Oxidative modification of LDL in the vascular wall seems to be a key factor in atherosclerosis development and thus lipid-soluble antioxidants that can protect LDLs may have a role in atherosclerosis prevention (Cherubim et al 2005); however, the relationship between lutein and zeaxanthin status and atherosclerosis is unclear.

Plasma levels of lutein, beta-cryptoxanthin and zeaxanthin were correlated to carotid intima-media thickness in a 3-year case-controlled study of 231 subjects (Iribarren et al 1997), as well as in an 18-month epidemiological study of 573 subjects, suggesting that these carotenoids may be protective against early atherosclerosis (Dwyer et al 2004). Lutein intake has also been found inversely associated with the risk of ischaemic stroke in an observational study involving 43,738 males (Ascherio et al 1999), as well as being inversely associated with the risk of subarachnoid haemorrhage in a cohort study of 26,593 male smokers (Hirvonen et al 2000). Serum levels of lutein and zeaxanthin, however, were not associated with atherosclerosis risk in a case-control study involving 108 cases of aortic atherosclerosis in an elderly population (Klipstein-Grobusch et al 2000).

The foregoing findings contrast with those from two case-controlled studies that found a positive correlation between lutein and zeaxanthin levels and cardiovascular risk. A nested, case-control study of 499 cases of cardiovascular disease with matched controls taken from the Physicians' Health Study found that concentrations of plasma lutein, zeaxanthin and retinol corresponded to a moderate increase in cardiovascular disease (Sesso etal 2005). Similarly, myocardial infarction risk was positively associated with lutein and zeaxanthin levels in adipose tissue and the diet in a case-controlled study of 1456 cases of first acute myocardial infarction and matched controls (Kabagambe et al 2005). The clinical significance of these findings is unclear and requires further investigation.


Dementia has been found to be associated with increased protein oxidative modification and the depletion of a large spectrum of antioxidant micronutrients, including lutein and zeaxanthin (Polidori et al 2004). A clinical study of 25 subjects with mild cognitive impairment, 63 subjects with AD and 56 healthy individuals found that serum lutein levels were lowest in the first two groups, particularly those with AD (Rinaldi etal 2003).

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