Obesity Linked to Faster Optic Nerve Atrophy in MS Patients
Since optic neuropathy correlates with greater nerve cell loss in the brain, tracking changes to the retina may be a feasible way to determine if healthier lifestyle choices can improve outcomes in MS.
The study, “Association of body mass index with longitudinal rates of retinal atrophy in multiple sclerosis,” was published in the Multiple Sclerosis Journal, and funded in part by the National MS Society.
MS is chronic neurodegenerative disease caused by a combination of genetic and environmental factors. Studies have suggested that obesity is associated with 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, the society states in a 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.
Researchers at Johns Hopkins University set out to investigate whether obesity in MS also increased the damage and loss of neurons in this region of the eye. This would support a link between obesity and worse outcomes of those with MS.
Their study included 513 participants from the Johns Hopkins MS Center who were classified either as having normal weight (214 patients), being overweight (153), or obese (146), depending on their body-mass index (BMI).
Damage to the optic nerve was assessed using a rapid, non-invasive, high-resolution method called optical coherence tomography (OCT), which uses light waves to acquire cross-section pictures of the retina. This allows ophthalmologists to map out and measure the thickness of layers in the eye.
Patients, grouped by distinct body fat measures, were 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 the other two groups, mostly because these patients had experienced more severe optic neuritis events — inflammation and loss of myelin (the protective coat around nerve fibers) in the optical nerve.
After a median follow-up of 4.4 years, however, obese patients exhibited a faster atrophy in the GCIPL layer than those with normal weight. In fact, these patients experienced a 0.57% reduction in GCIPL thickness each year, compared to 0.42% for patients of normal weight.
Atrophy rates in overweight patients, however, were not significantly different from those of normal weight (0.47% reduction per year versus 0.42% in the normal weight group).
In addition to body weight, factors like being African-American, male, and having progressive MS were all also found to be independently associated with a faster GCIPL degeneration.
When BMI was examined as a continuous variable, data showed that for each increase of one unit in BMI scores, GCIPL atrophy 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, the study showed 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 the outcomes of MS patients, and that measuring GCIPL atrophy may be a feasible way of monitoring effectiveness.