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Article

Olestra Consumption Is Not Associated with Macular Pigment Optical Density in a Cross-Sectional Volunteer Sample in Indianapolis^{1 ,2}

Dale A. Cooper^*3, Joanne Curran-Celentano, Thomas A. Ciulla^,4, Billy R. Hammond, Jr.^**, Ronald B. Danis, Linda M. Pratt, Karen A. Riccardi^* and Thomas G. Filloon^*

^* The Food and Beverage Products Division, The Procter & Gamble Company, Cincinnati, OH 45224; Department of Human and Animal Nutrition, University of New Hampshire, Durham, NH 03824; Department of Ophthalmology, University of Indiana Medical School, Indianapolis, IN 46202; and ^** Department of Psychology, University of Georgia, Athens, GA 30602

³To whom correspondence should be addressed.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
The associations between the intake of the fat-substitute olestra and the concentrations of macular carotenoid pigments and serum lutein and zeaxanthin were investigated in a volunteer cross-sectional sample in Indianapolis. The study was conducted in January through March, 1998 after olestra-containing savory snacks had been sold in central Indiana for a year. Volunteers (n = 280) aged 18–50 y were recruited to make a single clinic visit during which macular pigment optical density (MPOD) was determined by psychophysical flicker photometry, serum was obtained for determination of lutein and zeaxanthin concentration, usual intake of olestra, carotenoids and nutrients were assessed by 1-y food frequency questionnaire, and health habits including smoking, physical characteristics such as eye color, demographics and medical history were determined by questionnaire. Intake of olestra at least one time per month for the past year was reported by 81:280 subjects and their mean, median and 90^th percentile intakes were 1.09, 0.34 and 2.43 g olestra/d, respectively. Mean macular pigment optical density was not significantly different between olestra consumers and nonconsumers (0.213 ± 0.014 vs. 0.211 ± 0.010) nor was serum lutein and zeaxanthin concentration (0.361 ± 0.017 vs. 0.375 ± 0.013 µmol/L) or intake (1242 ± 103 mg/d vs. 1042 ± 58 mg/d) in one-way or two-way ANOVA. Olestra intake was not associated with MPOD or serum lutein and zeaxanthin before or after correction for significant covariates of MPOD. Thus, olestra intake over the past year in a cross-sectional volunteer sample in Indianapolis was not associated with MPOD.

KEY WORDS: • olestra • macular pigment • carotenoid • lutein • zeaxanthin • humans

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
In humans, the macula, or central area of the retina, contains the yellow pigments lutein and zeaxanthin but does not contain measurable concentrations of other dietary carotenoids. The concentration of macular carotenoid pigments can be determined psychophysically in human subjects by heterochromatic flicker photometry. The resulting measure, referred to as macular pigment optical density (MPOD),⁵ is variable between subjects (10–12-fold) but changed very little over periods of 1–16 y within several subjects with stable dietary patterns (Hammond et al. 1995 , 1997b ). MPOD is lower in individuals who smoke (Hammond et al. 1996c ), have light-colored irises (Hammond et al. 1996b ), are female (Hammond et al. 1996a ) and have lower visual sensitivity (Hammond et al. 1998 ).

Although no biological function for the macular carotenoid pigments has been established, they have been hypothesized to prevent light- and oxidative-damage to the macula and thereby reduce the risk of age-related macular degeneration (Snodderly 1995 ). This hypothesis is supported by the Eye Disease Case-Control Study that demonstrated an inverse association between the dietary intake of lutein-rich foods and risk of age-related macular degeneration (AMD) (Seddon et al. 1994 ). The fact that factors associated with increased risk for AMD are also associated with low MPOD, such as smoking, light-colored iris and being female, is consistent with this hypothesis as well. Contrary to the hypothesis, several studies have not found inverse associations between lutein intake or serum concentrations and risk of AMD (Alpers et al. 1995 ; Mares-Perlman et al. 1995 , 1996 ; Sanders et al. 1993 ). Moreover, lower MPOD may be a marker for carotenoid degradation by smoking or lower lutein intake rather than a mechanism for increased risk of AMD.

