Since optic nerve degeneration correlates with greater nerve loss in the brain, measuring changes in this tissue may be a feasible way to determine whether lifestyle changes that lead to body fat loss improve patient outcomes.
The study, “Association of body mass index with longitudinal rates of retinal atrophy in multiple sclerosis,” was published in the Multiple Sclerosis Journal, and supported by the National MS Society.
MS is chronic neurodegenerative disease caused by a combination of genetic and environmental factors. Studies suggest that obesity is linked to greater MS disability and disease progression, as well cognitive deficits.
Optical nerve tissue has been shown to mirror changes in overall brain health in people with MS, according to a society release. Degeneration in a particular layer in the back of the eye, called the ganglion cell and inner plexiform layer (GCIPL), appears to correlate with worse disability, increased disease activity, and greater brain atrophy in MS.
Johns Hopkins University researchers set out to investigate whether obesity also increased the damage to, and loss of, neurons in this region of the eye, as previous MS research has suggested.
Their study included 513 people being followed at the Johns Hopkins MS Center, who were classified as being of normal weight (214 patients), overweight (153), or obese (146) depending on their body-mass index (BMI).
Damage to the optic nerve was assessed using a rapid, non-invasive, and high-resolution method called optical coherence tomography (OCT). This method uses light waves to capture cross-sectional pictures of the retina, allowing ophthalmologists to map and measure the thickness of layers of the eye.
Each group of patients with distinct body fat measurements was fairly similar with respect to age, disease subtype, and disease duration. But women were more likely to be in the normal weight group, and African-Americans more likely to be obese.
In the first OCT assessment, those with normal weight had lower GCIPL thickness than did people in the other two groups. This was mostly because these patients had more serve optic neuritis events — meaning, more inflammation and loss of myelin (the protective coat around nerve fibers) in the optical nerve.
After a median followup of 4.4 years, however, obese patients showed a faster atrophy in the GCIPL layer than did those of normal weight. Obese patients experienced a 0.57% reduction in GCIPL thickness each year, compared to 0.42% for those of normal weight.
Atrophy rates in overweight patients (0.47%) were not significantly different from normal weight patients (0.42%).
In addition to body weight, factors like being African-American, male, and having progressive MS were all independently associated with faster GCIPL degeneration, the researchers wrote.
When BMI was examined as a continuous variable, data showed that for each one unit increase in BMI scores, GCIPL atrophy was accelerated by 0.011% each year. But when African-Americans were removed from the analysis — due to their higher representation in the obese group — this association was no longer significant.
Overall, results show that “baseline BMI is independently associated with an accelerated rate of GCIPL atrophy in MS,” the researchers wrote.
“Our study findings are in accordance with prior work demonstrating that MS patients with an elevated BMI exhibit more rapid disease progression, including accelerated brain atrophy and worse outcomes in ambulation and global disability,” the team concluded.
These findings also suggest that lifestyle changes aimed at reducing body fat may improve patient outcomes in MS, and that measuring GCIPL atrophy could be a feasible way of monitoring the effectiveness of a healthier lifestyle.
“If confirmed,” the society wrote in its release, “the findings show a link between a wellness factor — body weight — and MS progression, and support studies that would track whether reducing weight can improve outcomes in MS.”
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