Vitamin D has its receptors in everything!
outlines the excess of editorials about vitamin D today. It’s good, particularly
if it gets the word out that all of us Oxford folk need to inspect
and likely increase
our vitamin d levels. But for this Oxford chiropractic
clinic, articles about vitamin D and back pain are thrilling! Discover how
vitamin D impacts back pain
To step back a bit to make this link, Satterwhite Chiropractic
wants to point out that vitamin D receptors have been found in spinal nerve
roots, the spinal cord, the dorsal root ganglia and glial cells. They’re
everywhere in the spine! Researchers have even documented that vitamin D
metabolites are in the nucleus pulposus and annulus fibrosus cells of the
intervertebral disc. Vitamin D is a neurosteroid and influences immune and
inflammatory processes like lumbar disc herniation. (1) Isn’t this exciting?!
Further, intervertebral disc degeneration is a common cause
of lower back pain. In back pain for which there is no known cause, researchers
do tests for factors like vitamin D, glucose, calcium, etc. In one study, the
low back pain patients’ vitamin D levels were significantly lower. (2) Genetic
and environmental factors influence it as well with environmental factors
complicating already existing genetic factors. Vitamin D receptors are one of
many genetic differences from person to person that play a role in disc degeneration.
(3) But look at it this way, Satterwhite Chiropractic can be a positive environmental
factor in dealing with disc degeneration with our Oxford
chiropractic care approach involving gentle spinal manipulation in the form of
Cox Technic, gentle exercise, and nutrition including vitamin D.
So now how can vitamin D’s presence be optimized to relieve Oxford
back pain in our patients? Up its presence! In a placebo comparison study,
patients with musculoskeletal pain taking 4000 IU of vitamin D daily fare
better. Their pain scores declined faster as did levels of inflammatory and
pain-related cytokines (tumor necrosis factor alpha by 54.3% and prostaglandin
E2 by 39.2%). (4) This approach seems pretty simple, doesn’t it?