Why vitamin D production from sunlight has additional benefits to supplementation: The quantum nature of vitamin D

Feb 6

There’s been some debate as to whether it’s preferable to synthesize vitamin D naturally from sun exposure or from supplements.

The short answer is to think about how nature designed humans. Are we designed to take supplements or to be out in the sun? No.

Check out my previous post that explains how vitamin D is synthesized in the body and the numerous health benefits here. Yet, many physicians and dermatologists recommend avoiding sun exposure because it can increase the risk of melanoma. But is this really true?

Vitamin D Fun Facts You Weren’t Taught in School

Studies show that vitamin D deficiency (serum 25(OH)D ≤20 ng/mL/ ≤50nmol/L) is associated with a worse prognosis for metastatic melanoma and sun exposure is associated with increased survival of melanoma. Read that again.

More importantly, vitamin D deficiency has been associated with early death.

It’s important to note that blood tests measure serum 25(OH)D levels, whereas the active metabolite is actually 1,25-dihydroxyvitamin D3.

Adequate vitamin D levels have been found to prevent other types of cancer, but unfortunately, an estimated 50% of the world’s population is vitamin D deficient. I believe this is because modern society has moved humans indoors most hours of the day and we are living like zoo animals exposed to artificial light that’s messing with our physiology.

There are several factors that can affect vitamin D status such as skin color (melanin content), age, sex, BMI, chronic disease, vitamin D receptor (VDR) polymorphisms, sun exposure, sunscreen use, and latitude. For a full list of current expert recommendations for vitamin D, read this paper here. Depending on the study and population, intense sun exposure can synthesize anywhere between 600- 25,000 IU of vitamin D3 a day. You ideally need anywhere between 5-30 minutes of sun exposure a day depending on the amount of skin exposure and the other factors I mentioned above.

Vitamin D’s role in human health extends ways beyond its role in regulating calcium and phosphorus levels in the body, and I honestly don’t think we fully understand all the roles that vitamin D plays in our health. In fact, nearly every cell in our body has a vitamin D receptor (VDR).

The active form of vitamin D (calcitriol) increases renal sodium–phosphate cotransporters NPT2a expression and phosphate reabsorption, as well as intestinal NPT2b expression and phosphate absorption.

Interestingly, phosphorus means “bringer of light” in Greek and is essential to all living things. It forms the sugar-phosphate backbone of DNA and RNA and is the “P” in ATP (adenosine triphosphate), which is a major source of our body’s energy. Calories are NOT the main source of energy, and I’m starting to see more and more that we can access a lot of “free” energy from grounding (electrons in the Earth) and simultaneous sun exposure.

Now let’s dive deep into the nerdy science of vitamin D at the quantum level.

Why it’s better to make vitamin D from the sun

Although most experts recommend vitamin D supplements over sun exposure, supplements aren’t necessarily better. That said, I still think it’s important to supplement if a person is at risk for a deficiency, lives in a higher or lower latitude, or simply cannot get adequate sun exposure year-round. It’s also important to keep in mind that obtaining vitamin D from supplements requires healthy liver, kidney, and intestinal health, which unfortunately, most adults don’t have because chronic conditions are rampant and on the rise.

Otherwise, the best way to have sufficient levels of vitamin D is through sun exposure in small amounts regularly throughout the year. However, a lot of misinformed dermatologists (who are probably paid by pharmaceutical companies) claim that sun exposure is “bad” and can lead to melanoma. If this were true, why does vitamin D that is synthesized primarily in our skin, (remember, our ancestors didn’t have supplements), and can prevent melanoma? We also can’t get hypervitaminosis D from sun exposure because of built-in feedback mechanisms, but we can from supplements.

Why is it that our skin has photoreceptors called melanin that regulate our circadian rhythm? Nature doesn’t make any mistakes.

Why is it that melanoma rates have increased by 51% since 1999 despite the marked increase in the sunscreen industry? Could it be that NOT spending time in the sun is making us sick?

Of course, we want to avoid getting burned, but adequate sun exposure has numerous benefits that supplements cannot provide.

Vitamin D from the sun isn’t the same as supplements

Human bodies are basically like walking solar panels. We have photoreceptors on our eyes and skin that affect our circadian rhythm and a multitude of other factors that affect our health.

When the sun’s UVB rays (280- 320 nm) hit our skin, the photoreceptors on our skin photolyze 7-dehydrocholesterol to pre-vitamin D3 which in turn is isomerized by the body's temperature to vitamin D3. In our epidermis, keratinocytes, which are skin cells, are the only cells in our body that can directly produce the active form of vitamin D3, usually in about 16 hours. Otherwise, vitamin D3 is hydroxylated in the liver by a hydroxylase (CYP2R1 or CYP27A1) into 25-hydroxyvitamin D3 and after that, in the kidney by CYP27B1 into 1,25-dihydroxyvitamin D3 or calcitriol (the active form of vitamin D).

