In addition to the blood levels of vitamin D2 and 3, another criticism for the heart study, is that it was done in Scandinavia where a large percentage of people get their vitamin D from cod liver oil.1 A great explanation of how cod liver oil and vitamin A’s effects are found at #Dr. John Cannell #Vitamin D Counsel.2

There are high levels of vitamin A in cod liver oil.3 In fact a tablespoon of cod liver oil contains 136% of the tolerable upper limits of vitamin A and cod liver oil is a major source of vitamin D in Scandinavia where this heart study was done. Studies have shown that cod liver, and vitamin A, causes an 6-16% increased mortality rate. 4 Also, the Cochrane review shows an increased rate of mortality with increased vitamin A doses. 5 This is extensively explained in reference 4.

#Vitamin A in some ways blocks the effects of vitamin D.6,7 This was not considered in this study and is important, so it is a misleading study. In other studies, done outside of Scandinavian countries where cod liver oil is not the main source of vitamin D, there is no J-shaped curves on a statistics chart or increase in death rates with increased vitamin D.8 I get it. Digging through all these studies is time-consuming and then if you rely on those you think are experts, who do you trust? By looking at my personal case of optimal dosing after 6+ years of a blood level above 100ng/ml of vitamin D3, I think my health would not continue to improve if I supposed that these higher levels listed in this study were, and are dangerous.

However, if they studied people who were receiving optimal #vitamin D with optimal blood levels they would probably see, like I did in the thousands of patients who followed my recommendations, that their #osteoporosis would improve with fewer fractures. Of course, this did and would take time as they did not develop osteoporosis overnight and as we age, repairs take longer. More and appropriate studies at vitamin D3 doses that are optimal not those sure to fail are needed. Next post we will look at the specific claims against vitamin D that Tim makes.


  1. Durup D, Jorgensen HL, Christensen J, et al. A reverse J-shaped association between serum 25-hydroxyvitamin D and cardiovascular disease mortality: The CopD study. Journal Clin Endocrinology Metabolism, volume 100, issue 6, 1 June 2015, pages 2339-2346.
  5. Bjelakovic, G; Nikolova, D; Gluud, LL; Simonetti, RG; Gluud, C (2007). “Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: Systematic review and meta-analysis” (PDF). JAMA: The Journal of the American Medical Association. 297 (8): 842–57.
  6. MacDonald PN, Dowd DR, Nakajima S, et al. Retinoid X receptors stimulate and 9-cis retinoic acid inhibits 1,25-dihydroxyvitamin D3-activated expression of rat osteocalcin gene. Mol Cel Biol, 1993 Sep;13(9):5907-17.
  7. Thompson PD, Jurutka PW, Haussler CA, et al. Heterodimeric DNA binding by the vitamin D receptor and retinoid X receptors is enhanced by 1,25-dihydrovitamin D3 and inhibited by 9-cis-retinoic acid. Evidence for allosteric receptor interactions. J Bio Chem. 1998 April 3;(14):8483-91.
  8. Gaksch M, Jorde R, Grimmes G, et al. Vitamin D mortality: Individual participant data meta-analysis of standardized 25-hydroxyvitamin D in 26916 individuals from a European consortium. PLoS One. 2017; 12(2):e0170791.

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