CAN YOU POSTPONE YOUR DATE WITH CANCER AND MI

Do you have prostate cancer ? Will you get prostate cancer ? Do you have colon cancer ? Or get one sooner or later ? What about breast cancer ?

Even when you develop cancer excess vitamin D increases apoptosis and you survive longer. Not debatable.

Every one of your patients and ourselves and our spouses should be on vitamin D 2000 units a say for ever. There is no down side to it. Mind you I said vitamin D, not vitamin D with calcium.

Vitamin D decreases the incidence of all kind of cancers further all cancer patients should be on vitamin D also. Even after the diagnosis is made vitamin D increases the life span and it increases apoptosis. Remember there is no down side to vitamin D ingestion at that dose or even multiples of that dose, below may be a dose of 10,000 units a day
.

Milk from even well fed cows , how much vitamin D is there ? Zilch, zero- point is milk has no vitamin D unless you add it to milk. How many of you know that ?


Did you know that if you live in Atlanta , SanAntonio you have less chance of getting all kinds of cancers than in Boston .

FROM NEJM Volume 357:266-281 July 19, 2007 Number 3

Vitamin D Deficiency

Michael F. Holick, M.D., Ph.D.


Once foods were fortified with vitamin D and rickets appeared to have been conquered, many health care professionals thought the major health problems resulting from vitamin D deficiency had been resolved. However, rickets can be considered the tip of the vitamin D–deficiency iceberg. In fact, vitamin D deficiency remains common in children and adults. In utero and during childhood, vitamin D deficiency can cause growth retardation and skeletal deformities and may increase the risk of hip fracture later in life. Vitamin D deficiency in adults can precipitate or exacerbate osteopenia and osteoporosis, cause osteomalacia and muscle weakness, and increase the risk of fracture.

The discovery that most tissues and cells in the body have a vitamin D receptor and that several possess the enzymatic machinery to convert the primary circulating form of vitamin D, 25-hydroxyvitamin D, to the active form, 1,25-dihydroxyvitamin D, has provided new insights into the function of this vitamin. Of great interest is the role it can play in decreasing the risk of many chronic illnesses, including common cancers, autoimmune diseases, infectious diseases, and cardiovascular disease. In this review I consider the nature of vitamin D deficiency, discuss its role in skeletal and nonskeletal health, and suggest strategies for its prevention and treatment.

Sources and Metabolism of Vitamin D

Humans get vitamin D from exposure to sunlight, from their diet, and from dietary supplements. A diet high in oily fish prevents vitamin D deficiency. Solar ultraviolet B radiation (wavelength, 290 to 315 nm) penetrates the skin and converts 7-dehydrocholesterol to previtamin D3, which is rapidly converted to vitamin D 3 (Figure 1). 1 Because any excess previtamin D3 or vitamin D3 is destroyed by sunlight ( Figure 1), excessive exposure to sunlight does not cause vitamin D 3 intoxication.


During exposure to solar ultraviolet B (UVB) radiation, 7-dehydrocholesterol in the skin is converted to previtamin D3, which is immediately converted to vitamin D3 in a heat-dependent process. Excessive exposure to sunlight degrades previtamin D 3 and vitamin D3 into inactive photoproducts. Vitamin D2 and vitamin D3 from dietary sources are incorporated into chylomicrons and transported by the lymphatic system into the venous circulation. Vitamin D (hereafter "D" represents D 2 or D3) made in the skin or ingested in the diet can be stored in and then released from fat cells. Vitamin D in the circulation is bound to the vitamin D–binding protein, which transports it to the liver, where vitamin D is converted by vitamin D-25-hydroxylase to 25-hydroxyvitamin D [25(OH)D]. This is the major circulating form of vitamin D that is used by clinicians to determine vitamin D status. ..................

Few foods naturally contain or are fortified with vitamin D. The "D" represents D2 or D3 ( Figure 1). Vitamin D2 is manufactured through the ultraviolet irradiation of ergosterol from yeast, and vitamin D3 through the ultraviolet irradiation of 7-dehydrocholesterol from lanolin. Both are used in over-the-counter vitamin D supplements, but the form available by prescription in the United States is vitamin D2.

