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SOLGAR
Vitamins |
INNOVATION AND QUALITY
Since 1947
CAREFULLY MANUFACTURED
in the USA
BY SOLGAR LABORATORIES
Available from Independent Health stores and Healthcare practitioners
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At Solgar,
QUALITY ISN’T A WORD WE
USE CASUALLY
-
It’s a way of life.
IT HAS BEEN OUR GUIDING PRINCIPLE
since 1947
AND IS DEEPLY INGRAINED
IN EVERY STEP WE TAKE.
SA JOURNAL OF DIABETES & VASCULAR DISEASE
CONFERENCE REPORT
essential for the action of vitamin D are also
present in tissues not related to bone and
calcium metabolism, such as the immune
system. There is much evidence of non-classi-
cal targets, particularly an endocrine focus.
Tissue-specific deletions of VDR have now
better defined the role of vitamin D in different
tissues, with multiple implications for humans.
Research in mice with a calbindin deletion
found that in the absence of VDRs in the
intestinal endothelium, excess osteoid tissue is
produced. At only 20% of normal VDR levels
in the intestine, calcium homeostasis in the
gut normalises, with normal bone and growth
plates resulting. However, when there is a total
knockout of VDR in the gut, a massive loss of
bone results with an excess of osteoid tissue.
Deletion of VDR in the growth plate
affects kidney function. An increase in
sodium and phosphorous transport occurs,
as well as increased serum phosphate. Levels
of fibroblast growth factor are also affected.
The effects of VDR knockout in osteoblasts
differ depending on diet.With normal calcium
levels in the diet, calcium and phosphorous
transport remains normal, as does the bone.
In a low-calcium diet however, impaired bone
mineralisation is observed in the knockout
mice with osteoblast VDR deletion.
The native immune system is activated
by the vitamin D endocrine system. Immune
system VDR knockout in mice has vary-
ing effects. The acquired immune system is
damped down by receptor knockout, whereas
the natural immune system regulated by mac-
rophages is stimulated, with monocyte activa-
tion inducing the production of defensins.
Vitamin D deficiency can also affect the
survival of T cells. Individuals with low levels
of vitamin D are observed to have more
infections. A low VDR expression increases
the risk of
Mycobacterium tuberculosis
(MTB)
and other respiratory infections. Patients with
active MTB are found to have reduced levels,
and those who are HIV positive have very low
levels of vitamin D. Evidence has emerged that
vitamin D supplementation improves chronic
obstructive pulmonary disorder. Vitamin D or
VDR deficiency leads to increased sensitivity to
autoimmune diseases, such as inflammatory
bowel disease or autoimmune diabetes.
Vitamin D deficiency in early life has a
legacy effect in later life. Early life vitamin D
deficiency in mice doubles the diabetes risk
and Dr Bouillon postulated that a reduction
in incidence of type 1 diabetes mellitus of
70% could be achieved with vitamin D
supplementation in the first year of life.
An observational study has also reported
a doubling of risk of multiple sclerosis with
decreased vitamin D levels.
An increased incidence of cancer has been
observed in mice with VDR knockout in the
intestinal mucosa, breast and prostate. While
there was no spontaneous increase in cancer
in these mice, they were more prone to
oncogen-, chemocarcinogen- and ultraviolet
B-induced tumours. Observational data from
the NHANES III study found an increased risk
of colon cancer with low levels of vitamin D.
In terms of cardiovascular disease, VDR
knockout mice displayed higher renin hyper-
tension, increased cardiac hypertrophy and
increased thrombosis. Observational reports
associated increased risk of cardiovascular
events with decreasing levels of vitamin D in
humans. Cardiovascular mortality is increased
in those with vitamin D levels < 10–15 ng/mol,
however, interventional studies have shown
no effect on myocardial infarction and stroke.
Vitamin D deficiency is associated with
the metabolic syndrome. Vitamin D supple-
mentation has been associated with resolving
maturation problems (weakness) in skeletal
muscle. The elderly also benefit from supple-
mentation, with a decreased risk of falls.
Undoubtedly, vitamin D deficiency is
associated with increased mortality rates.
Supplementation could decrease mortality
rates by as much as 8%.
What is the optimal supplementation
level? One-third of the world’s population
falls below the threshold level of 25 ng/mol.
Dr Bouillon recommends 20 ng/mol as an
ideal supplementation level. Faced with the
question of possible harm in supplementation
doses > 90 ng/mol, he referred to a trial
where an increase in falls and fractures were
observed with vitamin D levels maintained at
> 90 ng/mol. His final response, ‘more is not
better’.
G Hardy
Source: Presentation at 2012 SEMDSA congress, Cape
Town, South Africa