A New Perspective on Diabetes

The State of Play in Diabetes

As of 2024, the global prevalence of diabetes has reached alarming levels, with over 537 million adults diagnosed with the condition and an additional 541 million classified as pre-diabetic. This dramatic increase underscores the urgent need for effective prevention and management strategies. Thirty years ago, in 1994, the global prevalence of diabetes was significantly lower, with approximately 135 million people affected. Sixty years ago, in 1964, the number was even lower, with around 30 million people diagnosed worldwide. This stark rise over the past several decades highlights the growing epidemic and the critical need for global health initiatives to address this issue.

The American Diabetes Association (ADA) defines Type 2 Diabetes Mellitus as a condition diagnosed when a patient's Hemoglobin A1C (HbA1C) level is 6.5% or higher, corresponding to an average blood glucose level of 140 mg/dL. In contrast, a normal HbA1C level is around 5.1%, equivalent to a blood glucose level of 100 mg/dL and an optimal level is around 4.6%. HbA1C measures the amount of glycosylated hemoglobin in the blood, providing an estimate of a person’s average glucose levels over the preceding 90 days. This definition is consistent with the diagnostic criteria used by many global health organizations, including the World Health Organization (WHO) and the International Diabetes Federation (IDF).

What is Diabetes Melitus?

"Diabetes Mellitus" is the original name for Diabetes which was appropriately named as it essentially means "sweet urine passing through," capturing the primary symptom of frequent urination and the presence of sugar in the urine that characterizes the disease. We will refer to this condition as simply diabetes to keep things simple. Diabetes has now been defined as a complex condition characterized by the body's inability to properly manage blood sugar levels, and it can manifest in several forms:

• Type 1 Diabetes: This form of diabetes occurs when the pancreas doesn’t produce enough insulin, a hormone necessary for alerting the body to the presence of sugar in the bloodstream. Without sufficient insulin, blood sugar levels remain high, leading to various health complications.

• Type 2 Diabetes: In Type 2 diabetes is the most common form and commonly called simply ‘diabetes’. In T2D the pancreas is able to produce insulin, but the body becomes resistant to it. This means that the insulin is not effective in lowering blood sugar levels. As a result, sugar remains free-floating in the blood, where it can caramelize proteins in the body, leading to various metabolic disturbances and complications.

• Type 3 Diabetes: Often referred to as Alzheimer's disease, Type 3 diabetes involves the brain's resistance to insulin and impaired glucose metabolism. This condition leads to neurodegeneration and cognitive decline due to disrupted insulin signaling and increased oxidative stress. The brain’s inability to properly utilize glucose exacerbates these issues, contributing to the progression of neurodegenerative diseases.

How does light govern metabolism?

When full spectrum sunlight made up of ultraviolet, purple, blue, green, red and infrared hits the surfaces of the eyes and skin, it triggers and powers every biochemical reaction in the body. Every biochemical reaction requires energy and information signalling in order to carry out its purpose. This means the intelligence within every single wavelength of light across this spectrum has a purpose when it reaches our eyes and skin in order to allow life to function well. For example, ultraviolet (UV) light exposure excites aromatic amino acids like tyrosine and tryptophan, leading to the production of neurotransmitters such as dopamine, serotonin, and melatonin and metabolic molecules such as nicotinamide adenine dinucleotide (NAD), and thyroid hormone T3, as well as the vasodilating nitric oxide and of course melanin one of the most important full spectrum photoreceptive substances covering the entire human body. Sulfated vitamin D3, histamine, and sulfhydryl groups of cholesterol in the skin are human photosynthetic chemicals activated by sunlight. Terrestrial UVA/UVB light controls the photolysis of adrenaline and sex steroid hormones.

UV and some visible light also create steroid hormones from LDL cholesterol requiring vitamin A and T3 as cofactors to lead to the creation of pregnenolone, DHEA and cortisol. Near-infrared (IR) light stimulates testosterone and progesterone production boosting leptin sensitivity and enhancing skin quality through the production of filaggrin and natural moisturising factor (NMF). It also creates highly structured water charge separating its molecules creating a battery within the water networks in the body. This IR light also stimulates mitochondrial energy and water production and activates stem cells. These processes not only support mitochondrial metabolism and efficient energy production reducing the risk of diabetes but also strengthen hormone levels, boost mood, cognitive function, and overall cellular health.

For diabetics, red blood cells (RBCs) play a crucial role in healing and regeneration. At the site of bone healing, RBCs act as ferry boats carrying UV light, which excites tryptophan a key amino acid. This UV light exposure can facilitate healing processes. Tryptophan is a precursor to important molecules like melatonin and serotonin, both of which are essential for regulating autophagy, the body's way of cleaning out damaged cells to regenerate newer, healthier cells. This autophagy process is critical for managing diabetes as it helps in the maintenance and function of pancreatic beta cells, improving insulin regulation and glucose metabolism.

Diabetics also often exhibit sleep dysfunction. Recent studies show a significant association between quantitative and qualitative sleep rhythm disturbances and an increasing prevalence of obesity. Furthermore, reduced sleep quality and duration lead to decreased glucose tolerance and insulin sensitivity, thus increasing the risk of developing type 2 diabetes. These findings highlight the importance of sleep and SCN circadian entrainment via light through the eye and skin in energy metabolism and diabetes management.

• Reference: This was from the January 2019 issue of Internist from the article ‘Importance of Sleep and Circadian Rhythm for Energy Metabolism’.

The below diagram from Hoff (1934) presents the complex interactions between different glands and their influence on bodily functions. Central to this model is the role of light as the primary controller of energy and informational signaling in all these processes. Full spectrum sunlight via its impact on the eyes and skin regulates all of these activities.

