Publications

OBJECTIVES

Describe tobacco companies' marketing strategies targeting low socioeconomic status (SES) females in the U.S.A.

METHODS

Analysis of previously secret tobacco industry documents.

RESULTS

Tobacco companies focused marketing on low SES women starting in the late 1970s, including military wives, low-income inner-city minority women, 'discount-susceptible' older female smokers and less-educated young white women. Strategies included distributing discount coupons with food stamps to reach the very poor, discount offers at point-of-sale and via direct mail to keep cigarette prices low, developing new brands for low SES females and promoting luxury images to low SES African-American women. More recently, companies integrated promotional strategies targeting low-income women into marketing plans for established brands.

CONCLUSIONS

Tobacco companies used numerous marketing strategies to reach low SES females in the U.S.A. for at least four decades. Strategies to counteract marketing to low SES women could include (1) counteracting price discounts and direct mail coupons that reduce the price of tobacco products, (2) instituting restrictions on point-of-sale advertising and retail display and (3) creating counteradvertising that builds resistance to psychosocial targeting of low SES women. To achieve health equity, tobacco control efforts are needed to counteract the influence of tobacco industry marketing to low-income women.

We explored associations between Plasmodium falciparum drug resistance-mediating polymorphisms and clinical presentations in parasitemic children enrolled in a cross-sectional survey in Tororo, Uganda, using a retrospective case-control design. All 243 febrile children (cases) and 243 randomly selected asymptomatic children (controls) were included. In a multivariate analysis adjusting for age, complexity of infection, and parasite density, the prevalence of wild-type genotypes was significantly higher in febrile children compared to asymptomatic children (pfcrt K76T: odds ratio [OR] 4.41 [95% confidence interval {CI}, 1.28-15.1]; pfmdr1 N86Y: OR 4.08 [95% CI, 2.01-8.31], and pfmdr1 D1246Y: OR 4.90 [95% CI, 1.52-15.8]), suggesting greater virulence for wild-type parasites.

Fatty acids are integral mediators of energy storage, membrane formation and cell signaling. The pathways that orchestrate uptake of fatty acids remain incompletely understood. Expression of the integrin ligand Mfge8 is increased in human obesity and in mice on a high-fat diet, but its role in obesity is unknown. We show here that Mfge8 promotes the absorption of dietary triglycerides and the cellular uptake of fatty acid and that Mfge8-deficient (Mfge8(-/-)) mice are protected from diet-induced obesity, steatohepatitis and insulin resistance. Mechanistically, we found that Mfge8 coordinates fatty acid uptake through αvβ3 integrin- and αvβ5 integrin-dependent phosphorylation of Akt by phosphatidylinositide-3 kinase and mTOR complex 2, leading to translocation of Cd36 and Fatp1 from cytoplasmic vesicles to the cell surface. Collectively, our results imply a role for Mfge8 in regulating the absorption and storage of dietary fats, as well as in the development of obesity and its complications.