A study published in the Journal of Neurosurgery: Spine indicates, in an animal model, a diet rich in docsahexaenoic acid (DHA; an omega-3 fatty acid) and curcumin (one of the principle components of turmeric) can neutralise the clinical and biochemical effects of myelopathy.
Langston Holly, Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, USA, and others reported that they examined the effects of a DHA and curcumin rich diet in promoting neuroprotection in an animal model of myelopathy because while several studies have shown dietary supplementation to have beneficial effects on cerebral function, “comparatively little information has been published regarding the use of dietary supplementation to enhance neural repair in disorders affecting the spine, and this represents a fertile area for study.”
In the study, 27 rats were equally divided into three groups: spinal compression (via surgical placement of thin epidural non-resorbable polymer in the mid-thoracic spine, designed to induce delayed neurological deficit) and a “Western society diet” (ie, one rich in saturated fats); spinal compression and a diet rich in DHA and curcumin; and no spinal compression and a standard diet.
Twenty-one days after the spinal compression procedure, using CatWalk XT software analysis (Noldus Information Technology), the rats in the Western diet group showed significant worsening in ambulatory parameters compared with the other two groups (such as cadence, p<0.02; mean stepping intensity, p<0.03; and print width, p<0.04). Rats in the Western diet group also had significantly worse gait at 21 days and 42 days (the end of the study) after surgery compared with their baseline levels, but there were no significant differences between postoperative gait parameters (at 42 days) and baseline gait parameters for rats in the DHA and curcumin group. Holly et al wrote: “Additionally, although the two groups started with statistically equivalent performance in these parameters, the DHA and curcumin group had significantly better gait function than the Western diet group at the final postoperative day 42 time point (p<0.05).”
They added that 4-HNE levels in the thoracic region at the site of compression were significantly elevated in the Western diet group, indicating “severe cellular membrane damage.”
The injury model used in the study, Holly et al wrote, reduced levels of brain-derived neurotrophic factor (BDNF). According to the authors, BDNF has been shown to have important roles in “axonal regeneration, promoting neuronal survival, regulating synapse formation and stabilisation, increasing dendritic complexity, and enhancing synaptic efficacy.” They added that one possible mechanism of neural repair in the present study was that the use of DHA and curcumin maintained levels of BDNF within the damaged spinal cord and potentiate its effects.
They concluded: “In an animal model of myelopathy, we have demonstrated that DHA and curcumin can counteract the effects of chronic spinal cord compression through several molecular mechanisms, resulting in the preservation of neurological function.”
Holly said: “Our findings suggest that diet can help minimise disease-related changes and repair damage to the spinal cord. We next want to look at other mechanisms involved in the cascade of events leading up to chronic spinal-cord injury. Our goal is to identify which stages will respond best to medical intervention and identify effective steps for slowing the disease process.”