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How important is Vitamin D?


Before taking Vitamin D3 you need to take the following test to check your levels!


Biochemistry university of wisconsin-Madison

Department of Biochemistry

Biological Partners
Vitamin D & Calcium

You CAN NOT get benefits from one without the other!

Do you suffer from an automimmune disease?



(#1) Sunlight Exposure causes Vitamin D Production
It is a known scientific fact that when UVB sunlight strikes the human skin, Vitamin D production occurs. When Vitamin D passes through the intestinal tract, it attaches itself to the VITAMIN D RECEPTORS that are found in very high quanities on the ends of the INTESTINAL VILLI that line the intestinal walls. The villi are small fingerlike projections that increase the surface area of the small intestine for maximum absorption. The result is dramatically improved Calcium absorption.

(#2) Calcium is difficult to absorb without Vitamin D
Calcium is a positively charged ion and is very difficult for the human body to absorb due to the fact that our intestinal walls are lined with positively charged villi that repel the positively charged ion, calcium. However, when Vitamin D passes through our digestive tract, Vitamin D attaches to the ends of the villi and changes the positive charge to a negative charge which then allows the villi to magnetically grab the Calcium ion as it passes by.

What is the result?
If the intestinal tract villi are full of Vitamin D, Calcium absorption can be improved by as much as 20 fold. Without Vitamin D, Calcium will simply pass through your body and you will get very little benefit from the Calcium you consume in your diet.


Diagram of the
Small Intestine & Intestinal Villi

The small intestine is crucial in the digestion & absorption of nutrients and spans about 22 to 25 feet.
This important organ is composed of the duodenum, jejunum, ileum, and villi

See Enlarged Diagram below of
Intestinal Villi & Calcium Absorption
Find Items in diagram below


Description of what is happening in




See Enlarged Diagram below of
Intestinal Villi & Calcium Absorption

Find Items in diagram below





Premenstrual Syndrome "PMS"

Readers Digest

"Premenstrual Syndrome (PMS)"

Reported that the Metabolic Bone Center at St. Lukes Hospital believes that "a chronic deficiency of calcium is largely responsible for premenstrual syndrome (PMS)" and that "a lot of women are avoiding the sun and their vitamin-D levels may be very low". In the same article, the Digest reported that "in 1997 the large federally financed trial found that a diet containing 1200 milligrams of calcium significantly lowered blood pressure in adults".

CNN Interactive Article

"Calcium may be the key to taming premenstrual pain"

"The research, funded in part by the maker of Tums, a popular antacid and calcium supplement, studied more than 400 premenopausal women across the United States....Within three months, there was a 50 percent reductions of symptoms,.....Symptoms such as mood swings, tension, headaches and cramping were all alleviated with calcium......Food cravings also dropped by half, and water retention decreased by more than one-third....PMS may be an early warning sign for osteoporosis....We've never really had a marker for this bone loss," Thys-Jacobs said. "Now I think we have it.....Now we have a premenstrual syndrome that is manifesting as a calcium deficient state."

Below is a list of other Scientific Facts
concerning Vitamin D

Scientific Fact
There are only 2 sources of Vitamin-D
Vitamin D3 (cholecalciferol) can be synthesized by humans in the skin upon exposure to ultraviolet-B (UVB) radiation from sunlight, or it can be obtained from the diet.


Scientific Fact
It has been estimated that nearly 95% of our vitamin D requirement comes from casual exposure to sunlight. Very few foods contain Vitamin-D, therefore less than 5% of vitamin-D levels actually comes from our diet.


Scientific Fact
Any process that either decreases the number of UVB photons(sunlight) entering the epidermis or decreases the amount of 7-dehydrocholesterol in the skin will result in a significant reduction in or the complete elimination of vitamin D3 production in the skin.


Scientific Fact
Elderly at risk for Vitamin-D deficiency
Aging decreases the amount of 7-dehydrocholesterol produced in the skin by as much as 75% by the age of 70.


Scientific Fact
Older people who are institutionalized or housebound are at a particularly high risk of vitamin D deficiency. For example, up to 80% of women and 70% of men living in hostels or nursing homes in Victoria, New South Wales and Western Australia were frankly deficient in vitamin D, and 97% had a 25-OHD level below the median value of the healthy reference range.


Scientific Fact
Because the zenith angle(of the sun) is dependent on time of day, season of the year, and latitude, those factors have a dramatic effect on the cutaneous production of vitamin D3.


Scientific Fact
Latitude dictates the level of year round exposure to UVB photons which dictates vitamin-d levels.
(1) Below 35°, the zenith angle is more direct, and therefore previtamin D3 synthesis can occur in the skin year-round.
(2) Above 35° latitude, the angle of the sun is so oblique during the winter months that most, if not all, of the UVB photons below 315 nm are absorbed by the ozone layer, thereby either reducing or completely preventing the production of previtamin D3 in the skin.


Scientific Fact
At latitudes greater than 40 N or S there is little conversion occurring from October to March, which is sometimes referred to as the 'vitamin D winter'.


