Low Vitamin D Levels Linked to Worse Movement Loss, but Not Disease Course

Low Vitamin D Levels Linked to Worse Movement Loss, but Not Disease Course

Low levels of vitamin D, found in the majority of patients with amyotrophic lateral sclerosis (ALS), are linked to more extensive loss of movement, but do not predict the course of disease over a year. Instead, researchers found that taking vitamin D supplements was associated with a faster decline.

The study’s results made the researchers suggest that low vitamin D levels were a consequence, rather than a cause, of poorer health in people with ALS.

The study, “Vitamin D levels are associated with gross motor function in ALS,” was published in the journal Muscle and Nerve.

Earlier studies of vitamin D have suggested that the vitamin may impact disease progression, but researchers at Harvard Medical School noted that small studies of clinic-based ALS patient groups came to different conclusions.

To overcome the restriction of single-center studies, the team turned to the Northeast ALS Consortium (NEALS) Multicenter Study for the Validation of ALS Biomarkers. Since the trial (NCT01495390) collects data in a structured manner and follows patients over time, it is a suitable source of information.

Researchers used vitamin D levels from 106 patients who had gone through physical and neurological exams. The severity of disease was measured with the ALS Functional Rating Scale-Revised (ALSFRS-R), and the team calculated what they referred to as the gross motor ALSFRS-R score by summing up the results of questions exploring turning in bed and adjusting bed clothes, walking, and climbing stairs.

Vitamin D levels were measured both as patients entered the study and at six months, with the team using an average of the two measurements for analysis. This was done to exclude seasonal variation of vitamin levels.

Researchers found that 69 percent of the patients had levels lower than what is recommended, with 50 percent having insufficient levels. The remaining 19 percent had levels so low they were considered vitamin D deficient.

Vitamin levels correlated with the gross motor ALSFRS-R score, but not with the total score, which also measured aspects such as speech, salivation, and breathing.

The team could not find links between the vitamin levels and any demographic factors of body mass index. Neither were the levels tied to the site of disease onset, disease duration, or treatment with Rilutek (riluzole).

Interestingly, patients who used vitamin D supplements had a faster rate of decline in the ALSFRS-R score. Those with higher levels of vitamin D at the start of the study did not have a slower disease progression when measured 18 months after the study’s start.

“The lack of an association between vitamin D levels and future disease progression argues against a role for vitamin D as a modifier of ALS outcomes. It is still possible that high-dose vitamin D supplementation, as used in pre-clinical studies, may have a role in neuroprotection. This hypothesis warrants future mechanistic and prospective investigations,” the researchers concluded.

2 comments

  1. John says:

    This information is really confusing.how can one make any decision based in this? Currently I take a liquid form of d3. Should I keep the status quo?

  2. David Hicks says:

    The reactions in ALS are cellular specific, so research should also be held in cellular specific conditions. The following comments relate to skeletal muscle cells and LMN ALS.
    In LMN ALS, the problem is not the change in Vitamin D levels per se, but the fact that the Vitamin D receptor is inhibited, stopping Vitamin D from entering skeletal muscle cells which are in a highly modified state. The Vitamin D levels in serum is not a cause of LMN ALS as the cause originates within the affected onset cell, i.e. striated skeletal muscle cell.
    The inhibition of the Vitamin D receptor occurs via an up regulated IL-1 beta which activates PLC beta and DAG in the cytosol. PARP is up-regulated causing the down regulation of GAPDH. The down regulated GAPDH allows DAG to bind with PKC and with the help of a phorbol ester (PMA), causes the inhibition of the Vitamin D receptor. If you wish to activate the Vitamin D receptor, the best way is to inhibit PARP, not increase Vitamin D levels. PARP inhibitors must be administered intermittently as they will also inhibit the cell cycle.

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