Background And Relevant Pharmacokinetics

Lutein and its isomer zeaxanthin are yellow-coloured, xanthophyll carotenoids that are not converted into vitamin A. The bioavailability of lutein and zeaxanthin from food sources is influenced by the food matrix and the type and extent of food processing, but most notably by the presence of fat in the diet (Castenmiller et al 1999), with dietary fat intake being inversely related to serum levels (Nolan et al 2004). Cooking may increase their bioavailability by disrupting the cellular matrix and protein complexes, and supplemental sources may be significantly more bioavailable than food sources (Castenmiller et al 1999). One clinical study found that plasma lutein was higher when lutein was consumed with a high-fat spread (207% increase) than with a low-fat spread (88% increase) (Roodenburg et al 2000). This was supported by a small in vitro study showing that dietary lutein is absorbed more efficiently with 24 g of avocado oil or 1 50 g of avocado fruit (Unlu et al 2005). For each 10% increase in dietary lutein and zeaxanthin, serum levels are seen to increase by 1 % (Gruber et al 2004).

When ingested, lutein and zeaxanthin are transported from the intestine to the liver via chylomicrons. They are then transported via LDL and HDL to various parts of the body (Yeum & Russell 2002). Lutein and zeaxanthin are present in the eye, blood serum, skin, cervix, brain, breast and adipose tissue. In the eye lutein is more prominent at the edges of the retina and in the rods (Bernstein 2001, Bone 1997). Lutein appears to undergo some metabolism in the retina to meso-zeaxanthin. Zeaxathin is primarily concentrated in the centre of the retina and the cones, where it is present in concentrations nearly 1000-fold those found in other tissues, thus giving the macula lutea or yellow spot of the retina its characteristic colour (Krinsky et al 2003).

Lower serum concentrations of zeaxanthin have been associated with male gender, smoking, younger age, lower non-HDL cholesterol, greater ethanol consumption and higher BMI (Brady et al 1996). Lutein and zeaxanthin, together with other carotenoids, have also been found to be lower in people with chronic cholestatic liver disease, which can be attributed to malabsorption of fat-soluble vitamins, as well as other mechanisms of hepatic release (Floreani et al 2000). In an epidemiological study involving 7059 participants, lower serum lutein and zeaxanthin levels was significantly Lutein and Zeaxanthin 808

associated with smoking, heavy drinking, being white, female, or not being physically

active, having lower dietary lutein and zeaxanthin, a higher percentage of fat mass, a higher waist-hip ratio, lower serum cholesterol, a higher white blood cell count, and high levels of C-reactive protein (Gruber et al 2004).

In a pharmacokinetic study involving 20 healthy volunteers, serum zeaxanthin levels were found to have an effective half-life for accumulation of 5 days and a terminal elimination half-life of around 12 days (Hartmann et al 2004). This was confirmed by another study that also found that lutein did not affect the concentrations of other carotenoids in healthy volunteers (Thurmann et al 2005). Similarly, high doses (50 mg) of beta-carotene over 5 years were not found to influence serum levels of lutein and zeaxanthin (Mayne et al 1998). It has been suggested that the associations between macula pigment density and serum lutein, serum zeaxanthin and adipose lutein concentrations are stronger in men (Broekmans et al 2002, Johnson et al 2000) and that the processes governing accumulation and/or stabilisation of zeaxanthin in fat tissue are different for males and females (Nolan et al 2004). This is supported by the finding that serum lutein and zeaxanthin concentrations vary with the menstrual cycle, with levels being higher in the late follicular than in the luteal phase (Forman et al 1998).

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