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© 2006 American Society for Nutrition J. Nutr. 136:2849-2855, November 2006

Nutrition and Disease

Supplementation with Fruit and Vegetable Soups and Beverages Increases Plasma Carotenoid Concentrations but Does Not Alter Markers of Oxidative Stress or Cardiovascular Risk Factors1

Elaine Paterson, Michael H. Gordon*, Chutamat Niwat, Trevor W. George, Laura Parr, Saran Waroonphan and Julie A. Lovegrove

Hugh Sinclair Unit of Human Nutrition, The University of Reading, Whiteknights, Reading, Berks, RG6 6AP, UK

* To whom correspondence should be addressed. E-mail: m.h.gordon{at}reading.ac.uk.


   ABSTRACT
TOP
 ABSTRACT
Introduction
 Subjects and Methods
 Results
 Discussion
 LITERATURE CITED
 
This study was aimed at determining whether an increase of 5 portions of fruits and vegetables in the form of soups and beverages has a beneficial effect on markers of oxidative stress and cardiovascular disease risk factors. The study was a single blind, randomized, controlled, crossover dietary intervention study. After a 2-wk run-in period with fish oil supplementation, which continued throughout the dietary intervention to increase oxidative stress, the volunteers consumed carotenoid-rich or control vegetable soups and beverages for 4 wk. After a 10-wk wash-out period, the volunteers repeated the above protocol, consuming the other intervention foods. Both test and control interventions significantly increased the % energy from carbohydrates and decreased dietary protein and vitamin B-12 intakes. Compared with the control treatment, consumption of the carotenoid-rich soups and beverages increased dietary carotenoids, vitamin C, {alpha}-tocopherol, potassium, and folate, and the plasma concentrations of {alpha}-carotene (362%), ß-carotene (250%) and lycopene (31%) (P < 0.01) and decreased the plasma homocysteine concentration by 8.8% (P < 0.01). The reduction in plasma homocysteine correlated weakly with the increase in dietary folate during the test intervention (r = –0.35, P = 0.04). The plasma antioxidant status and markers of oxidative stress were not affected by treatment. Consumption of fruit and vegetable soups and beverages makes a useful contribution to meeting dietary recommendations for fruit and vegetable consumption.


   Introduction
TOP
 ABSTRACT
 Introduction
Subjects and Methods
 Results
 Discussion
 LITERATURE CITED
 
There is considerable epidemiological evidence that a diet rich in fruit and vegetables may be protective against cardiovascular disease and cancer (1–5). Fruit and vegetables are a rich source of a wide range of potentially beneficial components including dietary fiber, folate, vitamins, minerals, and bioactive phytochemicals including carotenoids and phenolic compounds. Fruit and vegetable consumption increases the oxidative stability of LDL ex vivo (6,7) and reduces plasma concentrations of homocysteine (8). Effects on endothelial function, cell signaling, and gene expression have been less widely studied, although it is known that phytochemicals that occur in fruit or vegetables can affect these variables (9–11).

The observed protective effect of fruits and vegetables has prompted national bodies to recommend consumption of 5 portions of fruit and vegetables per day (12). The recommendation is that juice should not be considered as more than one portion because of decreased fiber and vitamin levels and the conversion of intrinsic sugars to extrinsic sugars that can result from processing. However, potentially beneficial effects of juice consumption have been demonstrated in several studies (13–15). In the case of carotenoids, it was demonstrated that these phytochemicals are more bioavailable from juices than from vegetables (16). Beneficial effects of soups and juices may arise either directly because of the provision of nutrients or indirectly because of the displacement of other foods, such as fatty foods, from the diet. The aim of this study was to investigate the effects of a daily increase of the equivalent of 5 portions (400 g) of fruit and vegetables in the form of soups and beverages upon markers of cardiovascular disease in free-living healthy subjects. The volunteers were asked to consume 4 g/d of fish oil in addition to the control or test intervention to afford a higher degree of oxidative stress. Fish oil increases the level of oxidative stress assessed by the oxidative stability of LDL ex vivo, increased apoptosis (17), or by the level of the DNA degradation product 8-hydroxy-2'-deoxyguanosine in the urine (18,19). However, other reports describe effects of fish oil in reducing oxidative stress by induction of antioxidant enzymes or by other mechanisms (20).


