Well-being and volunteering: Evidence from aging societies in Asia.

This study examines whether and how volunteering is associated with the well-being of older people in rapidly aging Asian societies; this topic has received remarkably little attention in the literature. Based on the severity of their population aging problem, five Asian societies are selected for an empirical study, namely Hong Kong, Japan, Singapore, South Korea, and Taiwan. We conduct analysis of the latest World Values Survey data set collected from 2011 to 2012 and the effect of volunteering on four aspects of well-being, namely self-reported life satisfaction, happiness, health, and life mastery. Given the ordinal nature of well-being, we establish ordered probit models that focus on voluntary work type, volunteer age, and the level of immersion in volunteer work. The findings indicate a significant positive relationship between active volunteering and well-being, which is valid for all well-being aspects. Active volunteering may have a more significant effect on well-being than inactive volunteering. Age is also a relevant factor affecting volunteering effect. No significant volunteering benefits are found for people younger than 54 years old. Voluntary work in charitable, humanitarian, and religious organizations is the most closely associated with higher well-being for relatively younger people. For people aged 65 and above, volunteering in self-help and cultural organizations is also associated with higher well-being. Moreover, immersion in volunteer work is crucial, particularly for retired people and people aged more than 65 in South Korea, Japan, and Taiwan. The results suggest people should be encouraged to engage in longer hours (or longer duration) of voluntary service. This study identifies the types of volunteer work that most effectively enhance the well-being of older people, which might help older adults transition to retirement and age with higher well-being and help aging societies alleviate their labor shortage problems by involving productive older people.

Docosahexaenoic acid reduces sterol regulatory element binding protein-1 and fatty acid synthase expression and inhibits cell proliferation by inhibiting pAkt signaling in a human breast cancer MCF-7 cell line.

BACKGROUND: Fatty acid synthase (FASN), the major enzyme in de novo fatty acid synthesis, is highly expressed in breast cancer and its expression is reduced by polyunsaturated fatty acids (PUFAs) in liver. We previously found a positive association between rat mammary tumor levels of the n-6 PUFA arachidonic acid (AA) and tumor weight. We examined the roles of the major n-3 PUFA, docosahexaenoic acid (DHA, 22:6n-3), and the major n-6 PUFA, AA, in FASN expression in, and proliferation of, human breast cancer MCF-7 cells. METHODS: The cells were treated for 48 h with BSA or 60 µM BSA-bound DHA, AA, or oleic acid (OA, 18:1n-9), then were incubated with or without estradiol or insulin. Western blot and 3H-thymidine incorporation assay were used to determine the role of DHA on FASN regulation and MCF-7 cell proliferation. RESULTS: DHA, but neither AA nor OA, inhibits estradiol-induced and insulin-induced expression of the precursor of sterol regulatory element binding protein-1 (p-SREBP-1), its mature form (m-SREBP-1), and FASN. Estradiol or insulin stimulation increased the pAkt/Akt and pS6/S6 ratios, expression of p-SREBP-1, m-SREBP-1, and FASN, and cell proliferation, and these effects were decreased by DHA. The DHA-induced decrease in FASN expression resulted from reduced pAkt/Akt signaling and not pERK1/2/ERK1/2 signaling. In addition, DHA enhanced the inhibitory effect of LY294002 on pAkt signaling and expression of p-SREBP-1, m-SREBP-1, and FASN. However, addition of rapamycin, an inhibitor of the mTOR signaling pathways, 1 h before addition of estradiol or insulin increased the pAkt/Akt ratio and FASN expression, and this effect was inhibited by addition of DHA 48 h before rapamycin. CONCLUSION: We conclude that, in MCF-7 cells, DHA inhibits pAKT signaling and thus expression of p-SREBP-1, m-SREBP-1, and FASN and cell proliferation.