Consumer food choices: the role of price and pricing strategies.

OBJECTIVE: To study differences in the role of price and value in food choice between low-income and higher-income consumers and to study the perception of consumers about pricing strategies that are of relevance during grocery shopping. DESIGN: A cross-sectional study was conducted using structured, written questionnaires. Food choice motives as well as price perceptions and opinion on pricing strategies were measured. SETTING: The study was carried out in point-of-purchase settings, i.e. supermarkets, fast-food restaurants and sports canteens. SUBJECTS: Adults (n 159) visiting a point-of-purchase setting were included. RESULTS: Price is an important factor in food choice, especially for low-income consumers. Low-income consumers were significantly more conscious of value and price than higher-income consumers. The most attractive strategies, according to the consumers, were discounting healthy food more often and applying a lower VAT (Value Added Tax) rate on healthy food. Low-income consumers differ in their preferences for pricing strategies. CONCLUSIONS: Since price is more important for low-income consumers we recommend mainly focusing on their preferences and needs.

Perceptions on the use of pricing strategies to stimulate healthy eating among residents of deprived neighbourhoods: a focus group study.

BACKGROUND: Pricing strategies are mentioned frequently as a potentially effective tool to stimulate healthy eating, mainly for consumers with a low socio-economic status. Still, it is not known how these consumers perceive pricing strategies, which pricing strategies are favoured and what contextual factors are important in achieving the anticipated effects. METHODS: We conducted seven focus groups among 59 residents of deprived neighbourhoods in two large Dutch cities. The focus group topics were based on insights from Rogers' Diffusion of Innovations Theory and consisted of four parts: 1) discussion on factors in food selection; 2) attitudes and perceptions towards food prices; 3) thinking up pricing strategies; 4) attitudes and perceptions regarding nine pricing strategies that were nominated by experts in a former Delphi Study. Analyses were conducted with Atlas.ti 5.2 computer software, using the framework approach. RESULTS: Qualitative analyses revealed that this group of consumers consider price to be a core factor in food choice and that they experience financial barriers against buying certain foods. Price was also experienced as a proficient tool to stimulate healthier food choices. Yet, consumers indicated that significant effects could only be achieved by combining price with information and promotion techniques. In general, pricing strategies focusing on encouraging healthy eating were valued to be more helpful than pricing strategies which focused on discouraging unhealthy eating. Suggested high reward strategies were: reducing the price of healthier options of comparable products (e.g., whole meal bread) compared to unhealthier options (e.g., white bread); providing a healthy food discount card for low-income groups; and combining price discounts on healthier foods with other marketing techniques such as displaying cheap and healthy foods at the cash desk. CONCLUSION: This focus group study provides important new insights regarding the use of pricing strategies to stimulate healthy eating. The observed perceptions and attitudes of residents of deprived neighbourhoods can be integrated into future experimental studies and be used to reveal if and how pricing strategies are effective in stimulating healthy eating.

A probabilistic model for simultaneous exposure to multiple compounds from food and its use for risk-benefit assessment.

A model is presented which allows to quantify the simultaneous distribution of the exposure to two compounds, for example a health-risk and a health promoting compound. The model considers the total dietary intake, and can be used as a first step to study the effects on the balance between risks and benefits following changes in the consumption pattern. The exposure is modelled separately for intake probabilities using a betabinomial model, and for intake amounts using a lognormal model, and these parts are afterwards integrated by Monte Carlo simulation. The model is illustrated using the risk-benefit case of dioxins and the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). High concentrations of both the health adverse compounds and the health promoting compounds are simultaneously present in fatty fish. Calculated exposures were compared with intake limits: the adequate intake for EPA+DHA and the tolerable daily intake (TDI) for dioxins. We estimate the probability that dioxin exposure is below TDI, the probability that EPA+DHA exposure is above the adequate intake, and the probability that both conditions occur simultaneously. We also model the dependence of these probabilities on age. In the studied population the exposure to both compounds is almost completely below the limits. A scenario study in which meat consumption was replaced by fatty fish consumption shows an increase in the fraction of the population with the recommended intake of EPA+DHA, however also the fraction of the population exceeding the TDI for dioxins is increased. For the example scenario the optimal amount of fatty fish consumption is derived.

Reversal of in vitro cellular MRP1 and MRP2 mediated vincristine resistance by the flavonoid myricetin.

In the present study, the effects of myricetin on either MRP1 or MRP2 mediated vincristine resistance in transfected MDCKII cells were examined. The results obtained show that myricetin can inhibit both MRP1 and MRP2 mediated vincristine efflux in a concentration dependent manner. The IC50 values for cellular vincristine transport inhibition by myricetin were 30.5+/-1.7 microM for MRP1 and 24.6+/-1.3 microM for MRP2 containing MDCKII cells. Cell proliferation analysis showed that the MDCKII control cells are very sensitive towards vincristine toxicity with an IC50 value of 1.1+/-0.1 microM. The MDCKII MRP1 and MRP2 cells are less sensitive towards vincristine toxicity with IC50 values of 33.1+/-1.9 and 22.2+/-1.4 microM, respectively. In both the MRP1 and MRP2 cells, exposure to 25 microM myricetin enhances the sensitivity of the cells towards vincristine toxicity to IC50 values of 7.6+/-0.5 and 5.8+/-0.5 microM, respectively. The increase of sensitivity represents a reversal of the resistance towards vincristine as a result of MRP1 and MRP2 inhibition. Thus, the present study demonstrates the ability of the flavonoid myricetin to modulate MRP1 and MRP2 mediated resistance to the anticancer drug vincristine in transfected cells, indicating that flavonoids might be a valuable adjunct to chemotherapy to block MRP mediated resistance.