   Subjects and Methods
TOP
 ABSTRACT
 Introduction
 Subjects and Methods
Results
 Discussion
 LITERATURE CITED
 
    Subjects. Subjects were recruited from the university and general public around the Reading area by the use of posters, advertisements in local newspapers, and leaflets. All potential study subjects had basic anthropometric measurements and fasting blood taken that was sent to the local hospital (Royal Berkshire Hospital, Reading, Berkshire, U.K.) for an analysis of full blood count, liver function status, lipid levels, and fasting glucose. Subjects were excluded from participation in the study if they were <20 or >70 y of age, suffered from liver disease, had gall bladder problems or abnormalities of lipid metabolism, diabetes mellitus, or a myocardial infarction. Subjects following a weight-reducing dietary regimen or taking any dietary supplements, including fatty acids, or vitamin and mineral supplements were also excluded. In addition, subjects were excluded if they were regular exercisers (>3 times/wk, >20 min each session) or consumed >150 mL of alcohol/wk. Blood pressure was required to be <150/90 mm Hg, hemoglobin >125 g/L for men and >115 g/L for women, gamma glutamyl transferase <80 IU/L, and plasma cholesterol <6.5 mmol/L. Suitable subjects were assigned to 1 of 2 groups by stratified randomization to produce an equal distribution of age, gender, and BMI to both groups. The study was approved by the University of Reading Ethics and Research Committee, and each volunteer gave written informed consent before participating.

    Study design. The study design was a single blind, randomized, controlled, crossover dietary intervention study. Volunteers consumed a daily supplement of fish oil (Boots the Chemist) containing 4 g/d fish oil that contained 2 g eicosapentaenoic acid (EPA)2/docosahexaenoic acid (DHA) throughout the study. Thirty-six volunteers (12 male, 24 female; 33 nonsmokers; 3 smokers; 29 Caucasian, 6 Asian, and 1 African) with low fruit and vegetable intake (<3 portions/d), between 20–67 y of age, were recruited and randomly assigned to 1 of 2 groups. After a 2-wk run-in period with fish oil supplementation, the volunteers consumed either carotenoid-rich or carotenoid-poor foods (see below for details) for a 4-wk period. Ten weeks later the volunteers repeated the above protocol, consuming the other intervention foods. Fasting plasma and early morning urine samples were collected at baseline prior to fish oil supplementation and at the start and end of the test or control intervention periods in each arm of the study. Anthropometric measurements were also made during the study.

    Study foods. Several choices of test and control intervention foods were offered to each subject. During the test intervention period the subjects were asked to consume 1 soup (500 mL) plus 1 juice (300 mL) or shot (fruit and vegetable preparation made from concentrated juices and purees) (100 mL) per day. This was equivalent to consuming 400 g/d of mixed fruit and vegetables. Soup choices were autumn vegetable; carrot and coriander; or tomato and red pepper, and beverage selections were purple carrot, apple and strawberry juice (300 mL); orange, banana and carrot shot (100 mL); apple, carrot and strawberry shot (100 mL); or carrot, banana and cherry shot (100 mL). For the control intervention, 1 packet soup (which made up to 500 mL) plus 1 portion of cordial (50 mL) diluted with water was consumed each day. Control soup selections were cream of mushroom, cream of herb, or cream of leek, and control juice selection was either Robinson's orange or lemon barley water (Robinson's Soft Drinks). All soups and fruit and vegetable beverages were supplied by Unilever.

Each subject was asked to consume a mixture of the different soups and beverages and complete a daily tick chart. This chart was used to calculate the exact products consumed and to measure compliance. In addition, any returned intervention foods and fish oil capsules were counted to assess compliance by each subject. To determine the dietary intake before and during the study intervention, each subject was asked to complete a 3-d estimated diet diary during wk 1, 5, 17, and 21.