Vitamin D from the skin and diet is metabolized in the liver to 25-hydroxyvitamin D ( Figure 1), which is used to determine a patient's vitamin D status. 25-hydroxyvitamin D is metabolized in the kidneys by the enzyme 25-hydroxyvitamin D-1 -hydroxylase (CYP27B1) to its active form, 1,25-dihydroxyvitamin D. The renal production of 1,25-dihydroxyvitamin D is tightly regulated by plasma parathyroid hormone levels and serum calcium and phosphorus levels. Fibroblast growth factor 23, secreted from the bone, causes the sodium–phosphate cotransporter to be internalized by the cells of the kidney and small intestine and also suppresses 1,25-dihydroxyvitamin D synthesis. The efficiency of the absorption of renal calcium and of intestinal calcium and phosphorus is increased in the presence of 1,25-dihydroxyvitamin D It also induces the expression of the enzyme 25-hydroxyvitamin D-24-hydroxylase (CYP24), which catabolizes both 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D into biologically inactive, water-soluble calcitroic acid.

Definition and Prevalence of Vitamin D Deficiency

Although there is no consensus on optimal levels of 25-hydroxyvitamin D as measured in serum, vitamin D deficiency is defined by most experts as a 25-hydroxyvitamin D level of less than 20 ng per milliliter (50 nmol per liter).
Hydroxyvitamin D levels are inversely associated with parathyroid hormone levels until the former reach 30 to 40 ng per milliliter (75 to 100 nmol per liter), at which point parathyroid hormone levels begin to level off (at their nadir). Furthermore, intestinal calcium transport increased by 45 to 65% in women when 25-hydroxyvitamin D levels were increased from an average of 20 to 32 ng per milliliter (50 to 80 nmol per liter). 13 Given such data, a level of 25-hydroxyvitamin D of 21 to 29 ng per milliliter (52 to 72 nmol per liter) can be considered to indicate a relative insufficiency of vitamin D, and a level of 30 ng per milliliter or greater can be considered to indicate sufficient vitamin D. 14 Vitamin D intoxication is observed when serum levels of 25-hydroxyvitamin D are greater than 150 ng per milliliter (374 nmol per liter).

With the use of such definitions, it has been estimated that 1 billion people worldwide have vitamin D deficiency or insufficiency. According to several studies, 40 to 100% of U.S. and European elderly men and women still living in the community (not in nursing homes) are deficient in vitamin D. More than 50% of postmenopausal women taking medication for osteoporosis had suboptimal levels of 25-hydroxyvitamin D — below 30 ng per milliliter (75 nmol per liter).

Children and young adults are also potentially at high risk for vitamin D deficiency. For example, 52% of Hispanic and black adolescents in a study in Boston 23 and 48% of white preadolescent girls in a study in Maine 24 had 25-hydroxyvitamin D levels below 20 ng per milliliter. In other studies, at the end of the winter, 42% of 15- to 49-year-old black girls and women throughout the United States had 25-hydroxyvitamin D levels below 20 ng per milliliter, 25 and 32% of healthy students, physicians, and residents at a Boston hospital were found to be vitamin D–deficient, despite drinking a glass of milk and taking a multivitamin daily and eating salmon at least once a week.

In Europe, where very few foods are fortified with vitamin D, children and adults would appear to be at especially high risk. People living near the equator who are exposed to sunlight without sun protection have robust levels of 25-hydroxyvitamin D — above 30 ng per milliliter. However, even in the sunniest areas, vitamin D deficiency is common when most of the skin is shielded from the sun. In studies in Saudi Arabia, the United Arab Emirates, Australia, Turkey, India, and Lebanon, 30 to

50% of children and adults had 25-hydroxyvitamin D levels under 20 ng per milliliter. Also at risk were pregnant and lactating women who were thought to be immune to vitamin D deficiency since they took a daily prenatal multivitamin containing 400 IU of vitamin D (70% took a prenatal vitamin, 90% ate fish, and 93% drank approximately 2.3 glasses of milk per day) .73% of the women and 80% of their infants were vitamin D–deficient (25-hydroxyvitamin D level, <20 ng per milliliter) at the time of birth.

Calcium, Phosphorus, and Bone Metabolism

Without vitamin D, only 10 to 15% of dietary calcium and about 60% of phosphorus is absorbed. The interaction of 1,25-dihydroxyvitamin D with the vitamin D receptor increases the efficiency of intestinal calcium absorption to 30 to 40% and phosphorus absorption to approximately 80%

In one study, serum levels of 25-hydroxyvitamin D were directly related to bone mineral density in white, black, and Mexican-American men and women, with a maximum density achieved when the 25-hydroxyvitamin D level reached 40 ng per milliliter or more.8 When the level was 30 ng per milliliter or less, there was a significant decrease in intestinal calcium absorption 13 that was associated with increased parathyroid hormone. Parathyroid hormone enhances the tubular reabsorption of calcium and stimulates the kidneys to produce 1,25-dihydroxyvitamin D. Parathyroid hormone also activates osteoblasts, which stimulate the transformation of preosteoclasts into mature osteoclasts (Figure 1). Osteoclasts dissolve the mineralized collagen matrix in bone, causing osteopenia and osteoporosis and increasing the risk of fracture.

