Page 132 - Vitamin D and Cancer

6 Vitamin D: Cardiovascular Function and Disease 119

this study include measurement of dietary intake in cases several years after their
heart attack since these individuals are likely to have changed their dietary patterns
after such a major medical event, and reliance on dietary vitamin D intake to
determine vitamin D status.

6.2.2.2 25-Hydroxyvitamin D and Myocardial Infarction

The small contribution of dietary vitamin D to overall body vitamin D levels was
revealed by the development in the 1970s of competitive protein-binding assays for
25-hydroxyvitamin D (25OHD), the main marker of vitamin D status [32]. Diet
was shown to contribute less than 20% of vitamin D stored in the body, with the
major component (more than 80%) coming from vitamin D synthesized in the skin
through sun exposure.[33, 34]
The first epidemiological study of cardiovascular disease to report results with
this new method of measuring vitamin D status was from Heidelberg, Germany [35].
The study recruited only 15 myocardial infarction cases, an unstated time after their
heart attack, and found that their mean serum 25OHD level (32 nmol/L) was within
the normal range for other controls at that time of year. The authors concluded,
somewhat surprisingly at the time, that “nutritional vitamin D status or exposure to
sunlight cannot account for the development of myocardial infarction.”
The next report came from a case control study in Copenhagen, Denmark [36].
The authors of this report, concerned about the possible effect of the acute-phase
reaction from a myocardial infarction on serum 25OHD levels, first showed in a
pilot study of 12 patients that 25OHD did not fluctuate in the first 4 days after onset
of symptoms. They then recruited 128 consecutive patients admitted with chest
pain (53 who had a myocardial infarction and 75 with angina) and compared them
with 409 controls, although no details are provided on how the latter were selected.
Mean serum 25OHD was slightly lower in cases (myocardial infarction 24.0 ng/mL,
angina 23.5 ng/mL) than in controls (28.8 ng/mL), with case–control differences
being statistically significant during May–August (p < 0.05). The authors concurred
with the conclusion of the earlier German report by stating that the “present results
do not support the theory that patients with ischaemic heart disease have a higher
vitamin D intake than the rest of the population.”
The third report came from the Tromso Heart Study, Norway, which had previ-
ously reported higher vitamin D intakes in cases [31]. This was a nested case–
control study which avoided possible bias, from a systematic error caused by the
effect of the disease on measures of vitamin D status, by measuring 25OHD levels
in blood samples collected at baseline interviews when participants were enrolled
into the study [37]. Mean serum 25OHD in 23 patients free of disease at baseline
who had myocardial infarctions during the 4-year follow-up period was again
slightly lower than in 46 controls matched for age and time of year (59.0 vs
63.4 nmol/L); with the case–control difference being significant after correcting for
vitamin D binding protein (p = 0.024), indicating that cases had a lower concentra-
tion of free-25OHD.