I want to embrace where the human species is today.
1 in 6 people globally affected by infertility. The number is close to 2.5 out of six in Americans. I consider infertility in humans as I would consider a mutation in DNA or mutant disease. Today we know we can rescue fruit flies from their genetic fate using light. The science of optogenetics is telegraphing us that our use of light today in technology is a huge problem. This implies that light maybe behind why humans are becoming infertile at record rates in a modern world that is blue lit, filled with RF and microwaves pulse radiation while blocking the healing rays of the sun in the visible spectrum.

Did you know oocytes have some unique characterisitics when it comes to light? Melanin levels in cells seem to control their backround fluorescence. When melanin is absent in a low concentration this decreases the intrinsic fluorescence of the oocyte. Conversely when melanin levles are raised in an oocyte, this increases the fluorescence of the oocyte. I'd like you to recall that in disease states associated with higher heteroplasmy, eukaryotes release more light. In health they tend to conserve their light release. Given these facts, do you see something unusually about the mammalian oocyte? Females are bron with all their eggs and this cell is the largest cell in their body and this cell is actively emitting UV light. This seems counterintuive to the centralized mindset. But it makes perfect sense to a decentralized thinker.

Melanin is a useful molecule in the lab for suppressing background fluorescence due to its wide range of absorbance of electromagnetic signals. In fact, it is well known in the literature that the expression of melanin in oocytes causes the animal pole to be darker visually and more light absorbent and thus have less fluorescent background compared with the lighter-colored vegetal pole.
Did you know human females at birth limit melanin in their oocytes? Did you know at puberty they change their melanin expression by using salt induced kinase inhibitors to increase melanin production in the oocyte which acts to conserve ultraweak UV light release during ovulation.
Salt-inducible kinase (SIK) inhibitors has been demonstrated to regulate the activity of the transcription factor CREB which is linked directly to the clock genes, and it plays a key role in controlling melanin pigment synthesis in the skin.

Do you know what kind of melanin the human oocyte makes to run this script? Did you know that neuromelanin is created from from regualr melanin stores in the neural crest derivatives from the oxidation of dopamine? (Zeise et al., 1992) Did you know that oocytes are loaded with dopamine?
Did you know that centralized science has no idea what oocytes are loaded with dopamine?
High levels of dopamine (DA) have been described in human ovary in 2005 and we now have evidence for DA receptors in granulosa and luteal cells, as well. However, neither the full repertoire of ovarian receptors for DA, nor their specific role, is established. What if I told you, the purpose of the dopamine was to age the germ line faster than the colony of the mitochondria in all other cell lines in a woman. Would you buy this?
It turns out mitochondria have small-molecule salt induced kinase inhibitors (SIK inhibitors) that when generated by endogenous light signals of the oocyte induce a topical change in melanin in an oocyte. Few people know that humans can inducing cutaneous pigmentation independently of UV irradiation in human skin using alterations in your salt concentration. I warned my audience about salt changes and UV fluorescence in my Vermont 2018 talk but y'all wanted it all dumbed down.
Well, soon you'll get the implication of the decentralized wisdom I gave in you 2018 Vermont with a new biophysics education on Patreon. Mujahid et al. 2017 was a key paper in me figuring out why infertility now affect 2.5 out of six Americans.

Is fecundity, fertility, and successful pregnancy all linked to circadian biology via melanin and melatonin biological control over apoptosis and autophagy in mitochondria? The answer appears to be a big YES, if you read the literature. This has huge implications for extinction level events in anything that alters melanin and melatonin levels in humans. It is now clear melanopsin function has a similiar effect on the light receptors of man. Blue light and nnEMF cause photoreceptor extinctions. I wonder how long it will take the non-Black Swans out there to get this rather simple, yet significant message?

Women give rise to the mitochondrial progenitors in the homo sapiens. Reproductive ageing in female mammals and women is characterized by a progressive decline of ovarian function, manifested by a decrease in the quantity and quality of oocytes with advancing age. The reproductive tract of women is one of the first organ systems to show hallmarks of ageing, in comparison to other organs.
Exposure to nnEMF/blue light has been shown to lead to early menarche and early reproductive decline. Human society has radically changed in its use of light to be sure. But our civilization has also changed globally in other ways in last 120 years. Women are now part of the work force, and they are delaying a family for their career. They are using birth control at early parts of their development that impact the circadian clock machinery in the mitochondria of their oocytes. All of these factors are playing a role in global infertility. In societies where women are irradiate earlier and often the rates of infertility are higher than we find inmore primative parts of the human clade in other parts of the world.

