The main outcomes of this study are as follows. Firstly, approximately 2/3 of individuals within the group of IBD patients with mild or inactive disease have insufficient or deficient 25[OH] vitamin D levels. However this is similar to that found in healthy controls. We confirm seasonal variation in 25[OH] vitamin D levels. Measurement of serum 25[OH] vitamin D during sunny months significantly affected patients levels. Overall consumption of vitamin D supplements increased patient’s serum levels (marginal statistical significance). Families of patients or controls and their families appeared to be less affected by these variables. The IBD families as a group, show higher mean 25(OH) vitamin D level and more often achieve replete status than patients. A modest but significant relationship with patients’ levels becomes evident during sunny months.

Our definitions of the distributions for 25[OH] vitamin D have an influence over the proportion of replete and insufficient number in groups. The controversy over acceptable levels of 25[OH] vitamin D continue and are accentuated by the recent decision of the Institute of Medicine (IOM) to endorse the 50 nmol/L as optimal value for skeletal health [41]. If we accept the IOM definition, 2/3 of patients and 3/4 of controls remain replete. However, there is controversy whether levels of 25[OH] vitamin D acceptable for skeletal health are also applicable to autoimmune or other diseases and the IOM decision was criticized [42]. Our hospital accepts 25[OH] vitamin D distributions at the higher levels as defined herein. In this way about 60% of IBD patients and 2/3 of controls remain insufficient. Other studies, including mostly active cases have reported lower levels in IBD [16, 17, 20–22], but others do report results similar to our study [43, 44]. In the current study, although only a few patients with CD had modestly elevated HBI scores, there was a weak inverse correlation with serum 25(OH) vitamin D levels, suggesting that perhaps active disease is the cause (or effect of) lower serum 25(OH) vitamin D in such cases.

The impact of seasons and vitamin D intake

Evaluating the most relevant variables affecting serum 25[OH] vitamin D levels, MVA ranked sunshine as the most influential on serum levels. The effect of seasons on serum 25[OH] vitamin D has been previously described [22]. Seasonal variation altered serum levels and the effect of vitamin D intake on levels. The effects were more evident in patients as sunshine compensated for intake in sunny months while vitamin D intake affected 25[OH] vitamin D levels in non sunny months. Still these effects did not as a whole compensate enough to achieve uniform replete levels.

In the current study patients who consumed vitamin D supplements had higher levels than those who relied solely on diet, but levels still did not reach desired values. About half the patients and controls consumed supplements but almost 60% did not achieve replete levels. Nevertheless the intake of supplements was disappointing. Only in the patient’s group was there an apparent important increase in levels seconday in vitamin D supplemental intake but did not reach conventional statistical significance. The explanation for the effect on patients is not clear, especially in the light of a recent finding that at least CD patients may have a 35% less efficiency in absorption of vitamin D [45].

Therefore, larger quantities of vitamin D intake may be needed in general and in winter in particular. At least 1200 IU/d (15 μg) is required for replete levels [25]. However, Aloia suggested that 3200 IU/d should be used for at least 2 months and a simulated model found that 4600 IU/d consistently achieved the 75 nmol/L mark [40].

The MVA also ranked Jewish ethnicity and dietary calcium as important determinants of serum vitamin D levels in this study. As explained in the results Jewish ethnicity frequency was similar in both patients and control groups. Their serum 25[OH] vitamin D levels were not significantly different from non Jewish groups but was more evident in the control group.

Dietary calcium was significantly related to serum vitamin D levels but a relationship was only observed in controls. The reason for this is not clear. It is possible that this variable reflected the increased dairy food consumption in controls with increased vitamin D added to such foods. Calcium intake can increase 25[OH] vitamin D levels, when the source of both is from milk but not other sources [46].

The impact of intrafamilial dynamics

Contrary to our expectations IBD family members as a group had the highest rather than lowest mean 25[OH] vitamin D levels. The levels in patient’s families were significantly higher than those in patients. The difference between them was significantly greater than the difference noted between controls and their families. Furthermore a modest but significant correlation in the IBD family unit emerged during sunny months which was less evident in the control family unit.

The reason(s) for these findings is (are) not clear. The possibilities include chance, because of relatively few participants in each group. Our control group may not have been as healthy as expected. 25(OH) vitamin D results of current controls were however, similar to those reported by others [43, 44] and were similar to another healthy control group reported from Montreal [47].

The inclusion of more non Caucasians in the control groups may have limited the 25[OH] vitamin D levels in the controls and their families. Non Caucasians may have lower 25[OH] vitamin D levels [48] However the numerical advantage of the IBD families was only modestly diminished by removal of the non Caucasians from controls. Furthermore the consistent relationships, observed in patients and the family unit rather than controls and their family unit, reduces somewhat the role of chance or the inclusion of excessive non Caucasians in the latter family unit. Still, it is possible that intra family dynamics are different between Caucasians and non Caucasians and this may have influenced intra family results.

In view of intra IBD family unit observations proposal of a genetic link unique to IBD patients and their families is tempting. However, failure to recruit both parents and inclusion of random single family members instead, dilutes ability to detect firm connections. Other undetected variables may also have contributed.

Limitations of study

Limitations in this study need to be considered. Firstly there are a paucity of participants and lack of homogeneity of the IBD group. The use of the combination of IBD patients rests on the similar 25[OH] vitamin D levels found in both groups. A second limitation is the use of clinical indexes to define clinical status of patients. Although, well recognized as markers of activity the HBI or SCCI do not preclude false judgment of remission or activity. The presence of symptoms may indicate irritable bowel related symptoms or those secondary to previous surgery (eg. diarrhea). In conjunction with this notion is that we evaluated patient’s status on a single blood test measurement, which does not allow any longitudinal assessment of clinical course. A third limitation is the absence of data in different categories. Most of these were inadvertent but data that were not available were not used to derive effects on serum vitamin D. In other situations however available data were used to answer questions pertaining to an outcome. For example intake of vitamin D was used to derive that particular information but was not used to relate to serum levels if those values were unavailable. Another limitation was in the way the data were analyzed (combination of patients and controls for effects of variables) may have precluded demonstration of disease effect on 25[OH] vitamin D levels. With the exception of a weak impact of corticosteroids, none of the previously shown effects of IBD on 25[OH] vitamin D levels were found [20, 49, 50]. However, the reason for lack of disease effect, may also relate to the clinical stability of our patients which mostly included inactive or mildly active disease. This suggests that disease activity is more likely an important determinant of serum 25[OH] vitamin D.