The welfare state determinants of health: Implications of regimes and pathways

Background. Population health within and between nations is heavily influenced by political determinants, yet these determinants have received significantly less attention than socioeconomic factors in public health. It has been hypothesized that the welfare state, as a political variable, may play a particularly prominent role in affecting both health indicators and health disparities in developed countries. The research, however, provides conflicting evidence regarding the health impact of particular regimes over others and the mechanisms through which the welfare state can most significantly affect health.^ Objective. To perform a systematic review of the literature as a means of exploring what the current research indicates regarding the benefits or detriments of particular regimes styles and the pathways through which the welfare state can impact heath indicators and health disparities within developed countries.^ Methods. A thorough search of the EBSCO, Pubmed, Medline, Web of Science, and Scopus electronic databases was conducted and resulted in the identification of 15 studies that evaluated the association between welfare state regime and population health outcomes, and/or pathways through with the welfare state influences health. ^ Results. Social democratic countries tended to perform best when infant mortality rate (IMR) was the primary outcome of interest, whereas liberal countries performed strongly in relation to self perceived health. The results were mixed regarding welfare state effectiveness in mitigating health inequities, with Christian democratic countries performing as well as social democratic countries. In relation to welfare state pathways, public health spending and medical coverage were associated with positive health indicators. Redistributive impact of the welfare state was also consistently associated with better health outcomes while social security expenditures were not.^ Discussion/Conclusions. Studies consistently discovered a significant relationship between the welfare state and population health and/or health disparities, lending support to the hypothesis that the welfare state is, indeed, an important non-medical determinant of health. However, it is still fairly unclear which welfare state regime may be most protective for health, as results varied according to the measured health indicator. The research regarding welfare state pathways is particularly undeveloped, and does not provide much insight into the importance of in-kind service provision or cash transfers, or targeted or universal approaches to the welfare state. Suggestions to direct future research are provided.^

Targeting AKT/mTOR Signaling Pathways During Murine Skin Tumor Promotion and the Impact of Dietary Energy Balance Manipulation

The prevalence of obesity has continued to rise over the last several decades in the United States lending to overall increases in risk for chronic diseases including many types of cancer. In contrast, reduction in energy consumption via calorie restriction (CR) has been shown to be a potent inhibitor of carcinogenesis across a broad range of species and tumor types. Previous data has demonstrated differential signaling through Akt and mTOR via the IGF-1R and other growth factor receptors across the diet-induced obesity (DIO)/CR spectrum. Furthermore, mTORC1 is known to be regulated directly via nutrient availability, supporting its role in the link between epithelial carcinogenesis and diet-induced obesity. In an effort to better understand the importance of mTORC1 in the context of both positive and negative energy balance during epithelial carcinogenesis, we have employed the use of specific pharmacological inhibitors, rapamycin (mTORC1 inhibitor) and metformin (AMPK activator) to target mTORC1 or various components of this pathway during skin tumor promotion. Two-stage skin carcinogenesis studies demonstrated that mTORC1 inhibition via rapamycin, metformin or combination treatments greatly inhibited skin tumor development in normal, overweight and obese mice. Furthermore, mechanisms by which these chemopreventive agents may be exerting their anti-tumor effects were explored. In addition, the effect of these compounds on the epidermal proliferative response was analyzed and drastic decreases in epidermal hyperproliferation and hyperplasia were found. Rapamycin also inhibited dermal inflammatory cell infiltration in a dose-dependent manner. Both compounds also blocked or attenuated TPA-induced signaling through epidermal mTORC1 as well as several downstream targets. In addition, inhibition of this pathway by metformin appeared to be, at least in part, dependent on AMPK activation in the skin. Overall, the data indicate that pharmacological strategies targeting this pathway offset the tumor-enhancing effects of DIO and may serve as possible CR mimetics. They suggest that mTORC1 contributes significantly to the process of skin tumor promotion, specifically during dietary energy balance effects. Exploiting the mechanistic information underlying dietary energy balance responsive pathways will help translate decades of research into effective strategies for prevention of epithelial carcinogenesis.