In women, the reproductive system ages early in life and this represents a key insight to understand how human female age in general. How you experiene menarche, peri menopause, and menopuase matters to a dectralized MD.
The oocyte is recognized as the largest cell in mammalian species and other multicellular organisms. Mitochondria represent a high proportion of the cytoplasm in oocytes and mitochondrial architecture is different in oocytes than in somatic cells, characterised by a rounder appearance and fragmented network. Although the number of mitochondria per oocyte is higher than in any other mammalian cell, their number and activity decrease with advancing age.
Mitochondria integrate processes essential for oocyte function, such as energy production, biosynthesis, and redox homeostasis.

Mitochondria integrate numerous processes essential for cellular function, such as metabolic processes related to energy production, biosynthesis, and waste removal, as well as Ca2+ signalling and reactive oxygen species (ROS) homeostasis. Further, mitochondria are responsible for the cellular adaptation to different types of stressors such as oxidative stress or DNA damage. When these stressors outstrip the adaptive capacity of mitochondria to restore homeostasis, it leads to mitochondrial dysfunction. This is how children are born with high disease burdens via transgenerational epigenetics.
Dysregulation of mitochondrial processes have been consistently reported in ageing and age-related diseases.
Reproductive ageing in female mammals and women is characterised by a progressive decline of ovarian function, manifested by a decrease in the quantity and quality of oocytes with advancing age. The reproductive tract of women is one of the first organ systems to show hallmarks of ageing, in comparison to other organs.
Difficulty conceiving and infertility are treated as taboo topics in most nations and lead to significant psychological stress for those experiencing them (Patel et al., 2018). Although assisted reproductive technologies (ART) such as cryopreservation (the freezing of oocytes, sperm, or embryos) and in vitro fertilization exist, they are not ubiquitously available or successful and require substantial financial investment (Katz et al., 2011). Furthermore, a fertilized oocyte derived from a woman of advanced age has a higher chance of resulting in miscarriage, and/or aneuploid offspring like trisomy of chromosome 21, commonly known as Down syndrome (Bittles et al., 2007). With advancing age, a decline in mitochondrial number and function is observed in oocytes. Mitochondria are exclusively maternally inherited and therefore the original population present in the oocyte will give rise to all future mitochondria in the offspring (Jansen and de Boer, 1998). Thus, elucidating the mechanisms underlying the loss of mitochondrial function with ageing and why oocytes age much earlier as compared to other organ systems, may lead to new lifestyle strategies to prolong oocyte fitness and fertility in humans who want to avoid reproductive extinction.

SUMMARY
QUESTION: When you read this blog what is your gut reaction? Just think about that answer now. I'll share my thought as I wrote it below.
Disturbing the molecular clock in animal models leads to abrogated mitochondrial rhythmicity and altered oxidative respiration. Moreover, mitochondrial-dependent production of reactive oxygen species (ROS/RNS), which plays a role in cellular signaling leading to early aging in different tissues. It has also been linked to the circadian clock mechanism dysfunction.

Note in the above picture and its description how the ROR receptor for Vitamin A begins the ticking of your circadian clock mechanism. What does blue light and nnEMF all liberate from opsins? Vitamin A. You starting to see my perspective yet?

My gut instinct tells me the light used in technology has been cultivated as a means of human behavioral & population control. Future militaries will consist of AI, drones, robotics, and lasers and it will be turned on We The People, and not the enemies of the state. Today's humans are the enemy of the political class. Humans, if they continue on their current trajectory, will be reduced to the status of cattle. Your government is cultivating you for a future they are building for you at your expense as you reach out your hands to allow the handcuffs of technology to be placed on your wrist no fight or revolution. It is Plato's Allegory of the Cave circa 2024.

Is there a way to tan your body without the sun if your child has precocious puberty? Yes. I have taken on new Farm clients for this treatment in 2024 on a case by case basis. Work by Mujahid et al. recently published in Cell Reports has described how topical administration of first and second generation SIK inhibitors, called HG 9-91-01 (HG), YKL 06-061 (YKL1) and YKL 06-062 (YKL2), can increase melanin production in vitro and in vivo to reverse the effect of blue light toxicity in high risk young adults and children with these risk factors.

UV from the sun induces tanning in keratinocytes and it engenders the production and secretion of alpha-melanocyte stimulating hormone (α-MSH) from POMC, which binds to the melanocortin 1 receptor (MC1R) in melanocytes. The subsequent increase in cAMP and activation of protein kinase A phosphorylates the cAMP-responsive-element-binding protein (CREB), resulting in increased microphthalmia-associated transcription factor (MITF) transcription and increased melanin production.

This is a new way to help people solve massive problems from tech abuse in infertility and precocious puberty. I did not include it in the Melanin Renovation Rx because it requires a knowledgeable MD to optimize the process.
CITES
1. https://www.cell.com/current-biology/fulltext/S0960-9822(20)31073-3
2. Mujahid N, et al. A UV-Independent Topical Small-Molecule Approach for Melanin Production in Human Skin. Cell Rep. 2017;19(11):2177–2184.
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