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Introduction The dietary carotenoids lutein (L) and zeaxanthin (Z) are transported in the bloodstream by lipoproteins, sequestered by adipose tissue, and eventually captured in the retina where they constitute macular pigment. There are no L&Z dietary intake recommendations nor desired blood/tissue concentrations for the Spanish general population. Our aim was to assess the correlation of L&Z habitual dietary intake (excluding food supplements), resulting serum concentrations and lipid profile with macular pigment optical density (MPOD) as well as the contrast sensitivity (CT), as visual outcome in normolipemic subjects (n = 101) aged 45-65. Methods MPOD was measured by heterochromatic flicker photometry, serum L&Z by HPLC, the dietary intake by a 3-day food records and CT using the CGT-1000-Contrast-Glaretester at six stimulus sizes, with and without glare. Results Lutein and zeaxanthin concentrations (median) in serum: 0.361 and 0.078 [mu]mol/L, in dietary intake: 1.1 mg L+Z/day. MPOD: 0.34du. L+Z intake correlates with their serum concentrations (rho = 0.333, p = 0.001), which in turn correlates with MPOD (rho = 0.229, p = 0.000) and with fruit and vegetable consumption (rho = 0.202, p = 0.001), but not with lutein+zeaxanthin dietary intake. MPOD correlated with CT, with and without glare (rho ranges: -0.135, 0.160 and -0.121, -0.205, respectively). MPOD predictors: serum L+Z, L+Z/HDL-cholesterol ([beta]-coeficient: -0.91±0.2, .sub.95% CI: -1.3,-0.5) and HDL-cholesterol (R.sup.2 = 15.9%). CT predictors: MPOD, mainly at medium and smaller visual angles (corresponding to spatial frequencies for which sensitivity declines with age) and gender ([beta]-coefficients ranges: -0.95,-0.39 and -0.13,-0.39, respectively). Conclusion A higher MPOD is associated with a lower ratio of L+Z/HDL-cholesterol and with a lower CT (higher contrast sensitivity). The HDL-cholesterol would also act indirectly on the CT improving the visual function.

Carotenoids are bioactive compounds with widely accepted health benefits. Their quantification in human faeces can be a useful non-invasive approach to assess their bioavailability. Identification and quantification of major dietary carotenoids in human faeces was the aim of the present study. Faeces and dietary intake were obtained from 101 healthy adults (45–65 years). Carotenoid concentrations were determined by HPLC in faeces and by 3-day food records in dietary intake. Carotenoids quantified in faeces (μg/g dry weight, median) were: β-carotene (39.5), lycopene (20), lutein (17.5), phytoene (11.4), zeaxanthin (6.3), β-cryptoxanthin (4.5), phytofluene (2.9). α-carotene (5.3) and violaxanthin were found 75.5% and 7.1% of the faeces. The carotenoids found in the highest concentrations corresponded to the ones consumed in the greatest amounts (μg/d): lycopene (13,146), phytoene (2697), β-carotene (1812), lutein+zeaxanthin (1148). Carotenoid concentration in faeces and in dietary intake showed correlation for the total non-provitamin A carotenoids (r = 0.302; p = 0.003), phytoene (r = 0.339; p = 0.001), phytofluene (r = 0.279; p = 0.005), lycopene (0.223; p = 0.027), lutein+zeaxanthin (r = 0.291; p = 0.04) and β-cryptoxanthin (r = 0.323; p = 0.001). A high proportion of dietary carotenoids, especially those with provitamin A activity and some of their isomers, reach the large intestine, suggesting a low bioavailability of their intact forms.

β-carotene, α-carotene and β-cryptoxanthin are greater contributors to vitamin A intake than retinol in the human diet for most people around the world. Their contribution depends on several factors, including bioavailability and capacity of conversion into retinol. There is an increasing body of research showing that the use of retinol activity equivalents or retinol equivalents could lead to the underestimation of the contribution of β-cryptoxanthin and of α-carotene. The aim is to assess their apparent bioavailability by comparing concentrations in blood to their dietary intakes and identifying the major food contributors to their dietary intake. Dietary intake (3-day 24-h records) and serum concentrations (by HPLC) were calculated in normolipemic subjects with adequate retinol status (≥1.1 µmol/L) from our studies (n = 633) and apparent bioavailability calculated from 22 other studies (n = 29,700). Apparent bioavailability was calculated as the ratio of concentration in the blood to carotenoid intake. Apparent bioavailabilities for α-carotene and β-cryptoxanthin were compared to those for β-carotene. Eating comparable amounts of α-carotene, β-cryptoxanthin and β-carotene foods resulted in 55% greater α-carotene (95% CI 35, 90) and 686% higher β-cryptoxanthin (95% CI 556, 1016) concentrations than β-carotene in blood. This suggests differences in the apparent bioavailability of α-carotene and β-cryptoxanthin and even larger differences with β-cryptoxanthin, greater than that of β-carotene. Four fruits (tomato, orange, tangerine, red pepper) and two vegetables (carrot, spinach) are the main contributors to their dietary intake (>50%) in Europeans.

