Vitamin D Deficiency

Vitamin D Deficiency is a topic covered in the 5-Minute Clinical Consult.

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This topic covers the commonly acquired vitamin D deficiency and not type II vitamin D–resistant rickets/type I pseudovitamin D–resistant rickets (both rare autosomal recessive disorders).


  • Vitamin D is a hormone and a vitamin.
  • Cholecalciferol (D3) is synthesized in the skin by exposure to ultraviolet B (UV-B) radiation. Ergocalciferol (D2) and D3 are present in foods.
  • D2 and D3 are hydroxylated in the liver to 25 vitamin D (calcidiol), the major circulating form.
  • Calcidiol is further hydroxylated in the kidney to the active metabolite 1,25 vitamin D (calcitriol).
  • Hypocalcemia stimulates parathyroid hormone (PTH) to be secreted, which prompts the increased conversion of 25 vitamin D to 1,25 vitamin D.
    • 1,25 vitamin D decreases renal calcium and phosphorus excretion, increases intestinal calcium and phosphorus absorption, and increases osteoclast activity. The net result is an increase in serum calcium.


  • A community cohort study of asymptomatic adolescents in Boston found 24% were deficient, with 5% severely deficient.
  • A study of hospitalized patients in Massachusetts found 57% vitamin D–deficient (VDD).
  • Women with history of osteoporosis/osteoporotic fracture have high prevalence of vitamin D deficiency.
  • A cohort study in Arizona found >25% of adults were VDD; highest rates among African Americans and Hispanics
  • A study of about 56,000 individuals across Europe found 13% to have vitamin D deficiency.

Pediatric Considerations
NHANES data suggest 70% of children do not have sufficient 25-OH vitamin D serum levels (9% deficient and 61% insufficient); associated with an increase in BP and decrease in high-density lipoprotein (HDL) cholesterol

Etiology and Pathophysiology

  • Insufficient dietary intake of vitamin D and/or lack of UV-B exposure (in sunlight) results in low levels of vitamin D.
    • This limits calcium absorption, causing excess PTH release.
  • PTH stimulates osteoclast activity, which helps to normalize calcium and phosphorous but results in osteomalacia.
  • Dietary deficiency
    • Inadequate vitamin D intake
  • Inadequate sunlight exposure
    • Institutionalized/hospitalized patients
  • Chronic illness: liver/kidney disease
  • Malabsorptive states

Vitamin D–dependent rickets type 1 occurs due to inactivating mutation of the 1α hydroxylase gene; as a result, calcidiol is not hydroxylated to calcitriol.

Risk Factors

  • Inadequate sun exposure
  • Female
  • Dark skin
  • Immigrant populations
  • Low socioeconomic status
  • Latitudes higher than 38 degrees
  • Elderly
  • Institutionalized
  • Depression
  • Medications (phenobarbital, phenytoin)
  • Gastric bypass surgery/malabsorption syndromes
  • Obesity

General Prevention

  • Adequate exposure to sunlight and dietary sources of vitamin D (plants, fish); many foods are fortified with vitamin D2 and D3.
  • Recommended minimum daily requirement is 600 IU/day from age 1 to 70 years and 800 IU/day for those >70 years. Up to 4,000 IU/day is safe in healthy adults without risk of toxicity.
  • For ages 51 to 70 years, minimally recommended supplementation is 800 IU/day to prevent nonvertebral fractures.
Pediatric Considerations
  • The American Academy of Pediatrics recommends all breastfed babies receive 400 IU/day of vitamin D beginning “within the first few days of life.”
  • 2016 Global Consensus Recommendations suggest all infants, regardless of feeding method, begin vitamin D 400 IU within a few days of birth (1).

Pregnancy Considerations
Insufficient data to recommend routine screening of all pregnancies; only “at risk” should be screened; it is safe to take 1,000 to 2,000 IU/day during pregnancy (2)[B].

Commonly Associated Conditions

  • Osteomalacia, osteoporosis
  • Premenstrual syndrome
  • Rickets
  • Celiac disease
  • Gastric bypass
  • Chronic renal disease
  • Bacterial vaginosis in pregnant women
  • Hypertension
  • Cohort study found that vitamin D deficiency is correlated with increased risk of all-cause mortality.

Vitamin D deficiency is associated with risk of myocardial infarction (MI) and all-cause mortality (3)[A].

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