Thanks for this, Mrs.D. I'm inclined to agree with you, including about physicians. I haven't been able to find any such research supporting the claim.
Anyway, I read the long study you sent. Good summary of it all. This is the relevant bit for me:
"MEASURES ASSOCIATED WITH VITAMIN D: SERUM 25OHD
Serum 25OHD level is widely considered as a marker of vitamin D nutriture, and consideration of serum 25OHD measures for the purposes of nutrient reference value development has generated notable interest. There is agreement that circulating serum 25OHD levels are currently the best available indicator of the net incoming contributions from cutaneous synthesis and total intake (foods and supplements) (Davis et al., 2007; Brannon et al., 2008; Davis, 2008). Thus, the serum 25OHD level may function as a biomarker of exposure; it is a reflection of the supply of vitamin D to the body and can be a useful adjunct to examining the intake level of vitamin D if the confounders and the measure's variability depending upon a range of variables are kept in mind. However, what is not clearly established is the extent to which 25OHD levels serve as a biomarker of effect. That is, there is some question as to whether levels of 25OHD relate to health outcomes via a causal pathway and can serve as predictors of such outcomes.
Research recommendations in the previous Dietary Reference Intake (DRI) review of vitamin D (IOM, 1997), as well as an Institute of Medicine (IOM) workshop on DRI research needs (IOM, 2007), called for studies to evaluate the intake requirements for vitamin D as related to optimal circulating 25OHD concentrations across life stage and race/ethnicity groups of U.S. and Canadian populations, taking into account variability in UVB radiation exposures. The issue of the role of serum 25OHD concentrations was also identified by the sponsors of this current study on vitamin D and calcium DRIs as central to the development of DRIs for vitamin D (Yetley et al., 2009). Much in the way of this information gap for serum 25OHD concentrations has not yet been addressed. Nonetheless, measures of serum 25OHD are important considerations in developing DRI values for vitamin D intake. The sections below highlight factors affecting serum 25OHD level and methodologies for its measurement. It is important to note that these discussions refer to 25OHD, not to calcitriol (i.e., 1,25-dihydroxyvitamin D). Calcitriol, the active hormonal form of the nutrient, has not been used typically as a measure associated with vitamin D nutriture or as an intermediate related to health outcomes. Calcitriol is not useful as such a measure, for several reasons. Its half-life is short (hours), its formation is not directly regulated by vitamin D intake, its levels are regulated by other factors (such as serum PTH), and, even in the presence of severe vitamin D deficiency the calcitriol level may be normal or even elevated as a result of up-regulation of the 1α-hydroxylase enzyme."
The key point is in the first paragraph: "However, what is not clearly established is the extent to which 25OHD levels serve as a biomarker of effect." We don't have a way to effectively measure what's happening on a cellular level, and to what extent serum levels are related to or effective at the cellular level. Of course, this is an aside from the D3 v 2 debate, and the more important issue. Sound about right?
Quote:
Originally Posted by mrsD
I don't think the doctor is correct. 40+ yrs ago the only D available was D2 on RX ergocalciferol, and was made by Lilly and called Deltalin. This was the go to treatment for rickets. Many of the therapeutic manuals still have this in them, and that is why doctors continue to prescribe it. Lilly sold its patent long ago and the D2 is now brand Drisdol and many generics.
However I will look again. I am reminded of a fellow I ran into at an HMO clinic who took FOUR 50,000 IU D2s a day, for his medical problems. I have to say I suspected him of mailing them abroad, as many patients get doctors to do prescribe high for them as a favor.
Either that or his D2 was not really working well for him?
Doctors sometimes make stuff up, to impress patients, when they are caught without a good answer based in fact.
I'll come back here later today...
edit:
http://press.endocrine.org/doi/full/...0/jc.2004-0360
This article is from 2004. It is pretty clear.
But as it states, few studies get done on this subject.
This is a 2011 article... very long and very complex:
http://www.ncbi.nlm.nih.gov/books/NBK56061/
The way I look at this issue is this:
Claims are D2 is "less toxic"... well if that is true and
no studies are done on the claim, it suggests that D2 is not acting in the tissues hence is eliminated from the body.
Also D3 is the form made in the skin from sunlight. So it is natural to assume that it is more biologically compatible with the body.
The claims about "rickets" suggests only that the lower end of serum values really need to be met for success.
The ricket level usually is given as 30. The therapeutic levels today from research suggest 50-100, the 100 being mostly targeting MS patients. We see now that most foods in the US are fortified now with D3, and the D2 has been discarded.
If people insist on using D2 today, that is their choice. But studies are showing D3 to be superior to it.
And the bottom line? The comment by en bloc's doctor about the "cellular level" ? Both forms D2 and D3 have to undergo conversion to the active form called calcitriol.
This is considered a drug also on RX for people with kidney disease who do not convert the other two forms properly by the kidneys.
Its brand name is Rocaltrol (by Roche).
So D2 and D3 are not working on the cellular level until converted by the kidneys to the active calcitriol. The links I put up here, seem to say that D2 is slower in this regard. |