Thread by @DrJackKruse

What do you know about the Stiles-Crawford effect in a healthy eye? What if I told you this effect is how we sharpen central vision and narrow the periphery of the retina from too much blue light. Would you believe it? Did you know melanopsin has a specific topographic map on a healthy retina? A lesson no has taught you is incoming.

2. All opsins are topologic insulators. You might want to read that threadroll above now to understand topology well.

Topology changes in a cell = geometry change of cristae = UPE change from mitochondria = the optical signal changes in the same tissue altering physiology.

So what happens if you sustain mitochondrial damage in your retina's colony of mitochondria to the Stiles Crawford effect?

What are the implications?

3. The Stiles–Crawford effect (SCE) is the human eye's phenomenon of reduced light sensitivity when light enters the pupil from its periphery compared to the pupil's center. This effect is due to the optical properties of photoreceptors, which act as waveguides and are aligned to channel light towards the fovea, the central point of vision. The SCE makes vision less sensitive to light entering the periphery, thus reducing glare and improving visual clarity. It also keeps a lid on the amount of blue light the periphery the retina gets.

This sharpens vision, makes myopia, glaucoma, cataracts, hyperopia, and AMD almost impossible to get. Makes one resistant to mental illness too. Makes one impervious to diabetic transformations. Makes neurodegeneration rare.

You feeling me yet?

4. Since blue light destroys all photoreceptors what happens to the optics of the eye to the brain?

Mammalian photoreceptors aggregate numerous mitochondria, organelles chiefly for energy production, in the ellipsoid region immediately adjacent to the light-sensitive outer segment to support the high metabolic demands of phototransduction. However, these complex, lipid-rich organelles are also poised to affect light direction, polarization, and passage into the outer segment of the photoreceptor.

Did you know mitochondria in cone photoreceptors act as microlenses to enhance photon delivery and confer directional sensitivity to light? What if I told you that altering the passage of light through the eye is the first step in changing the size of the ventricles of your brain would believe that? Is this how people develop Normal Pressure hydrocephalus?

Is this why people with concussion get immediate photosensitivity as part of the TBI? Yep

5. No one in centralized medicine is making these connections because the labs studying UPEs are looking at bioelectricity instead of UPE transformation and topologic changes happening the eye.

these tightly packed mitochondria “focus” light for entry into the outer segment and that mitochondrial remodeling affects such light concentration. This “microlens”-like feature of cone mitochondria delivers light with an angular dependence that determines retinal photoreceptor damage. That damage then is propagated via electric resistance changes to the rest of the connectome via current flow.

Why are kids becoming more crazy than at any time in human history? This post explains it in detail.

Stack the lessons.

6. In primates and human cells, mitochondria form a reticular network surrounding the nucleus. However, cone photoreceptors of the retina in humans have an abundance of tightly packed mitochondria, which are arranged into an elongated bundle as seen below.

This bundle occupies the ellipsoid, the distal portion of the cone inner segment (IS), immediately proximal to the light-sensitive outer segment (OS).

7. Why has centralized opthalmology failed you?

Generally, they have assumed that such a high density of mitochondria at this unusual location is optimally situated to supply ample adenosine triphosphate (ATP) to support phototransduction in the cone OS because that is what is in the BigHarma medical school curriculum.

They never pushed back on BigHarma education because the evidence for 50 years has shown that photoreceptors ALWAYS rely more on glycolysis than mitochondrial oxidative phosphorylation for their energy needs. In fact the retina uses more Warburg emtabolism than any other organ per volume in humans.

This is another reason why biochemist Seigfried beliefs that Warburg metabolism is pathologic. If he was right every humans should have cancerous retinas. We don't. The reason we use it is because this part of the retina does not get much oxygen from the RBCs.

So this means, there must be another reason that mitochondrial cones receptors in our retina operates this peculiar way, no?

Is this why the RPE is loaded with melanin? Is it an fire wall for this design?

