This morning I read this: http://ajcn.nutrition.org/content/84/4/694.full. And just recently En Bloc mentioned on here that she had a argument with her doctor about D3 versus D2, where she says her doctor claimed D3 may raise the serum levels but D2 works and maintains itself on a cellular level. I'm not sure how to interpret this: how would he measure that? Or more generally, what's the basis for such a claim? Are there studies supporting such a claim?

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.

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?

I had read numerous articles that MrsD posted long ago about the difference between the two and when the subject come up in the doctor's office, I felt like I had a good case. However, he quickly took the wind out of my sail and said that the D3 only raises it quick for the short term and that long term results needed the D2...and then made the comment about D3 not working at the cellular level. I sort of blew him off as exactly what MrsD said (he was just trying to impress me), but when I got to the pharmacy to pick up my Rx of D2 I asked the pharmacist the same question. guess what: I got the SAME answer! He told me almost the same thing (didn't focus on the 'cellular level', but made same reference to the D3 raising levels quick and for short term while D3 is better for long term results.

So my conclusion now must be that this must be what the doctors and others are taught at some point in training. I have read some the articles MrsD posts and this is newer info. I don't think my doctor is intentionally giving me wrong info (this is a doctor I trust emphatically and has always been up front about everything), but more like this is what he truly believes based upon training years ago. He may not have been advised on newer info out there now.

I will add that today I went back to my PCP for continued problems with my URI and he had run some other labs at my last visit that I wasn't aware of. I thought he was doing my Vit D & B12 at my upcoming Feb 17th visit, but he had done them 2 weeks ago with some other labs...and gave me my results today. After 12 weeks of D2, my level has gone from 26 to 58! So apparently the D2 does something good. I have absorption issues and this time I took a long course of Rifaximin for my SIBO before starting the D2 in hopes I would have better absorption...and it worked. I know in many ways I have had improvement in how I feel overall, but it's been overshadowed by the infection for the last 2 months and hard to really see at times. But I must say that this at least shows that D2 does work in some ways. I have NEVER had a level of 58 before...even on D3. I'm sure the treatment for SIBO and improved absorption is key to my new level. So the jury is still out for me now that i have this huge improvement and proof that D2 will increase vitamin D. I will be very interested in seeing what David's numbers come back after use of D3.

I don't know if I would have believed this if I didn't have the results right in front of me. But clearly, D2 works as well...quite well too, for increasing a level from 26 to 58.

I would continue to have testing for that D.

Lab error has dogged vitamin D testing considerably
In the recent past. For example, Quest labs have had
2 episodes of erroneous D results, one for a year long
due to wrong calibration technique. Who knows therefore
How much lab errors with this still remain undiscovered?

In fact people are coming here now saying doctors are
No longer testing and insurances not paying for it because
of questions about validity.

If D2 works for you I'd get retested .

I think your conclusion is right, En Bloc. Physicians rarely go beyond what they learned in med school, many, perhaps most at any rate. I have two in my family, and I make sure they know what I think about that!

More importantly, congratulations on getting those numbers up! I don't doubt that D2 can increase numbers. I know a number of people who have used it to increase their numbers. None of the studies doubt that it can work, just that it works less effectively than D3. What were you doses like again? How many and how much?

I'm not sure what my numbers will be like, since I can't seem to tolerate the high doses I need. If the insomnia continues at this low does, like 1000-2000 IU per day, I may have to try D2, and see what I can do with that. But one step at a time: first I'll retest in a month after this low does of D3, all I can really tolerate, and then if I don't see results, I'll like try oral D2. I don't think I'll do high dose 50 000 IU, as I always like to start off slowly.

Does one have to come off the supplements before testing to not skew the results? MrsD., how does this go with D testing? I recall you saying something about B12 testing along these lines.

