Physiologia, Vol. 5, Pages 55: Gravity in the Eye: How ‘Gravitational Ischemia’ in the Retina May Be Released and Resolved Through Rapid Eye Movement (REM), a Component of Gravity Opposition Physiology

Physiologia doi: 10.3390/physiologia5040055

Authors:
J. Howard Jaster
Joshua Ong
Giulia Ottaviani

This narrative review of rapid eye movement (REM) focuses on its primary etiology and how it fits into the larger framework of neurophysiology and general physiology. Arterial blood flow in the retina may be sensitive to the full overlying ‘weight’ of its adjacent and contiguous vitreous humor caused by the humoral mass effect in the Earth’s gravitational field. During waking hours of the day, this ‘weight’ is continuously shifted in position due to changing head position and eye movements associated with ordinary environmental observations. This reduces its impact on any one point on the retinal field. However, during sleep, the head may maintain a relatively constant position (often supine), and observational eye movements are minimal, leaving essentially one retinal area exposed at the ‘bottom’ of each eye, relative to gravity. During sleep, REM may provide a mechanism for frequently repositioning the retina with respect to the weight it incurs from its adjacent (overlying) vitreous humor. Our findings were consistent with the intermittent terrestrial nocturnal development of ‘gravitational ischemia’ in the retina, wherein the decreased blood flow is accompanied metabolically by decreased oxygen tension, a critically important metric, with a detrimental influence on nerve-related tissue generally. However, the natural mechanisms for releasing and resolving gravitational ischemia, which likely involve glymphatics and cerebrospinal fluid shifts, as well as REM, may gradually fail in old age. Concurrently associated with old age in some individuals is the deposition of alpha-synuclein and/or tau in the retina, together with similar deposition in the brain, and it is also associated with the development of Parkinson’s disease and/or Alzheimer’s disease, possibly as a maladaptive attempt to release and resolve gravitational ischemia. This suggests that a key metabolic parameter of Parkinson’s disease and Alzheimer’s disease may be a lack of oxygen in some neural tissues. There is some evidence that oxygen therapy (hyperbaric oxygen) may be an effective supplemental treatment. Many of the cardinal features of spaceflight-associated neuro-ocular syndrome (SANS) may potentially be explained as features of gravity opposition physiology, which becomes unopposed by gravity during spaceflight. Gravity opposition physiology may, in fact, create significant challenges for humans involved in long-duration space travel (long-term microgravity). Possible solutions may include the use of artificial gravitational fields in space, such as centrifuges.

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