Thread by @DrJackKruse

Photoreceptors are useless without retinal, which is produced in the eye. When retinal is liberated oxygen becomes a toxin and Fe is a wrecking ball.
phys.org/news/2018-08-c…

nnEMF activates VGCCs, flooding cells with Ca²⁺ and ROS/RNS, damaging mtDNA and heme proteins (cytochromes, CYP11A1, CYP19A1). Blue light liberates retinal, impairing melanopsin and dehydrating melanin, lowering éR and DDW production. This stalls StAR (STARD1)-mediated cholesterol import via TOM/TIMM/VDAC2, blocking pregnenolone synthesis.

Dehydrated melanin disrupts microtubule dynamics and protein synthesis, exacerbating "pregnenolone steal" toward cortisol, depleting sex steroids. The retina, as a "window to the brain," thins under suboptimal light causung blindness, degenerating brain tissue (e.g., frontotemporal dementia precursors). nnEMF/lack of sun alters AMO in skin/eye, changing central retinal pathways. Oxidative stress increases peroxide (ROS) levels, altering UPE signatures and heme construction, and is linked to hormone-related disorders by disordered UPE transformation in the CYP enzyme system.

In humans, iron is a double-edged sword, especially in the brain. It’s essential for energy production in mitochondria and for synthesizing neurotransmitters like dopamine, which governs movement and reward. Iron accumulates naturally in the brain as we age, particularly in regions like the basal ganglia, globus pallidus, and substantia nigra. These areas, rich in gray matter, hold two to four times more iron than white matter, where myelin insulates nerve fibers.

But when iron accumulates excessively, trouble brews. In neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and Friedreich’s ataxia, iron overload in neurons triggers oxidative stress, resulting in the production of reactive oxygen species (ROS) that damage lipids, proteins, and DNA. This process, known as ferroptosis, is particularly devastating in the retina, where photoreceptors and intrinsically photosensitive retinal ganglion cells (ipRGCs) are particularly vulnerable.

These cells, which detect light to regulate our circadian rhythms, rely on iron-containing proteins and melanin, a pigment that chelates iron to protect against oxidative damage. When this balance falters, ferroptosis destroys neurons, disrupting circadian signaling and contributing to diseases such as Parkinson’s, where the loss of dopamine-producing neurons in the substantia nigra is linked to iron overload and reactive oxygen species (ROS).

Why does iron accumulate in sick or dying neurons? The answer echoes the stars. Just as a star amasses iron in its core as it runs out of energy, neurons hoard iron when their energy production falters, often due to mitochondrial dysfunction. In both cases, iron signals a system on the brink, teetering between stability and collapse.

2. 95% of melatonin is made from mitochondria. So what happens when mitochondria are damaged from blu elight toxicity? You get high blood glucose and insulin and flatlined cortisol.

What happens when you knock out melatonin receptors via melanopsin dysfunction from the liberation of Vitamin A? You get insulin resistance and set the stage for many mitochondrial diseases like diabetes and cancer.
Do you know what I'm talking about? Light shapes life. How is it shaping yours? The link below should open your mind.
onlinelibrary.wiley.com/doi/full/10.10…

3. Here are more links of blue light and photoreceptor damage.

4. We only have what we give to others. Lift another up today with your wisdom.

5. Retinal is also tied to the circadian clock and photorepair. Disruptions to RBP4 rhythms is often from poorly timed light exposure, (no sunrise) and can elevate or desynchronize RBP4, contributing to insulin resistance, glucose dysregulation, and even immune imbalances. The link between RBP4 (retinol-binding protein 4) levels and the timing of sunlight exposure is primarily mediated through the circadian system, where light acts as a key zeitgeber (time-giver) to synchronize internal clocks that regulate RBP4 expression and function.

RBP4, a carrier protein for vitamin A (retinol) mainly produced in the liver. It isn't just a static metabolic player, its levels oscillate diurnally, peaking and troughing in alignment with the light/dark cycle.

This rhythm is driven by core clock genes like BMAL1, DBP, and REV-ERBα (heme photoreceptor), which control hepatic RBP4 transcription and its downstream effects on insulin sensitivity via the STRA6 receptor in adipose tissue.

6. Does melatonin control the epigenetic clock in humans? It does. One component it controls is DNA methylases. DNA demethylation is the process of removal of a methyl group from nucleotides in DNA. DNA methylation on cytosine at CpG sites on a gene promoter leads to the silencing of gene expression, while DNA demethylation of a gene promoter is linked to transcriptional activation and gene expression. Most diseases of aging are associated with hypermethylation of the brain and brainstem and this correlates with low NAD+ and low melatonin levels as the pictures above show.

TET2 gene epigenetically controls the onset of this process in humans and apes.

7. TET2 gene epigenetically controls the onset of this process in humans and apes. The Ten-Eleven Translocase-2 (TET2) enables elevated levels of GnRH gene expression and maintenance of male reproductive function. This is important for infertility, use of the baldness drugs which induces hypermethylation, and in cancers of the male genitals like testicular cancer. Blue light and nnEMF stimulate hypermethylation in man.......

Reproduction depends on the establishment and maintenance of elevated GnRH neurosecretion. The elevation of primate GnRH release is accompanied by epigenetic changes. Specifically, cytosine residues within the GnRH gene promoter are actively demethylated, whereas GnRH mRNA levels and peptide release rise. It has been found that TET2 expression increases with age in the developing preoptic area-hypothalamus and is substantially higher in a mature (GT1–7) than an immature (GN11) GnRH cell lines.

This indicates to those paying attention to why infertility and pregnenolone steal syndrome occurs when free T3 is low or Vitamin A is running wild in the plasma due to an altered light environment become a wrecking ball to all these proteins.

Accumulation of higher oxidation products depended on TET, which ultimately is linked back to the global effect of melatonin in a cell to scavenge free radicals that are driving the oxidation of TET enzymes which alter the methylation pattern of the entire genome. Science has once again underestimated the human epigenetic toolbox and its ability to lead to disease or wellness. 5-methyl- cytosine (mC) can be oxidized to 5-hydroxy-methylcytosine (hmC) by TET enzymes, members of the α-ketoglutarate–dependent oxygenase family. This family is deeply related to anions generated in the TCA cycle. This was discussed in my Kreb's bicycle blogs on Patreon.

Sunlight unmethylates our genome to provide longevity. nnEMF exposure does the opposite as the slide below shows. AM sunlight is more critical to get right than PM sunset but in cases where you are trying to renovate a disease both must be used in unison.