This light-driven regulation impacts various endocrine glands, including the parathyroid, adrenal, thyroid, gonads, and pancreatic islets. Light also governs the sympathetic and parasympathetic nervous system which play a crucial role in modulating these glands. The diagram below outlines this light mediated physiological functions, such as vegetative innervation (autonomic nervous system control), mineral balance, acid-base regulation, hemogram/leukogram tendencies (related to blood composition and immune function), body temperature, metabolic rate, and blood glucose levels. Light, through its interaction with the skin and eyes, directly influences the hypothalamus, setting off a cascade of hormonal signals that regulate these bodily functions. This demonstrates that light is not just a passive environmental factor but an active driver of the body's internal regulatory systems, governing both energy balance and informational signaling pathways crucial for maintaining homeostasis.

You now know that light exposure affects glucose metabolism through neural pathways. Activation of intrinsically photosensitive retinal ganglion cells (ipRGCs) by light can influence the hypothalamic suprachiasmatic nucleus (SCN) and subsequently affect brown adipose tissue (BAT) thermogenesis, thereby modulating glucose tolerance. [https://pubmed.ncbi.nlm.nih.gov/36669474]. The sun contains 42% infrared light and 16% red light demonstrating nearly 60% of sunlight is red and infrared light. It just so happens that this light is best at reducing high blood sugar levels, whilst high energy visible unbalanced artificial blue light is the light which raises blood glucose dramatically. Unbalanced artificial blue light from 420 nm to 455nm has been shown to suppress mitochondrial respiration/metabolism, leading to elevated systemic glucose levels, while red/infrared light (660-900 nm) can increase ATP production and reduce glucose levels. [https://pubmed.ncbi.nlm.nih.gov/36327250] This modulation of mitochondrial activity by light can directly influence systemic glucose concentrations.

Light governs leptin regulation through its interaction with the eye and skin, influencing the hypothalamus's leptin signaling pathway. Leptin, a hormone produced by subcutaneous fat, communicates energy status to the brain, particularly the hypothalamus. In fact, leptin is the energy accountant of the brain acting as the key hormone controlling growth and metabolism within the human living system. The light absorption spectrum of light relevant to leptin regulation primarily includes ultraviolet (UV) and infrared (IR) ranges. Leptin and insulin are like siblings, with leptin acting as the big brother who oversees energy storage and utilization, while insulin, the younger sibling, manages blood sugar levels, both working together to maintain the body's energy balance. They influence each other and are entangled; when one is influenced, so is the other.

UV and IR light emitted from our sun reach subcutaneous fat cells, modulating leptin production, which in turn signals the hypothalamus about the body's energy status. Light is a supplemental energy to food supporting all bodily functions allowing leptin in the brain and skin to communicate to increase satiety when under the power of sunlight. Light exposure through the eye influences the suprachiasmatic nucleus (SCN), the master clock of the body, orchestrating the release of various hormones, including leptin, and aligning them with the day-night cycle. By affecting both local production in subcutaneous fat and central signaling pathways in the brain, UV and IR light play critical roles in the biophysical process of leptin regulation. So, we now know that leptin is a solar driven hormone operating on a circadian cycle with low levels in the morning and high levels at night cluing us into the body requiring a large amount of sunlight in the AM and no light after sunset towards bed. And a somewhat minor indication by comparison, Leptin also indicates food consumption to be more important in the AM than the PM.

Leptin action in the central nervous system (CNS) exerts a powerful effect on blood glucose homeostasis. Early evidence demonstrated that leptin contributes directly to glucose regulation through experiments in leptin or leptin receptor-deficient mice. Both ob/ob and db/db mice, which lack leptin or its receptor, exhibit marked hyperglycaemia, hyperinsulinemia, and glucose intolerance, independent of their excessive body weight. Remarkably, the hyperglycaemia in ob/ob mice can be normalized by infusing leptin into the brain, highlighting that leptin’s effects on blood glucose homeostasis are mediated primarily via the CNS. The hypothalamus, including the arcuate nucleus (ARC), plays a critical role in leptin-dependent regulation of glucose homeostasis. Restoration of leptin action within the ARC alone is sufficient to normalize blood glucose levels in LepRb-deficient mice, implicating arcuate AgRP neurons in this regulatory process. Research indicates that PI3K signaling, rather than STAT3, mediates leptin’s effects on glucose homeostasis. Pharmacological inhibition of PI3K signaling prevents leptin-enhanced insulin sensitivity and glucose tolerance, and POMC-specific ablation of PI3K signaling disrupts glucose homeostasis.

Leptin's effects on blood glucose homeostasis extend beyond direct regulation to influence downstream systems that control the autonomic nervous system. In the hypothalamus, leptin suppresses hepatic glucose production via vagal innervation of the liver, a vital component of this effect. Leptin also impacts glucose and lipid metabolism in peripheral tissues through sympathetic outflow and activation of AMPK signaling. Furthermore, leptin indirectly influences blood glucose levels by limiting carbohydrate intake through its anorexic effects and by altering peripheral lipid metabolism alongside insulin. The glucose-lowering effect of brain leptin action involves both insulin-dependent and insulin-independent mechanisms. Leptin improves insulin sensitivity, enhancing its established role in blood glucose regulation. Importantly, leptin also lowers glucose levels independently of insulin, as demonstrated in mice and rats with ablated pancreatic β-cells treated with streptozotocin, where central leptin fully normalizes severe hyperglycemia.