Dietary carotenoids influence the concentration of macular carotenoid pigments because these substances are derived solely from the diet. Thus, both the intake and serum concentrations of lutein and zeaxanthin are positively associated with MPOD (Hammond et al. 1996a ). Also, when lutein intake is increased beyond usual dietary intakes by spinach or supplement feeding, MPOD increases and then declines after cessation of feeding (Hammond et al. 1997a , Landrum et al. 1997 ). Effects of other nutritional factors on MPOD have not been well studied.

Olestra, a fat substitute approved for use in savory snacks, has the potential to affect MPOD based on clinical studies that demonstrate it can reduce serum concentrations of carotenoids (Schlagheck et al. 1997 ). The serum effects are larger in studies where olestra is consumed frequently with the main sources of dietary carotenoids and more lipophilic carotenoids such as ß-carotene are more affected than less lipophilic ones like lutein. The current study was conducted to determine if olestra consumption as it actually occurs among consumers is related to reduced serum and tissue concentrations of carotenoids, measured as MPOD.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Subject recruitment and clinic visits.

A cross-sectional volunteer sample of 280 adults was obtained in the Indianapolis, IN, area from January through March 1998. This location was chosen because it was the national test market site for Olean®-containing savory snacks and because Olean® snacks were marketed through all outlets (e.g., stores, restaurants, vending). Olean®-containing savory snacks had been available from February 1997 through the study period in these counties. The study protocol was approved by the Indiana University Institutional Review Board.

Advertisements for volunteers were placed in community newspapers and newsletters and on billboards throughout the area. Volunteers were admitted to the study if they were 18–50-y-old, residents of Marion County, IN, or bordering counties for the past year, free of known ocular disease or life threatening disease as determined by medical history, and not a student or employee of Indiana University-Purdue University at Indianapolis (IUPUI). Individuals over 50 y of age were excluded to minimize the possibility of confounding effects of age-related eye changes on MPOD measurement.

Subjects that qualified for the study based on a prescreening telephone interview completed a food frequency consumption questionnaire and a demographics, lifestyle, medical and health history questionnaire prior to making a single clinic visit to IUPUI. During the visit, the questionnaires were reviewed and subjects provided a fasting blood sample, their visual acuity was measured and macular pigment density was determined by psychophysical flicker photometry.

The questionnaires provided data on sex, age, height and weight, education, income, smoking habits, passive smoke exposure, occupation, light exposure, physical activity, eye health history, use of corrective lenses, iris color, ethnic background, skin color by subjective rating, sensitivity to the sun, medical history, current prescription and over-the-counter medication use, nutritional supplement use, menopausal status and current pregnancy or lactation. Visual acuity was measured by Snellen chart, and refractive error was measured on current prescription lenses.

Determination of MPOD.

MPOD was measured psychophysically with a one-degree test stimulus as described (Hammond et al., 1996a , 1997a , 1998 ; Werner and Steele 1988 ). The one-degree test stimulus was presented near the center of a six-degree, 1.5 log Td., 470-nm circular background. The test stimulus was alternately composed of a 460-nm measuring field (peak macular pigment absorbance) and a 570-nm, 1.7 log Td, reference field (minimal macular pigment absorbance). The measuring and reference fields were superposed and presented out of phase at an alternation rate of 11–12 Hz in the foveal condition, and 6–7 Hz in the parafoveal condition. Subjects adjusted the radiance of the 460-nm measuring field in order to achieve minimal flicker with the 570-nm reference. This measurement was done in the fovea (where macular pigment is most dense) and four-degrees in the parafovea (where light absorption by macular pigment is negligible). A 5-min opaque fixation point was located on the left edge of the background, and subjects fixated on this point when making the parafoveal measurement. Subtracting the foveal from the parafoveal sensitivity measurement yields an optical density measure of macular pigment. For an extended discussion of the macular pigment measurement procedure, see the recent methods chapter by Snodderly and Hammond (1999) .