Scientific Fact
Vitamin-D Levels in the Northern States are lower than Southern States. Cancer rates in Northern States are higher than cancer rates in southern states


Scientific Fact
Melanin is a natural sunscreen that evolved to protect humans from blistering solar radiation as they evolved in equatorial regions of the world. This skin pigment is an extremely effective sunscreen with absorption properties from the ultraviolet C (200-280 nm) into the visible range (> 700 nm), and it competes quite well with 7-dehydrocholesterol for UVB photons. Thus, people of color who have greater amounts of melanin in their epidermis than do whites are less efficient in producing vitamin D3 than are whites. A person with skin type 5/6 (dark skin, never develops a sunburn) requires 10-50 times the exposure to sunlight to produce the same amount of vitamin D3 in their skin as does a white person with skin type 2 or 3.


Scientific Fact
Effects on cancer rates due to changing geographical residence
In 1968 an epidemiological study indicated that dietary habits and environmental influences are the chief determinants of the world's varying cancer rates and not genetic factors. Data showed that in the course of three generations, Japanese migrants in the United States contracted colon cancer at the same rates as the general American population. In contrast, the regular colon cancer rate in Japan remained about one-fourth the American incidence.


Scientific Fact
Vitamin D deficiency is widespread among U.S. population, expectant mothers are deficient and giving birth to deficient infants. Vitamin-D levels are past from the mother to the infant. The infant will maintain 1/2 of the vitamin-D level of the mother. Therefore, if the mother is vitamin-D deficient, this deficiency will be past onto the child.


Scientific Fact
Recent studies have found that women who cover most of their body for religious reasons, such as Muslims and Orthodox Jews, risk vitamin D deficiencies. As one example, Turkish researchers reported that veiled Muslim women had lower levels of vitamin D compared with nonveiled women. Recent studies show a prevalence of Vitamin D deficiency in Muslim women, and children born to Muslim women.


Scientific Fact
"We absolutely have a huge problem with vitamin D deficiency," said Dr. Bess Dawson-Hughes, director of the Bone Metabolism Laboratory at Tufts University


Scientific Fact
"If everyone had adequate vitamin D levels in their bloodstreams, it would be equivalent to eliminating a big portion of cancer." Harvard School of Public Health


Scientific Fact
The most common autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, have all been successfully prevented in models using mice that were prone to these diseases if they received vitamin D early in life.


Scientific Fact
Infants and young children who are vitamin D deficient may be imprinted for the rest of their lives with increased risks of type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and many common cancers.


Scientific Fact
Vitamin D deficiency is often misdiagnosed as fibromyalgia.


Multiple Sclerosis

Vitamin D and multiple sclerosis.
Hayes CE, Cantorna MT, DeLuca HF.
Department of Biochemistry, University of Wisconsin-Madison 53706, USA.

Recently, it has been clearly demonstrated that exogenous 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D3, can completely prevent experimental autoimmune encephalomyelitis (EAE), a widely accepted mouse model of human multiple sclerosis (MS).

This finding has focused attention on the possible relationship of this disease to vitamin D. Although genetic traits certainly contribute to MS susceptibility, an environmental factor is also clearly involved.

It is our hypothesis that one crucial environmental factor is the degree of sunlight exposure catalyzing the production of vitamin D3 in skin, and, further, that the hormonal form of vitamin D3 is a selective immune system regulator inhibiting this autoimmune disease.

Thus, under low-sunlight conditions, insufficient vitamin D3 is produced, limiting production of 1,25-dihydroxyvitamin D3, providing a risk for MS. Although the evidence that vitamin D3 is a protective environmental factor against MS is circumstantial, it is compelling.

This theory can explain the striking geographic distribution of MS, which is nearly zero in equatorial regions and increases dramatically with latitude in both hemispheres. It can also explain two peculiar geographic anomalies, one in Switzerland with high MS rates at low altitudes and low MS rates at high altitudes, and one in Norway with a high MS prevalence inland and a lower MS prevalence along the coast.

Ultraviolet (UV) light intensity is higher at high altitudes, resulting in a greater vitamin D3 synthetic rate, thereby accounting for low MS rates at higher altitudes. On the Norwegian coast, fish is consumed at high rates and fish oils are rich in vitamin D3.

Further, experimental work on EAE provides strong support for the importance of vitamin D3 in reducing the risk and susceptibility for MS.

If this hypothesis is correct, then 1,25-dihydroxyvitamin D3 or its analogs may have great therapeutic potential in patients with MS.

More importantly, current research together with data from migration studies opens the possibility that MS may be preventable in genetically susceptible individuals with early intervention strategies that provide adequate levels of hormonally active 1,25-dihydroxyvitamin D3 or its analogs.

