Journal of Endocrinological Investigation

, Volume 37, Issue 11, pp 1127–1130 | Cite as

Toward a physiological referent for the vitamin D requirement

  • R. P. HeaneyEmail author

Current approaches to setting nutrient intake recommendations are based in a disease-prevention paradigm. The disease to be prevented is typically the disorder classically associated with the nutrient concerned: scurvy for vitamin C, polyneuritis for thiamine, bone disease for vitamin D (D). And the method used is the randomized, controlled trial. While there is growing recognition that nutrients affect many systems, the disease-prevention approach continues, in most cases, to focus on one, or at most two, body systems. For D (cholecalciferol), that system is the skeleton [1].

In contrast, there is general recognition that most nutrients, particularly the micro-nutrients, function to sustain health basically at a molecular-biological level. Logically, the criteria for setting intake requirements should be based on the actual function of the nutrients concerned, not on diseases that they might arguably prevent. In other words, intake recommendations should be based in physiology.



Cholecalciferol Human Milk Scurvy Intake Recommendation Increase Calcium Absorption 
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Conflict of interest



  1. 1.
    IOM (Institute of Medicine) (2011) Dietary reference intakes for calcium and vitamin D. The National Academies Press, Washington DCGoogle Scholar
  2. 2.
    Liu PT, Stenger S, Li H et al (2006) Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science 311(5768):1770–1773PubMedCrossRefGoogle Scholar
  3. 3.
    Franceschi RT, Li Y (2011) Vitamin D regulation of osteoblast function. In: Feldman D, Pike W, Adams J (eds) Chapter 17 in “vitamin D”, 3rd edn. Academic Press, San DiegoGoogle Scholar
  4. 4.
    Lieben L, Masuyama R, Torrekens S et al (2014) Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. J Clin Invest 122:1803–1815CrossRefGoogle Scholar
  5. 5.
    Heaney RP (2012) The nutrient problem. Nutr Rev 70:165–169PubMedCrossRefGoogle Scholar
  6. 6.
    Szent-Gyorgi A, Hyman M (2004) Paradigm shift: the end of “normal science” in medicine. Altern Ther 10(10–15):90–94Google Scholar
  7. 7.
    Sahota O, Mundey MK, Godber IM, Hosking DJ (2006) Vitamin D insufficiency and the blunted PTH response in established osteoporosis: the role of magnesium deficiency. Osteoporos Int 17:1013–1021PubMedCrossRefGoogle Scholar
  8. 8.
    Chapuy M-C, Preziosi P, Maamer M, Arnaud S, Galan P, Hercberg S, Meunier PJ (1997) Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int 7:439–443PubMedCrossRefGoogle Scholar
  9. 9.
    Aloia JF, Talwar SA, Pollack S, Feuerman M, Yeh JK (2006) Optimal vitamin D status and serum parathyroid hormone concentrations in African American women. Am J Clin Nutr 84:602–609PubMedPubMedCentralGoogle Scholar
  10. 10.
    Ginde AA, Wolfe P, Camargo CA, Schwartz RS (2012) Defining vitamin D status by secondary hyperparathyroidism in the US population. J Endocrinol Invest 35:42–48PubMedGoogle Scholar
  11. 11.
    Hollis BW, Wagner CL (2013) The role of the parent compound vitamin D with respect to metabolism and function: why clinical dose intervals can affect clinical outcomes. J Clin Endocrinol Metab 98:4619–4628PubMedCrossRefGoogle Scholar
  12. 12.
    Heaney RP, Armas, LAG. Quantifying the vitamin D economy. Nutr Rev (in press) 2014Google Scholar
  13. 13.
    Heaney RP, Armas LAG, Shary JR, Bell NH, Binkley N, Hollis BW (2008) 25-hydroxylation of vitamin D3: relation to circulating vitamin D3 under various input conditions. Am J Clin Nutr 87:1730–1737Google Scholar
  14. 14.
    Luxwolda MF, Kuipers RS, Kema IP, Dijck-Brouwer DAJ, Muskiet FAJ (2012) Traditionally living populations in East Africa have a mean serum 25-hydroxyvitamin D concentration of 115 nmol/L. Br J Nutr 108:1557–1561PubMedCrossRefGoogle Scholar
  15. 15.
    Hathcock JN, Shao A, Vieth R, Heaney RP (2007) Risk assessment for vitamin D. Am J Clin Nutr 85:6–18PubMedGoogle Scholar

Copyright information

© Italian Society of Endocrinology (SIE) 2014

Authors and Affiliations

  1. 1.Creighton UniversityOmahaUSA

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