    Sample collection. Fasting blood samples were collected from all subjects by venepuncture from the antecubital vein. The blood samples were immediately wrapped in foil and kept on ice for transport to the laboratory. Following centrifugation at 1560 x g for 10 min at +4°C, aliquots of plasma were prepared in cryogenic vials for storage at –80°C. Early morning urine samples were collected, mixed, measured, prepared into aliquots, and frozen at –20°C before analysis. Analyses did not commence until the full intervention study was complete, and all samples from each subject were analyzed within one batch to reduce interbatch variation.

    Plasma ascorbic acid and uric acid. Plasma samples were mixed with an equal volume of metaphosphoric acid (10%) and stored at –80°C prior to analysis for ascorbic acid by HPLC with UV detection (21) and a simultaneous determination for uric acid (22).

    Plasma carotenoids and tocopherols. Plasma carotenoids and tocopherols were measured by the method of Thurnam et al. (23) using a Hewlett Packard 1050 HPLC system with a Nucleosil 100–5C18, 25 cm x 4.6 cm column (Hichrom) with a flow rate of 1.5 mL/min.

    FRAP, TEAC, and ORAC. The ferric-reducing anitioxidant potential (FRAP) was analyzed with the method of Benzie and Strain (24) using a Cecil Instruments 1000 series spectrophotometer. Plasma trolox-equivalent antioxidant capacity (TEAC) was measured using the method of Re et al. (25). Plasma oxygen radical absorbance capacity (ORAC) was measured using the principle described by Huang et al. (26) adapted for semiautomated measurement on a Perkin-Elmer Luminescence Spectrometer LS-50B with 96-well reading capability.

    LDL oxidation (ex vivo). LDL was isolated from plasma using ultra centrifugation (2 stage separation at 416,000 x g for 50 min) (27). The susceptibility of LDL to copper induced oxidation was measured as the lag phase before oxidation by monitoring the increase in conjugated dienes at 234 nm (28).

    Plasma lipids, CRP, glucose hexokinase, and insulin. Analysis of plasma lipids, CRP, and glucose hexokinase were performed using an Instrument Laboratory ILAB 600 autoanalyzer. Standard kits and appropriate sero-normal, low, and high, quality control standards were purchased from Instrument Laboratories Ltd (Warrington, UK) and included in all batches. LDL cholesterol was calculated from Friedwald's equation. Insulin was assessed by ELISA (Dako Cytomation, Ely, Cambs, UK) with in-house pooled plasma controls in each batch.

    Plasma VCAM, ICAM, GSH, PON, and GPx. Both vascular cell adhesion moloecule-1 (VCAM) and endothelial intercellular adhesion molecule-1 (ICAM) were analyzed using quantitative sandwich enzyme immunoassay (EIA) (R & D Systems). In-house pooled plasma samples were included in each batch. Plasma homocysteine, cysteine, and GSH were analyzed by HPLC using the method of Pfeiffer et al. (29) at the University of Aberdeen. Paraoxonase (PON) activity was determined by measuring the increase in absorbance at 412 nm using paraoxon as substrate (30). Plasma glutathione peroxidase (GPx) was determined by an ELISA (Oxis Research) using a biotinylated-polyclonal antibody with amplification by a biotin-streptavidin coupling. In-house pooled plasma controls were used in each batch.

    Urinary isoprostanes and 8-OHdG. Urinary isoprostanes and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured using commercially available competitive ELISA kits (Oxford Biomedical Research). In-house pooled urine samples were used in each batch to standardize interbatch variation, and both 8-OHdG and isoprostane values were corrected for urinary creatinine levels. These were analyzed using a colorimetric microplate assay (Oxford Biomedical Research) with pooled urine controls being included throughout the procedure.

    Dietary analysis. Estimation of portion sizes was completed by use of the photographic atlas (31) and portion size book (32). Diet records were then analyzed using nutrition analysis software package (Diet Cruncher, Way Down South Software) combined with an electronic version of McCance and Widdows on the 6th edition food composition database (Food Standards Agency, London).

    Statistical analyses. Initial investigations on data were applied to assess normality of distribution. Those data that were not normally distributed were log transformed and reassessed. Categorical data were assessed by the chi-square test to determine whether there was equal distribution of subjects between groups. Data were tested by repeated-measures ANOVA with post hoc Bonferroni correction to reduce the likelihood of chance findings from multiple comparisons. A value of P ≤ 0.05 was used to define significance and a 95% CI. The baseline in the 2 arms of the study did not differ (P > 0.05) and hence no carryover effects were present. Values in the text are means ± SD.