Leptin receptor expression in GABA and POMC neurons is sufficient to mediate leptin's glucose-lowering effects, implicating AgRP and POMC neurons as key players in leptin’s antidiabetic action. However, the majority of leptin receptor-expressing neurons are GABAergic, suggesting other non-ARC neurons might also contribute to leptin’s glucose-regulating effects. Collectively, these data demonstrate leptin's powerful role in controlling blood glucose via mechanisms that are independent of, yet synergize with, the classic insulin-dependent model of glucose homeostasis. Leptin’s ability to regulate blood glucose, independent of food intake and body weight, underscores its critical role beyond appetite and obesity regulation. It coordinates a series of physiological responses, with blood glucose homeostasis as a significant endpoint. Leptin has shown promise in reducing hyperglycemia in leptin-deficient lipodystrophy and holds potential as a clinical treatment for insulin-deficient Type 1 diabetes.

• https://pubmed.ncbi.nlm.nih.gov/10485707 

• https://pubmed.ncbi.nlm.nih.gov/19574396

• https://pubmed.ncbi.nlm.nih.gov/18779578

• https://pubmed.ncbi.nlm.nih.gov/20855609

• https://pubmed.ncbi.nlm.nih.gov/24201279

• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670357/ 

• Farr, O. M., Gavrieli, A., & Mantzoros, C. S. (2015). Leptin’s Role in the Hypothalamic-Pituitary Axis and Other Systems. Neuroendocrinology, 102(3), 265-271.

• Klok, M. D., Jakobsdottir, S., & Drent, M. L. (2007). The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obesity Reviews, 8(1), 21-34.

The Diabetes Problem: Modern Light Alterations: Unbalanced artificial light and nnEMF

Unbalanced artificial light, particularly light at night (LAN), sends signals to the brain that it's still daytime. This suppresses melatonin, increases cortisol, and ruins sleep factors crucial for maintaining metabolic homeostasis. Disruption of circadian endocrine bioenergetics impairs glucose tolerance and insulin sensitivity. For example, exposure to LAN has been shown to acutely impair glucose tolerance in a time-, intensity-, and wavelength-dependent manner in rats [https://pubmed.ncbi.nlm.nih.gov/28374068]. This effect is mediated through the suprachiasmatic nucleus (SCN) of the hypothalamus, which acts as the master biological clock. The SCN instructs the hypothalamus, paraventricular nucleus, and pituitary, governing the sympathetic/parasympathetic nervous system, acid/alkaline regulation (pH), mineral balance (such as calcium and potassium), Red Blood Cell (RBC) to White Blood Cell (WBC) balance, body temperature, metabolic rate, and blood glucose levels [https://pubmed.ncbi.nlm.nih.gov/24673196].

LAN exposure affects the suprachiasmatic nucleus, which regulates circadian biology and rhythmicity, thereby impacting glucose and lipid metabolism. This disruption can result in increased body weight, glucose intolerance, and insulin resistance. A study on Chinese adults found that higher outdoor LAN exposure was significantly associated with increased fasting glucose, HbA1c, and insulin resistance, leading to a higher prevalence of diabetes in that test group [https://pubmed.ncbi.nlm.nih.gov/36372821]. These fields are particularly detrimental to our health if exposure occurs at night when our bodies are designed to be healing. A study demonstrated that light exposure during sleep increases insulin resistance and affects heart rate variability, suggesting a link between light exposure and cardiometabolic dysfunction [https://pubmed.ncbi.nlm.nih.gov/35286195]. Chronic exposure to LAN and EMFs is associated with metabolic disturbances, including increased triglycerides and a higher risk of diabetes. These effects are mediated through disruptions in biological clock mechanisms within the hypothalamus and alterations in glucose and lipid metabolism.

Most of the fields included in the broad category of nnEMF include non-visible radiation which also has a dramatically disruptive cascade of impacts for cell biology. When these nnEMFs reach our skin and eye surfaces and disrupt our visual and non-visual photoreceptor biology, they oxidize vitamin A, reduce vitamin D levels, dysregulate calcium signaling, decrease insulin secretion, increase blood glucose (independent of food intake), and interrupt nitric oxide homeostasis. Visual photoreceptors allow us to see, while non-visual photoreceptors enable us to determine biological time and regulate all biochemical processes, including hormone creation, release, and breakdown. Non-visual photoreceptors such as neuropsin (the UV light photoreceptor), melanopsin (the blue light circadian entrainment photoreceptor), and encephalopsin (the purple light entrainment photoreceptor) suffer collateral damage from nnEMF exposure. This damage leads to altered endocrine and fertility signaling, adverse nuclear gene expression, photophobia, and an inability to effectively capture and utilize full-spectrum sunlight to regulate biochemical reactions. These disruptions establish the metabolic conditions for diabetes, independent of food consumption.

Diabetes is closely associated with melanopsin dysfunction, with individual risk varying based on the redox state of the melanopsin-leptin axis. The human circadian system's response to light after sunset is highly susceptible and variable, largely dependent on the extent of melanopsin/retinol dysfunction present. This is crucial as the mechanisms by which exposure to non-native electromagnetic fields (nnEMFs) and artificial light can influence blood glucose and insulin levels significantly contribute to diabetes through several pathways.