The apparatus used for the macular pigment measurement delivered the stimulus in natural view, but used a stimulus configuration that was similar to configurations used in past studies where the stimulus was presented in Maxwellian view. Preliminary data on 32 subjects (age range, 18–72 y) have shown, however, that macular pigment density measured in natural view, and with slight differences in stimulus configuration (e.g., this study used a four-degree rather than a six-degree parafoveal reference), provides the same values as macular pigment measured in Maxwellian view (Snodderly and Hammond 1999 ). Light for the ten-degree background was produced by three light-emitting diodes (LED), packed tightly in a triangular array, with peak energy at 470-nm and half-widths of about 20-nm. Light for the 570-nm reference field was produced by an LED with peak energy at 570-nm (half-width = 20 nm). Light for the 460-nm measuring field was produced by two LED with peak energy at 458-nm (half-width = 20-nm). Light from the LED sources was collimated with planoconvex lenses and was then passed through polycarbonate diffusers (high-efficiency, holographic type; Physical Optics Corp., Torrance, CA), which served essentially as back projection screens.

The size of the background and test stimulus was defined by circular apertures (constructed by computer-generated images exposed on high-density, photographic mylar film) placed after the collimating lenses. The background and test stimulus were then combined and reflected to the subject by a 5.1-cm beamsplitter whose front surface was located 40.6 cm from the subject’s eye. The entire optical system was contained in a rectangular, black plexiglass box. One side of the box contained a one-inch hole centered on the subject’s optical axis through which the stimulus could be viewed. Head alignment was accomplished by the use of an adjustable head-and-chin-rest assembly and, when properly aligned, the subject viewed the hole in the box as slightly larger and concentric with the background field.

Stimuli were calibrated using a photocell (PIN-10, UDT Sensor, Inc., Hawthorne, CA). The LED were driven by a constant current power supply. Radiance variation was achieved by varying the frequency of a 1.5-ms pulse over a range of 300–300,000 Hz. Our calibration of the high-frequency pulse rate shows that the frequency delivery is nearly perfectly proportional to the radiance output. Thus, macular pigment density values could be derived by simply calculating the log ratio of the frequencies of the 460-nm measuring field at the foveal and parafoveal eccentricities, respectively.

MPOD was measured in the right eye of all subjects. If needed, subjects wore their own corrective lenses or trial lenses so their visual acuity was 20:25 or better during the test. Subjects were given brief instructions on the method and a practice trial before five foveal and five parafoveal measurements were made. In a few cases either the foveal or parafoveal readings were repeated because the foveal readings had a range > 100 U or the parafoveal > 75 U. The foveal and parafoveal values were calculated to be the average of the final five readings.

Dietary intake estimation.

Dietary intake of olestra, lutein and zeaxanthin, as well as other dietary components was determined by means of a food frequency questionnaire (FFQ) that assessed dietary intake during the preceding 1-y. The FFQ used is the same as the one being used in the Women’s Health Initiative program (Patterson et al. 1999 ). It includes questions about the usual intakes over the past year of 122 foods and food groups as well as adjustment and summary questions. The FFQ also contained a snack-food addendum that obtained information about the intake of 16 categories of snack foods, including regular, fat reduced or Olean®-containing potato chips, tortilla and corn chips, cheese puffs, curls, combos and bugles, other snacks and crackers. These questions were followed by one that asked how frequently savory snacks of any type were consumed. The snack-food addendum and FFQ were developed by the Fred Hutchinson Cancer Research Center (FHCRC) for use in the Olestra Post Marketing Surveillance Study (Kristal et al. 1998 ). The FFQ were processed at the FHCRC, and average daily intakes of nutrients and olestra were determined by use of their database for average nutrient content of food categories which was derived from the University of Minnesota Nutrition Coordinating Center’s nutrient database (Minneapolis, MN) and the 1993 USDA-NCI carotenoid database for U.S. foods (Mangels et al. 1993 ).

