Common Names
- Xanthophyll
- Dihyroxycarotenoid
- Nonprovitamin A carotenoid
For Patients & Caregivers
How It Works
Current evidence is not sufficient to know if lutein is useful in preventing macular degeneration or cataracts. A diet containing lutein-rich vegetables and fruits may lower the risk of some cancers.
Lutein is a natural pigment synthesized by plants and microorganisms. Because it is an antioxidant, cancer prevention activity has been proposed, but no studies have proved this. Scientists also think that lutein may stimulate the immune system, stop DNA from mutating, or stop the growth of pre-cancerous cells. Lutein has been associated with a decreased risk of macular degeneration and cataracts, but there is not enough evidence to draw definite conclusions. There is some early evidence that increased lutein levels in the blood may protect against heart disease, but more studies are needed.
Purported Uses
- To prevent cancer
One population-based study showed that higher intake of foods rich in lutein is associated with a lower risk of developing colon cancer, but another review of clinical trials suggests this effect is small. Dietary lutein does not reduce the risk of lung or prostate cancer, and its effects on cervical cancer are mixed. There is no proof that lutein can treat cancer. - To treat cataracts
Population-based studies in humans found that eating lutein-rich foods was associated with reduced risk of developing cataracts. There is no evidence that lutein can treat cataracts or that lutein supplements could have the same effect as dietary lutein. - To prevent and treat macular degeneration
A few clinical trials support this use, but others have found no effect of dietary lutein on macular degeneration. Also, there is not enough evidence that lutein can treat macular degeneration. - To increase visual acuity
Clinical trials support this use in patients with degenerative diseases of the retina. - To prevent heart disease
One small study indicates that taking lutein supplements may protect against heart disease, but additional studies are needed.
For Healthcare Professionals
Clinical Summary
Lutein is a natural carotenoid pigment synthesized by plants and microorganisms. Carotenoids are classified as either provitamin A (alpha-carotene, beta-carotene, and beta-cryptoxanthin, which can be converted into retinol) or nonprovitamin A (lutein, lycopene, and zeaxanthin). Lutein has antioxidant (1) (2) and anti-inflammatory (3) activities, and supplements are marketed as protection against ocular diseases such as age-related macular degeneration (AMD) and for general eye health.
Dietary lutein may protect against DNA damage but this may be due to concomitant intake of other micronutrients (4). However, preliminary evidence suggests that supplemental lutein may reduce biomarkers for coronary vascular disease (CVD) in healthy nonsmokers (5), and increase serum lutein in patients with early atherosclerosis, thereby regulating serum lipids and reducing inflammatory cytokines (6).
Epidemiologic studies also suggest an association between increased lutein consumption and decreased incidence of atherosclerosis (7) and cataracts (8) (9), although the effects of dietary lutein on macular degeneration are inconsistent (10) (11) (12). Other long-term studies found no effects with lutein/zeaxanthin supplementation on cognitive function (31), or risk for cataract surgery or vision loss (32) (33).
Preliminary studies suggest lutein supplementation may increase plasma lutein concentrations and physical activity in sedentary older adults (34). It may also improve visual field in patients with retinitis pigmentosa (15). Other studies show increased macular pigment optical density (MPOD) with lutein-containing supplements in patients with Alzheimer’s disease (35), but not in healthy volunteers (36) or offspring of parents with neovascular AMD (37). Although lutein/zeaxanthin improved retinal function in patients with early AMD (38), the current evidence is insufficient to support its use (12) (13) (14).
Increased lutein consumption may decrease the risk of renal cell carcinoma (16), nonaggressive urothelial cell carcinoma (17), and breast cancer (18). Data on the effects of dietary lutein intake and risk of cervical or colon cancer are conflicting (19) (20) (21) (22), whereas no association was found between lutein and lung cancer risk (23) or prostate cancer risk (39).
Food Sources
Kale, spinach, winter squash, cruciferous vegetables, cabbage, green beans, yellow/orange fruits, mangoes, papayas, peaches, oranges (1). Lutein is absorbed best with meals that are higher in fat.
Mechanism of Action
Lutein is one of the predominant carotenoids that accumulates in both the lens and retinal macula (24). It scavenges reactive oxygen species, preventing damage to DNA and protein molecules (19) (25). As an oxycarotenoid, its structure is less hydrophobic than beta-carotene and lycopene. This enables lutein to react with free radicals in a membrane’s aqueous phase, resulting in increased membrane integrity, which may in turn affect tissue permeability to oxygen and other molecules (19). It may also protect against ocular damage by reducing the amount of blue light that reaches photoreceptors (25).
As a nonprovitamin A carotenoid, lutein does not have any vitamin A activity, but does have antioxidant, anti-inflammatory, and immune-enhancing properties. In an obese rat model, lutein independently reduced superoxide dismutase activity, and also raised glutathione peroxidase activity in lean rats when combined with ascorbic acid (26). In vitro and atherosclerotic mouse models demonstrate the ability of lutein to inhibit monocyte inflammatory responses to low-density lipoprotein (LDL) in the artery wall and reduce monocyte migration (7). In humans, lutein supplementation decreases lipid peroxidation and inflammatory response (5).
Carotenoids including lutein inhibit mutagenesis and transformation, and premalignant lesions (1). In murine mammary cancer models, dietary lutein selectively modulated apoptosis and inhibited angiogenesis by increasing p53 and Bax proapoptotic gene expression, while decreasing Bcl-2 antiapoptotic gene expression with a subsequent increase in Bax:Bcl-2 ratio in tumors (27). Lutein-mediated AP-1 suppression and anti-inflammatory effects are due to its antioxidative and p38/c-Jun-N-terminal kinase inhibitory activities (3). In a hepatocellular carcinoma animal model, lutein reduced γ-glutamyl transpeptidase activity, a marker of cellular proliferation (2).