Exposure to nnEMFs, such as those from Wi-Fi and other wireless radiation, has been shown to impair insulin secretion and increase oxidative stress in pancreatic islets. This can lead to hyperglycemia and altered glucose metabolism. For instance, a study demonstrated that Wi-Fi radiation (2.45 GHz) caused hyperglycemia and reduced insulin secretion in rats, accompanied by increased lipid peroxidation and decreased antioxidant enzyme activities [https://pubmed.ncbi.nlm.nih.gov/29913098]. Additionally, exposure to a 60-Hz magnetic field was found to induce hyperglycemia by altering the insulin/glucagon ratio and increasing oxidative stress [https://pubmed.ncbi.nlm.nih.gov/34083675].

nnEMFs can significantly disrupt the body's biophysics, particularly affecting the eye, skin, and gut. The eye, as the front side of the brain, has a direct connection to the hypothalamus and habenula nucleus, which govern biological timing and frontal lobe functions. nnEMF exposure dysregulates this otherwise carefully governed tract, oxidizes docosahexaenoic acid, creates oxidative free radicals, lowers the charge in cell membranes making them permeable to toxins, causes mast cell activation, leads to calcium influx into cell cytoplasm, and unstructured and dehydrates the body's water networks (blood is 93% water, cerebrospinal fluid is 99% water, etc.).

The skin, rich in photoreceptors and sensitive to electromagnetic fields, can also be disrupted, affecting cellular processes such as immune T and B cell repair and regulation. In the gut, nnEMF exposure can alter the microbiome and interfere with the gut-brain axis, impacting digestion and hormonal regulation involving gastrin, ghrelin, and leptin. These disruptions lead to cellular stress and oxidative damage, impairing insulin production by pancreatic beta cells and dramatically contributing to metabolic disorders like diabetes. This cascade of effects underscores how nnEMF exposure can undermine cellular function and overall metabolic health.

Dr. Nora Volkow's research at the National Institute on Drug Abuse has revealed that cell phone radiation increases blood glucose around the exposure site. Research involving school children exposed to higher levels of radiofrequency nnEMF from cell phone base stations found an increased risk of type 2 diabetes and higher average blood glucose levels compared to children with lower exposure [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4661664/]. Elevated blood glucose and insulin resistance due to nnEMF exposure lead to higher HbA1c levels over time with regular exposure to Wi-Fi, cell towers, Bluetooth devices, 4G and 5G reception, and wireless smart devices like Apple Watches, baby monitors, and wireless robotic vacuum cleaners.

Exposure to extremely low-frequency EMFs (e.g., 60-Hz magnetic fields) has been shown to induce hyperglycemia and alter lipid metabolism in animal models. This is mediated through changes in the insulin/glucagon ratio and cellular redox state. These magnetic fields are emitted by the power lines outside our homes, the copper electrical wires throughout our homes, and in our bedroom walls behind our heads where we sleep, and the technology devices we use every day [https://pubmed.ncbi.nlm.nih.gov/34083675].

In our modern world, these alterations in blood glucose, insulin secretion, and HbA1c due to various types of nnEMFs including light from phone screens, Wi-Fi routers, and electrical wires in your bedroom walls also raise triglycerides. As part of this metabolic cascade of destructive damage, it’s a biological certainty that reducing your exposure to these numerous fields will lower your triglycerides to around 75 mg/dL, which is considered a healthy range. Remarkably, this can occur independent of changing your diet! If you have tried minimizing carbohydrate intake and your triglycerides, fasting glucose, or HbA1c has not dropped materially, you likely have issues with unbalanced artificial light, wireless radiation, and other nnEMF in your environment.

We can now see that visible and non-visible light alterations within our environment impact our brains via our eyes and skin to destroy mitochondrial metabolism and dramatically dysregulate blood glucose and insulin secretion, the hallmarks of all 3 types of diabetes. Leptin, the master hormone, is intertwined in this process because insulin resistance and leptin resistance go hand in hand. Leptin resistant is a hallmark of metabolic processes, including glucose regulation and insulin sensitivity, becoming skewed, contributing to dysregulated blood glucose levels and broader metabolic dysfunction. Leptin, a crucial hormone for managing blood glucose levels, relies on precise signaling in the brain to regulate glucose homeostasis and energy balance. Disruptions caused by artificial light and nnEMF can impair leptin’s ability to accurately gauge and manage energy demands, leading to leptin resistance. This resistance blinds the body to its true energy needs and utilization, independent of food intake.

Food is created via photosynthesis which uses light and water to create what we eat. Missing either the light or the water from natures growth recipe and the food never grows. When we consume this food, we unpack the light and water inside our digestive tract with the electrons containing the light fingerprint of light it grew under and the protons containing the water fingerprint it grew with. So, what happens if someone consumes electrons and protons from glucose within carbohydrates that are out of season and grown in a different zip code requiring long-distance transport just to get to your location? The glucose metabolism pathways within the cytoplasm and mitochondria become impaired. The most important pathway affected here is metabolic complex 1 in the mitochondrial electron transport chain (NAD+/NADH). This is where highly excited electrons (food grown in strong light like bananas) from carbohydrates enter the mitochondria. The carbs here are the fuel and the exhaust here is the free radical called superoxide. As someone continues to eat these foods out of season whilst living under the influence of unbalanced artificial light and other nnEMFs their mitochondrial lose their ability to effectively metabolize fats and ketones and the superoxide radicals produced become excessive and the metabolic complex within the mitochondria gets worn out and breaks. This broken superoxide pulse within the mitochondrial respiratory chain is a hallmark of all diabetics.

At the same time, the body is becoming more insulin-resistant and leptin-resistant, meaning it becomes less effective at responding to food consumption. This results in poorer signaling of satiety and an inability to accurately monitor energy intake and expenditure within the brain and metabolic pathways. Consequently, blood glucose levels, triglycerides, and glycation of blood cells (measured as HbA1c) rise, leading from pre-diabetes to type 2 diabetes.

