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10/01/2026

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CBD / Cannabis Potential To Protect & Treat Traumatic Brain Injury

✔️ Study Overview

• Preclinical research investigated the effects of cannabidiol on traumatic brain injury

• Focused on cognitive recovery and cellular mechanisms underlying brain protection

• Identified a previously unrecognized molecular pathway involved in neuronal survival

✔️ Key Findings

• Cannabidiol significantly improved learning and memory performance after traumatic brain injury

• Treatment reduced neuronal cell death in brain regions critical for cognition

• Oxidative stress markers were markedly decreased following cannabidiol administration

✔️ Newly Identified Mechanism

• Cannabidiol directly binds to a cellular protein called SET

• This interaction alters the shape and location of SET within neurons

• SET is retained in the cytoplasm rather than entering the nucleus

• This modulation influences PP2A signaling and promotes activation of the Akt survival pathway

• The mechanism operates independently of the classical PI3K pathway

✔️ Why This Matters

• Traumatic brain injury has limited effective treatments for cognitive impairment

• Secondary injury processes such as oxidative stress and programmed cell death drive long term damage

• Cannabidiol targets these secondary processes rather than the initial mechanical injury

✔️ Neuroprotective Effects of Cannabidiol

• Supports neuronal survival under stress conditions

• Reduces oxidative damage that contributes to progressive brain injury

• Engages endogenous cell survival signaling pathways

✔️ Safety and Translational Context

• Cannabidiol has an established safety profile in humans for other medical indications

• It is non intoxicating and does not produce THC associated psychoactive effects

• Findings are based on animal models and require validation in human clinical trials

✔️ Clinical and Research Implications

• Identifies SET and related signaling pathways as potential therapeutic targets

• Supports further investigation of cannabidiol as a treatment for traumatic brain injury

• Highlights the importance of timing and dosing in future clinical studies

This study provides a clear molecular foundation for cannabidiol CBD as a promising candidate in Protecting and Treating traumatic brain injury research.

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January 3, 2026
Link 🔗 to Study / Source in First Comments Below ⬇️

23/12/2025

2-AG is one of the body’s first responders when the brain is threatened. When an insult happens, whether that is trauma, ischemia, inflammation, or excitotoxic stress, the brain does not wait for outside help. It makes its own medicine, fast. That medicine is 2-arachidonoylglycerol, better known as 2-AG.

2-AG is an endocannabinoid, a lipid-based signaling molecule produced on demand in the brain and nervous system. Unlike neurotransmitters that sit stored in vesicles waiting to be released, 2-AG is synthesized in real time from membrane lipids the moment neurons sense danger. That speed matters. It allows the ECS, our Master Regulator, to respond within seconds to injury and begin damage control before secondary injury cascades take over.

When released, 2-AG primarily activates CB1 receptors in the brain and CB2 receptors on immune and glial cells. At CB1, 2-AG reduces excessive glutamate release, which is one of the main drivers of neuronal death after injury. Too much glutamate overstimulates neurons until they burn out. 2-AG reduces that volume, protecting neurons from excitotoxic damage. At CB2, it calms inflammatory signaling, limiting microglial overactivation that would otherwise expand the injury zone.

2-AG also stabilizes the blood-brain barrier, reduces oxidative stress, and helps preserve mitochondrial function inside neurons. This keeps cells alive long enough to repair rather than collapse. In short, 2-AG does not directly repair damage; it creates a protective window in which repair is possible.

This mechanism was clearly demonstrated in the peer-reviewed study “Endocannabinoid 2-arachidonoylglycerol protects against cerebral ischemia by reducing inflammation and neuronal damage,” published in 2003. The researchers showed that increasing 2-AG levels after brain ischemia significantly reduced brain edema, infarct size, and neuronal death, while blocking 2-AG worsened outcomes.

What this tells us is profound. The brain already knows how to protect itself. It uses 2-AG as an emergency signal to restore order when chaos hits. Supporting ECS balance does not introduce something foreign; it amplifies a system designed for survival. When the brain is injured, 2-AG shows up first, quietly doing the work most never see, keeping neurons alive long enough for healing to begin.

-Mike Robinson, The Researcher OG

23/12/2025

Billy has now lived twenty Christmas’s on this earth when all the odds were stacked against him. So many things they said he wouldn’t do. So many years they said he may not see.

I did not know if he would live to see
one,
two,
three or four years old. And here he is today celebrating twenty whole Christmase’s on this earth.

The only words to describe it are breathtaking. Absolutely unbelievable that he just keeps making it …. ZERO seizures!
Plant medicine is quite literally gifting Billy year on year.

Happy Christmas, my amazing, courageous boy. I love you with all my heart.

Mummy ….. 💜

21/12/2025

Asthma has never been just an airway problem. It is a spasm, an inflammatory, and a nervous system problem layered together, which is why so many patients feel tightness long before wheezing ever shows up. The smooth muscle surrounding the bronchial tubes locks down, inflammation adds pressure, and the nervous system stays stuck in a reactive loop that keeps the chest from fully opening.

This is where cannabis enters the conversation, not as smoke versus lungs, but as pharmacology versus physiology. Long before legalization debates, researchers were already documenting the antispasmodic and bronchodilatory effects of cannabinoids, especially THC, on airway smooth muscle.

A landmark study published in 1975 in The New England Journal of Medicine titled “Bronchodilator effect of delta9-tetrahydrocannabinol in humans” demonstrated that THC produced significant bronchodilation in both asthmatic and non-asthmatic subjects. The effect was rapid, measurable, and directly tied to smooth muscle relaxation rather than sedation. In simple terms, the airways opened because the muscle stopped spasming.

This matters because asthma attacks are not always driven solely by mucus or allergies. They are often driven by involuntary contraction of the airway muscle, triggered by stress, inflammation, or nervous system overactivity. Cannabinoids interact with the ECS, our Master Regulator, which plays a role in smooth muscle tone, immune signaling, and autonomic balance. When that system is supported, the body is better able to release tension instead of clamping down.

Cannabinoids also influence mast cell activity and the release of inflammatory mediators, which contribute to bronchial hyperreactivity. That does not mean cannabis replaces rescue inhalers or medical oversight, but it does explain why many patients report easier breathing, reduced chest tightness, and fewer stress triggered flare ups when cannabinoids are used thoughtfully and appropriately.

It is also why delivery method matters. Antispasmodic benefits do not require combustion, and many patients find relief with non-inhaled forms of CBG and CBD that still support systemic signaling and nervous system regulation.

Asthma is about control, not force. When the body feels safe, muscles relax, air moves, and panic fades. Cannabinoids do not bully the lungs open. They help the system remember how to let go.

That distinction is everything when it comes to real respiratory balance.

-Mike Robinson, The Researcher OG

20/12/2025