   Results
TOP
 ABSTRACT
 Introduction
 Subjects and Methods
 Results
Discussion
 LITERATURE CITED
 
    Anthropometric data. Subjects were allocated to the control and test intervention groups so they were not different with respect to weight, BMI, systolic or diastolic blood pressure (Table 1), number of smokers, or ethnic groups. Ages of the groups were 35.3 ± 13.9 y and 38.2 ± 15.1 y. There were no significant changes in anthropometric variables following the control or test intervention.


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  		TABLE 1 Anthropometric and blood pressures of subjects before and after control and fruit and vegetable interventions1

 
    Compliance and dietary intakes. Compliance with the study protocol as assessed by the return of unused products at the end of each intervention period was 92%. Nutrient intake of the study subjects as assessed by 3-d diet diaries (Table 2) was representative of the general population (31). The number of portions of fruit and vegetables habitually ingested was 2.8 ± 1.9 and 2.2 ± 1.3 before the control and test interventions, respectively. The intake of fruit and vegetables increased during the test food period to 6.3 ± 2.6 portions (P < 0.01) with no increase during the control food period, which remained at 2.8 ± 1.1 portions.


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  		TABLE 2 Daily intakes of macronutrients and key vitamins by subjects during the control and test interventions from 3-d diet diaries1

 
The diet diaries provided evidence of an increase in carbohydrates and a decrease in protein and vitamin B-12 intakes during both the control and test intervention periods (Table 2). However, the test intervention increased the intake of dietary carotenoids, potassium, vitamin C, {alpha}-tocopherol and folate (Table 2). The daily intake of carotenoids from the test intervention products was 17.5 mg (Table 3).


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  		TABLE 3 Carotenoid concentrations of test soups and beverages1

 
    Plasma concentrations of micronutrients and markers of antioxidant status. The dietary intervention increased plasma concentrations of {alpha}-carotene, ß-carotene, lycopene, and total carotenoids (Table 4). The increases in plasma concentrations of {alpha}-carotene, ß-carotene, lycopene, and lutein during the test intervention period were 1.05, 0.8, 0.27, and 0.14 µmol/L, respectively. Plasma vitamin C, {alpha}-tocopherol, or uric acid, and GSH concentrations did not change, nor did activities of plasma PONS or GPx.


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  		TABLE 4 Plasma concentrations of micronutrients and biochemical markers of antioxidant status of subjects before and after the test interventions1

 
    Intervention biochemical data. The levels of urinary 8-isoprostanes and 8-hydroxy-2'-deoxyguanosine (8-OHdG), the ORAC, TEAC and FRAP values of plasma, and the oxidative stability ex vivo were determined as biomarkers of oxidative stress and antioxidant capacity during the study (Table 5). Although the levels of 8-OHdG increased from baseline during the 2-wk run-in period during which the subjects consumed 4 g fish oil/d (P < 0.01) (from 5.94 ± 3.2 to 8.59 ± 7.42 µmol/mol creatinine in the control period and from 6.04 ± 2.8 to 8.41 ± 5.3 µmol/mol creatinine in the test period), there was no effect of the test intervention.


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  		TABLE 5 Urinary and plasma biomarkers in subjects before and after the intervention1

 
FRAP values were reduced following both control and test interventions as shown by a within-subject effect of time, but these findings were not a result of the consumption of the soups and beverages rich in carotenoids because there was no effect of treatment. The oxidative stability of LDL ex vivo was reduced by the fish oil (from 59.4 ± 9.7 min to 49.2 ± 10.5 min using data from all volunteers, P < 0.01), but it was not affected by the intervention (Table 5). No other changes occurred in these variables, and the inflammatory biomarkers, plasma ICAM, VCAM, and CRP also were not affected by treatment (data not shown).

Consumption of soups and beverages rich in carotenoids reduced the plasma total cholesterol concentration (P = 0.03). This reduction was due to the unexpected reduction in HDL cholesterol as shown by within-subject effects of treatment (P = 0.05) and time (P = 0.01) (Table 5).

