My onc check-up today

Sally- You don't need a presciption--any health food store will have it.  I've been taking it for

over 2 years and about a half year ago increased to 2400 mg daily.  

Will get blood levels taken next month.

Here is a link to iherb----very reputable online source and the link has many quality brands at very good prices. I just ordered something BBS suggested regarding cognitive problems. 

http://www.iherb.com/Search.aspx?c=1&kw=vitamin+d3 

Hope this helps 

Hi Sally--You don't mention how much D3 is in your Calcium and Supplement?

If it says cholecalciferol-it is D3.

Here is an eye-opener from the NIH about how useful this stuff may really be.

I Could not get the chart reprinted on here so just a few exerpts. 

http://www.nlm.nih.gov/medlineplus/druginfo/natural/patient-vitamind.html

Vitamin D deficiency has been associated with muscle weakness and pain in both adults and children. Limited research has reported vitamin D deficiency in patients with low-back pain, and supplementation may lead to pain reduction in many patients.

Without sufficient vitamin D, calcium absorption cannot be maximized and the resulting elevation in parathyroid (PTH) secretion by the parathyroid glands results in increased bone resorption, which may weaken bones and increase the risk of fracture. Vitamin D supplementation has been demonstrated to slow bone loss and reduce fracture, particularly when taken with calcium

Renal osteodystrophy is a term that refers to all of the bone problems that occur in patients with chronic kidney failure. Oral calcifediol or ergocalciferol may help manage hypocalcemia and prevent renal osteodystrophy in people with chronic renal failure undergoing dialysis.

Limited research suggests that synthetic vitamin D analogs may play a role in the treatment of human cancers. However, it remains unclear if vitamin D deficiency raises cancer risk, or if an increased intake of vitamin D is protective against some cancers. Until additional trials are conducted, it is premature to advise the use of regular vitamin D supplementation to prevent cancer.

Type 1 diabetes: It has been reported that infants given calcitriol during the first year of life are less likely to develop type 1 diabetes than infants fed lesser amounts of vitamin D. Other related studies have suggested using cod liver oil as a source of vitamin D to reduce the incidence of type 1 diabetes. There is currently insufficient evidence to form a clear conclusion in this area.Type 2 diabetes: In recent studies, adults given vitamin D supplementation were shown to improve insulin sensitivity. Further research is needed to confirm these results.

Hypothyroidism (low blood levels of parathyroid hormone) is rare, and is often due to surgical removal of the parathyroid glands. Oral doses of dihydrotachysterol (DHT), calcitriol, or ergocalciferol at high doses can assist in increasing serum calcium concentrations in people with hypoparathyroidism or pseudohypoparathyroidism.

Some patients may develop secondary hyperparathyroidism due to low levels of vitamin D. The initial treatment for this type of hyperparathyroidism is vitamin D. For patients with primary or refractory hyperparathyroidism, surgical removal of the parathyroid glands is commonly recommended.

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There are many reasons to consider upping D3 and alot of them seem to be therapeutic. 

For me, even if the idea of Cancer preventative should prove not to hold up,  there are still more than enough reasons to supplement. 

If this can help reduce musculoskeletal pain, help prevent osteoporosis, heck, maybe even help retain your teeth,--the list seems to be endless---maybe not a panacia--but then what is?

The experts seem to be all over the map as to what may finally considered the optimum dose. 

As to the dose you don't mention what dose is contained in your Multi---And I am not going to make Joan nuts by mentioning a certain Doctor on Her thread (his stance on multis)---LOL

Sufficient to say it was the Ask the Expert at the October conference on metastatic disease and this expert and Edge apparently are in some agreement in this issue.

October 2007: Living with Metastatic Breast Cancer

Question from Lisab:

What are your recommendations as far as taking vitamins during chemo treatment?

Answer:
"HE WHO SHALL BE NAMELESS"

I actually have very strong views on this. The only vitamin supplementation I recommend is Vitamin D. I am advising Vitamin D-3 at 2000 units a day. It may turn out that higher doses are actually preferable, but we do know for sure that 2000 units is safe. Almost everybody in the world who does not live at the equator is Vitamin D deficient. Vitamin D is made by the skin by exposure to the sun, but those of us in the far north or far south and who wear clothes do not have enough skin exposure to make enough Vitamin D. I do not advise excessive sun exposure because of risk of skin aging and skin cancer. Hence Vitamin D supplementation makes sense. 2000 units a day is not a very big dose. If one takes one's shirt off and goes in the sun for half an hour, your body will make 10,000 units. We do not find toxicity from Vitamin D until people take hundreds of thousands of units for prolonged periods.

And this from EDGE

RCC Risk and Sunlight / Vitamin D
In addition there appears to be a positive role of both sunlight exposure via solar ultraviolet B (UV-B) radiation and Vitamin D in renal cell cancer risk reduction: WB Grant28 assessed the protective role of UV-B radiation and dietary factors in an multi-country ecologic study of cancer mortality rates in Europe, finding an inverse correlation of UV-B radiation with a number of cancers, including renal cancer, as well as bladder, breast, endometrial, ovarian, and prostate, with the strongest correlations between UV-B and multiple myeloma, and NHL (also WB Grant29 on the inverse association of UV-B and Vitamin D, and RCC risk) using latitude as an index of solar UVB irradiance, and finding that five-year survival rates south of 50 degrees N were 20%-50% higher than those near 55 degrees latitude), and the adverse association between obesity and enhanced RCC risk may itself be at least partly mediated by Vitamin D and UV-B, as obese individuals may also have lower serum levels of vitamin D30; note of course that obesity and excess energy intake are known etiologic risk factors for both renal cell and non–renal cell cancer16.