Now remember, here’s the kicker. With exposure to nnEMF including Wi-Fi, Bluetooth, cell phone radiation, artificial lighting especially after dark, AC powered devices and flickering lighting, electric cars, solar inverters, 5G, Alexa, Google Voice, airplane travel, power transmission lines, satellites and family members or neighbours’ devices, are powerful enough to create diabetes by themselves even if a healthy diet is consumed. Living in this modern AC electrically powered wireless digitally connected world under the power of artificial light is destroying brain health, creating a chronic alteration in metabolism and resulting in the presence of a completely preventable and reversable disease, diabetes.

Modern-day diabetes can be viewed as an environmental disease caused by unbalanced artificial light and non-native electromagnetic field (nnEMF) exposure. This condition is closely linked to melanopsin damage in the arterial tree within the body, leading to stiff vessels that fail to deliver adequate blood, oxygen, and electrons to distal tissues.

Unbalanced artificial light, such as that emitted from phone and computer screens or LED lights in homes and offices, along with wireless radiation from Wi-Fi routers, smartwatches, and Bluetooth earbuds, causes melanopsin, a crucial circadian photoreceptor, to break from its covalent bond with vitamin A. This disruption leads to an impaired ability to detect environmental light and an aldehyde radical of vitamin A that steals electrons from hemoglobin, initiating an oxidative cascade throughout the biological system.

Melanopsin photoreceptors are present in the eyes, arteries, and subcutaneous fat within the skin. Thus, both visual and skin exposure to nnEMFs are detrimental to our biological system. The increase in vitamin A analogues in the blood triggers a corresponding drop in vitamin D levels, weakening the immune system. Chronic exposure to unbalanced artificial light and nnEMFs can lead to autoimmune conditions like Type 1 Diabetes.

When artificial unbalanced light and other nnEMFs destroy melanopsin photoreceptors in our skin and eyes, the circulatory system suffers. Vascular calcification in humans can occur in either the intimal or medial layers of the arterial wall. Intimal calcification is associated with atherosclerosis, characterized by lipid accumulation, inflammation, fibrosis, and focal plaques development. Medial calcification is linked to arteriosclerosis, which involves age- and metabolic disease-related structural changes in the arterial wall, resulting in increased arterial stiffness. It is hypothesized that vascular calcification, whether intimal or medial, may directly increase arterial stiffness.

Both types of vascular calcification are likely linked to the extent of melanopsin damage in the system. By restoring melanopsin/retinol function in the arterial bed, we can potentially restore the return of nitric oxide (NO), melanopsin, and natural cannabinoids to the lipid membrane rafts, increasing their redox potential in these vessels. Enhancing their charge potential can reverse the calcification process without invasive procedures. These areas are rich in carbonic anhydrase and ascorbate, which help control protons, thus maintaining the shape and function of red blood cells (RBCs).

Diabetes is characterized by hyperglycemia and unbalanced artificial light damage. Hyperglycemia in diabetes leads to lower RBC ascorbate levels, increased RBC rigidity, and greater osmotic fragility, making them less likely to navigate small capillary beds. As melanopsin damage increases, RBC ascorbate levels drop, and RBCs morph into echinocytes. Consequently, melanopsin becomes a key candidate for driving microvascular angiopathy in diabetes. Research supports the link between nnEMF exposure and elevated blood glucose levels in diabetics.

Diabetics often suffer from poor DC electric current because they live indoors under artificial light. This sedentary, indoor lifestyle under artificial light and nnEMF leads to the destruction of Complex 1 (NAD/NADH) in mitochondria. Carbohydrates, which typically enter at Complex 1, can no longer be utilized efficiently, resulting in insulin resistance.

NAD/NADH is derived from vitamin B3 (niacin), which is synthesized from tryptophan, an aromatic amino acid with an absorption spectrum between 200nm and 400nm (UVC, UVB, UVA). Lack of sunlight exposure disrupts the electrical integrity of Complex 1 within mitochondria.

Deuterium, a heavy isotope of hydrogen, belongs in the blood, where it can absorb ultraviolet light and promote growth. However, nnEMF exposure lowers cell membrane electrical integrity, allowing deuterium to leak into the cytoplasm and enter metabolic pathways. One key area it impacts is the intersection of the TCA and urea cycles. Deuterium's extra neutron makes it twice as heavy as hydrogen, clogging cellular metabolism and tanking bioenergetics, leading to disease susceptibility. This misplacement of deuterium is a hallmark of metabolic diseases, including diabetes, autoimmune diseases, and cancer.

Within mitochondria, when Cytochrome C Oxidase (Complex 4) functions poorly due to deuterium infiltration, water conduction at the inner mitochondrial membrane is lost. This impairs nanoscopic protein folding of Complex 1 (NAD+), making quantum tunnelling of electrons inefficient and increasing reactive oxygen species (ROS), resulting in metabolic syndrome. While vitamin B3 can help with NAD+, it only addresses part of the issue. Natural sunlight in the ultraviolet spectrum is also required to activate NAD+ and allow it to function properly. Understanding vitamin B3 from a biochemical substrate viewpoint is only half the equation; the other half involves light's effect on these substrates, programming their electrons to create proper physiological effects.

In Type 2 Diabetes (T2D), exogenous niacin can be beneficial as it acts as a ketone mimic drug. Niacin, also known as vitamin B3, nicotinic acid, and vitamin PP, is an organic compound essential for human health. Niacin deficiency causes pellagra, a pandemic disease condition. Vitamin B3 can bypass a "broken" Complex 1 due to chronic ATP deficiency. It serves as a precursor to NAD+/NADH, crucial for proper mitochondrial function and activating the Pentose Phosphate Pathway (PPP), which is vital for restoring Complex 1 and optimal mitochondria. The aromatic amino acid tryptophan, absorbing full-spectrum UV light, forms the base of niacin, NAD+, and NADP+. Without UV light, none of these work as they should in cells.

