The course of PD can be quite variable, and it is difficult for clinicians to predict what will happen to an individual person with PD, but identifying prognostic factors ought to help practitioners answer their patients’ questions and potentially improve the understanding of mechanisms underlying the disease pathogenesis.
If vitamin B12 is related to the progression of PD as suggested in the study by Christine et al., its replacement may slow the decline of the disease. But there are several issues that need to be addressed in the context of their findings.
First, what constitutes a low vitamin B12 level is not a simple issue. If the evaluation is limited to measurement of vitamin B12 concentration, the diagnosis of genuine deficiency is unreliable. Most experts agree that combined measurement of vitamin B12 with determination of homocysteine levels is necessary and while Christine et al. measured both levels, their statistical analysis and subsequent conclusions are exclusively based on the levels of the vitamin.
Moreover, 34 patients in the study were classified as having “borderline-low” vitamin B12 levels, and 14 had both borderline-low B12 level and high homocysteine concentration. This brings into question whether the researchers identified PD patients who actually had low B12 levels.
The design of the DATATOP trial could also introduce some bias into the findings. At the time of publication, the study was criticized for disregarding the symptomatic effect of selegiline and for a lack of objective definition of criteria for the trial’s primary endpoint – introduction of levodopa.
This could have led to the termination of individuals at different stages of the disease, introducing a potential bias in the sample of patients who remained in the study for enough time to undergo subsequent determination of B12 levels.
The findings in the current study are also in contrast to previous research, and the underlying mechanism of vitamin B12 in PD is also unclear.
Nevertheless, the results of the study by Dr. Christine and his colleagues are intriguing and further investigations to address this hypothesis are warranted.
Francisco Cardoso, MD, PhD, is with the movement disorders unit within the neurology service at the Federal University of Minas Gerais, Belo Horizonte, Brazil. His comments are derived from an editorial accompanying the study by Dr. Christine and colleagues (Movement Dis. 2018 Mar 6. doi: 10.1002/mds.27366). He had no relevant disclosures.
