Lutein Side Effects, safety, toxicity, adverse effects

Lutein Side Effects, safety, risks, danger and toxicity

Many elderly individuals are now taking lutein supplements daily for many years, and perhaps decades. Do we really know whether it is safe to take a lutein supplement for prolonged periods? Does lutein have any short term or long term side effects? One study evaluated lutein side effects for a period of six months and did not show side effects. However, if people are planning to take lutein supplements for decades, we don't know the potential long term adverse reactions. It may be a good idea, until further lutein studies, to limit lutein supplement intake to two or three times a week as opposed to daily.

Lutein supplement
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Lutein is a potent antioxidant carotenoid found in abundance in fruits and green leafy vegetables. In the macula, lutein is selectively accumulated from plasma and filters out visible blue light. Recent studies suggest this filtering process serves to protect the retina from damage caused by light or oxidation.

Six month lutein study shows no side effects
The effect of lutein and zeaxanthin supplementation on metabolites of these carotenoids in the serum of persons aged 60 or older.
Invest Ophthalmol Vis Sci. 2006. Khachik F, de Moura FF, Ferris FL 3rd, Kim J, Thompson DJ. Department of Chemistry and Biochemistry, Joint Institute for Food Safety and Applied Nutrition (JIFSAN), University of Maryland, College Park, MD, USA.
To investigate the effect of lutein supplementation at doses of 2.5, 5.0, and 10 mg/d for 6 months on distribution of these carotenoids and their metabolites in the serum of elderly human subjects, with and without age-related macular degeneration. To determine whether supplementation with lutein can interact with the serum levels of other dietary carotenoids, retinol, and alpha-tocopherol. Forty-five subjects received daily supplements of lutein (containing 5% zeaxanthin) for 6 months and were followed up for another 6 months after supplementation. Blood was collected at various intervals and lutein, zeaxanthin, and their metabolites in the sera were quantified by normal-phase high-performance liquid chromatography (HPLC)-UV/visible detection. After 6 months of supplementation with 10 mg of lutein, the increases in the mean serum levels from baseline were: 210 to 1000 nM/L for lutein and 56 to 95 nM/L for zeaxanthin. Similarly, the mean concentrations (nM/L) of carotenoid metabolites increased from 49 to 98 for 3-hydroxy-beta,epsilon-caroten-3'-one (3'-oxolutein); 31 to 80 for 3'-hydroxy-epsilon,epsilon-caroten-3-one; and 19 to 25 for epsilon,epsilon-carotene-3,3'-dione. The serum levels of these carotenoids gradually decline within 6 months after supplementation. The increase in the serum levels of lutein / zeaxanthin correlates with increases in the serum levels of their metabolites that have previously been identified in the ocular tissues. Elderly human subjects with and without AMD can safely take supplements of lutein up to 10 mg/d for 6 months with no apparent toxicity or side effects.

Lutein supplement side effects
At this point, it appears that taking a lutein supplement daily for many months does not lead to side effects. However, it is best to limit use to less than 10 mg a few times a week until we have research from longer studies. One possible lutein side effect is the possibility that taking too high a dose may displace the other carotenoids in the retina and cause an imbalance in the retina. You may wish to skip taking your supplement once or twice a week to see if your vision improves on the days when you are not taking it. This way you will know if your daily lutein dose is too high.

Safety study of lutein on rodents
Toxicity profile of lutein and lutein ester isolated from marigold flowers (Tagetes erecta).
Int J Toxicol. 2008: Harikumar KB, Nimita CV, Preethi KC, Deshpande J. Harikumar KB, Nimita CV, Preethi KC, Kuttan R, Shankaranarayana ML, Deshpande J. Amala Cancer Research Centre, Amala Nagar, Thrissur, Kerala, India.
As the dietary lutein concentration is much lower compared to the actual requirement to reduce macular degeneration, supplementation of lutein is under consideration. There are very few data on the toxicity of lutein. In the present study, we evaluated the short-term and long-term toxicity profile of lutein and its esterified form isolated from marigold flowers (Tagetes erecta) in young adult male and female Wistar rats. Lutein and its ester form administered orally at doses of 4, 40, and 400 mg/kg body weight for 4 weeks for short-term toxicity study and 13 weeks for a subchronic toxicity study did not produced any mortality, change in body weight, food consumption pattern, organ weight, and other adverse side reactions. Administration of lutein and ester form did not alter the hepatic and renal function, and did not produce any change in the hematological parameters and in lipid profile. Histopathological analysis of the organs supported the nontoxicity of lutein and its ester form.

Curr Eye Res. 2009;
Genotoxic effects of carotenoid breakdown products in human retinal pigment epithelial cells.
Kalariya NM, Ramana KV, Srivastava SK. AMD Center, Department of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, Texas, USA.
To investigate the genotoxic effects of lutein (LBP) and beta -carotene breakdown products (beta -apo-8-carotenal, BA8C) and the preventive role of GSH in human retinal pigment epithelial cells (ARPE-19). LBP- and BA8C-induced DNA damage in human retinal pigment epithelial cells (ARPE-19) was determined by comet assay. The DNA damage was quantified by the image analysis system using Comet Score software. ARPE-19 cell viability was determined by CellTiter 96 AQ(ueous) one-solution cell proliferation assay kit. Intracellular GSH levels were measured by Ellman's reagent. RESULTS: Incubation of serum-starved ARPE-19 cells with LBP and BA8C caused significant DNA damage in a dose- and time-dependent manner. The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by alpha -tocopherol + ascorbic acid (T + AA). Furthermore, BSO-induced GSH depletion in ARPE-19 cells caused a significant elevation in LBP- and BA8C-induced DNA damage, whereas increased GSH levels in ARPE-19 cells prevented it. Our results suggest that breakdown products of dietary carotenoids could be genotoxic in ARPE-19 cells. lutein induced genotoxic effects could worsen oxidative stress. The intracellular GSH pool in ARPE-19 cells might play a critical role in carotenoid breakdown products-induced genotoxicity.