Calculations of dietary exposure to acrylamide.

In this paper we calculated the usual and acute exposure to acrylamide (AA) in the Dutch population and young children (1-6 years). For this AA levels of different food groups were used as collected by the Institute for Reference Materials and Measurements (IRMM) of the European Commission's Directorate General Joint Research Centre (JRC) from April 2003 up to May 2004. This database contained about 3500 AA levels received from mainly Germany, The Netherlands, Ireland, Greece, Austria, UK and from food industry. Food consumption levels used were derived from the Dutch National Food Consumption Survey of 1997/1998 (n=6250 of which 530 children aged 1-6 years). The exposure was estimated using the probabilistic approach. The results of the exposure calculations are discussed in relation to different methodological aspects of AA exposure calculations and possible uncertainties related to this. The items discussed include quality of the AA levels measured in food items, the allocation of AA levels to food categories, the quality of food consumption levels, and relevant exposure model in relation to reported toxicity of AA. Furthermore, we demonstrate that scenario studies and probabilistic modelling of exposure are potential useful tools to evaluate the effect of processing techniques to reduce AA levels in food on AA exposure. The scenarios studied reduced total AA exposure ranging from <1% up to 17%.

Economic incentives and nutritional behavior of children in the school setting: a systematic review.

The aim of the present review was to examine the existing literature on the effectiveness of economic incentives for producing sound nutritional behavior in schools. Studies published in the English-language literature that included baseline and/or outcome data regarding food and beverage intake of schoolchildren were eligible for inclusion. A systematic search of the literature was conducted to identify relevant primary studies and relevant systematic reviews of primary studies. Altogether, 3,472 research publications were identified in the systematic search, of which 50 papers were retrieved. Of these, 30 publications representing 28 studies fulfilled the criteria for inclusion. The studies addressing price incentives suggest that such incentives are effective for altering consumption in the school setting. Other types of economic incentives have been included in combined intervention schemes, but the inclusion of other intervention elements makes it difficult to draw conclusions about the effectiveness of the economic incentive instruments per se in these studies.

Dietary exposure to dioxins and dioxin-like PCBs in The Netherlands anno 2004.

In this study, representative occurrence data for PCDD/Fs and dioxin-like PCBs in food were obtained and used to estimate dietary exposure of the Dutch population. Food composite samples were analyzed as well as single fish and vegetables samples. Total dioxin concentrations in animal products ranged from 0.05 pg TEQ/g product in poultry to 2.5 pg TEQ/g product (using TEF(2006)) in fish (shrimp), with 0.12pg TEQ/g product being the lowest concentrations measured in fish (tuna). In vegetable products, concentrations ranged from 0.00002 pg TEQ/g product (white kale) to 0.19 pg TEQ/g (oils and fats). A long-term dietary exposure distribution was calculated using Monte Carlo Risk Assessment software. The lower bound median exposure of the Dutch population to PCDD/Fs and dioxin-like PCBs was estimated at 0.8 pg WHO-TEQ/kgbw/d, half of which were dioxin-like PCBs. Dairy was the main source (38%) due to its high consumption. Time-trend analysis shows that the exposure to dioxins has further decreased by 35% over the past five years. This is due to lower levels of dioxin-like compounds in most of the foods, mainly influenced by lower levels in meat and milk. The use of the new TEFs gives an exposure reduction of 10% with respect to TEF(1998). Still, 4% of the Dutch population exceeds the exposure limit of 14 pg/kgbw/week as set by the EU.

Dietary intake and risk evaluation of polybrominated diphenyl ethers in The Netherlands.

The current study aims at estimating the dietary intake of PBDEs in the Netherlands and evaluating the resultant risk. Dietary intake was estimated using results of PBDE analyses in Dutch food products from 2003/2004 and consumption data of the third Dutch National Food Consumption Survey (1997/1998). Assuming that non-detects represent levels of half the detection limit, the median long-term intake of the Dutch population of the sum of five major PBDEs (namely PBDEs 47, 99, 100, 153+154) is 0.79 ng/kg body weight bw/day (P97.5: 1.62 ng/kg bw/day). When non-detects are considered as zeros the values are 0.53 (median) and 1.34 (P97.5) ng/kg bw/day. Environmental concentrations of PBDEs in Europe are expected to decline in the near future because of the ban on penta- and octaBDE technical products. However, it will take at least a decade before this will result in lower PBDE concentrations in food products. Hence, a regular monitoring program for PBDEs is recommended. A risk evaluation at the most sensitive endpoints of BDE 99 carried out in this paper indicates that, although the long-term exposure to BDE 99 is well below the human exposure threshold level for neurodevelopmental toxicity, it may be close to that for reproductive toxicity.