In the data analyses described below, nutrient data were excluded from 10 individuals who had total energy intakes of <2,090 kJ/d or >20,900 kJ/d, because these values indicate that the data may not be valid. In calculating olestra intake, the intake of olestra from various snacks was added and multiplied by the ratio of the frequency of consumption of any savory snack to the total of the frequency of individual snack-food categories reported. This same procedure is commonly used in cases where a large number of food categories are studied and the number of servings of individual categories of a type of food can exceed number of individual snacks consumed, such as in calculation of total fruit and vegetable intake.

Serum carotenoid analysis.

Blood samples were collected into serum separator tubes and protected from direct light exposure during processing. Clotted blood was separated with refrigerated centrifugation at 2000 x g at 4°C for 15 min. Serum was divided up into cryovials for storage at -80°C. An aliquot of each sample was archived in Indianapolis. The remaining samples were shipped, packed with dry ice, to the University of New Hampshire, where they were stored at -80°C prior to analysis.

The separation and quantification of carotenoids were performed by reversed-phase HPLC methodology. Serum was precipitated with ethanol containing the internal standard and extracted into hexane. The hexane layer was removed and transferred to an amber vial, and the hexane extraction was repeated twice. The combined hexane extract was evaporated under a stream of nitrogen to dryness, and the sample was resuspended in 200 µL of ethanol and 20 µL were injected for analysis. The HPLC system was a gradient reversed-phase system equipped with an HP 1100 (Hewlett-Packard, Burlington, MA) photodiode array detector set at 292, 325, and 452 nm for tocopherol, retinol and carotenoids, respectively. The analytical column was a 4.6 x 250 mm Bakerbond C18 column (Mallinckrodt Baker, Phillipsburg, NJ) following a Vydac (Western Analytical Products, Murieta, CA) high performance 5-micron C18 guard column. The mobile phase consisted of 100% methanol buffered with 1% ammonium acetate with a flow rate of 1.5 mL/min which transitioned to 80:20 methanol/methylene chloride over the first 10 min and remained set for the remainder of the 15-min run before switching back to 100% methanol. A Hewlett-Packard HP 3365 Series II ChemStation was used to control the HPLC method and data handling. Quantification was performed using peak height ratios to internal standards and comparison to concentration curves using reference standards. Accuracy was assessed using the National Institutes of Standards and Technology (NIST) Standard Reference Material SRM 986 and by participation in the NIST Micronutrients Measurement Quality Assurance Program.

Statistical analysis.

Differences in MPOD and serum carotenoids between olestra users and nonusers were compared by means of one-way and two-way ANOVA (SAS, Cary, NC). The association between olestra intake and MPOD was determined with or without adjustment of MPOD for covariates. A multivariable model that did not include olestra intake was developed by screening potential covariates using stepwise maximum r-squared regression ( = 0.25) for continuous variables, and Spearman’s correlation ( = 0.15) for categorical variables. Covariates that were statistically significantly related to MPOD were included in the final general linear model except for serum lutein and zeaxanthin (SAS). The association between olestra intake and MPOD was performed with and without adjustment of MPOD for covariates included in the final general linear model. The Jonckheere-Terpstra test for trend was used to compare crude and adjusted MPOD between olestra nonconsumers and consumers by quartile of olestra intake (Hollander and Wolfe 1973 ). The association between olestra intake and serum lutein and zeaxanthin was also performed with and without adjustment of serum lutein and zeaxanthin for the same covariates.

	RESULTS

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Characteristics of study subjects.

The study subjects were heterogeneous regarding key characteristics including sex, race, age, smoking status, education and body weight (Table 1 ). Consumption of at least one serving of olestra-containing foods per month over the previous year was reported by 30% of volunteers and mean, median and 90^th percentile olestra intakes among these consumers were 1.09, 0.34 and 2.43 g/d (range = 0.03–14.5 g/d). Olestra consumers tended to be female (P = 0.063), Caucasian (P = 0.126) and overweight or obese (P = 0.090 with more years of education (P = 0.034).