I have had numerous tests done over the last 1.5 years (4 tests, I think) with all them coming back between 22-28...consistently in this range, so I would have to conclude the labs are accurate. Then after clearing up my absorption issues (which I know worked because my GI issues also improved) and completing a course of D2 and now have a much higher level. I would have no reason to suspect inaccuracy all of a sudden. That just wouldn't make sense after numerous accurate tests all in the same range. If it was still low, we wouldn't suspect the lab to be inaccurate...we would likely suspect the D2 not working. But since my level improved, we should at least consider it worked...isn't that reasonable? I can request a retest, but I'm not sure why unless there is documented problems with testing these days. I do plan on being retested in 3-6 months....just to check the level again and see if it has dropped, or whether I'm maintaining a stable level. If my level is still increased then I'd consider it proven that D2 worked and the test accurate.

The standard RX dose of D2 is 50,000 iu...one capsule a week. I took this for 12 weeks, then a 6 week course taking two a week. I also stopped 3 weeks ago, so I was not taking it when the test was run.

Well, if D2 is 'less effective' than D3, I wonder how high my level would have been with D3...probably toxic. I think a 32 point increase with D2 is pretty 'effective'.

Agreed on all counts.

By more effective I meant you wouldn't need such high doses, which is what the few studies that have differentiated between the two have indicated.

Like I said, I'll see what my levels are like in a month and I may take that route. I'll look into what D2 is exactly. I know it's synthetic, that's all.

I'm glad your numbers went up so effectively. Keep it up, it's working. I don't know if I'd like to go off D3 for 3 weeks before testing. I may feel like **** again, since I don't take enough for it to stay in my system too long. Perhaps I'm wrong. But it's impressive that the D2 stayed in your system enough for those levels even after having stopped 3 weeks prior to testing.

Here is one article that goes into detail about Quest's problems with Vit D testing.

http://www.nytimes.com/2009/01/08/bu...08labtest.html

And another from more recently 2012:
http://www.webmd.com/women/news/2012...accurate-study

and:
http://www.sciencedaily.com/releases...0625152310.htm

These are the only oral products of ergocalciferol in the FDA orange book (on RX)
The D2 sources I am finding are Vegan made.
like this one...
http://www.vitacost.com/source-natur...u-60-tablets-1
800IU to 2,000IU only.

And this was posted yesterday on our MG forum:
http://neurotalk.psychcentral.com/thread231959.html

To get around the testing dilemma for Vit D, one might track their calcium serum levels instead. Something to think about.

I honestly have never seen anything comparing the two (D2 & D3) equally, with the only difference being the amount needed for effectiveness. They are completely different substances and the amount needed is not in question...as far as I can tell. My doctors point was actually the opposite...that D2 stays longer than D3. He argued that D3 makes for quick short term increases in levels, whereas D2 takes longer to achieve the level desired, but it lasts longer and is more effective in the long run.

I argued (at length) MrsD's data/info to no avail. In the end, he asked me to give his point a try (using D2 for 12 weeks) and see what the results show before making my conclusion. So I did. And my results certainly proved his point. That doesn't mean I discount MrsD's data...actually I think the points in those articles are valid. But the fact is: taking D2 really worked for me and I cannot just assume that because it did that my labs must be in error now. Had it not worked and my levels stayed low, I doubt there would be discussion that the lab was in error. I'm sure if my levels had not increased that we would all be confirming that it was simply because it was the ineffectiveness of D2.

I have finished the prescription course, so don't plan to take any more D2 at this point. Then I plan to retest in 3 months to see if my level stays or drops...and by how much. I think follow up testing is important in this regard. Of course, if my level is once again in the 20's, then I would have to question the validity of the 58 level lab. Does that make sense?

I have to ask you: If you are afraid of coming off the D3 for just 3 weeks, doesn't that indicate that it would, in fact, be only a short term fix? Certainly, D3 should last longer than that. If it doesn't, then that would confirm exactly what my doctor stated...that it only increases numbers quick and short term...not long term. I know that D2 is Rx and NOT taken every day/week/month, etc...because it's supposed to last in the body (or cells, maybe, as he stated).

Frankly I think I'm confusing myself, the more I write about this and give it more thought...LOL I'm intrigued by this thread and all the info involved.