Vitamin D Insufficiency Common in Early Parkinson's

Susan Jeffrey

March 16, 2011

March 16, 2011 — Vitamin D levels are frequently low among patients with early Parkinson's disease (PD), a new study shows. However, no decrease in levels over time was seen as the disease progressed; levels stayed the same or actually increased.

"So that offers at least some support for the notion that it's not the disease itself that is causing the vitamin D deficiency, or if it is, it's occurring months to years before they actually have clinical symptoms," lead study author Marian L. Evatt, MD, from Emory University School of Medicine and the Atlanta Veterans Affairs Medical Center in Georgia, told Medscape Medical News.

The results are published in the March issue of Archives of Neurology.

Several Lines of Research

Vitamin D is now considered a hormone that regulates a variety of physiologic processes, the study authors note. The potential pathologic role of vitamin D deficiency has lately been the focus of research across a number of diseases, including multiple sclerosis, diabetes, and some forms of cancer, they note.

Dr. Marian L. Evatt

In 2007, a hypothesis article was published postulating that low vitamin D levels may have something to do with either the pathogenesis or progression of PD, Dr. Evatt explained (Mov Disord. 2007;22:461-468). "They outlined several lines of research that would support that hypothesis."

Her own work has focused on nutrition in the setting of PD and whether there might be supplements or other nutritional measures that might affect management or prevention of the disease, she said.

Previously, her group examined the prevalence of vitamin D deficiency in a cohort of PD patients, Alzheimer's disease patients, and healthy controls. "To our surprise, the prevalence of vitamin D deficiency was much higher in the Parkinson's patients than in the health controls or the Alzheimer's patients," Dr. Evatt said, although unlike previous work, they found no correlation of vitamin D levels with disease duration in either the PD or Alzheimer's disease patients ( Arch Neurol. 2008;65:1348-1352).

Another article published last July, for which Dr. Evatt wrote an accompanying editorial, used data from the population-based Mini-Finland Health Survey and showed a protective effect against PD for those with levels above 50 mmol/L, with a 65% risk reduction vs those with levels less than 25 mmol/L, as well as an apparent dose-response effect (Arch Neurol. 2010;67:808-811).

In the current study, Dr. Evatt and colleagues examined the prevalence of vitamin D insufficiency in untreated patients with early PD, diagnosed within 5 years of entry into the study. They conducted a survey of vitamin D status in stored blood samples from 157 patients with PD who were enrolled in the placebo group of the Deprenyl and Tocopherol Antioxidative Therapy of Parkinsonism (DATATOP) trial.

DATATOP is a previously reported randomized factorial trial that investigated the effect of selegiline or tocopherol or both in the setting of early nondisabling PD (Arch Neurol. 1989;46:1052-1060). Patients had a baseline and an endpoint or final visit measurement of 25-hydroxyvitamin D available.

"The nice thing about this group is that they are early in their disease and they don't need medicine, so you can't argue that they're disabled enough to impact their vitamin D levels," Dr. Evatt noted. "And we confirmed that there was still a high prevalence of vitamin D deficiency in those patients."

At baseline, most participants (69.4%) were deemed vitamin D insufficient, defined as a 25-hydroxyvitamin D level of less than 30.0 ng/mL. Vitamin D deficiency, a level of less than 20 ng/mL, was seen in 26.1%.

"Contrary to our expectation that vitamin D levels might decrease over time because of disease-related inactivity and reduced sun exposure, vitamin D levels increased over the study period," they write.

Vitamin D insufficiency was seen at the final examination in 51.6% and frank deficiency decreased to 7%. "These findings are consistent with the possibility that long-term insufficiency is present before the clinical manifestations of PD and may play a role in the pathogenesis of PD," the study authors conclude.

'Sweet Spot'

Dr. Evatt said she'd like to see whether these findings could be replicated in other cohorts. "If that's the case, then there's a lot of ground work that's going to need to be laid," she added.

For example, it's not clear what the optimal levels of vitamin D may be for disease prevention vs bone health. A recent report by the Institute of Medicine put the level conservatively at greater than 20.0 ng/mL, whereas the endocrinology community generally uses greater than 30.0 ng/mL as an optimal level at least for bone health. There may be other disease-specific optimal or "sweet spot" levels that haven't yet been established, Dr. Evatt speculated.

"There's not enough evidence in a whole cadre of chronic diseases to suggest that getting it above that level is better in those diseases, even though there's several ecologic and cross-sectional studies to suggest that low vitamin D may have something to do with many diseases, not just Parkinson's," she added.

The role vitamin D plays may not end up being simple, she said, "but there's certainly enough evidence there that I think it warrants looking into more closely."

This data-mining project was supported by the Parkinson's Disease Foundation's Advancing Parkinson's Treatments Innovations Grant to the Parkinson's Study Group. Dr. Evatt receives salary support from the Atlanta Veterans Affairs Medical Center. Disclosures for coauthors appear in the original article.

Arch Neurol. 2011;68:314-319.

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