Lutein is mainly supplied by dietary fruit and vegetables, and they are commonly jointly assessed in observational and interventional studies. Lutein bioavailability and health benefits depend on the food matrix. This study aimed to assess the effect of dietary intervention with lutein-rich fruit or vegetables on lutein status markers, including serum and faecal concentrations (by high pressure liquid chromatography), dietary intake (24 h recalls ×3), and macular pigment optical density (MPOD) and contrast threshold (CT) as visual outcomes. Twenty-nine healthy normolipemic subjects, aged 45–65 y, consumed 1.8 mg lutein/day supplied from fruits (14 subjects, 500 g/day of oranges, kiwi and avocados) or vegetables (15 subjects, 180 g/day of green beans, pumpkin, and sweet corn) for four weeks. Serum lutein concentration increased by 37%. The effect of the food group intervention was statistically significant for serum lutein+zeaxanthin concentration (p = 0.049). Serum α- and β-carotene were influenced by food type (p = 0.008 and p = 0.005, respectively), but not by time. Serum lutein/HDL-cholesterol level increased by 29% (total sample, p = 0.008). Lutein+zeaxanthin/HDL-cholesterol increased, and the intervention time and food group eaten had an effect (p = 0.024 and p = 0.010, respectively) which was higher in the vegetable group. The MPOD did not show variations, nor did it correlate with CT. According to correlation matrixes, serum lutein was mainly related to lutein+zeaxanthin expressed in relation to lipids, and MPOD with the vegetable group. In faecal samples, only lutein levels increased (p = 0.012). This study shows that a relatively low amount of lutein, supplied by fruit or vegetables, can have different responses in correlated status markers, and that a longer intervention period is needed to increase the MPOD. Therefore, further study with larger sample sizes is needed on the different responses in the lutein status markers and on food types and consumption patterns in the diet, and when lutein in a “pharmacological dose” is not taken to reduce a specific risk.

BACKGROUND & AIMS: Lutein and zeaxanthin accumulate in retina (macular pigment). Their nutritional status can be assessed using dietary or biochemical markers and both have been associated with macular pigment optical density. We proposed to assess dietary and status markers of lutein and zeaxanthin in a group of healthy Spanish volunteers, considering the potential influence of age, gender and serum lipids to investigate the predictors of the macular pigment optical density. METHODS: Serum lutein and zeaxanthin concentrations, dietary intake and macular pigment optical density were determined in 108 healthy men and women (20–35 and 45–65 years), using high-performance liquid chromatography, 3-day food records and heterochromic flicker photometry, respectively. Mann–Whitney U-test, Spearman correlation coefficient and multivariate regression analysis were used for the statistical study. RESULTS: Serum concentrations and dietary intake of lutein plus zeaxanthin (p < 0.0001 and p = 0.001, respectively) were higher in older vs younger subjects, whereas macular pigment optical density was lower (p = 0.038). The highest correlation coefficients between intake and serum were for fruit and serum lutein (ρ = 0.452, p < 0.0001) and for fruit and lutein + zeaxanthin (ρ = 0.431, p < 0.0001) in the younger group. Macular pigment optical density correlated with serum xanthophylls (ρ = 0.223, p = 0.02) and fruit and vegetable intake (ρ = 0.350, p = 0.0002), showing highest correlations when lutein and zeaxanthin were expressed in relation to serum lipids in older subjects (ρ = 0.262, p = 0.006). Multivariate regression analysis identified age and serum lutein as major predictors of macular pigment optical density (total sample), and a coefficient of determination of 29.7% for the model including lutein + zeaxathin/cholesterol + triglycerides, sex and fruit + vegetables in the older group. CONCLUSIONS: The establishment of normal/reference ranges for serum lutein and zeaxanthin should consider age ranges and be expressed in relation to lipid concentrations, at least in subjects over 45 years, as this could influence macular pigment optical density. The macular pigment optical density showed age-specific correlations with lutein plus zeaxanthin expressed in relation to serum lipid concentrations as well as with the fruit and vegetable intake.

The dietary carotenoids lutein (L) and zeaxanthin (Z) are transported in the bloodstream by lipoproteins, sequestered by adipose tissue, and eventually captured in the retina where they constitute macular pigment. There are no L&Z dietary intake recommendations nor desired blood/tissue concentrations for the Spanish general population. Our aim was to assess the correlation of L&Z habitual dietary intake (excluding food supplements), resulting serum concentrations and lipid profile with macular pigment optical density (MPOD) as well as the contrast sensitivity (CT), as visual outcome in normolipemic subjects (n = 101) aged 45-65. MPOD was measured by heterochromatic flicker photometry, serum L&Z by HPLC, the dietary intake by a 3-day food records and CT using the CGT-1000-Contrast-Glaretester at six stimulus sizes, with and without glare. Lutein and zeaxanthin concentrations (median) in serum: 0.361 and 0.078 [mu]mol/L, in dietary intake: 1.1 mg L+Z/day. MPOD: 0.34du. L+Z intake correlates with their serum concentrations (rho = 0.333, p = 0.001), which in turn correlates with MPOD (rho = 0.229, p = 0.000) and with fruit and vegetable consumption (rho = 0.202, p = 0.001), but not with lutein+zeaxanthin dietary intake. MPOD correlated with CT, with and without glare (rho ranges: -0.135, 0.160 and -0.121, -0.205, respectively). MPOD predictors: serum L+Z, L+Z/HDL-cholesterol ([beta]-coeficient: -0.91±0.2, .sub.95% CI: -1.3,-0.5) and HDL-cholesterol (R.sup.2 = 15.9%). CT predictors: MPOD, mainly at medium and smaller visual angles (corresponding to spatial frequencies for which sensitivity declines with age) and gender ([beta]-coefficients ranges: -0.95,-0.39 and -0.13,-0.39, respectively). A higher MPOD is associated with a lower ratio of L+Z/HDL-cholesterol and with a lower CT (higher contrast sensitivity). The HDL-cholesterol would also act indirectly on the CT improving the visual function.