UVB light makes up only about 5% of the sun’s energy but is very effective at exerting important biological effects on the body, especially on the skin. Not only that, the positive effects that sun exposure has on our health are numerous (reviewed here), including releasing those feel-good beta-endorphins, improving immune health, and balancing our hormones and circadian rhythm.

Sulfate is produced in the skin from sun exposure which produces vitamin D sulfate and cholesterol sulfate are synthesized. Vitamin D sulfate and cholesterol sulfate are water soluble so they don’t need to be transported around the body by a carrier lipid protein like LDL. The health benefits of sulfate are varied including blood vessel health and delivering important molecules such as cholesterol, vitamin D, dopamine, and melatonin. The authors of one study also hypothesized that sulfated calcitriol (vitamin D metabolite) may play a role in regulating the physiological activity of calcitriol. It’s important to know that sunscreen blocks sulfate synthesis in the skin.

The Vitamin D-Melanin-Light Connection

If humans weren’t meant to synthesize vitamin D from sunlight, why do we have photoreceptors on our skin and eyes that use vitamin D?

I believe vitamin D, its metabolites, and VDRs play a major role in circadian rhythm function mostly through its interaction with melanin. Vitamin D also plays a role in neurotransmitter production that is derived from aromatic amino acids (phenylalanine, tryptophan- serotonin, melatonin, histamine, and tyrosine- dopamine, norepinephrine), which absorb UV light, but that’s another topic for another post. Let’s get back to the light-vitamin D-melanin connection.

Melanin is what gives our skin pigment (more melanin = darker skin), but it’s also found mostly inside our brains (substantia nigra), our eyes, our intestines, and even in the cochlea of our ears. Vitamin D can enhance melanin synthesis, and conversely, melanin in the skin affects vitamin D synthesis. Vitamin D controls melanin synthesis by regulating the enzyme tyrosinase in response to UV light exposure, which catalyzes the initial step of melanogenesis (melanin synthesis). So the more melanin you have in your skin, the more UV light you block, and therefore, less vitamin D is synthesized in the skin.

Besides protecting our skin from free radical damage, melanin affects inflammatory responses directly and/or indirectly by influencing the host cytokine/chemokine production ((IL)-1, IL-6, interferon γ (IFN-γ), and tumor necrosis factor-α (TNF-α).

Several studies now show that vitamin D and its metabolites can protect against melanoma. Vitamin D3 exerts photoprotective activities in both melanocytes and keratinocytes via the VDR in these cells. Inside the nucleus, the VDR creates a heterodimer with RXRα and RXRβ which regulates melanocyte homeostasis and inhibits melanoma formation in the skin and tumor microenvironment.

A study in human eye melanoma showed that the levels of VDR were always the lowest in the cells of uveal melanoma and higher in normal uveal melanocytes (melanin cells) and other normal uveal cells. The authors concluded that this could be because vitamin D acts through VDR and activates various anti-tumor effects such as inhibiting cell proliferation, increasing apoptosis (programmed cell death), regulating the Wnt-β/catenin pathway, etc. which are all related to tumor growth. Moreover, vitamin D deficiency has been associated with an increased risk of age-related macular degeneration (AMD), dry eye syndrome, diabetic retinopathy, and impaired corneal healing after surgeries and traumas, and VDRs are found in the cells of protective barriers of the human eye such as the adult retinal pigment epithelial.

VDRs are found in the brain including dopamine receptors in the substantia nigra region of the brain. Vitamin D can also regulate the enzyme tyrosine hydroxylase, which synthesizes dopamine. Substantia nigra contains a lot of neuromelanin, thus further linking vitamin D with melanin. It also raises the question of whether vitamin D also acts as a neurosteroid in the brain. Interestingly, bright light exposure reduces tyrosine hydroxylase-positive dopamine neurons in the substantia nigra, which connects artificial light disruption of the circadian rhythm and Parkinson’s disease.

Lastly, vitamin D has recently been found to regulate melatonin production, and sleep disturbances have been associated with circadian rhythm disruption caused by a lack of sun exposure and too much artificial light exposure. Additionally, VDRs are found throughout the eye including in the retinal pigment epithelium, which is a major circadian rhythm regulator.

Putting all this together, we can see that vitamin D’s role extends way beyond bone and immune health and can be considered a key factor in circadian rhythm regulation.

Vitamin D is also tied to the leptin-melanocortin pathway

I consider Dr. Jack Kruse to be the expert on this, but in a nutshell, adequate sunlight exposure on your eyes and skin regulates this pathway which controls metabolism and circadian rhythm. Firstly, UVB light stimulates the production of 1,25(OH)2D3, and noncalcemic vitamin D analogs, which then triggers the expression of corticotropin-releasing hormone (CRH), urocortins, and most importantly POMC, and their receptors in human skin. Therefore, UVB-synthesized vitamin D can activate the leptin-melanocortin pathway.

