Serum cholesterol may have a protective effect in multiple sclerosis (MS) via the blood-brain barrier, although researchers are unsure as to the mechanism of action, reports a study in The Journal of Lipid Research. This could indicate that modifiable lifestyle factors may help to reduce the risk of MS and progression of the disease.

Previous findings suggested that higher low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) levels are positively associated with worsening disability on the Expanded Disability Status Scale (EDSS) and MS Severity Scale (MSSS), however the impact of high-density lipoprotein (HDL) on the disease has not been clear. A team that included researchers from the University of Buffalo designed a multicenter, prospective, longitudinal observational study of 154 patients aged 18–55 with MS who were enrolled within four months from their first demyelinating event, had presence of ≥2 T2-hyperintense lesions on diagnostic MRI, and presence of ≥2 OCB in CSF obtained prior to corticosteroid treatment and Expanded Disability Status Scale (EDSS) ≤0.5. Patients received 3–5g of methylprednisolone for the first symptom and baseline MRI was performed ≥ 30 days after steroid administration; once-weekly, intramuscular interferon beta 1-a treatment 30µg, at baseline was also initiated. Analyses for serum lipid and apolipoprotein were also conducted over the course of the study.

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Higher levels of serum HDL-C and apolipoprotein A-1 (ApoA-I) were associated with lower CSF total protein level, but the possible mechanisms of action remain unknown. However, the findings could be applied in the development of future lifestyle guidelines for prevention and treatment of MS. “Cholesterol profiles can be affected by several factors including genetics, diet, smoking and physical activity,” stated lead author Murali Ramanathan, PhD. “A better understanding of this key class of modifiable factors could be leveraged both as clinical advice to MS patients seeking to reduce the risk of progression and as the basis of guidance to healthy individuals with genetic and other known risk factors for MS.”

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