Mean MPOD in olestra consumers and nonconsumers did not differ (Table 2 ). Mean MPOD also was not different between olestra consumers and nonconsumers based on two-way ANOVA in subgroups with potentially differing MPOD responses including sex, race, age, smoking status, years of education, overweight status and lutein + zeaxanthin intake (Table 2) . Likewise, mean MPOD adjusted for covariates (next paragraph) was not significantly different between olestra consumers (0.214 ± 0.012) and nonconsumers (0.212 ± 0.009).

View larger version (13K): [in this window] [in a new window]   Figure 1. Lack of a relationship between macular pigment optical density (MPOD) and olestra intake among (A) 81 olestra consumers in a cross-sectional volunteer sample in Indianapolis, without adjustment of MPOD, and (B) olestra consumers after adjustment of MPOD and olestra intake for sunglass use, lutein and zeaxanthin intake, hat use, eye color, fiber intake, fruit consumption, current medical condition, cigarette smoking and physical activity. The line indicates the median MPOD for olestra nonconsumers.

Mean serum lutein and zeaxanthin concentrations of olestra consumers and nonconsumers were 0.361 ± 0.017 µmol/L and 0.375 ± 0.013 µmol (P = 0.535). Mean lutein and zeaxanthin intakes of olestra consumers and nonconsumers did not differ at 1242 ± 103 mg/d and 1042 ± 58 mg/d, respectively. Olestra intake was not correlated with serum lutein and zeaxanthin concentration (P = 0.6737) or intake (P = 0.1290) in Spearman correlation analyses.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
We found that olestra consumption is not associated with reduced macular carotenoid pigment optical density in a volunteer sample of the free-living population in Indianapolis where olestra had been consumed over the course of a year. This was based on the absence of significant associations in one- and two-way ANOVA and on correlations before and after adjustment for covariates of MPOD. There were also no significant associations between olestra consumption and serum lutein and zeaxanthin concentrations.

These results are consistent with those of the Olestra Post-Market Surveillance Study (OPMSS) (Thornquist et al. 1998 ). The OPMSS found no association between olestra intake and serum lutein or zeaxanthin concentrations in a population cross-sectional sample of 947 adults in Indianapolis identified by random digit dial almost 1 y after introduction of olestra products in central Indiana. Also, in a cohort of 402 adults, 80% of whom reported consumption of olestra, serum lutein and zeaxanthin were not lower 1 y after introduction of olestra into the market compared to just prior to introduction into the market, even in the highest 10 percentile of olestra intake.

The absence of an association between olestra intake and MPOD in Indianapolis may be due to relatively infrequent concurrent consumption of olestra and carotenoid-containing foods. Less frequent concurrent consumption would limit interaction in the gut, the means by which olestra can inhibit absorption of carotenoids (Cooper et al. 1997 ). The median and 90^th percentile olestra intakes of olestra consumers in this study were 9.5 and 68.0 g/mo, equivalent to about 0.34 and 2.4 g/d. Weststrate and van het Hof (1995) demonstrated that a similar intake of sucrose polyester, 3 g/d, consumed at the main meal decreased serum ß-carotene by 20%; data were not provided regarding lutein. Even though olestra intakes were similar in the current study, there was no evidence of reduction in serum lutein. The difference may be due to less frequent consumption of olestra with sources of dietary carotenoids in real-world studies compared to clinical studies.

The absence of an association between olestra consumption and serum or macular carotenoids is consistent with premarket estimates of potential reductions in serum carotenoids based on food intake diaries (Cooper et al. 1997 ). Utilizing these diaries, the assumption that all savory snacks would contain Olean® and that reductions in serum carotenoids within meals would be the same as controlled clinical studies, the estimated potential reduction in serum ß-carotene at the 50^th and 90^th percentile consumption of olestra was calculated to be 5.9 and 9.5%. In making these estimates, the average and 90^th percentile number of olestra eating occasions were found to be 10 and 20 times per month and the number of ß-carotene eating occasions 34 and 46 times per month. Furthermore, olestra and carotenoids were estimated to be eaten together only 8 or 12 times per month at the mean and 90^th percentile. Although the same estimate was not performed for lutein and zeaxanthin, lutein is found in many of the same foods as ß-carotene. Also, since it is less lipophilic than ß-carotene, one would expect the effect on lutein absorption when concurrent consumption occurs to be less than that for ß-carotene. In spite of these estimates, some investigators have predicted the effects would be much larger (Kelly et al. 1998 , Weststrate and van het Hof 1995 ).

