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The authors estimated that in order for subjects with body mass indexes (BMIs) above the normal range to obtain an increase in serum 25OHD level similar to that of subjects with weight in the normal range, an additional 17 percent increase in vitamin D above the administered dose of 700 IU/day would be needed for every 10 kg increase in body weight above baseline in their study population.

The implication of these studies is that vitamin D deposited in fat tissue is not readily available, and obese individuals may require larger than usual doses of vitamin D supplements to achieve a serum 25OHD level comparable to that of their normal weight counterparts. In support of the hypothesis that vitamin D is stored in adipose tissues, weight reduction studies show that serum 25OHD levels rise when obese individuals lose body fat (Riedt et al., 2005; Zitterman et al., 2009; Tzotzas et al., 2010). Conclusive statements regarding changes in serum 25OHD levels after gastric bypass surgery cannot be made, as a result of confounding factors, such as weight change, possible malabsorption, and diet. There is evidence of a rise in serum 25OHD levels after surgery (Mahdy et al., 2008; Aasheim et al., 2009; Goldner et al., 2009; Bruno et al., 2010), as well as evidence that there is no change after surgery (Riedt et al., 2006; Fleischer et al., 2008; Valderas et al., 2009). Gehrer et al. (2010) indicated that serum 25OHD levels decrease after gastric bypass surgery, although the quality of the methods used is questionable.


As described previously, the products of vitamin D metabolism are excreted through the bile into the feces, and very little is eliminated through the urine. This is in part due to renal reuptake of vitamin D metabolites bound to DBP, as mediated by the cubilin–megalin receptor system (Willnow and Nykjaer, 2005).

Excess Intake

Excess intake of vitamin D—but not sun exposure, which is associated with a series of thermal and photoisomerization reactions (see Figure 3-2) —can lead to a state of vitamin D “intoxication” or “hypervitaminosis D.” Chemically synthesized vitamin D became available late in the third decade of the 20th century; reports of vitamin D intoxication were first found from 1928 to 1932 and continued throughout most of the 20th century (DeLuca, 2009). The condition of hypervitaminosis D leads to hypercalcemia and eventually to soft tissue calcification and resultant renal and cardiovascular damage (DeLuca, 1974). In the case of animal models, at necropsy, vitamin D–intoxicated rats show widespread calcification of organs and tissues.

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