I am a bit bothered by the fact that it isn’t using D3 instead. There is no reason to not have used cholecalciferol, and there is definitely enough evidence to support using D3 instead. Fortifying food with D2 did help to eliminate infantile rickets - but that’s about it.
Just in case you don’t know what the cochrane review is:
"Cochrane contributors - 37,000 from more than 130 countries - work together to produce credible, accessible health information that is free from commercial sponsorship and other conflicts of interest. Many of our contributors are world leaders in their fields - medicine, health policy, research methodology, or consumer advocacy - and our groups are situated in some of the world’s most respected academic and medical institutions.Our work is recognized as representing an international gold standard for high quality, trusted information. "
The link to the Cochrane Review:
There’s TONS of results/studies done all pretty much going along the same lines
(in summary, D2 does not have anywhere near as much benefit as D3 does and D3 is what should be regarded as a nutrient worthy of fortification or supplementation - I skimmed the history of how D2 even began as the go-to form of supplementation but will spare you those ‘big pharma’ details)
Just a few snippets (out of many) below and I’ve tried to highlight pertinent things in red for you to see.
*Dose of vitamin D3
A dose of vitamin D3 less than 800 IU a day significantly decreased mortality (RR 0.92 (95% CI 0.87 to 0.97); P = 0.005; I2 = 0%; 50,437 participants; 13 trials; Analysis 1.11). A dose of vitamin D3 equal to or greater than 800 IU a day had no statistically significant effect on mortality (RR 0.96 (95% CI 0.92 to 1.00); P = 0.07; I2 = 0%; 25,558 participants; 26 trials; Analysis 1.11). The difference between the estimate of the effect of vitamin D3 on mortality in the trials using a low dose of vitamin D3 and the trials using a high dose of vitamin D3 was not statistically significant by the test of interaction (Chi2 = 1.37; P = 0.24; Analysis 1.11).
*Intervention effect of vitamin D3 according to vitamin D status at entry
Vitamin D3 significantly decreased mortality in the trials including participants with vitamin D insufficiency (RR 0.95 (95% CI 0.91 to 0.99); P = 0.009; I2 = 0%; 55,883 participants; 20 trials; Analysis 1.13). Vitamin D3 had no statistically significant effect on mortality in the trials including participants with vitamin D adequacy (RR 0.92 (95% CI 0.80 to 1.07); P = 0.29; I2 = 0%; 4979 participants; 10 trials; Analysis 1.13). The difference between the estimate of the effect of vitamin D3 on mortality in the trials including participants with vitamin D insufficiency and the trials including participants with vitamin D adequacy was not statistically significant by the test of interaction (Chi2= 0.1; P = 0.75; Analysis 1.13)
*Dose of vitamin D2
A dose of vitamin D2 less than 800 IU a day, tested in one trial, had no statistically significant effect on mortality (RR 0.82 (95% CI 0.17 to 3.98); P = 0.81; 101 participants; Analysis 1.17). A dose of vitamin D2 equal to or greater than 800 IU a day had no statistically significant effect on mortality (RR 1.02 (95% CI 0.95 to 1.10); P = 0.51; I2 = 9%; 18,273 participants; 12 trials; Analysis 1.17). The difference between the estimate of effect of vitamin D2 on mortality in the trials using a high dose of vitamin D2 and the trial using low-dose vitamin D2 was not statistically significant by the test of interaction (Chi2 = 0.07; P = 0.79; Analysis 1.17).
*Intervention effect of vitamin D2 according to vitamin D status
(now this is a bit disturbing)
Vitamin D2 significantly increased mortality in the trials including participants with vitamin D insufficiency (RR 1.20 (95% CI 1.05 to 1.37); P = 0.008; I2 = 0%; 4413 participants; 6 trials; Analysis 1.19). Vitamin D2 had no statistically significant effect on mortality in the trials including participants with vitamin D adequacy (RR 0.97 (95% CI 0.86 to 1.10); P = 0.62; I2 = 0%; 10,496 participants; 5 trials; Analysis 1.19). The difference between the estimates of effect of vitamin D2 on mortality in the trials including participants with vitamin D insufficiency and the trials including participants with vitamin D adequacy was statistically significant by the test of interaction (Chi2 = 5.23; P = 0.02; Analysis 1.19).
— The review later notes slight potential for bias (but not for certain)
Part of the discussion:
Our review identified a possible difference between the two forms of supplemental vitamin D, that is, vitamin D3 and vitamin D2. Vitamin D3 seemed to significantly decrease mortality, while the effect of vitamin D2 may be neutral or even detrimental. The World Health Organization officially regards these two forms as equivalent, based on the results of quite old studies on rickets prevention (World Health Organization 1950). Biological differences between vitamins D3 and D2 are found in some species such as birds and monkeys (Hoy 1988; Marx 1989). Evidence on biological differences between the two vitamins in humans has been sparse and contradictory. A number of recently published clinical trials found evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than vitamin D2 (Armas 2004; Heaney 2011; Leventis 2009; Romagnoli 2008; Trang 1998). However, a randomised clinical trial found that vitamin D3 and vitamin D2 were comparable in maintaining serum 25-hydroxyvitamin D levels (Holick 2008b). A recently published systematic review and meta-analysis indicated that vitamin D3 is more efficacious than vitamin D2 in raising serum 25-hydroxyvitamin D concentrations (Tripkovic 2012). An emerging body of evidence suggests several plausible explanations for this observation. The plasma half-life of vitamin D3 is longer, and it has higher affinity to the vitamin D binding protein, hepatic vitamin D hydroxylase, and the vitamin D receptor (The fact that it’s absorbed better alone is a good enough reason to have used D3 instead of D2 in my opinion) (Holmberg 1986; Houghton 2006; Mistretta 2008). Vitamin D3 is the only naturally occurring form of vitamin D produced endogenously in our body, while vitamin D2 can be obtained only through the diet (Norman 2008). Vitamin D2 seems to upregulate several enzymes that degrade administered vitamin D2 and endogenous D3 (Heaney 2008). Our result could be of interest to health policy makers in different countries. The predominant supplemental form of vitamin D in the United States is vitamin D2 (Houghton 2006). In Europe, Japan and Canada, vitamin D supplements principally contain vitamin D3 (Holick 2008a), although in some European countries, like France and Great Britain, vitamin D2 is also available on the market.
Another article and it’s abstract here:
Full Article: http://ajcn.nutrition.org/content/84/4/694.full
“Supplemental vitamin D is available in 2 distinct forms: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Pharmacopoeias have officially regarded these 2 forms as equivalent and interchangeable, yet this presumption of equivalence is based on studies of rickets prevention in infants conducted 70 y ago. The emergence of 25-hydroxyvitamin D as a measure of vitamin D status provides an objective, quantitative measure of the biological response to vitamin D administration. As a result, vitamin D3 has proven to be the more potent form of vitamin D in all primate species, including humans. Despite an emerging body of evidence suggesting several plausible explanations for the greater bioefficacy of vitamin D3, the form of vitamin D used in major preparations of prescriptions in North America is vitamin D2. The case that vitamin D2 should no longer be considered equivalent to vitamin D3 is based on differences in their efficacy at raising serum 25-hydroxyvitamin D, diminished binding of vitamin D2 metabolites to vitamin D binding protein in plasma, and a nonphysiologic metabolism and shorter shelf life of vitamin D2. Vitamin D2, or ergocalciferol, should not be regarded as a nutrient suitable for supplementation or fortification.”