, including Parkinson’s disease (tremor), obstructive sleep apnea, sudden cardiac death, epilepsy, and fetal distress syndromes.