Niacin cannot be directly converted to nicotinamide, but both compounds can be converted to NAD+ and NADP+ in vivo, provided the redox potential is greater than -200mV. Redox potential measures the charge from one end of the mitochondria to the other, from Complex 1 to oxygen. Red/IR light stimulates cells to replace defective mitochondrial engines, while unbalanced artificial light damages them.

When Complex 1 has misfolded electron transport proteins due to poor redox (e.g., quinolone issue of CoEnQ10), fats that feed into Complex 2 (FADH2) must be consumed predominantly to avoid massive ROS production that overwhelms the cell's redox potential, dropping it from -400mV. This raises blood retinol (vitamin A) levels while lowering vitamin D levels and causes pregnenolone steal syndrome, which lowers all hormones. Chronic pregnenolone steal syndrome eventually shortens telomeres, leading to cellular signaling problems that cause senescence or advanced early aging.

Chronic loss of NAD+ indicates a loss of negative feedback control of the ubiquitin cycle, directly affecting our molecular circadian clock and peripheral clock genes (CCGs). As mitochondrial redox charge drops, NAD+ accumulates relative to NADH levels.

In a lifestyle dominated by unbalanced artificial light, redox potential drops below -200mV, and a ketogenic diet can worsen the situation by exacerbating obesity if unbalanced artificial light and nnEMF exposure persist, especially during spring and summer. When mitochondrial redox drops below this threshold, it indicates a proton problem, usually related to excessive deuterium leaking into the mitochondrial matrix via the UCP-2 mechanism. The solution involves mitigating artificial light frequencies with unbalanced artificial light blocking glasses, protecting skin from these frequencies, reducing other nnEMFs like wireless radiation, and increasing natural sunlight exposure

How do we know type 2 diabetics are solar deficient?

Every type 2 diabetic is vitamin D deficient, as demonstrated in these studies: https://pubmed.ncbi.nlm.nih.gov/34017921/ and https://pubmed.ncbi.nlm.nih.gov/27114101/. We generate vitamin D from UVB sunlight exposure, which can help protect human metabolism and potentially reverse type 2 diabetes. Sunlight has many more benefits on the immune system and metabolism beyond vitamin D synthesis. It stimulates nitric oxide production, lowering blood pressure and improving cardiovascular health. Sunlight also modulates the immune system, reducing inflammation and benefiting conditions like multiple sclerosis and type 1 diabetes. Additionally, sunlight regulates circadian rhythms by influencing melatonin and serotonin levels, enhancing mood and mental health. Regular sunlight exposure may reduce the risk of certain cancers, including colorectal, breast, and prostate cancers. It also supports a healthy endocrine system, circadian rhythm, mitochondrial health, nervous system regulation, blood pressure regulation, and sleep, among other benefits. Relevant studies include https://pubmed.ncbi.nlm.nih.gov/23264189/, https://pubmed.ncbi.nlm.nih.gov/28009891/, https://pubmed.ncbi.nlm.nih.gov/27876126, and https://pubmed.ncbi.nlm.nih.gov/33376202. An excellent study on the Vitamin D-independent benefits of safe sunlight exposure as it relates to type 1 and type 2 diabetes, multiple sclerosis, and cancer can be found here: https://pubmed.ncbi.nlm.nih.gov/34329737/.

Vitamin B12 and Vitamin D3 are linked to solar exposure. A lack of sunlight can lead to leptin resistance and diseases that damage the NAD+/NADH redox couple at complex 1. The absence of artificial light at night is critical for the solid-state conversion of serotonin via methylation, which mediates circadian clock plasticity in both the SCN and peripheral clocks in all organs. This biochemical process requires a coherent domain of structured water within the body's water networks and the presence of Vitamin B12 and folate. B12 is synthesized in the liver under sunlight exposure, while folate is destroyed by full-spectrum sunlight and produced in the dark when artificial light is absent. This differentiation helps determine solar deficiency versus artificial light toxicity. B12 deficiency can result in leptin resistance, as noted in http://www.medscape.com/viewarticle/872008.

Non-native electromagnetic fields (nnEMFs), including unbalanced artificial light exposure, contribute to metabolic syndrome and diabetes by creating the Melanopsin/Vitamin A problem. This leads to low melatonin levels, poor mitochondrial DNA function, and problems in the eye and skin, constituting an unbalanced artificial light hazard. When the circadian mechanism is disrupted, enterocytes do not turn over every 24-48 hours, allowing deuterium to enter the liver, which significantly contributes to diabetes. The process begins with artificial light exposure in the eye and skin, disrupting the peripheral clock mechanism in the gut and liver. Insulin, a solar hormone, has a diurnal rhythm independent of glucose intake. Artificial light via the eye or skin can activate digestion and stimulate insulin secretion without food in the gut, as melanopsin lowers melatonin by altering retinol function, ruining photoreceptor function that controls the circadian mechanism.

Diabetics with age-related macular degeneration (AMD) and/or cataracts are expected to have significantly different plasma glucose changes than patients without eye disease. Ambient light's entry into the eye has a massive influence on glucose balance regulation in humans, as demonstrated by Hollwich and Diekhues in 1967 and 1971. Oral or IM injections fail to reverse these issues because pharmaceutical solutions typically act on gut hormones and do not address the eye or skin.