Vitamin D & Calcium:
The reversal of 5 Autoimmune Diseases

(1) EAE(Similar to Human Multiple Sclerosis) (2) Rheumatoid arthritis (3)Systemic Lupus
(4) Inflammatory Bowel Disease (5) Type I Diabetes


Vitamin D:
its role and uses in immunology

Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA; and Department of Nutrition, Pennsylvania State University, University Park, Pennsylvania 16802, USA

Diseases Prevented or Reversed using Vitamin D
vitamin D compounds = 1,25-(OH)2D3

Experimental Autoimmune Encephalomyelitis (EAE)
(Similar to Human Multiple Sclerosis)

We focused on the disease, experimental autoimmune encephalomyelitis (EAE) in mice. We selected B10.PL mice as the model because the sequence of neural degenerative symptoms that result in these mice after myelin basic protein injection is similar to human multiple sclerosis (MS). We succeeded in establishing EAE and showed there was an incidence of 100% in B10.PL mice fed a 0.87% calcium diet containing dietary vitamin D. However, the provision of 1,25-(OH)2D3 at 50-200 ng/day could prevent the appearance of the EAE lesions. If the vitamin D compound was given postimmunization, it prevented further development of the disease (28) . By now we have carried out extensive experiments on this experimental model of autoimmune disease and have found that the vitamin D compounds (including some important potent analogs) are extremely effective in blocking the development of EAE.

In our attempt to reduce the hypercalcemic effects of 1,25-(OH)2D3, we provided this compound to animals maintained on a very low calcium diet (29) . To our surprise, the low calcium diet produced a lower incidence of disease that was resistant to treatment with the vitamin D hormone (29) (see Fig. 2 ). On the other hand, when similar examinations were followed in the high calcium diet, the vitamin D compounds were effective (Fig. 3 ).

Thus, it became clear that calcium is required for the vitamin D suppression of the autoimmune disease, EAE. Our initial clinical trial with the analog 19-nor-1,25-(OH)2D2 (30) revealed little effectiveness in preventing new MS lesions primarily because we failed to simultaneously provide a normal to high calcium intake. The results, therefore, imply that a high calcium diet is required for the vitamin D hormone to be effective in the treatment of EAE.

Rheumatoid arthritis

The success with EAE suggested that vitamin D compounds could be used to treat other autoimmune disorders. Rheumatoid arthritis proved to be another example of an autoimmune disorder that can be largely prevented by the administration of the 1-hydroxylated vitamin D compounds, including 1,25-(OH)2D3 (31) . Two autoimmune models of rheumatoid arthritis were used. One is the disorder caused by Lyme's disease or the organism Borrelia burgdorferi; the other is collagen-induced arthritis. An example of collagen-induced arthritis and its prevention by the administration of 1,25-(OH)2D3 is illustrated in Fig. 4 . Although little more was done in studying this disorder, high calcium intakes were not required for vitamin D compounds to prevent the lesions.

Systemic Lupus Erythematosus (SLE)

Another example not yet reported in the literature from our group is systemic lupus erythematosus (SLE). In 1992, Lemire et al. described an attenuation of this disorder by 1,25-(OH)2D3 injected three times a week to MRL mice (32) . In our research group, MRL mice were placed on either a 0.87% calcium, 0.3% phosphorus diet or a 0.02% calcium, 0.3% phosphorus-purified diet.
As shown in Fig. 5 , the severity of the MRL symptoms was also markedly prevented by the administration of 1,25-(OH)2D3. Again, the results illustrate that a high calcium background is required for the vitamin D hormone to prevent the development of this autoimmune disorder in the MRL mice. This, then, agrees with the results obtained with EAE.

Inflammatory Bowel Disease (IBD)

The laboratory of Margherita Cantorna has investigated the possible treatment or prevention of inflammatory bowel disease (IBD) by vitamin D (33) . Vitamin D deficiency accelerated the appearance of symptoms and increased the severity of IBD in interleukin 10 (IL-10) knockout (KO) mice. Vitamin D-deficient IL-10 knockout mice developed symptoms of IBD within 6-8 wk (Fig. 7 ). This was essentially prevented by the administration of 1,25-(OH)2D3, again under conditions of high calcium intakes.

Type I Diabetes

Vitamin D deficiency markedly accelerated the appearance and increased the incidence of type I diabetes in the NOD mice (Fig. 8 ). Addition to the diet of 1,25-(OH)2D3 at 50 ng/day for females and 200 ng/day for males prevented the appearance of the diabetic lesions. In any case, the autoimmune disorder in the NOD mice can be prevented by the administration of 1,25-(OH)2D3 if animals are receiving a normal to high calcium diet.

The sum of these findings in whole animals clearly illustrates that T cell-mediated immunity can be regulated by exogenous administration of 1-hydroxylated vitamin D compounds. The absence of vitamin D from the diet might also increase the incidence and severity of autoimmune diseases, pointing to important regulatory actions of the vitamin D hormone. Clearly, we are just beginning to probe the mechanisms whereby vitamin D hormone and its analogs can act as selective immunosuppressants. We do not understand the mechanism whereby the vitamin D hormone can act as an immunosuppressant especially of T cell-mediated inflammatory responses.

Suppression of autoimmune disease requires
not only the active form of vitamin D and its analogs,
but also adequate or high calcium intakes.