The test intervention significantly reduced plasma homocysteine concentration (Table 5). This reduction correlated weakly with the increase in dietary folate during the test intervention (r = –0.35, P = 0.04).


   Discussion
TOP
 ABSTRACT
 Introduction
 Subjects and Methods
 Results
 Discussion
LITERATURE CITED
 
The major aim of this study was to determine whether soups and juices provided an effective vehicle for the provision of 400 g/d (equivalent to 5 portions) of fruit and vegetables and the dietary components such as micronutrients and phytochemicals contained within them. In addition, the study investigated whether the dietary intervention had a beneficial effect on markers of oxidative stress and CVD risk factors. Subjects who habitually consumed <3 portions of fruit and vegetables per day were recruited, and the oxidative challenge of the background diet was increased by including a fish oil supplement in both the control and test interventions. Fish oil is rich in the polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and several studies have shown that fish oil consumption increases oxidative stress when assessed by the oxidative stability of LDL (17,33–35), or the effect on excretion of 8-OHdG (19). All groups were given fish oil supplements and it was observed that consumption of fish oil resulted in a significant increase in susceptibility of LDL to oxidative damage with a reduction in lag phase from 59.4 ± 9.7 min to 49.2 ± 10.5 min, in addition to a significant increase in 8-OHdG excretion from 6.0 ± 2.5 µmol/mol creatinine at baseline to 8.27 ± 4.9 µmol/mol creatinine. These observations support previous findings about the effects of fish oil (17,19,33–35).

Analysis of the diet diaries indicated that there was a significant increase in the number of portions of fruit and vegetables consumed after the test soups and juices. The test soups and juices increased dietary intake of fruits and vegetables by the equivalent of 400 g/d (5 portions of fruit and vegetables). A decrease in protein and vitamin B-12 intake during both the control and test intervention periods occurred in part because of the replacement of a meat-containing meal by the soup. Although it is not desirable to have a reduction in dietary vitamin B-12 or protein, the dietary intakes of these nutrients after both interventions were still higher than the U.K. reference nutrient intake (RNI), and were therefore not a cause for concern in this study.

The major carotenoids in plasma at baseline were lycopene, lutein + zeaxanthin (not separated), ß-carotene, {alpha}-carotene, and ß-cryptoxanthin. The plasma total carotenoid concentration at baseline was similar to that reported previously (36). The test intervention provided a significantly higher dietary intake of the carotenoids lutein, lycopene, {alpha}- and ß-carotene, vitamin C, {alpha}-tocopherol, and folate, which caused significant increases in plasma concentrations of {alpha}-carotene, ß-carotene and lycopene. The increases in {alpha}-carotene, ß-carotene, lycopene, and lutein + zeaxanthin were 362%, 250%, 31% and 24% above the baseline value. The ratios of increases in plasma carotenoids (µmol/L): dietary carotenoids from the soups and juices (expressed as mg/d) during the test intervention period were 0.15, 0.06, and 0.54 for carotenes, lycopene, and lutein + zeaxanthin, respectively. The high ratio for lutein is consistent with a study that showed lutein to be 5 times more bioavailable than ß-carotene (37). The increase in total carotenoids from the diet diaries was 26.4 mg/d, of which the test intervention contributed 17.5 mg/d. This increased the plasma carotenoid concentration from 2.17 µmol/d at baseline to 4.44 µmol/d. The software used to analyze the diet diaries reported levels of ß-carotene and total carotenoids but not other individual carotenoids.

The lack of an increase in plasma concentrations of vitamin C after the test intervention was surprising, particularly as there was a significant increase in the dietary vitamin C intake. However, the baseline concentrations of plasma vitamin C were relatively high and it is known that plasma vitamin C concentration reaches an upper limit in the range of 70–95 µmol/L (38). A small but significant reduction in HDL cholesterol due to the treatment was observed. This undesirable change is not consistent with reports from other intervention studies involving consumption of fruits and vegetables (1,7), and the finding is unexpected. The reasons for this are unclear.

