Lutein and Zeaxanthin: Actions


Lutein and zeaxanthin are both powerful antioxidants, with activity having been demonstrated in a number of in vitro tests. In vitro studies of human lens epithelial cells also indicate that their antioxidant activity may protect the lens from UVB radiation. According to animal studies, lutein increases glutathione levels and reduces retinal apoptosis following ischaemic reperfusion.


The yellow colour of lutein and zeaxanthin is due to their ability to absorb blue light, which is believed to contribute to their protective function because blue light is at the high energy, and therefore the most damaging, end of the visible spectrum. Lutein and zeaxanthin thus serve as an optical filter for blue light, reducing chromatic aberration and preventing damage to the photoreceptor cell layer.


Lutein and zeaxanthin are entirely of dietary origin and are initially absent in newborns but gradually accumulate over time (Nussbaum et al 1981). It has been generally accepted that macular pigment density decreases with age; however, there are conflicting results. In one prospective, observational study involving 390 patients, macular pigment density was not found to change significantly with age, even when elderly subjects with cataracts and ARMD were considered. Other studies, however, have found that macular pigment does indeed decline with age in both normal eyes and those with ARMD and Stargardt macular dystrophy, but not in retinitis pigmentosa or choroideremia.

Although lutein and zeaxanthin levels in the serum, diet, and retina correlate, the nature of the relationships between lutein and zeaxanthin in foodstuffs, blood and the macula are confounded by many variables, including processes that influence digestion, absorption, and transport and accumulation and stabilisation of the carotenoids in the tissues. It is suggested, however, that lutein and zeaxanthin are transported into an individual’s retina in the same proportions found in his or her blood.

Two clinical studies have demonstrated that increasing lutein intake will increase macular pigment density within 4 weeks. More recently, a clinical study confirmed the association between macular pigmentation, dietary lutein intake and serum lutein levels.


Lutein modulates cellular and humoral-mediated immune responses, according to animal studies. In particular, high levels of C-reactive protein and a high white blood cell count have been identified in individuals with low serum levels of lutein. In a case-controlled study serum lutein and zeaxanthin, together with other carotenoids, were also found to be lower in children with acute phase infections compared to healthy controls.


According to an animal study, lutein reduces the risk of sunburn, as well as the local UVB-radiation-induced immune suppression and reactive oxygen species generation that are implicated in photocarcinogenesis. A protective effect on skin cancer, however, has not been observed in human cohort studies. One prospective cohort study involving 43,867 men and 85,944 women found no significant inverse association between intake of lutein and squamous cell carcinoma, and an increased risk of squamous cell carcinoma was observed for people with multiple prior non-melanoma skin cancers and high serum levels of lutein and zeaxanthin. The clinical significance of these findings is uncertain.