- nonprovitamin A carotenoid
For Patients & Caregivers
Bottom Line: 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.
- 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 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 certain laboratory markers used to determine risk for heart disease.
In this large study, 35,551 women were followed for 10 years to compare the intake of dietary lutein and cataracts. Those who reported high intakes of dietary lutein were less likely to develop cataracts, indicating that eating lutein-rich foods may reduce cataract risk. Further clinical studies of patients taking lutein supplements or placebo are needed to determine if these protective effects were due to dietary lutein alone.
This study involved 856 patients with newly diagnosed urothelial cell carcinoma (UCC) who were matched with 856 members by sex, age at baseline, study center, date and time of blood collection, and fasting status. Blood levels of carotenoids were measured, including alpha- and beta-carotenes, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin. Researchers report that the risk of UCC decreased with greater blood concentrations of lutein and beta-carotene.
For Healthcare Professionals
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). Current evidence is insufficient to support the use of lutein to prevent early age-related macular degeneration (12)(13)(14). A preliminary study suggests that lutein supplementation may improve visual field in patients with retinitis pigmentosa, but larger confirmatory trials are also needed (15).
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).
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 activity 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).
Absorption: Intestinal absorption of carotenoids, including lutein, is facilitated by the formation of bile acid micelles containing carotenoids. The presence of fat in the small intestine stimulates the secretion of bile acids from the gall bladder and improves the absorption of carotenoids by increasing size and stability of the micelles, thus allowing more carotenoids to be solubilized. Bioavailability of lutein is affected by the dose and presence of other carotenoids such as beta-carotene. Lutein bioavailability from vegetables is approximately 70% (28).
Distribution: Carotenoid concentrations in human serum and tissues are highly variable and depend on food sources, efficiency of absorption, and amount of fat in the diet. Lutein is transported by high-density lipoprotein (HDL) and, to a lesser extent, by very low LDL. Carotenoid serum concentrations after a single dose peaks at 24–48 h postdose. The average lutein concentration in human serum is 280 nM (1). Lutein is primarily stored in adipose tissue and the liver. Of all the carotenoids circulating in the body, only two polar species – lutein and zeaxanthin – are contained in the macula (29).
Metabolism/Excretion: It is assumed that lutein is excreted through the bile and kidneys (30).
Wang MX, et al. Lutein supplementation reduces plasma lipid peroxidation and C-reactive protein in healthy nonsmokers. Atherosclerosis. 2013;227:380-385.
In this randomized, double-blind, placebo-controlled trial, the effects of lutein supplementation on CVD biomarkers was evaluated in healthy nonsmokers. A total of 117 subjects were randomly assigned to receive either lutein 10 mg/d, lutein 20 mg/d, or placebo for 12 weeks. Plasma carotenoid concentrations, total antioxidant capacity (TAOC), lipoprotein profiles, and antioxidant enzyme levels were determined at baseline, as well as Weeks 6 and 12 after treatment initiation. Protein and lipid oxidative damage and C-reactive protein (CRP) concentrations were also measured at baseline and post-supplementation. During the 12-week treatment period, significant increases in plasma lutein and TAOC were observed for both treatment groups. In addition, malondialdehyde levels were significantly reduced in the 20-mg lutein group, indicating a decrease in lipid peroxidation. Decreases in CRP concentration were dose-dependent with lutein, with significant between-group differences for lutein 20 mg/d versus placebo. For both active treatment groups, serum CRP was directly related to changes in plasma lutein and TAOC. Investigators concluded these findings preliminarily support a reduction in CVD biomarkers with lutein supplementation.
Ros MM, et al. Plasma carotenoids and vitamin C concentrations and risk of urothelial cell carcinoma in the European Prospective Investigation into Cancer and Nutrition. Am J Clin Nutr. 2012 Oct;96(4):902-10.
This study involved 856 patients with newly diagnosed urothelial cell carcinoma (UCC) who were matched with 856 cohort members by sex, age at baseline, study center, date and time of blood collection, and fasting status. Plasma carotenoids including alpha- and beta-carotenes, beta-cryptoxanthin, lycopene, lutein, and zeaxanthin were measured by using reverse-phase HPLC. Plasma vitamin C was measured by a colorimetric assay. Incidence rate ratios (IRRs) were estimated using conditional logistic regression with adjustment for smoking status, duration, and intensity. Researchers reported that risk of UCC decreased with greater concentrations of plasma carotenoids (IRR for highest quartile compared with the lowest: 0.64; 95% CI: 0.44, 0.93; P-trend = 0.04). Plasma lutein was inversely associated with risk of nonaggressive UCC (IRR: 0.56; 95% CI: 0.32, 0.98; P-trend = 0.05). Plasma beta-carotene was also inversely associated with aggressive UCC (IRR: 0.51; 95% CI: 0.30, 0.88; P-trend = 0.02), but no association was observed between plasma vitamin C and risk of UCC. Investigators concluded there is some evidence of a protective role with greater concentrations of plasma lutein and beta-carotene to reduce the risk of UCC, but that residual confounding by smoking and other factors could not be excluded.
Christen WG, et al. Dietary carotenoids, vitamins C and E, and risk of cataract in women: a prospective study. Arch Ophthalmol . Jan 2008;126(1):102-109.
To determine the effects of dietary carotenoids on cataract formation in women, this prospective observational study was undertaken with 35,551 female participants for 10 years. Cataract formation and visual acuity were the primary outcome measures. Increased dietary lutein/zeaxanthin was associated with an 18% reduced risk of cataract formation. Randomized clinical trials of lutein/zeaxanthin in both men and women are necessary to determine if lutein supplementation may also reduce cataract risk.