• Reference: Studies by Jarrett (1974), Lakatuna et al. (1974), Lestradet et al. (1974), Reinberg et al. (1974), and Thum (1975) support these recommendations.

Childhood Type 1 Diabetes Mellitus (CT1DM)

In a comprehensive 2017 study on Childhood Type 1 Diabetes Mellitus (CT1DM) encompassing data from 72 countries, researchers found a concerning global increase in the incidence of CT1DM. This rising trend is particularly alarming given that children under the age of seven with diabetes are at a high risk of cognitive dysfunction and poor glycemic control. Such poor glycemic control can induce hypoglycemia, which has the potential to adversely affect the developing nervous system.

Additionally, the study highlights a geographic and environmental component to the incidence of CT1DM. Specifically, the incidence is notably higher in regions with higher latitudes and lower sunshine durations. This correlation suggests that reduced sunlight exposure, increased indoor living under unbalanced artificial light and surrounded by invisible nnEMF such as Wi-Fi has negative effects on leptin and insulin regulation, vitamin D synthesis, melanopsin circadian entrainment, G6PD function, mitochondrial metabolism and proper brain blood sugar regulation. Burying the full rainbow of sunlight from reaching your eyes and skin and introducing artificial frequencies of light whilst eating food out of season are the reasons we are seeing the increased prevalence of childhood diabetes in these areas.

Understanding these factors is crucial for developing targeted strategies to manage and prevent CT1DM, emphasizing the importance of considering environmental influences on disease incidence and glycemic control.

Cite 1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634499/#CR1

Cite 2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634499/#CR3 

Cite 3: https://pubmed.ncbi.nlm.nih.gov/15864338

Cite 4: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7500018/

Cite 5: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337255/ 

Cite 6: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4149588/ 

Eating Out of Season and Its Link to Diabetes

In diabetics increased glycosylation of haemoglobin increases its affinity for oxygen, thus, oxygen delivery is altered. Diabetics suffer from poor superoxide levels and tend to have very low levels of sulfated Vitamin D3 naturally. They are usually unbalanced artificial light toxic, and they rarely are out in normal sunlight to harness the UV and IR powers in sunlight. Food exacerbates the diabetic person, but a lack of sunlight and too much fake light are behind why it really happens.

Carbohydrates don’t cause type 2 diabetes by themselves; they just make it worse. 

Artificial light and non-native electromagnetic fields (nnEMF) disrupt photoreceptor biology in the skin and eyes, leading to oxidative stress, reduced vitamin D levels, dysregulated calcium signaling, and increased blood glucose levels independent of food intake. These disruptions impact insulin secretion and nitric oxide homeostasis, further contributing to metabolic dysfunction. Non-visual photoreceptors like neuropsin, melanopsin, and encephalopsin play crucial roles in regulating biochemistry, including hormone creation and release. Exposure to nnEMF leads to altered endocrine signaling and adverse gene expression, contributing to conditions like diabetes.

Diabetics and those with fatty liver disease can benefit from consuming eggs and seafood due to their choline content. Choline is an essential nutrient that plays a critical role in liver function, fat metabolism, and cellular structure. It is a key component of phosphatidylcholine, a major phospholipid that makes up cell membranes and lipoproteins. In the liver, choline helps prevent the accumulation of fat by promoting the export of triglycerides and cholesterol. This process reduces the risk of non-alcoholic fatty liver disease (NAFLD), which is common in individuals with diabetes. Choline also supports the synthesis of acetylcholine, a neurotransmitter involved in various metabolic processes. For diabetics, choline helps maintain insulin sensitivity and glucose metabolism. It supports methylation reactions necessary for DNA repair and gene expression, which are crucial for proper cellular function and energy production. Dietarily this is a wiser move compared with consuming a high intake of glucose and fructose which inhibits glucose-6-phosphate dehydrogenase (G6PD), which leads to increased oxidative stress and pancreatic beta-cell apoptosis, contributing to diabetes. However, just the consumption of high glucose/fructose foods is not going to cause diabetes, instead it’s the consumption of these out-of-season that exacerbate these issues. Remember, the light the body unpacks from these equatorial foods compared with the light your eyes and skin are receiving is at a mismatch regulating insulin, leptin and delivering incoherent signals to the body’s metabolic organs the mitochondria., resulting in metabolic dysfunction. Artificial light and non-native electromagnetic fields (nnEMF) provide further incoherent environmental light signals to the body, further inhibiting G6PD and increasing blood glucose levels.

G6PD is crucial in the pentose phosphate pathway (PPP), providing D-ribose as an alternative fuel for cellular processes. Disruption of G6PD by unbalanced light exposure and eating out-of-season foods results in a lack of proper cellular energy metabolism, highlighting the importance of mitigating these artificial sources of visible and non-visible light, experiencing full spectrum natural light exposure and consuming seasonally appropriate diets for optimal metabolic health.

When one eats a diet high in fructose (which contains a lot of deuterium), this will also lower zinc levels in cells. This lowers testosterone in men. Higher fructose levels also cause a transient magnesium deficiency in all cells in both sexes when this occurs chronically.  Acutely, it changes it at the intestinal brush border. This lowers the magnesium available to make ATP (energy) if it goes on too long. Therefore, magnesium deficiency is so common in people who eat carbohydrates in a low light mismatched environment (out-of-season) (T2D alert!).  This is also why most diabetics suffer from low magnesium stores and over time this will destroy their sleep and cause peripheral neuropathy too.