Deficiencies of calcium and vitamin D in utero and in childhood may prevent the maximum deposition of calcium in the skeleton. As vitamin D deficiency progresses, the parathyroid glands are maximally stimulated, causing secondary hyperparathyroidism. Hypomagnesemia blunts this response, which means that parathyroid hormone levels are often normal when 25-hydroxyvitamin D levels fall below 20 ng per milliliter. Parathyroid hormone increases the metabolism of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D, which further exacerbates the vitamin D deficiency. Parathyroid hormone also causes phosphaturia, resulting in a low-normal or low serum phosphorus level. Without an adequate calcium–phosphorus product (the value for calcium times the value for serum phosphorus), mineralization of the collagen matrix is diminished, leading to classic signs of rickets in children and osteomalacia in adults.

Whereas osteoporosis is unassociated with bone pain, osteomalacia has been associated with isolated or generalized bone pain. The cause is thought to be hydration of the demineralized gelatin matrix beneath the periosteum; the hydrated matrix pushes outward on the periosteum, causing throbbing, aching pain. Osteomalacia can often be diagnosed by using moderate force to press the thumb on the sternum or anterior tibia, which can elicit bone pain. One study showed that 93% of persons 10 to 65 years of age who were admitted to a hospital emergency department with muscle aches and bone pain and who had a wide variety of diagnoses, including fibromyalgia, chronic fatigue syndrome, and depression, were deficient in vitamin D.

Osteoporosis and Fracture

Approximately 33% of women 60 to 70 years of age and 66% of those 80 years of age or older have osteoporosis. It is estimated that 47% of women and 22% of men 50 years of age or older will sustain an osteoporotic fracture in their remaining lifetime. Chapuy et al. reported that among 3270 elderly French women given 1200 mg of calcium and 800 IU of vitamin D3 daily for 3 years, the risk of hip fracture was reduced by 43%, and the risk of nonvertebral fracture by 32%. A 58% reduction in nonvertebral fractures was observed in 389 men and women over the age of 65 years who were receiving 700 IU of vitamin D3 and 500 mg of calcium per day.

A meta-analysis of seven randomized clinical trials that evaluated the risk of fracture in older persons given 400 IU of vitamin D3 per day revealed little benefit with respect to the risk of either nonvertebral or hip fractures (pooled relative risk of hip fracture, 1.15; 95% confidence interval [CI], 0.88 to 1.50; pooled relative risk of nonvertebral fracture, 1.03; 95% CI, 0.86 to 1.24). In studies using doses of 700 to 800 IU of vitamin D3 per day, the relative risk of hip fracture was reduced by 26% (pooled relative risk, 0.74; 95% CI, 0.61 to 0.88 ), and the relative risk of nonvertebral fracture by 23% (pooled relative risk, 0.77; 95% CI, 0.68 to 0.87) with vitamin D3 as compared with calcium or placebo. 8 A Women's Health Initiative study that compared the effects of 400 IU of vitamin D3 plus 1000 mg of calcium per day with placebo in more than 36,000 postmenopausal women confirmed these results, reporting an increased risk of kidney stones but no benefit with respect to the risk of hip fracture.

The Women's Health Initiative study also showed that serum levels of 25-hydroxyvitamin D had little effect on the risk of fracture when levels were 26 ng per milliliter (65 nmol per liter) or less. However, women who were most consistent in taking calcium and vitamin D3 had a 29% reduction in hip fracture. 43 Optimal prevention of both nonvertebral and hip fracture occurred only in trials providing 700 to 800 IU of vitamin D3 per day in patients whose baseline concentration of 25-hydroxyvitamin D was less than 17 ng per milliliter (42 nmol per liter) and whose mean concentration of 25-hydroxyvitamin D then rose to approximately 40 ng per milliliter.

Evaluation of the exclusive use of calcium or vitamin D3 (RECORD trial) showed no antifracture efficacy for patients receiving 800 IU of vitamin D3 per day. However, the mean concentration of 25-hydroxyvitamin D increased from 15.2 ng per milliliter to just 24.8 ng per milliliter (37.9 to 61.9 nmol per liter), which was below the threshold thought to provide antifracture efficacy.8 Porthouse and colleagues, 45 who evaluated the effect of 800 IU of vitamin D3 per day on fracture prevention, did not report concentrations of 25-hydroxyvitamin D. Their study had an open design in which participants could have been ingesting an adequate amount of calcium and vitamin D separate from the intervention. This called into question the conclusion that vitamin D supplementation had no antifracture benefit. 8

Muscle Strength and Falls

Vitamin D deficiency causes muscle weakness.Skeletal muscles have a vitamin D receptor and may require vitamin D for maximum function.

