Performance
Vitamin D slowed muscle loss after spinal cord injury in mice
By Life and Health Today Staff, . Life and Health Today.
Vitamin D reduced muscle wasting in mice that had suffered a complete spinal cord injury, according to research published in the Journal of Cachexia, Sarcopenia and Muscle. The finding is preclinical, meaning it has not yet been tested in a human trial, and the authors say it establishes a rationale for doing so rather than a treatment ready for use.
Skeletal muscle atrophy, the progressive loss of muscle mass and function, is a common and serious secondary complication of spinal cord injury, for which no established treatment currently exists. The study used adult male C57BL/6 mice that underwent a complete surgical cut of the spinal cord at the tenth thoracic vertebra, a level that causes paralysis of the hindlimbs. Starting three days after injury, one group of mice received daily oral doses of vitamin D at 150 international units per kilogram of body weight; a control group received coconut oil. Treatment continued for 25 days.
Compared with the control group, the vitamin D-treated mice showed significantly less loss of body weight and better motor recovery, according to the journal. Hindlimb muscle mass was better preserved, and the cross-sectional area, a measure of individual muscle fibre size, was significantly larger in three muscles: the gastrocnemius, the extensor digitorum longus, and the soleus. The journal also reported that vitamin D reduced a pathological shift in muscle fibre type, from the oxidative fibres associated with endurance toward the glycolytic fibres associated with disuse and wasting.
The researchers used proteomic analysis, a technique that maps the proteins a cell is producing, to look for a mechanism. They found that vitamin D was associated with increased activity of a metabolic regulator called TIGAR, a protein involved in how cells manage energy. That increase was linked to a higher number of mitochondria, the structures inside cells that generate energy, and to improvements in their physical structure as seen under an electron microscope.
The journal's published conclusion states that vitamin D "mitigates skeletal muscle atrophy following SCI by restoring metabolic and mitochondrial homeostasis through the upregulation of TIGAR," and that the findings "establish a strong preclinical rationale for investigating VD supplementation as a therapeutic strategy to preserve muscle health in SCI patients."
The study also included a human component: serum vitamin D levels were measured in spinal cord injury patients and compared with their muscle index, a measure of muscle mass assessed by dual-energy X-ray examination. The journal reported a significant positive correlation between the two, with an R-squared value of 0.6495. A correlation, however, does not establish that low vitamin D causes muscle loss; people with more severe injuries or less sun exposure might have lower vitamin D for reasons unrelated to muscle health, and the study was not designed to separate those possibilities.
What this research does not show is whether vitamin D supplementation preserves muscle in people with spinal cord injuries. The mouse model used a complete spinal cord transection, which is one of the most severe injury types, and the dose used in the animals cannot be directly translated to a human regimen. The study does not report whether the motor recovery seen in mice reflects anything that would be meaningful in a human clinical context.
The open question is whether a randomised controlled trial in spinal cord injury patients would replicate the muscle-preservation effect seen here. That is the step the authors are calling for, and it has not yet been done. Anyone considering vitamin D supplementation in the context of a spinal cord injury or any other condition should discuss it with a clinician who knows their individual history.