Serum Lutein and Macular Pigment Density in Retinitis Pigmentosa

Serum Lutein and Macular Pigment Density in Retinitis Pigmentosa

Lutein Studied in Retinitis Pigmentosa

It has been suggested that increasing macular pigment optical density (MPOD) with lutein supplementation might shield cone photoreceptors from UV-related oxidative damage and possibly slow the rate of cone degeneration over the long term. Previous studies have raised the possibility that lutein may be a potential treatment for retinitis pigmentosa, with one trial showing that supplemental lutein helped preserve visual function (1).

However it has also been reported that macular pigment optical density (MPOD) is not directly related to serum lutein in patients with retinitis pigmentosa, as it is in healthy individuals. This report led researchers from Harvard Medical School and the USDA Human Nutrition Research Center on Aging at Tufts University to further investigate the relationship between MPOD and serum lutein in retinitis pigmentosa patients (2). Their findings shed light on what factors influence MPOD in people with this disease.

Study Design

The authors measured MPOD with heterochromatic flicker photometry, serum lutein and serum zeaxanthin by high performance liquid chromatography and central foveal retinal thickness by optical coherence tomography in 176 patients aged 18–68 years with typical forms of retinitis pigmentosa. Thirty seven (21%) of these patients had cystoid macular edema (CME).

The researchers adjusted for potentially confounding variables such as age, sex, iris color, central foveal thickness and, in some analyses, serum total cholesterol.

Results

MPOD increased with increasing serum lutein (P = 0.0017, see figure 4) and decreased with increasing serum total cholesterol (P = 0.0025) but was unrelated to serum zeaxanthin.

MPOD was higher in patients with brown rather than lighter irises (P = 0.014). MPOD was also related to central foveal retinal thickness (P < 0.0001), being lower in eyes with more photoreceptor cell loss and in eyes with moderate to marked CME.

The relationship between MPOD and serum lutein tended to be stronger in men than in women, which is compatible with some previous results in healthy subjects based on measurements of serum lutein.

In summary, this study found MPOD to be independently related to serum lutein, serum total cholesterol, iris color, and central foveal retinal thickness in patients with retinitis pigmentosa.

Comments

The authors offer some possible explanations for a number of their observations. The lack of an association between MPOD and serum zeaxanthin, for example, may be explained by the observations that lutein is more abundant in the diet, and that about half of the zeaxanthin in the center of the fovea is derived from lutein. This raises the possibility that it may be easier to increase macular pigment in the axons of cone photoreceptor in patients with retinitis pigmentosa by focusing on supplemental lutein rather than zeaxanthin.

The inverse relationship between MPOD and serum cholesterol suggests that higher serum cholesterol levels impede transport of lutein into the retina.

Finally, the linear relationship observed between MPOD and central foveal thickness when data from patients with CME were excluded, could mean that moderate to marked edema hinders the uptake of lutein into the macula or distorts the radial arrangement of the foveolar cone axons.

References

  1. Bahrami H, et al. Lutein supplementation in retinitis pigmentosa: PC-based vision assessment in a randomized double-masked placebo-controlled clinical trial. BMC Ophthalmology 6:23, 2006.
  2. Sandberg MA, et al. The relationship of macular pigment optical density to serum lutein in retinitis pigmentosa. Invest Ophthalmol Vis 51:1086–91, 2010.