Possible Contradictions and Our Explanations
Our hypothesis is new. Very new. So naturally, along the way, we’ve come across many contradictions, surprises, and frequently asked questions. We share them here openly, along with explanations and our opinions, hoping to spark deeper understanding, debate, and further research within the scientific community.
We considered many possible fallouts and had explanations for each, which is why we believe this research path is worth pursuing.
Microgravity leads to accelerated aging.
We know from thousands of spaceflight simulation experiments that the absence of gravity accelerates aging. Astronauts in microgravity experience bone loss, muscle wasting, vascular stiffening, and immune dysfunction at rates significantly higher than those observed on Earth. Humans evolved for life on Earth, and deviations away from Earth’s gravity (1G) affect us negatively.
Our hypothesis does not claim that microgravity is good. We have analyzed the impact of Earth’s gravity on us, and we hypothesise that 1G – despite it being the ideal gravity – shortens our lifespan. The real challenge isn’t escaping the Earth’s gravity, but learning how to live longer within it.
Scientists could not have missed something so simple.
It only seems simple. The physics (a head–heart hydrostatic gradient) is basic, but the biology is not. We likely missed it because:
- Studies have only been done on the impact of extreme gravitational forces, or their absence. Research on the impact of terrestrial gravity is lacking.
- Most brain data is collected supine, without varying posture or tightly controlling CO₂/BP.
- Some researchers may have assumed that autoregulation/collaterals were sufficient and underweighted venous pressure limits.
- The effect is subtle but cumulative, so it doesn’t appear in shorter studies.
- If the hypothesis is correct, we should find posture-dependent, region-specific, reversible signatures; however, studies haven’t been designed to look for them.
Aging occurs even in organisms without brains, and different organs exhibit varying rates of aging.
It’s true – even individual cells in culture undergo senescence. This shows that aging has local, built-in mechanisms. But in complex organisms like humans, there’s also central coordination. The brain, especially the hypothalamus and brainstem, helps regulate how rapidly or slowly aging unfolds across the body. It achieves this by regulating key systems, including hormones, metabolism, inflammation, and circadian rhythms. Simpler organisms, though lacking a brain, still exhibit forms of systemic coordination. So yes, aging would still happen without gravity. But counteracting the effects of gravity’s cumulative impact on brain perfusion and regulatory degradation, we believe it would happen more slowly.
The brain has massive collateral circulation.
Extensive collateral vessels help in acute problems in the larger arteries, but they can’t ensure uniform microvascular oxygen delivery. Tissue perfusion is dependent on the cerebral perfusion pressure (CPP = MAP − ICP). In deep, perforator-supplied regions with limited redundancy, thin CPP margins can cause reduced perfusion despite normal inflow in the major arteries.
Our hypothesis, therefore, focuses on chronic and region-specific shortfalls in oxygen delivery. These are subtle, subthreshold deficits that accumulate over time, rather than overt starvation. These cumulative shortfalls in neuroendocrine control hubs offer a plausible pathway by which gravity’s head-to-heart hydrostatic load could contribute to brain-directed systemic aging.
The effects of reduced CBF could be combatted through increased oxygen extraction.
When there is a reduction in cerebral blood flow, Oxygen extraction factor (OEF) rises to keep the brain’s oxygen supply steady. However, this can only be done up to a ceiling set by capillary transit and diffusion limits. In small, perforator-supplied deep regions, repeated small drops in cerebral perfusion pressure (CPP) can push OEF toward that ceiling for long periods. This could produce a chronic strain experienced within those regions that doesn’t result in immediate failure. Further studies need to be done to establish the relationship between chronic cerebral blood flow reductions and hypoperfusion.
Hyperperfusion has negative effects too.
There’s no universal threshold for “too much” cerebral blood flow. It’s relative to metabolic demand and the physiological cost of delivery. Perfusion is excessive when it exceeds metabolic needs (lowering oxygen extraction), raises intracranial pressure (reducing CPP, where CPP = MAP − ICP), disrupts capillary transit dynamics, impairs blood-brain barrier integrity, or leads to venous congestion. Our framework aims to find methods for optimising deep-region CPP with minimal ICP and CO₂ burden, i.e., postural and ventilation changes that enhance nutrient delivery.
There is no direct empirical proof for this theory.
We completely agree, and that is why we present it as a highly plausible hypothesis that needs to be investigated further. Proving a causal relationship would require proving each link in the chain of causation. Lack of prior research and technological limitations on brain imaging further hinder our ability to make a definitive claim on this phenomenon.