Excess Vitamin D: Too Much of A Good Thing?

Excess Vitamin D: Too Much of A Good Thing?

Vitamin D is known as the “sunshine vitamin.” This is because 90 percent of our D requirements naturally comes from the sun. Bioavailable vitamin D3 is created in the skin through the action of the sun’s UV-B rays on cholesterol (7-dehydroxycholesterol), as one of five forms.

Diet offers Vitamin D2 and D3 as the remaining ten percent (i.e., fish liver oils, fatty fish, egg yolks, and as fortified foods), though these forms are not biologically active. Vitamin D2, added to “D-fortified foods,” is produced synthetically by exposing the mold ergot (ergosterol) to ultraviolet light. This process was patented and licensed to pharmaceutical companies which is used as prescription vitamin D. D4 and D5 are synthetic analogues of D3 being tested in vitro for the treatment of cancer.

Vitamin D’s reputation as a potent cancer fighter is mainstream news. A lack of vitamin D is also reported to be behind increased rates of infections, heart disease, stroke, diabetes, osteoporosis, and autoimmune disorders. Models and studies have most of us convinced that excess vitamin D intake could reduce cancer deaths by 75 percent. Why else would the government add vitamin D2 to fortify food?  Meanwhile, as cancer rates rise, we are urged to cover up with sunscreen against the sun which nature intended as the truest source of vitamin D. Why the contradiction?[1]

Much of the research, to date, conceptualizes vitamin D as a resource which gets used up which must be replenished through supplementation – like supplying gasoline to a car. However, this assumes vitamin D acts like a vitamin when in fact it is a secosterid hormone (cholecalcipherol) that functions like other steroid hormones, such as cortisol and testosterone. It is converted to its active form by two hydroxylations:

the first conversion is in the liver to become 25(OH)D (calcidiol), the inactive, primary storage hormone. This is the most abundant circulating form and is therefore the most common measure of serum levels by the medical community primarily because active D3 has a short half-life, so is not considered a reliable measurement of vitamin D.
the second conversion is in the kidneys to form 1,25(OH)2D (calcitriol), This 1,25-D active form binds to  vitamin D-binding protein, a carrier protein in the plasma before going to the vitamin D receptor (VDR) on target cells to activate important functions such as calcium absorption in the intestines, phosphorous metabolism, and the activation of the innate and adaptive immune systems. In addition to the kidneys, calcitriol is also synthesized by monocyte–macrophages in the immune system. When synthesized by monocyte-macrophages, calcitriol acts locally as a cytokine, defending the body against microbial invaders by stimulating the innate immune system.
The real story on Vitamin D has shifted, even if its translation in the press and in practice has been slow. Evidence shows that the assumption that low D levels cause inflammatory diseases is flat out wrong. Rather, when we see D in its true light, it is as a marker and a consequence of the inflammatory disease process. That is a game changer by itself and deserves its own headline. So it is no surprise that going a step further to say that vitamin D supplementation can potentially exacerbate disease proliferation might challenge even the most open-minded practitioners.

One of the great mysteries in human biology is the fact that most human breast milk is considered deficient in vitamin D. Yet why would Nature overlook such an important nutrient in the “perfect food?”

Case in point: when lactating mothers take all but exceedingly high levels of vitamin D – 6,000 IU which is 15 times the United States Recommended Daily Intake – the vitamin D content in breast milk remains low.[2]

The medical community measures inactive 25-D and deems “healthy “ to equal a serum level between 35-50 ng/ml. Some consider a level between 50-80 ng/ml to be optimal. Suggested daily doses range from 4,000 iu and as high as 50,000 iu for short periods in order to reach “optimal” (30-80 ng/L) serum levels. The jury is still out on what an optimal serum 25-D level should be.

If D levels differ within the body, do they also differ among cultures?  In a 2004 study in India, researchers postulated that a group considered to be “healthy” hospital workers must have sufficient D levels from their exposure to the sun. However, when results showed that only 34% had 25-D concentrations above 15 ng/ml and 20 percent had levels below 5 ng/ml, (well below the 30-80 ng/ml range) researchers deemed the entire staff as “deficient.”

The authors did not consider an alternative hypothesis. They did not question that “healthy” from one measure (inactive 25-D) may not tell the whole story. They didn’t consider that their “normal range” might be unnaturally adjusted upward to accommodate the high levels of consumption of fortified D-products in the West. Neither did they question the fact that secosteroids work differently from vitamins, or that cultural differences, themselves, might account for the differences in hormones.

Further studies showed similar “low 25-D” status in African Americans when compared with Eastern Europeans. Mainstream science says that low 25-D in African Americans and other groups with dark skin results primarily because pigmentation reduces vitamin D production in the skin. Current beliefs suggest “healthy African Americans do not achieve optimal (inactive) 25D concentrations at any time of year.”  However, the study showed that “healthy blacks” are indeed healthy when considering levels of D-binding protein and other hormones. When looking at the broader picture, concentrations of bioavailable 25-D are similar between blacks and whites based on differences in genetic polymorphisms[3] and environmental variables.[4]

As a secosteroid, vitamin D is controlled by multiple delicate feedback pathways through the vitamin D receptor (VDR). The VDR is the heart of the innate immune system at the site of each cell, responsible for the expression and regulation of 2000 genes, turning up the expression of some, turning down the expression of others. Under most conditions, the active 1,25-D form acts as the “on” switch to activate the VDR and immunity, while the inactive form acts as the “off” switch. 25-D is not completely inactive, but it cannot activate the VDR. According to Trevor Marshall, author of The Marshall Protocol, not only does the inactive 25-D inactivate VDR, but so does supplemented vitamin D which can go on to suppress innate immunity.

Melanin in the skin affects the synthesis of vitamin D through specialized cells called melanocytes, located at the base of the epidermis by specialized cells called melanocytes. These cells have photosensitive receptors, similar to those in the eye that detect UV radiation from the sun and other sources.  Within a few hours of UV exposure, melanin is produced as the number and size of melanin granules increase.

More than a sun shield, not only does melanin reduce the chances of skin cancer, but it also helps preserve the body’s supply of folate which prevents the risk of miscarriage and babies with neural tube defects. (Too much UV may cause the breakdown of folate). Because folate is required for DNA replication in dividing cells, its absence has an affect on many processes in the body. Hormonal changes during pregnancy stimulate the production of melaninas seen by darkened skin (i.e.,  linea nigra).

Melanin is a key to life because it is present in both sperm and egg and supervises the growth of the developing fetus. It is present at the inception of life, and needed for reproduction. Melanocytes resemble nerve cells and are essential for transferring energy. Lack of or insufficient melanin in the embryo causes the mother to lose her baby.

The production of active 1,25-D is also increased by prolactin, a hormone which stimulates lactogenesis (the formation of milk in mammary glands), which requires large amounts of calcium. Prolactin also acts like a cytokine by binding to cytokine-like receptors and is, therefore, an important regulator of the immune system.

Why does most reporting on D fail to connect the dots that lead to the healing sun? Could it be that the Vitamin D Council is driving vitamin D science to suit its own agenda even while the concept of vitamin D “deficiency” is rapidly becoming obsolete? In fortifying the food chain with unnatural vitamin D, have we fooled with mother nature and come to the point where we no longer know what the body’s natural level of vitamin D is? Could “D-deficient” really be “D-sufficient?”