FRONTOTEMPORAL DYSPLASIA AND GLP-1 DRUGS: WHY IS THERE A LINK?

The retina thins from the effect of man-made light and a lack of sunlight, and then your risk of Frontotemporal dementia rises. The OCT test is the best screening test for FTD. We have familial and mtDNA FTD.

The OCT test tells us the retina acts as a ‘window to the brain," and that window changes the photolithography of the retinal cells via the central retinal pathways. When the light is not optimal, the retina thins and the brain degenerates. Retinal degeneration has been detectable in mutation carriers prior to the onset of cognitive symptoms, establishing retinal thinning as one of the earliest observable signs of familial (frontotemporal dementia). nnEMF (man-made light) and a lack of sun lead to neural degeneration, which is primarily driven by the abnormal accumulation of misfolded proteins within neurons.

Light controls the confirmation bending of proteins. The DNA code controls the AA sequence and secondary bending, but quantum processing determines tertiary and quaternary bending by UPE transformation in cells. The most common protein abnormality in FTD is the tau protein, also known as TDP-43. These protein aggregates damage and kill nerve cells, leading to brain atrophy (shrinkage) and the resulting behavioral, personality, language, and movement problems characteristic of FTD. I believe this protein also thins the retina. Excess Manufactured Light is the main offender, but a lack of healing sunlight is the next big risk factor. The State enforced these changes during the Obama administration in 2008, and his vice president put the final nail in the coffin because it is set to become permanent in 2028. Now, governments are forcing people to use GLP-1 drugs to reduce light-induced obesity, and this will make FTD and other neurodegenerative conditions explode. None of these things are on the MAHA playlist because the people RFK Jr has hired are all ignorant when it comes to quantum biology and mitochondrial medicine.

Blue light increases RBC turnover in the retina and changes the oxidation state of iron, and this affects the synthesis of new heme proteins in the retina and brain. Oxidative stress is a key trigger in this disease because it increases peroxide production (ROS), which alters the UPE signature of cells in the construction of the heme proteins, which changes the photolithography inside the retina and brain. Changing the photolithography = altered protein folding via the Golgi apparatus and RER. TDP-43 is a biomarker of redox imbalance in FTD-related UPEs.

The path of energy in life, based on the evidence we have as a species now, is that Optical photonics began 13.8 billion years ago. The photoelectric effect was born from the rudimentary physics present in the early universe. Photonics precedes all chemistry of all types. Functional medicine does not realize this or teach it. Molecules were and are innovated by redox chemistry, and each one has an electromagnetic barcode to program its possible states around the star it evolved in. All living things release light in the form of biophotons, which is shown below. Biophotons and UPEs are two different terms for the same phenomenon.

The TDP-43 molecule is codified by light in its absorption and emission spectra. This links it to aberrant UPE production in the central retinal pathways, as blue light increases heme turnover to alter its biophotonic signal. Look at all the places a UPE can be made from in a cell to cause this disease on the slide. You'll also see that light carries spin information that can create this disease.

Where there is a change in matter (TDP-43), there must also be a change in atomic molecular geometry in that tissue. Where normal cellular geometry ceases to exist, we will find light as the key agent of change. When both exist in simultaneity, you'd better understand Fermat's law and the photoelectric effect to understand what a disease really is. Right now, in centralized ophthalmology, none of them do. See Bruce Willis story or Wendy Williams story to make sense of this science and it modern situation.

The new GLP-1 drugs also cause retinal thinning and blindness, which is why their use is linked to FTD.

THE BIOPHYSICAL CODA of FTD: When Turing realized morphology in all living things had a photonic timeline in Nature, he wrote a key paper on morphogenesis. Light signaling predates the emergence of biochemistry and molecular creation from redox chemistry. This paper suggested that a system of chemical substances, called morphogens, could react together as a symphony does and subsequently diffuse their electromagnetic, electrochemical, and photobiolelectric information through a tissue to sculpt it, changing its morphology without using the nuclear genome.

Turing stated in 1951 that this set of circumstances is adequate to account for the main phenomena of morphogenesis. In such a dissipative system, although the cells may originally be quite homogeneous at the embryo stage, this information upload may later develop a pattern or structure in the embryo due to the instability of the homogeneous equilibrium caused by light pollution in the parents' germ line, which is triggered by random disturbances in the tissue.

Those random disturbances are UPEs. The random disturbance he hypothesized about turned out not to be random at all. UPEs are created in cells through light-induced AMO interactions via redox chemistry, which directs their own sculpting from the nuclear genome. The UPE energy transformation is driven by the mitochondrial genome, which is subject to light in the environment to create UPEs and eventually by reactive chemicals like ROS/RNS inside all cells. Any disease linked to aberrant UPEs will always present as having a spectrum of maladies. FTD has that optical signature. So do many other neurodegenerative conditions.

CITES

https://www.ncbi.nlm.nih.gov/books/NBK559286/