The number of subjects in this study (280) was higher than any previous study of MPOD in order to include as many olestra consumers as possible (81) and power to detect associations between olestra intake and other dietary variables and MPOD. Based on our power calculations, an observed correlation coefficient of r = 0.10 would be declared statistically significant at the one-sided P = 0.05 significance level. This corresponds to an r-squared value of 0.01, which implies a 1% reduction in variability of the dependent variable, MPOD. Although a significant association was not demonstrated for olestra, dietary intake and serum concentrations of lutein and zeaxanthin intake, as well as other lifestyle and medical factors, were found to be key determinants of MPOD in these subjects (Ciulla et al., unpublished data). In spite of these significant associations, the total variance explained by the main dietary, medical, physical and lifestyle factors was <20%. Thus, it is not surprising that a single food ingredient is not associated with MPOD.

This population was studied about 1 y following the introduction of olestra-containing savory snacks into the central Indiana marketplace to allow changes in tissue concentrations of lutein and zeaxanthin in the macula to occur if they would. The rates of turnover of macular carotenoids in the usual dietary intake range are not well characterized, and published studies have focused on the rate at which MPOD increases above baseline. For instance, one study showed that MPOD increases in most subjects in response to high dietary intake of lutein from food sources (Hammond et al. 1997a ). The increase was seen in 4 wk and MPOD remained elevated for at least 1 mo following cessation of treatment. Another study in two subjects showed an increase in MPOD following intakes exceeding normal dietary intake by roughly 10-fold to 30 mg/d after 1 mo of supplementation (Landrum et al. 1997 ). Taken together, previous studies suggest that 1 y is adequate time for increases, but not necessarily decreases, in MPOD to become manifest in response to dietary manipulation. Thus, the duration of olestra consumption may be a limitation of this study.

The absence of an association between olestra intake and serum lutein and zeaxanthin suggests olestra was not associated with MPOD because serum lutein and zeaxanthin concentrations were not affected by olestra. Since macular carotenoids are presumably transported from serum to the macula, one would expect changes in serum lutein and zeaxanthin to precede changes in MPOD. Possibly, however, the macular carotenoids reflect average serum carotenoid levels over a period of weeks or months, whereas serum carotenoids reflect shorter term fluctuations in dietary intake.

In summary, olestra consumption by a cross-sectional sample of free-living individuals consuming typical mixed diets in Indianapolis was not associated with reduced MPOD or serum lutein and zeaxanthin.

	FOOTNOTES

 
¹ Presented in part at the Association for Research in Vision and Ophthalmology Meeting, Ft. Lauderdale, FL [Cooper, D A., Ciulla, T. A., Hammond, B. R., Riccardi, K. A., Filloon, T. G. & Curran-Celentano, J.; 1999 Macular carotenoid pigment density and olestra consumption in a cross-sectional volunteer sample in Indianapolis. Inv. Ophthalmol. Vis. Sci. 40: S165 (abs.)].

² Supported by the Procter & Gamble Company.

⁴ Dr. Ciulla is a recipient of a career development award from Research to Prevent Blindness, New York, NY.

⁵ Abbreviations used: AMD, age-related macular degeneration; FFQ, food frequency questionnaire; FHCRC, Fred Hutchinson Cancer Research Center; IUPUI, Indiana University-Purdue University at Indianapolis; LED, light emitting diode; MPOD, macular pigment optical density; NIST, National Institute of Standards and Technology; OPMSS, Olestra Post-Market Surveillance Study; USDA-NCI, United States Department of Agriculture-National Cancer Institute.

Manuscript received July 16, 1999. Initial review completed September 23, 1999. Revision accepted November 16, 1999.

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