8. The more likely reason is topology and polarization effects. This situation explains why our retina's are built backward. It allows the mitochondria to act as a posterior lens in the eye to improve the signal in light and reduce the noise. This helps craft the perfect UPE signal as an output.

9. The decentralized explanation for this precise arrangement of cone mitochondria lies in their role in shaping the path of light as it passes toward the Outer segment of cones.

The vertebrate retina has an inverted structure with many neural layers through which light must pass before successful detection by the photoreceptor OS.

Thus, there placed substantial evolutionary pressure upon the retina to facilitate light delivery to the OS for detection. This is why you always hear me rail against PhDs touting their data in nocturnal animals and thinking it links to humans.

They say it because they do not understand every tweet in this thread. They are ignorant of evolution, light, and how all the pieces fit together.

For instance, in nocturnal mammals, the compact arrangement of chromatin in rod photoreceptor nuclei is believed to minimize light scatter.

CITE

Solovei, M. Kreysing, C. Lanctôt, S. Kösem, L. Peichl, T. Cremer, J. Guck, B. Joffe, Nuclear architecture of rod photoreceptor cells adapts to vision in mammalian evolution. Cell 137, 356–368 (2009).

In addition, Müller glia, support cells that axially span the retina from its inner surface to the base of the photoreceptor IS, have been shown to have optical fiber–like light guidance properties. I told people this in my Vermont 2018 talk and showed them a cover of a journal that showed this relationship. Note the dates on the cites below.

CITES

1. K. Franze, J. Grosche, S. N. Skatchkov, S. Schinkinger, C. Foja, D. Schild, O. Uckermann, K. Travis, A. Reichenbach, J. Guck, Müller cells are living optical fibers in the vertebrate retina. Proc. Natl. Acad. Sci. U.S.A. 104, 8287–8292 (2007).

2.S. Agte, S. Junek, S. Matthias, E. Ulbricht, I. Erdmann, A. Wurm, D. Schild, J. A. Käs, A. Reichenbach, Müller glial cell-provided cellular light guidance through the vital guinea-pig retina. Biophys. J. 101, 2611–2619 (2011).

3. A. M. Labin, S. K. Safuri, E. N. Ribak, I. Perlman, Müller cells separate between wavelengths to improve day vision with minimal effect upon night vision. Nat. Commun. 5, 4319 (2014).

This is not a new idea. It was ignored by centralized opthalmology at your peril.

The photoreceptor inner segmentconstitutes the last structure that light must pass through before reaching the OS. There, the SHAPE of photoreceptors and their elevated average refractive index have been recognized for their similarity to the design of miniature dielectric antennas. SHAPE and SIZE = topology effect folks. 2016 they gave a Nobel for it.

You starting to see what they all missed?

10. Where is my Vermont 2018 talk to fact check me?

patreon.com/posts/nourish-…

11. What else did they miss? The UPE story. patreon.com/c/DrJackKruse

12. Here is the Muller Cell paper. pnas.org/doi/10.1073/pn…

The picture of the Muller cells is on the cover of Proceedings of the National Academy of Sciences (PNAS) featured on June 12, 2007, issue of the journal.
The cover illustration by Andreas H. Reichenbach accompanies a study in the issue that found Muller cells act as living optical fibers, guiding light through the vertebrate retina to the photoreceptors. The artwork showing Muller cells as fiber optic cables

The cover shows stylized Muller cells functioning as a high-tech fiber optic plate, a striking visual metaphor for the biological discovery.

The featured article, "Müller cells are living optical fibers in the vertebrate retina," demonstrated that these glial cells, which span the entire thickness of the retina, act as waveguides. This mechanism efficiently transports light to the light-sensitive rods and cones, minimizing scattering and distortion.

The context: This discovery helped explain how the vertebrate eye's "inverted" retinal structure, where light must pass through several layers of cells before reaching photoreceptors, is optimized to prevent image degradation.

13. When these things are all jacked up this is how eye disease like keratoconus, AMD, and cataracts occur. Centralized Opthalmology has no answers for these conditions. patreon.com/posts/decentra…