Page 137 - Vitamin D and Cancer

124 R. Scragg

after treatment [106]. Consistent with these case reports, vitamin D supplementation
(with 1-a-hydroxyvitamin D) of hemodialysis patients was found to improve left
ventricular cardiac function, as measured with echocardiography, by increasing
fractional fiber shortening [107] and decreasing end-systolic and end-diastolic
diameter [108]; although the results from the latter two studies are not entirely
consistent with each other, perhaps because of their limited statistical power due to
very small samples (12 and 5, respectively). Benefits in cardiac function have also
been reported for 1,25(OH) D. This metabolite reduced end-systolic diameter and
2
increased fractional shortening, but only in hemodialysis patients (n = 5) with very
high PTH levels in a Finnish report [109]; and reduced measures of cardiac size
(intraventricular wall thickness and left ventricle mass), without any change in
blood pressure or cardiac output, in 15 hemodialysis patients compared with 10
control patients from Korea [110]. In a US case series of 101 patients with severe
congestive heart failure undergoing evaluation for cardiac transplantation, patients
with more severe disease had significantly lower 25OHD levels, although this
could have been a consequence from less outdoor sun exposure due to feeling
unwell from their disease [111].

6.3.3.3 Calcification

Research using very high doses of vitamin D to produce vascular and cardiac
lesions from calcification continued throughout this period with animal models
[112–117]. However, human studies reported either inverse associations [118, 119],
or no association [120], between blood levels of 1,25(OH) D and coronary
2
calcification. Since blood levels of 1,25(OH) D can be influenced by a number of
2
variables, including dietary calcium and vitamin D status [121], the significance of
these findings was unclear in the absence of studies of the relationship of 25OHD
and calcification.

6.3.4 Summary

Although animal studies of vitamin D toxicity and arteriosclerosis continued during
the 1980s and 1990s, this period was characterized by a shift in emphasis from
studies of adverse effects toward those looking at potential beneficial effects of
vitamin D on CV function. The identification of vitamin D receptors in cardiac and
smooth muscle was compelling evidence for a role by vitamin D in regulating CV
function. However, the number of epidemiological studies, which are essential for
determining etiology, was still limited, with the majority of reports being either
animal studies or human studies of patients. The latter often had very small num-
bers which limited their statistical power for evaluating vitamin D, or selected
groups of patients and controls who may have not been representative of the wider
populations from which they were sampled. These deficiencies in design are