Dataset Information

Why don't poor men eat fruit? Socioeconomic differences in motivations for fruit consumption.

ABSTRACT:

Background

Those of lower socioeconomic status (SES) tend to have less healthy diets than those of higher SES. This study aimed to assess whether differences in motivations for particular foods might contribute to socioeconomic differences in consumption.

Methods

Participants (n = 732) rated their frequency of consumption and explicit liking of fruit, cake and cheese. They reported eating motivations (e.g., health, hunger, price) and related attributes of the investigated foods (healthiness, expected satiety, value for money). Participants were randomly assigned to an implicit liking task (Single Category Implicit Association Task) for one food category. Analyses were conducted separately for different SES measures (income, education, occupational group).

Results

Lower SES and male participants reported eating less fruit, but no SES differences were found for cheese or cake. Analyses therefore focused on fruit. In implicit liking analyses, results (for income and education) reflected patterning in consumption, with lower SES and male participants liking fruit less. In explicit liking analyses, no differences were found by SES. Higher SES participants (all indicators) were more likely to report health and weight control and less likely report price as motivators of food choices. For perceptions of fruit, no SES-based differences were found in healthiness whilst significant interactions (but not main effects) were found (for income and education) for expected satiety and value for money. Neither liking nor perceptions of fruit were found to mediate the relationship between SES and frequency of fruit consumption.

Conclusions

There is evidence for social patterning in food motivation, but differences are modified by the choice of implicit or explicit measures. Further work should clarify the extent to which these motivations may be contributing to the social and gender patterning in diet.

SUBMITTER: Pechey R

PROVIDER: S-EPMC4262578 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Cancer stands as one of the prominent global causes of death, with its incidence burden continuously increasing, leading to a substantial rise in mortality rates. Cancer treatment has seen the development of various strategies, each carrying its drawbacks that can negatively impact the quality of life for cancer patients. The challenge remains significant within the medical field to establish a definitive cancer treatment that minimizes complications and limitations. In the forthcoming years, exploring new strategies to surmount the failures in cancer treatment appears to be an unavoidable pursuit. Among these strategies, immunology-based ones hold substantial promise in combatting cancer and immune-related disorders. A particular subset of this approach identifies "eat me" and "Don't eat me" signals in cancer cells, contrasting them with their counterparts in non-cancerous cells. This distinction could potentially mark a significant breakthrough in treating diverse cancers. By delving into signal transduction and engineering novel technologies that utilize distinct "eat me" and "Don't eat me" signals, a valuable avenue may emerge for advancing cancer treatment methodologies. Macrophages, functioning as vital components of the immune system, regulate metabolic equilibrium, manage inflammatory disorders, oversee fibrosis, and aid in the repair of injuries. However, in the context of tumor cells, the overexpression of "Don't eat me" signals like CD47, PD-L1, and beta-2 microglobulin (B2M), an anti-phagocytic subunit of the primary histocompatibility complex class I, enables these cells to evade macrophages and proliferate uncontrollably. Conversely, the presentation of an "eat me" signal, such as Phosphatidylserine (PS), along with alterations in charge and glycosylation patterns on the cellular surface, modifications in intercellular adhesion molecule-1 (ICAM-1) epitopes, and the exposure of Calreticulin and PS on the outer layer of the plasma membrane represent universally observed changes on the surface of apoptotic cells, preventing phagocytosis from causing harm to adjacent non-tumoral cells. The current review provides insight into how signaling pathways and immune cells either stimulate or obstruct these signals, aiming to address challenges that may arise in future immunotherapy research. A potential solution lies in combination therapies targeting the "eat me" and "Don't eat me" signals in conjunction with other targeted therapeutic approaches. This innovative strategy holds promise as a novel avenue for the future treatment of cancer.