This study did not demonstrate that the increase in 8-OHdG induced by fish oil can be partly offset by the test soup and juice intervention. Kiokias et al. (19) reported that consumption of a mixture of natural carotenoids (30 mg/d) can offset the increase in urinary 8-OHdG induced by fish oil. Halliwell (39) commented that the available evidence suggests that in Western populations, intake of certain fruit and vegetables can decrease oxidative DNA damage, whereas ascorbate, vitamin E, and ß-carotene cannot.

The current study found no evidence that consumption of the equivalent of 400 g of fruit and vegetables in the form of soups and beverages increased the oxidative stability of plasma or LDL. There were no changes in plasma ORAC, TEAC or FRAP values, or in the oxidative stability of LDL ex vivo. It is notable that the ORAC values of the 2 groups were similar after the intervention, but the test group was lower than the control group before the intervention. The FRAP values fell by a similar amount for both test and control groups during the intervention period, whereas the TEAC values were unchanged by both the control and test intervention. These 3 methods are mainly dependent on water-soluble antioxidants and metabolites, but the FRAP value primarily measures reducing activity, whereas the TEAC and ORAC assays are measures of radical-scavenging activity. The sensitivity of the assays to different plasma components (e.g., albumin and bilirubin) is variable (40). Roberts et al. (7) provided evidence that consumption of 4 g fish oil/d reduced the oxidative stability of LDL ex vivo and of plasma, assessed by the ORAC assay, but the effects were partially offset by the consumption of 5 portions of fruit and vegetables. The study design used volunteers who smoked, and consequently, the levels of oxidative stress would have been higher than in the current study, where only 3 of 36 volunteers smoked.

The reduction of plasma homocysteine concentrations may be at least partly due to the known effect of dietary folate in reducing this variable, although the increase in dietary folate was calculated to be 7 µg/d during the test group intervention, based on the diet diaries. The database may be incomplete in respect of the folate content of the foods consumed, so the true increase may have been greater. Also, the bioavailability of folate from different foods varies widely (41), and the reduction in dietary folate during the control period was partly due to the reduction in meat consumed. During the test period, the increase in dietary folate was due to an increase in folate from vegetable sources, which exceeded the reduction in intake from meat. Broekmans et al. (8) showed that consumption of 400 g additional fruit and vegetables plus 200 mL fruit juice for 4 wk caused an 11% reduction in plasma homocysteine concentrations. The change in plasma homocysteine during the test intervention of the present study was a 9% reduction.

This study provides evidence that plasma carotenoid concentrations can be increased by the consumption of carotenoid-rich fruit and vegetable beverages and vegetable soups, but whether this change had an effect on disease risk was not established. There was a significant reduction in plasma homocysteine concentrations after dietary intervention with the carotenoid-rich soups and beverages, which is suggested to be beneficial insofar as high plasma homocysteine concentrations are a risk factor for cardiovascular disease (42), although other risk markers were not affected. Despite the use of a range of methods of assessing antioxidant status, no significant effect of the dietary intervention on oxidative stability of plasma or LDL was detected.


   ACKNOWLEDGMENTS
 
The authors acknowledge Jackie Carsson-Long for her help with study days and diet diary coding and Dr. Frank Thies for the analysis of PONS.


   FOOTNOTES
 
1 This research was supported by grants from Unilever Bestfoods and the University of Reading Research Endowment Trust Fund. Back

2 Abbreviations used: DHA docosahexaenoic acid; EPA eicosapentaenoic acid; FRAP, ferric-reducing anitioxidant potential; GSH, glutathione; GPx, glutathione peroxidase; ICAM, endothelial intercellular adhesion molecule-1; 8-OHdG, 8-hydroxy-2'-deoxyguanosine; ORAC, oxygen radical absorbance capacity; PON, human serum paraoxonase; TEAC, trolox-equivalent antioxidant capacity; VCAM, vascular cell adhesion moloecule-1. Back

Manuscript received 2 May 2006. Initial review completed 10 June 2006. Revision accepted 22 August 2006.


   LITERATURE CITED
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 ABSTRACT
 Introduction
 Subjects and Methods
 Results
 Discussion
 LITERATURE CITED
 

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