INFORMATION FOR SPECIALISTS


Marigold flower -
source of dietary
Lutein/Zeaxanthin

Precautions / Warnings / Contraindications:

- Use cautiously in patients at risk for cardiovascular disease due to results from an epidemiological study suggesting increased cardiovascular disease risk in those with higher plasma Lutein levels.
- Use cautiously in patients at risk for cancer due to results from epidemiological studies suggesting increased cancer risk in those with higher plasma Lutein levels.
- Avoid in patients hypersensitive to Lutein or Zeaxanthin.

Pregnancy & Lactation:
 
- Generally not recommended due to lack of sufficient data.
- Increased plasma Lutein is associated with decreased preeclampsia risk.
- Plasma Lutein decreased in pregnancy until one-month postpartum and remained stable until three months postpartum. Studies have also shown decreases in plasma Lutein during lactation.
- Median Lutein concentrations in human milk were 4.79 (range 0.42-9.98) nM/g fat. Breast milk Lutein increased from one to three months postpartum. Studies suggest changes in breast milk Lutein with increases in dietary carotenoids and duration of lactation.
- Beta-carotene supplementation of pregnant women resulted in increased Lutein/Zeaxanthin concentrations during pregnancy and post-partum.

Drug Interactions:
 
Alcohol: In humans, moderate consumption of various types of alcoholic beverages (red wine, beer, and spirits) has counteracting effects on plasma antioxidant components, resulting in no significant effect on overall antioxidant status). Serious alcohol consumption decreases plasma Lutein/Zeaxanthin.
Antidiabetic agents: In humans, postload plasma glucose concentrations and fasting insulin concentrations decreased significantly as serum Lutein/Zeaxanthin increased.
Antilipemics: In vitro, pretreatment of cells with Lutein inhibited LDL-induced monocyte migration in a dose-dependent manner. In an animal model, chow plus lutein (0.2% by weight) reduced atherosclerotic lesion size by 44% in apoE-null mice and 43% in LDL receptor-null mice.
Antioxidants: Lutein and Zeaxanthin have antioxidant effects.
Antineoplastic agents: In vitro, Lutein protected normal cells, but not transformed cells, from apoptosis induced by the chemotherapy agents etoposide and cisplatin. The mechanism of action was suggested to be based on an increased ratio of Bcl-xL:Bax protein expression in normal cells but not transformed mammary cells.
Cholestyramine resin: Concomitant intake of Lutein/Zeaxanthin and cholestyramine may decrease the absorption of Lutein/Zeaxanthin.
Colestipol: Concomitant intake of Lutein/Zeaxanthin and colestipol may decrease the absorption of Lutein/Zeaxanthin.
Cytochrome P450 metabolized agents: Lutein content in the diet is at least partially responsible for variability in CYP1A2 according to a study in humans. Plasma Lutein explained the largest portion of the variance (7%) and was negatively associated with CYP1A2.
Mineral oil: Concomitant intake of mineral oil and Lutein/Zeaxanthin may reduce the absorption of Lutein/Zeaxanthin.
Nicotine (tobacco): In humans, smokers have lower levels overall of plasma Lutein than non-smokers.
Orlistat: Orlistat may decrease the absorption of Lutein/Zeaxanthin.
Retinoids: In humans, retinol supplementation caused a significant increase in the plasma concentrations of Lutein.

Herbs and Suplements interactions:

Alpha-tocopherol: In humans, consumption of a Lutein-containing supplement resulted in lower serum alpha-tocopherol concentration.
Antilipemics: In vitro, pretreatment of cells with Lutein inhibited LDL-induced monocyte migration in a dose-dependent manner. In an animal model, chow plus Lutein (0.2% by weight) reduced atherosclerotic lesion size by 44% in apoE-null mice and 43% in LDL receptor-null mice.
Antineoplastics: In vitro, Lutein induced apoptosis in transformed but not normal human mammary cells. Lutein also protected normal cells, but not transformed cells, from apoptosis induced by the chemotherapy agents etoposide and cisplatin. The mechanism of action was suggested to be based on an increased ratio of Bcl-xL:Bax protein expression in normal cells but not transformed mammary cells.
Beta-carotene: Results from various human studies suggest that beta-carotene may reduce or increase bioavailability of Lutein. In humans, Lutein reduced beta-carotene absorption when the two were given simultaneously.
Carotenoids (general): In humans, adding a second carotenoid (supplement form) to a meal providing a first carotenoid (food form) reduced absorption of the first carotenoid.
Cytochrome P450 metabolized herbs and supplements: Lutein content in the diet is at least partially responsible for variability in CYP1A2 according to a study in humans.
Essential fatty acids: The antioxidant activity of Lutein/Zeaxanthin has the potential to inhibit fatty acid oxidation and increase levels of polyunsaturated fatty acids from supplements.
Dietary fiber: Dietary fiber decreases the antioxidative effect supplementary carotenoids due to reduced bioavailability in the gut.
Hypoglycemics: In humans, postload plasma glucose concentrations and fasting insulin concentrations decreased significantly as serum Lutein/Zeaxanthin increased.
Retinol: In humans, retinol supplementation caused a significant increase in the plasma concentrations of Lutein.
Zeaxanthin: In humans, Zeaxanthin is capable of being converted to Lutein. Thus, Zeaxanthin supplementation is expected to increase plasma Lutein levels.

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