Our primary source of vitamin D is sun exposure. 20 minutes of exposure of one quarter of the body to midday sun will produce about 4,000 i.u. in a Caucasian. Darker skinned persons will need two to three times as long to produce the same amount. The only food sources are cod liver oil, fatty fish, eggs and the fortified foods, primarily milk and some cereals. Deficiency is associated generalized myalgias, bone and joint pain, sweating of the head at nite, sore scalp with hair brushing or combing, and sensitive teeth.

Vitamin D enhances calcium absorbtion, thereby preventing rickets, osteomalacia, osteoporosis and secondary hyperparathyroidism. Sufficient Vitamin D may prevent psoriasis and seasonal affective disorder. Activated Vitamin D is involved in a number of diverse cellular processes including inhibition of proliferation of breast, colon and prostate cancer cells. Supplementation may prevent type I diabetes and rickets in children, and weight gain, diabetes, heart disease and multiple sclerosis in adults.


50ug/2000 iu/day.
No Observed Adverse Effect Level[1] (NAS)
95 ug/3800 iu/day.
Lowest Observed Adverse Effect (NAS)

Vieth[2] recommends:

LOAEL: >1000ug (40,000 iu)/d
NOAEL: >250ug (10,000 iu)/day for prolonged intake.


To assure >100 nmol/L, take 100 ug (4000 iu)/day. Patients with Oat cell carcinoma, Non Hodgkins Lymphoma, Tuberculosis, or Sarcoid should avoid any dietary or environmental Vit. D.

Patients with no sunlight exposure should get at least 1,000 iu/day (Holick)


1 nmol/L =1ng/ml x 2.5

Toxicity mild with serum:
350 ng/dl (140 nmol/L) (Vieth)
310 ng/dl (125 nmol/L) (Adams and Lee)
220 nmol/L levels in some lifeguards w/o supplementation
To minimize PTH: > 100 nmol/L, which corresponds to 4000 iu/day intake
Optimal: 40-80 nmol/L; 35-55 ng/ml (Cannell, Dir. Vit D Council)
30-50 ng/ml (Holick)[3]
40-60 nmol/L (Rowen)[4] has lower risk of Prostate Ca; Above 80 nmol/L risk starts to increase again.[5]
> 30 ng/ml (75 nmol/L) for persons with osteoarthritis[6]
Moderate deficiency:
<20 ng/ml (50 nmol/L)
< 15 ng/ml level at which serum PTH levels increase[7]
Severe deficiency: <8 ng/ml (20 nmol/L)[8]


John H Juhl, DO


My clinical experience over the last 18 months is that for vitamin D 1400-1800 i.u. by mouth per day, I have had no adversely elevated levels either at the trough (Feb) or peak (Aug) seasons. Persons with irritable bowel or malabsorbtion syndromes may need considerably higher doses to get optimal blood levels. One patient had a 15 point increase in Vit D25-OH levels after adding bile salt capsules to his major meal.


Based on the recent paper by Hollis[9], I am now increasing the bottom of the optimal range for serum Vitamin25(OH)-D from 40 to 50 ng/ml.


I am increasing baseline recommendation to 2,400 i.u./day.

[1] Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.. Dietary reference intakes: calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington DC: National Academy Press,1997.

[2] Vieth Rheinhold, Vitamin D supplementation, 25-hydroxyvitamin concentrations, and safety,AM J Clin Nutr 1999;69:842-56.

[3] Holick Michael F, Vitamin D deficiency: What a pain it is, Mayo Clin Proc, 2003;78(12):1457-59.

[4] Rowen Robert J, Are you getting too much Vitamin D? Second Opinion, May 2004;XIV,#5.

[5] Int J Cancer, Jan 1, 2004;108(1):104-8.

[6] McAlindon TE, Felson DT, Zhang Y, et al, Relation of dietary intake and serum levels of vitamin D to progression of osteoarthritis of the knee among participants in the Framingham study, Ann Intern Med, 1996;125:353-59.

[7] Thomas MK, Lloyd-Jones DM et al, Hypovitaminosis D in Medical Inpatients, NEJM 1998; 338#12: 777-83.

[8] Plotnikoff Gregory A,, Prevalence of Severe Hypovitaminosis D in Patients with Persistetnt, Nonspecific Musculoskeletal Pain,, Mayo Clin Proc, 2003:78:1463-70.

[9] Cannell JJ, Hollis BW, Use of vitamin D in clinical practice, Alt Med Review, 2008; V 13 # 1, p 6-33.