Living in a strong solar environment can mitigate the effects of a high-fructose and carbohydrate diet by raising vitamin D, T3, LDL, DHEA, and melatonin levels. Fructose naturally appears in foods grown in strong photosynthetic environments with full-spectrum sunlight. Therefore, consuming fructose without corresponding UV/IR light exposure is unnatural and harmful. Nitric oxide, produced by UV light, counteracts the inhibitory effects of fructose on endothelial nitric oxide synthase which would otherwise lead to lower quality blood and circulatory health. Nature couples’ fructose and sunlight to balance their effects, emphasizing the importance of eating seasonally appropriate foods.

Healing Diabetes

Healing type 2 diabetes involves healing the brain via light exposure through the eyes and skin to balance blood glucose, eating in season food optimizing light signalling in the gut and at the same time mitigating the effects of artificial light and non-native electromagnetic fields (nnEMF). Type 2 diabetes is reversible through restoring the photoreceptor system in the eyes and skin, depleting deuterium from the mitochondrial matrix, restoring dopamine/melatonin/serotonin/NAD via experiencing all parts of the full spectrum of sunlight from ultraviolet to infrared which restores the function of the suprachiasmatic nucleus (SCN), enhances leptin signaling in the hypothalamus and reducing inflammation in the gut via coherent internal light signals via consuming in-season food. This process balances blood glucose levels and regulates insulin, a solar-driven circadian hormone. Blocking excessive blue light, especially from artificial sources, aids in healing by preventing the disruption of leptin and glucose signaling pathways, thus maintaining hormonal balance and proper metabolic function.

Type 1 diabetes is much harder to reverse due to the significantly worse state of mitochondrial health in affected individuals. In type 1 diabetes, the autoimmune destruction of insulin-producing beta cells in the pancreas. The mitochondria in these individuals are often more damaged, inheriting more damaged mitochondria from their parents and being gifted a higher mitochondrial DNA mutation rate thus a lowered ability to produce water and energy effectively at a cellular level resulting in higher oxidative stress. This fundamental difference in the disease mechanism makes type 1 diabetes more challenging to manage and reverse compared to type 2 diabetes.

The reversal of Type 1 Diabetes hinges on the regrowth of islet cells in the pancreas, which are responsible for insulin production. The possibility of reversing Type 1 Diabetes depends on the extent of damage to these cells. There are many anecdotes of those with T1D altering their lifestyles and spending time in tropical zones recovering some insulin secretion. The question of how long they need to spend or how much function they can recover is case specific and based around the extent of the metabolic and immunologic dysfunction. To evaluate this, one can measure the basal release of insulin while exposed to UV light, which can provide insight into the capacity for reversing the condition. The goal is to encourage the pancreas to begin producing insulin again, which is a testable outcome. A stronger solar environment stimulates the regrowth and function of islet cells in the pancreas due to increased UV light exposure, which enhances the body's natural insulin production. Additionally, tropical environments help mitigate complications associated with Type 1 Diabetes, such as neuropathy and nephropathy, by promoting overall metabolic and immunologic health through natural light exposure and vitamin D synthesis.

Conclusion

150 years ago, human life was naturally aligned with the rhythms of the environment. In winter, embracing the cold, utilizing available sunlight, consuming local foods typically more ketogenic during the winter and adjusting sleep patterns and water intake according to seasonal changes were integral to maintaining metabolic health. Specifically, people would consume more deuterium-depleted water in winter and less during summer, gain some fat mass in summer, and lean out in winter. These seasonal adaptations supported robust mitochondrial function and metabolic stability throughout the year.

In contrast, the modern world presents a vastly different environment. Today, approximately 30 billion artificial light sources are active globally at any given time, collectively emitting over 1,000 gigawatts of artificial light. Alongside this, there are roughly 10,000 functional satellites orbiting Earth, contributing to our electromagnetic exposure. On the ground, around 80 million radiofrequency-transmitting cell phone antennas connect 5.3 billion mobile phone users, while an additional 21 billion wirelessly connected devices, including tablets, smartwatches, televisions, and portable computers, further increase the electromagnetic load. This unprecedented exposure to non-native electromagnetic fields (nnEMF) marks a significant departure from the conditions our ancestors experienced. The rapid proliferation of artificial radiation and EMF in our environment has occurred with little time for our biological systems to adapt. Consequently, we now find ourselves navigating a technologically connected and artificially illuminated existence, with the long-term impacts on health and well-being still being assessed.

These form the basis of modern-day environmental stressors collectively called nnEMF which include radiofrequency radiation, microwaves, dirty electricity/electromagnetic interference, alternating current (AC) electric and magnetic fields and low-level currents, along with artificial high energy narrow-band visible light (HEVL) and light flicker. These are mitochondrial toxins as they collapse the electrical membrane potential, alter the oxidative radical signalling magnetically and provide unbalanced photonic energy and information signals forming a complete electromagnetic destruction of our water and energy producing power plants within our cells. Less energy is produced, less water is produced, less carbondyoxide is produced and more biophotons are released as the body begins to drop in energy levels and structural coherence. Less energy for the body to do work, repair and grow means less energy for the brain, heart, kidneys, liver, endocrine, immune and musculoskeletal systems as the body’s key energy reliant systems, leading to more toxicity and disease. Less structural coherence means poor tissue (bone, joint, muscle, organ) quality and more susceptibility to tears, breaks and biomechanical issues.  

Realizing the dramatic alteration to light signals we experience in this modern world via our eyes, skin, and gastrointestinal tract, and its consequential alteration in metabolism favouring the creation of diabetes, is a key first step to reversing the chronic disease. The reversal and prevention of diabetes is now within our reach.

References

• N. Volkow et al. Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. Journal of the American Medical Association. Vol. 305, February 23, 2011. Available online:

• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782876/