Performance speed and proximal muscle strength were markedly improved when 25-hydroxyvitamin D levels increased from 4 to 16 ng per milliliter (10 to 40 nmol per liter) and continued to improve as the levels increased to more than 40 ng per milliliter (100 nmol per liter).8 A meta-analysis of five randomized clinical trials (with a total of 1237 subjects) revealed that increased vitamin D intake reduced the risk of falls by 22% (pooled corrected odds ratio, 0.78; 95% CI, 0.64 to 0.92) as compared with only calcium or placebo. 8 The same meta-analysis examined the frequency of falls and suggested that 400 IU of vitamin D3 per day was not effective in preventing falls, whereas 800 IU of vitamin D3 per day plus calcium reduced the risk of falls (corrected pooled odds ratio, 0.65; 95% CI, 0.4 to 1.0).8 In a randomized controlled trial conducted over a 5-month period, nursing home residents receiving 800 IU of vitamin D2 per day plus calcium had a 72% reduction in the risk of falls as compared with the placebo group (adjusted rate ratio, 0.28%; 95% CI, 0.11 to 0.75).

Nonskeletal Actions of Vitamin D

Brain, prostate, breast, and colon tissues, among others, as well as immune cells have a vitamin D receptor and respond to 1,25-dihydroxyvitamin D, the active form of vitamin D. In addition, some of these tissues and cells express the enzyme 25-hydroxyvitamin D-1 -hydroxylase.

Directly or indirectly, 1,25-dihydroxyvitamin D controls more than 200 genes, including genes responsible for the regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis. It decreases cellular proliferation of both normal cells and cancer cells and induces their terminal differentiation. One practical application is the use of 1,25-dihydroxyvitamin D3 and its active analogues for the treatment of psoriasis.

1,25-Dihydroxyvitamin D is also a potent immunomodulator.

Latitude, Vitamin D Deficiency, and Chronic Diseases

Cancer ---LET ME HIGHLIGHT SOME OF THE POINTS AGAIN

People living at higher latitudes are at increased risk for Hodgkin's lymphoma as well as colon, pancreatic, prostate, ovarian, breast, and other cancers and are more likely to die from these cancers, as compared with people living at lower latitudes.

More than 50% of postmenopausal women taking medication for osteoporosis had suboptimal levels of 25-hydroxyvitamin D — below 30 ng per milliliter (75 nmol per liter).
-............healthy students, physicians, and residents at a Boston hospital were found to be vitamin D–deficient, despite drinking a glass of milk and taking a multivitamin daily and eating salmon at least once a week.
Also at risk were pregnant and lactating women who were thought to be immune to vitamin D deficiency since they took a daily prenatal multivitamin containing 400 IU of vitamin D
Directly or indirectly, 1,25-dihydroxyvitamin D controls more than 200 genes, including genes responsible for the regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis.It decreases cellular proliferation of both normal cells and cancer cells and induces their terminal differentiation."

Is 30- 50% higher incidence of cancer good enough to convince us to take more vitamin D ?

"People living at higher latitudes are at increased risk for Hodgkin's lymphoma as well as colon, pancreatic, prostate, ovarian, breast, and other cancers and are more likely to die from these cancers, as compared with people living at lower latitudes.Both prospective and retrospective epidemiologic studies indicate that levels of 25-hydroxyvitamin D below 20 ng per milliliter are associated with a 30 to 50% increased risk of incident colon, prostate, and breast cancer,
along with higher mortality from these cancers.

In a study of men with prostate cancer, the disease developed 3 to 5 years later in the men who worked outdoors than in those who worked indoors. Pooled data for 980 women showed that the highest vitamin D intake, as compared with the lowest, correlated with a 50% lower risk of breast cancer . Children and young adults who are exposed to the most sunlight have a 40% reduced risk of non-Hodgkin's lymphoma 65 and a reduced risk of death from malignant melanoma once it develops , as compared with those who have the least exposure to sunlight.

To answer your question what is the dose needed to prevent cancer my answer is whtever it takes to bring the blood 25 OH D3 level to 30 or higher. That is the scientific answer.

""Cardiovascular Disease
Living at higher latitudes increases the risk of hypertension and cardiovascular disease . In a study of patients with hypertension who were exposed to ultraviolet B radiation three times a week for 3 months, 25-hydroxyvitamin D levels increased by approximately 180%, and blood pressure became normal (both systolic and diastolic blood pressure reduced by 6 mm Hg). Vitamin D deficiency is associated with congestive heart failure 54 and blood levels of inflammatory factors, including C-reactive protein and interleukin-