Monday 12th January 2026 brought mild 12° weather, so my day-5 plantar fasciitis was mildly better, especially if I judged my heel strike well, so off we went to the Pleiades. Earthing got rained off twice, but I was lucky on my third try and I made a note to record how much more conductive grass is after rain. Total time was 45’, just enough to reset or at least alleviate the torque on my foot. Then I took the obligatory molecular hydrogen tablet. H₂, in theory, targets some of the very biological roadblocks (oxidative stress, inflammation, low cellular energy) that hinder nerve repair and neuroplasticity after a stroke. I compared molecular H₂ with the Redox supplement from ASEA I used to take and these four points came up for H₂
Selective Antioxidant : Unlike many antioxidants that neutralize all reactive oxygen species (ROS), H₂ is proposed to selectively target only the most harmful and cytotoxic ROS, like the hydroxyl radical (•OH). This is important because some ROS are needed for normal cellular signalling. After a stroke, oxidative stress runs rampant in the brain and nervous system, damaging cells.
Anti-inflammatory: H₂ appears to modulate signalling pathways (like NF-κB) that reduce the production of pro-inflammatory cytokines. Chronic inflammation is a major impediment to recovery after brain injury.
Cell Signalling & Hormesis : H₂ may act as a gentle stressor that triggers protective cellular pathways, a concept known as hormesis. It can influence the release of beneficial hormones like ghrelin and potentially upregulate the body’s own antioxidant systems.
Mitochondrial Support: There is evidence H₂ helps protect and improve the function of mitochondria (the cell’s energy powerhouses), which are often damaged after a stroke. Better mitochondrial function means more energy (ATP) for repair and nerve signalling.
I judged chronic excitotoxicity due to calcium overload to be the issue with my foot (plantar fasciitis on day-5.) This is a subtle, persistent issue about impaired network function and hindered recovery. Network Imbalance: The stroke damages inhibitory interneurons (which use GABA) as much as excitatory ones. This chronic imbalance where excitation is relatively unopposed in the peri-infarct (area surrounding the dead core) and connected regions. Chronic, low-grade excess glutamate can lead to excessive, poorly targeted synaptic strengthening. Think of it as “noisy” signals in the network, which can contribute to issues like spasticity, dystonia, or learned non-use.
Excitotoxicity is a pathological process in which nerve cells (neurons) are damaged or killed by excessive stimulation by neurotransmitters, most notably glutamate. It is a major mechanism of brain injury in a stroke. Think of it as a lethal case of “overexcitement” for brain cells.
Overstimulation is due to glutamate which floods the synapses and over-activates receptors on the receiving neuron, especially the NMDA receptor and AMPA receptor. These receptors act like gateways. When excessively activated, they open wide, allowing a massive, uncontrolled influx of calcium ions (Ca²⁺) into the neuron.
My 4th and 5th right hand fingers were burning strongly by the evening, if not so much at the start of the day. My strategy for now is Earthing, Exercise, Qigong breathing, Magnesium (for GABA), Aloe Vera, Hydrogen, Epsom salts, selected essential oils (Frankincense and Copaiba)
