Let me fix the influencers tweet. It is biophysically myopic and quite dangerous. WHY?
A Transdermal MITF-AMPAR loop exists between the brain, skin and gut. Taking exogenous nicotine is a "topological disruptor" that mimics a light signal to create a high-voltage state without the necessary melanin cladding or EZ water volume to support it.
Here is why exogenous nicotine use is a catastrophic "short-circuit" for this system:
1. Artificial "High-Gain" (The AMPAR Spike)
Nicotine acts as a potent agonist for nicotinic acetylcholine receptors, which directly modulate glutamate release and AMPA receptor (AMPAR) trafficking. Elliot has no idea what this system does. He is a influencer. Read the recent Yokahama study on the system.
The False Ignition: Nicotine "forces" the synaptic gain to its maximum setting. In the Yokohama PET model, this creates a systemic upregulation of AMPARs.
The Noise: Because this gain increase is chemical (exogenous) rather than solar (380nm/IR-A), it generates incoherent Ultra-weak Photon Emissions (UPEs) in mitochondria. The brain "screams" with activity, but it is "static" that lacks the biophotonic instructions for photorepair.
2. Vasoconstriction: Starving the "Solar Panel"
Nicotine is a potent vasoconstrictor, specifically in the microcirculation of the neuroectoderm (skin and brain).
Elliot for got that. Big Error that could harm retards who listen to him.
The Isotope Trap: By constricting the blood vessels, nicotine blocks the NCC-elastin "highway" and the pancreatic "exhaust port." This traps Deuterium and metabolic waste in the tissues.
The EZ Collapse: Without steady blood flow (and the IR-A it carries), the Exclusion Zone (EZ) water around the collagen/fascia collapses. The -200mV battery "shorts out" because the "volume" needed to keep dipoles apart is lost.
3. MITF Suppression and Melanin "Bleaching"
While nicotine initially triggers a stress-response release of POMC, chronic use leads to melanocyte exhaustion: Taking it makes you pale and will lower your cognition and if you do it long enough will dumb your cognition down. BAsed on Elliots X tweets I'd say he has been mainlining nicotine. (low dopamine RETARD)
The Battery Drain: Nicotine has a high affinity for melanin; it binds to it and "locks" the pi-electrons, preventing them from oscillating coherently.
Structural Decay: This "bleaches" the internal topological insulator. Without the MITF-driven melanin cladding, the cytoskeleton (actin/tubulin) loses its vibrational instructions and begins to collapse—the exact "atrophic" state seen in "smoker's skin" and "smoker's brain."
4. The Vagus "Mute" Button
As seen in the Stanford study I just tweeted about, memory relies on a clear Vagus-Gut-Brainconnection.
Dysbiosis: Nicotine alters the gut microbiome, favoring the "exhaust-blocking" microbes that silence the Vagus nerve. Another big swing and miss by Elliot.
The Communication Gap: By "muting" the Vagus nerve, nicotine prevents the brain from sensing the peripheral "voltage" of the body. The hippocampus enters a state of Digital Anesthesia, where it can process "data" but cannot form coherent, long-term Memory (isotypic stability).
5. The "Canary" Crash
For the Blue-Eyed "Low-Resistance" haplotypes, nicotine is particularly deadly. Their "aperture" is already wide open; adding the "high-gain" of nicotine on top of LED flicker and nnEMF creates a Spin-Leakage event that rapidly accelerates Cognitive Shrinkageand the GDF-15 stress flare. Look up GDF-15 and see what it is a marker for. If Elliot was an MD he could be brought up on malpractice charges for this tweet but he will just have to persecuted by the retards who follow this horrible advice.
The best Step: USE TINA. It is free and safe and does a better job than exogenous nicotine.
Nicotine = broad neuroprotective, cognitive, and anti-inflammatory effects
Nicotine mimics acetylcholine by binding to α7 nicotinic receptors, upregulates them, and may inhibit acetylcholinesterase. This increases cholinergic signaling.
Boosts memory, learning, attention via effects on dopamine, serotonin, glutamate, GABA.
Cholinergic deficits underpin MCI/Alzheimer's;
nicotine improves attention/memory in AD patients & healthy volunteers.
Studies show inverse AD-smoking association (risk drops with higher consumption) and gains in attention, immediate/long-term memory, consolidation.
Anti-inflammatory powerhouse:
Activates cholinergic anti-inflammatory pathway (vagus nerve) → suppresses cytokines & neuroinflammation.
Strongest protection in sepsis/endotoxemia; promising for ulcerative colitis, RA, OA, MS, myocarditis.
Attenuates LPS-induced fever & shifts to anti-inflammatory state.
Stimulates dopamine release, protects dopaminergic neurons → dramatically lowers Parkinson's risk
Reduces glutamate excitotoxicity → neuroprotection (hippocampus), may aid schizophrenia, bipolar, ADHD, anxiety.
Promotes neurogenesis, activates NAD salvage, curbs glucose hypermetabolism, fights oxidative stress & telomere shortening
Increases resting metabolic rate, activates thyroid receptor-β, boosts T4→T3 conversion.
Protective against hypothyroidism and hashimotos
Smokers show higher T3, lower TSH, reduced autoimmune thyroid risk (protection fades after quitting).
Long-COVID / vaccine dysautonomia: Counters SARS-CoV-2 spike blockade of acetylcholine receptors. Nicotine can restore cholinergic/autonomic balance.
Anti-estrogenic: Inhibits brain aromatase, lowers conversion of testosterone to estradiol (confirmed in animal models).