Thread by @DrJackKruse

Check out my latest article: WHY ARE ALS AND ATRIAL FIBRILLATION LINKED? linkedin.com/pulse/why-als-…

The oculomotor nerve (CNIII) is responsible for controlling the pupillary size.  It contains several parasympathetic functions related to the eye. The oculomotor PNS fibers originate in the Edinger-Westphal nucleus in the central nervous system and travel through the superior orbital fissure at the base of the orbit to synapse in the ciliary ganglion located just behind the orbit (eye). From the ciliary ganglion, the postganglionic parasympathetic fibers leave via short ciliary nerve fibers, a continuation of the nasociliary nerve (a branch of the ophthalmic division of the trigeminal nerve). The trigeminal nerve is critical in the mammalian dive reflex.  This is why the astute quantum clinician can use cold water on the face to help people.  The short ciliary nerves innervate the orbit to control the ciliary muscle (responsible for accommodation) and the iris sphincter muscle, responsible for miosis or constriction of the pupil (in response to light or accommodation).  

As bright light enters the pupil, the carotid circulatory system must provide blood flow, and the superior cervical ganglion optimizes this coordination.  This is often not appropriately yoked with circadian mismatches in heme proteins Rev Erb Alpha and beta.  This is especially true in diabetics and children with cyanotic heart disease.  This means this ganglion controls blood flow to the CNS due to a light-activated mechanism.  Since the brain gets 20% of cardiac output, this has a massive effect on the quantum abilities of the eye. It also means that when bright light does not increase cerebral blood flow, we know we have a patient with a serious circadian mismatch in the local environment.

2. Why don't I listen to people who wear sunglasses or contacts? BECAUSE THEY CANNOT THINK WELL.

How does a brain surgeon know this and prove it to the public?

DECENTRALIZED SCIENCE.

3. Normally, bright light from the sun increases metabolic demand in the retina and visual cortex, triggering SCG-mediated vasodilation to increase CBF. This is part of neurovascular coupling, where neural activity drives blood flow (e.g., via nitric oxide release, as discussed in my blogs at length). Sunlight also stimulates PER clock genes. This is important for cardiac function.

Circadian Mismatch Indicator: If CBF does not increase with bright light, it suggests:
SCN Dysfunction: Inadequate light exposure (e.g., UV blockage) impairs circadian entrainment.

4. Sympathetic Dysregulation: The SCG fails to adjust blood flow, possibly due to circadian misalignment of Rev-Erb-alpha/beta/beta or CCO dysfunction. Mitochondrial Stress: Low NAD+ and pseudohypoxia impair vascular responsiveness, as mitochondria in endothelial cells (e.g., in the carotid system) rely on CCO for energy and signaling.

Note the bottom line of the slide.

5. Clinical Relevance: This mismatch should manifest as visual symptoms (e.g., poor adaptation to light), neurological symptoms (e.g., fatigue, cognitive impairment), or systemic issues (e.g., arrhythmias in Afib).
It’s a diagnostic clue for clinicians to assess light exposure, circadian health, and mitochondrial function.

Relevance to My Thesis: This aligns with my focus on light as a critical environmental input for mitochondrial and autonomic health. It also supports my earlier point about UV light’s role in nitric oxide release and vascular tone, which directly influences CBF.

6. Without proper cerebral blood flow, one cannot think well, so when your profile pic shows you wearing them, I ignore you and your opinion. Why? Because I know I am wiser than you.

7. @threadreaderapp make me a roll