Proopiomelanocortin (POMC) is a key component of the leptin-melanocortin pathway because it produces the melanocyte-stimulating hormones (MSHs), corticotrophin (ACTH), and β-endorphin. ACTH produces the main stress hormone cortisol, MSHs influence pigmentation and immune reactions, and β-endorphins are those feel-good chemicals. POMC can be cleaved into α-MSH, which is made up of primarily aromatic amino acids (tyrosine, tryptophan, and phenylalanine), which if you remember from what I previously said, absorb UV light. POMC also contains leptin receptors which regulate our satiety and hunger sensations.

The leptin-melanocortin pathway is closely tied to our circadian rhythm. As I previously posted, when UV light hits the eye, it gets absorbed by photoreceptors in our eyes (retinal pigment epithelium or RPE), and this light information gets transferred to the suprachiasmatic nuclei (SCN) in the hypothalamus via the retinohypothalamic tract and onto key metabolic areas that express melanocortin-4 receptor (Mc4r), such as α-MSH. Mc4r is associated with fat storage, glucose tolerance, and sexual function, and has been most recently linked to obesity. Remember POMC can get cleaved and turn into α-MSH.

Digging further, serum vitamin D levels have also been linked with leptin levels independent of adipose (fat) tissue where leptin resides. Importantly, 1,25-dihydroxyvitamin D3 binds to vitamin D responsive element (VDRE) in the nucleus where it can regulate tryptophan hydroxylase 2 mRNA expression in the brain, which is the enzyme that controls serotonin synthesis. 1,25-dihydroxy vitamin D3 can also control leptin mRNA expression in the brain. 5-HT, which is just another way to say serotonin, can activate POMC in the brain via its receptor 5-HT2C. So, vitamin D regulates serotonin production in the brain, and 5-HT/ serotonin can stimulate POMC.

For more information about the importance of proper sunlight exposure and the leptin-melanocortin pathway, watch these interviews with Dr. Jack Kruse here and here.

The quantum nature of vitamin D: It’s all about sunlight

What most aren’t taught in school is that vitamin D improves mitochondrial function by facilitating energy production and promoting redox balance.

As I mentioned in my previous blog post, the active form of vitamin D, 1,25(OH)2D, regulates a ton of gene expression in humans by binding to vitamin D receptors in the nucleus, some of which have to do with mitochondrial function and energy production. In another blog post I wrote, I talked about how mitochondria absorb UV light and are light-controlled. Reader’s Digest version is red light is better and artificial blue light is not good for mitochondrial health. Keep this in mind as I continue.

One of my favorite papers I’ve co-authored investigates the connection between the gut microbiome and mitochondrial function. Another paper I also co-wrote discusses how vitamin D can modulate the gut microbiota, and how a lack of sun exposure and overly hygienic lifestyle might be contributing to the rise in autoimmune diseases.

What’s super cool about vitamin D is that it has quantum properties through light activation. Vitamin D has existed in phytoplankton and zooplankton for at least 750 million years. The authors of this paper hypothesize that the provitamin D prebiotic system has quantum entanglement properties which can potentially enhance photosynthetic properties. In other words, vitamin D might enhance energy production by absorbing sunlight. More studies are needed to prove this theory and translate it to human health, but it’s an interesting theory to ponder.

Taken all of this together, it doesn’t surprise me that several recent studies have since come out describing how vitamin D improves mitochondrial function. For example, vitamin D deficiency can lead to mitochondrial dysfunction, which can lead to less ATP production (less complex I expression of the mitochondrial electron transport chain), inflammation, and increased oxidative stress (ROS), which have all been observed in chronic illnesses and aging.

Some of the main ways in which vitamin D supports mitochondrial function is by:

Improving mitochondrial integrity and respiration via VDR activities.
Protecting cells from an overproduction of reactive oxygen species (ROS), which can lead to cellular and DNA damage
Regulating mitochondrial respiration via VDR activity which could improve cardiovascular health such as decreasing hypertension.
Enhancing muscle repair and mitochondrial function
Enhancing can enhance mitophagy, ROS defense, and epigenetic gene regulation involved in non-oxidative energy metabolism and can regulate mTOR gene function via the active form of vitamin D (1,25-dihydroxy vitamin D, 1,25(OH)2D3).

In conclusion, we can see just how dynamic vitamin D is for our mitochondrial, circadian, and immune health, most of which are activated by or at least enhanced by sunlight exposure. My hope is that after reading this you will realize that sun is not the enemy and that humans rely on adequate sun exposure for overall health. Vitamin D is just one of the pieces of the puzzle, and its benefits stem way beyond supplements.

Sources

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5351676/

https://academic.oup.com/jnci/article/97/3/195/2544082
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https://febs.onlinelibrary.wiley.com/doi/10.1002/1873-3468.12767

https://pubmed.ncbi.nlm.nih.gov/29374749/

https://pubmed.ncbi.nlm.nih.gov/28994020/

https://pubmed.ncbi.nlm.nih.gov/32918212/

https://www.rsc.org/periodic-table/element/15/phosphorus

https://www.sciencedirect.com/science/article/pii/S0085253815550692

https://www.mdpi.com/2079-7737/8/2/30

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8771003/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444280/