The following is a direct quote from the Mayo Clinic’s
website on Parkinson’s disease: “Parkinson's
disease is a progressive disorder of the nervous system that affects your
movement. It develops gradually, sometimes starting with a barely noticeable
tremor in just one hand. But while tremor may be the most well known sign of
Parkinson's disease, the disorder also commonly causes stiffness or slowing of
movement. In early stages of Parkinson's disease, your face may show little or
no expression, or your arms may not swing when you walk. Your speech may become
soft or slurred. Parkinson's disease symptoms worsen as your condition
progresses over time. Although Parkinson's disease can't be cured, medications
may markedly improve your symptoms. In occasional cases, your doctor may
suggest surgery to regulate certain regions of your brain and improve your
symptoms”.
A recent paper in the American Journal of Clinical Nutrition[1]
looked at the role of vitamin D in Parkinson’s disease (PD). The authors, from the Jikei University Medical
School in Tokyo, present at the outset a summary of the existing data. Those
who suffer from PD have lower blood levels of vitamin D. They also have lower
bone mineral density and a higher risk of falls. In the US, there is a North-South
gradient in the incidence of PD, which may reflect a North-South gradient in
sunshine bearing in mind that vitamin D is the sunshine vitamin. They also
point out that the enzymes responsible for the synthesis of the active form of
blood vitamin D are expressed in highest concentration in that part of the
brain where there is most neuronal damage in PD (substantia nigra). Finally, they point out that in mice, where
the vitamin D receptor, which transports vitamin D into cells is deleted using
genetic knock out technology, show characteristics of PD.
All of this, while interesting, is entirely correlational in
nature and does not prove cause and effect. The authors therefore set out to
test the hypothesis that vitamin D is directly related to PD by conducting a
randomized, double blind placebo controlled study. Patients with PD were
randomly assigned to receive either a placebo or a vitamin D supplement for 12
months. Neither the patients nor the investigating physicians knew which was
which since this was a blinded study. The patients were followed every 2 to 12
weeks and were clinically examined to ascertain the progression or otherwise of
their condition using the Hoehn and Yahr (HY) scaling system. The average age
of the patients was 72 years.
Compared to those given the placebo, those given the vitamin
D supplement showed a highly statistically significant slowing down of the rate
of progression of PD. No adverse effects were observed. The authors rightly
take a conservative view of these results, They point out that in this age
group, vitamin D supplementation generally improves muscle strength and overall
balance and the extent to which the improvement in PD symptoms might be
influenced by this non-specific effect is unknown. The authors also included a
genetic component to their studies. They showed that those PD patients with a
particular genetic variation of the vitamin D receptor (FokI T allele)
responded best. A related editorial in this edition of the AJCN[2],
researchers from The Queensland Brain Institute also adds to the general
argument that vitamin D has a neuroprotective role. Supporting the arguments of
the authors of the intervention study, they add that vitamin D supplementation
reduces the side effects of some drugs used in the therapy of PD. They also go
on to argue that if the findings of the intervention study are replicated and
if no adverse effects are seen then “there is a case to translate this
treatment promptly. Even if optimal vitamin D status delays PD progression by a
small degree, this treatment is cheap, simple to access, relatively safe and
publicly acceptable”.
This is yet another example of a study which flies in the
face of the high priests of dietetics who constantly argue that a health diet
will provide all of an individual’s nutrient requirements. It also highlights
the need to marry an individual’s genetic make-up to their response to a
nutritional intervention. Regrettably, the ruthless supplement industry will
exploit this paper and make absurdly exaggerated claims about vitamins.
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