Group items matching

in title, tags, annotations or url

"Thursday, 17 December 2009 This blog is in response to Dr Briffa's post here. as I keep having problems commenting on his blogs. While 44ng/ml is sufficient to not only maximize uptake of calcium (>32ng/ml) and ensure maximum bone mineral density (>42ng/ml), pregnant and nursing mothers should be aware that in order to maximize the amount of vitamin D3 in human breast milk 6400iu/daily was found to be necessary to raise (>58ng/ml) at latitude 32. This is detailed in the Taylor, Wagner and Hollis paper. Vitamin D supplementation during lactation to support infant and mother. Although 4000iu/daily met the mothers daily needs in full it left babies being born with lower 25(OH)D status than required for optimum calcium absorption They also found DAILY use of supplements was required by pregnant and nursing mothers to ensure an even daily Vitamin D3 supply to the foetus & baby. It makes virtually no measurable difference for everyone else if you supplement daily or weekly. While Dr Briffa will not be lactating he may be interested seeing in the Grassrootshealth chart showing disease incidence by 25(OH)D status. this may encourage him to go just another 10ng/ml higher and a bit nearer to the natural level at which human breast milk flows replete with D3."

"Let's shine some sunlight on these knowledge deficiencies: * Serum vitamin D levels have been dropping (as chronic inflammation has been increasing) over the last three decades -- has something changed in our diets? * Vitamin D deficiencies occur globally (not restricted to Northern latitudes or winter) -- related to diet? * Women are more vulnerable, because of cultural modesty in some countries, but males are still D-deficient. * A subset of people exposed to ample sunshine are still D-deficient. * Vitamin D deficient individuals also have elevated TNF. * Vitamin D deficiency and inflammation are risk factors in the same diseases. It seems that the simplest conclusion is that chronic inflammation leads to vitamin D deficiency, even though vitamin D deficiency may also contribute to inflammation."

Addressing the health benefits and risks, involving vitamin D or skin cancer, of increased sun exposure.\nMoan J, Porojnicu AC, Dahlback A, Setlow RB.\nProc Natl Acad Sci U S A. 2008 Jan 15;105(2):668-73. Epub 2008 Jan 7.\nPMID: 18180454

Vitamin D and skin physiology: a D-lightful story.\nHolick MF, Chen TC, Lu Z, Sauter E.\nJ Bone Miner Res. 2007 Dec;22 Suppl 2:V28-33.\nPMID: 18290718 \ndoi: 10.1359/jbmr.07s211\n

Evolution and function of vitamin D. Holick MF. Recent Results Cancer Res. 2003;164:3-28. Review. PMID: 12899511

In vivo threshold for cutaneous synthesis of vitamin D3. Matsuoka LY, Wortsman J, Haddad JG, Hollis BW. J Lab Clin Med. 1989 Sep;114(3):301-5. PMID: 2549141

Geographic variation of prostate cancer mortality rates in the United States: Implications for prostate cancer risk related to vitamin D. Grant WB. Int J Cancer. 2004 Sep 1;111(3):470-1; author reply 472. No abstract available. PMID: 15221981 10.1002/ijc.20220 The implications of our results and those of Tuohimaa et al.[1] include the following. Vitamin D supplementation should be undertaken in wintertime, a period when it is impossible to produce vitamin D by solar UVB exposure in northeastern states.[13] Given these new results, the optimal vitamin D intake and production and serum 25(OH)-vitamin D3 levels for prostate cancer appear to be lower than for other cancers. However, when developing guidelines for vitamin D fortification, many factors should be included in the analysis, including all of the potential health benefits and possible risks of vitamin D, as well as age, sex, residence, child-bearing status, etc.[14] Also, the suggestion that daily vitamin D3 supplement doses of 100 g (4,000 IU)/day are safe[15] should be reexamined. Finally, in terms of preventing prostate cancer, more attention should be given to diet, which has the greatest environmental impact on risk of prostate cancer, with animal products being important risk factors and vegetable products, especially onions and other allium family members, being important risk-reduction factors.[16]

Ecological studies of ultraviolet B, vitamin D and cancer since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Jul;19(7):446-54. Epub 2009 Mar 9. PMID: 19269856 CONCLUSION: These findings provide strong evidence that vitamin D status plays an important role in controlling the outcome of cancer. Support for the UVB-vitamin D-cancer theory is now scientifically strong enough to warrant use of vitamin D in cancer prevention, and as a component of treatment. More research studies would help to explore whether there are benefits beyond the substantial effects that have been observed.

Global vitamin D status and determinants of hypovitaminosis D. Mithal A, Wahl DA, Bonjour JP, Burckhardt P, Dawson-Hughes B, Eisman JA, El-Hajj Fuleihan G, Josse RG, Lips P, Morales-Torres J; on behalf of the IOF Committee of Scientific Advisors (CSA) Nutrition Working Group. Osteoporos Int. 2009 Jun 19. [Epub ahead of print] PMID: 19543765 CONCLUSION: Reports from across the world indicate that hypovitaminosis D is widespread and is re-emerging as a major health problem globally.

The review, published in Osteoporosis International, provides a global perspective of vitamin D status across different regions of the world and identifies common and significant determinants of hypovitaminosis D. Six regions of the world were reviewed-Asia, Europe, Middle East and Africa, Latin America, North America, and Oceania-through a survey of published literature.

Vitamin D and multiple sclerosis. Hayes CE, Cantorna MT, DeLuca HF. Proc Soc Exp Biol Med. 1997 Oct;216(1):21-7. Review. PMID: 9316607

Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Mar 6. [Epub ahead of print] PMID: 19269856

Ecological Studies Of Ultraviolet B, Vitamin D And Cancer Since 2000. Grant WB, Mohr SB. Ann Epidemiol. 2009 Mar 6. [Epub ahead of print] PMID: 19269856 doi:10.1016/j.annepidem.2008.12.014

Chen TC, Chimeh F, Lu Z, Mathieu J, Person KS, Zhang A, Kohn N, Martinello S, Berkowitz R, Holick MF. Factors that influence the cutaneous synthesis and dietary sources of vitamin D. Arch Biochem Biophys. 2007 Apr 15;460(2):213-7. Epub 2007 Jan 8. PMI

Seasonality of UV-radiation and vitamin D status at 69 degrees north. Brustad M, Edvardsen K, Wilsgaard T, Engelsen O, Aksnes L, Lund E. Photochem Photobiol Sci. 2007 Aug;6(8):903-8. Epub 2007 Jun 27. PMID: 17668121 The generally high dietary intakes of vitamin D, especially in winter, mask largely the effect of seasonal variation in UV-exposure, causing an atypical seasonal variation in vitamin D status. The UV-hour variable significantly predicted 25(OH)D levels in blood when adjusted for intakes and artificial UV-radiation exposure and sun holidays abroad.

sunlightD.org Grassroots Health and ZRT Labs are working together to help us all make sure we have enough vitamin D. Participate in understanding vitamin D. Visit grassrootshealth.net and join the research project. You'll get your D tested twice a year for five years. The cost is just $40 a test, $80 a year, more than reasonable for accurate D testing, and you'll help provide real answers, for yourself and for us all, about how much D we get and how much we need. Join now. Do commit to the full 5 years if you decide to sign on. If not joining for the full test period please use the testing links below.

"I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control. By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few)."