Finally, there is the issue of amount of Vitamin D intake, as it now appears the current level recommendations are insufficient for optimal health: Heike Bischoff-Ferrari33 of the Harvard School of Public Health and coresearchers have examined this issue comprehensively, concluding that a daily intake for all adults of greater than 1000 IU (40 µg) vitamin D (cholecalciferol) is needed to bring vitamin D concentrations in no less than 50% of the population up to 75 nmol/L, the starting point of a blood level optimized for BMD and fracture risk reduction, lower-extremity function, dental health, and colorectal cancer prevention; but they further found that the best concentrations are between 90 and 100 nmol/L (36–40 ng/mL), entailing a daily oral dose of 2000 IU (50 µg/d) as both safe and optimal. Finally, John Hathcock from the Council for Responsible Nutrition and coresearchers have valuably derived a revised safe Tolerable Upper Intake Level (UL) for vitamin D, as 250 µg/d (10,000 IU vitamin D3)64, and concluding that the most recent clinical trial data are sufficient to establish that vitamin D is nontoxic at intakes much higher than those previously considered unsafe, and that this demonstrated safety profile should allow the safe increase of Vitamin D intakes necessary to obtain additional benefits at higher levels than previously recognized.

These recent findings are a necessary corrective to long-standing perceptions that low levels of Vitamin D - that is, hypovitaminosis D - are uncommon, or at least so in developed parts of the world. This is in error - Elina Hyppönen and Chris Power34 of the Centre for Paediatric Epidemiology and Biostatistics, Institute of Child Health in London found that the prevalence of hypovitaminosis D was highest during the winter and spring, when 25(OH)D concentrations <25, <40, and <75 nmol/L were found in 15.5%, 46.6%, and 87.1% of participants, respectively, and they conclude that the prevalence of hypovitaminosis D in the general population is alarmingly high during the winter and spring, and often still inadequate but less so at other times of the year, warranting action at a population level rather than at a risk group level.

And it should be further noted that the current recommended allowanceof 400 IU for vitamin D 400 IU for mature adults (aged 50–70 years) is inadequate even to maintain skeletal health35 and is almost certainly too low for any meaningful anticancer activity36. Noting that solar ultraviolet B (UVB) irradiance and/or vitamin D have been demonstrated to be inversely correlated with incidence, mortality, and/or survival rates for breast, colorectal, ovarian, and prostate cancer, and Hodgkin's and non-Hodgkin's lymphoma, with evidence emerging that at least 19 types of cancer are likely to be vitamin D-sensitive including leukemia, and cancers of the small intestine, and vulva37, WB Grant38 of the Sunlight, Nutrition and Health Research Center has estimated that assuring a minimal level of 1,000 IU of oral vitamin D would yield reductions in cancer mortality of 7% for males and 9% for females in the US, and 14% for males and 20% for females in Western European countries below 59 degrees. Lower vitamin-D production from solar ultraviolet-B irradiance in part help explain some differences in cancer survival rates, especially among Black Americans who typically have only 50-75% as much serum 25(OH)D as white Americans39. Indeed the research of Edward Giovannucci and his Harvard colleagues40 strongly suggests that the now documented high frequency of hypovitaminosis D in Blacks - primarily a result of a higher degree of skin melanin effectively filtering out UV-B radiation41 - may be an important, and relatively easily modifiable, contributor to the higher risk of cancer incidence and mortality (2-fold higher compared to Whites) observed in this population, especially given the rapidly accumulating evidence that hypovitaminosis D may increase both cancer incidence and cancer progression42-58.

It is now well established that (1) sunlight ultraviolet radiation produces Vitamin D in the skin, to be subsequently hydroxylated in the liver into 25(OH)D, the primary circulating form of vitamin D, that (2) many types of cell, including some cancerous ones, are able to convert (by by 1-a-hydroxylase) this 25(OH)D into 1,25(OH)2D, the most active form of this vitamin, a function also performed by the kidneys, and that (3) that circulating vitamin D activates vitamin D receptors located on many cells, both cancerous and noncancerous59.
From this foundation, Edward Giovannucci60 has put forward and argued for the biological plausibility of the vitamin D hypothesis, that this Vitamin D receptor activation induced by circulating Vitamin D effectively arrests tumor progression and metastasis, with the variable efficacy of the vitamin D conversion function by different organs and cell types likely accounting for the perceived variation in risk seen across different cancer sites, although it may be as, or more, plausible that observed differences between incidence and mortality are related to solar UV-B exposure, as suggested by Francis Boscoe and Maria Schymura in their previously cited work37, and we know that sunlight exposure is a considerably stronger determinant of 25(OH)D level than is typical dietary intake61. It should be noted that although the preference to achieve optimal internal levels is for Vitamin D supplementation, as opposed to heightened UV-B sunlight exposure, largely out of the concern for risk of melanoma, nonetheless it should be kept in perspective that melanoma accounts fro approximately 7,900+ deaths annually, it is estimated that if the predicted 25(OH)D level is increased 25 nmol/L, this would results in approximately a 29% lower cancer mortality rate, translating into 85, 550 fewer deaths62.

Finally we note that although the WHI trial on calcium and Vitamin D supplementation63 is oft-cited as having demonstrated that Vitamin D does not influence colorectal cancer risk, the study is in fact severely methodologically flawed: it deployed a dose of 400 IU of vitamin D3, but that low level is known to raise serum levels of 25(OH)D3 very modestly, approximately 7 nmol/L, or less than 3 ng/m36, and the use of this nonoptimal low supplementation level coupled with the trial's relatively short duration is likely to explain the perceived failure of vitamin D to reduce the colorectal cancer incidence.

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So bottom line ---Looks like 2000mg seems to be in the ball park if not still low until the FDA ups their recommendation from the 400 that is woefully inadequate.---May be worth it to not freak out your physician--by getting your D levels checked periodically. 

Take care