What causes Evans index and lateral ventricles size to increase on a brain MRI and how to slow/reverse it

And how can this increase be slowed

ventriculomegaly

"For brain structure

A 2026 randomized trial gave 2 g/day DHA to 365 older adults at elevated dementia risk. DHA clearly reached the central nervous system and increased the CSF DHA-to-arachidonic-acid ratio, so absorption into the relevant compartment was real. Yet after 24 months there was no detectable benefit in brain volumes or cognition. That is sobering direct evidence against assuming “more DHA automatically preserves MRI volume.”

re-analysis of meditation => brain volume data also shows that many of the early studies are low-quality…

Ventricles first, because it’s mostly not about ventricles. They enlarge passively. The skull is a fixed box — Monro-Kellie — so brain + blood + CSF sums to a constant. Lose parenchyma, CSF floods in because something has to occupy the volume. Ex vacuo. The ventricles aren’t doing anything; they’re a cast of what left.

Two active contributions on top of that, both underrated. Periventricular white matter is watershed territory — long penetrating arterioles, lousy collateral supply — so the tissue immediately hugging the ventricles is the most ischemia-vulnerable tissue in the brain. Ventricles therefore enlarge disproportionately to global loss. And CSF turnover slows badly with age (roughly 4x/day in young adults, much less later) as arachnoid granulations and glymphatic clearance degrade, while the ependymal lining denudes. So there’s a hydrodynamic component layered on the mechanical one.

Brain mass: the thing everyone gets wrong is that it’s mostly not neuron death. “You lose 100,000 neurons a day” is folklore. Stereological counts — Terry, West, Pakkenberg, Morrison & Hof — show neocortical and hippocampal neuron number is largely preserved in healthy aging. What’s actually lost:

  • Neuropil. Dendritic arbors retract, spines vanish, somata shrink. Neurons wither in place rather than dying. Gray matter loss is mostly the connective felt between cell bodies, not the cell bodies.
  • White matter — and this is the bigger volumetric contributor in later life. Myelin is lipid-rich and bulky. WM volume peaks around 40–50 (much later than gray) then falls steeply. Late-myelinating regions go first: prefrontal, association cortex. Last in, first out.
  • Capillary rarefaction, and some fraction is just tissue water.

maybe greg fahy’s protocol!!

A small controlled longitudinal study of adults with genuine GH deficiency found that GH treatment increased cerebral volume and reduced ventricular volume over six months. Cross-sectional MRI work in people with pathological GH/IGF-1 excess also found greater MRI-derived GM and WM volumes and lower CSF volume.

So Fahy’s claim is not biologically absurd. GH could plausibly influence:

  • oligodendrocytes and myelin maintenance
  • protein and lipid synthesis
  • vascular or extracellular compartments
  • tissue water
  • inflammatory signaling
  • MRI tissue contrast and segmentation

The irritating scientific problem is that several of those mechanisms can make white matter look larger on MRI without representing regeneration of lost axons.

The central ambiguity: regeneration versus volume inflation

Somatropin commonly causes dose-dependent fluid retention in adults. Hydration and tissue-water changes can alter MRI-derived GM, WM, CSF and ventricular volumes, sometimes enough to mimic structural change. Controlled dehydration/rehydration studies have shown reversible changes in measured white-matter volume, cortical thickness and ventricular size.