Browsing by Author "Page R"

Now showing 1 - 3 of 3
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    Dietary practices, physical activity and social determinants of non-communicable diseases in Nepal: A systemic analysis.
    (PLOS, 2023-02-06) Sharma S; Matheson A; Lambrick D; Faulkner J; Lounsbury DW; Vaidya A; Page R; Kushitor SB
    Unhealthy dietary habits and physical inactivity are major risk factors of non-communicable diseases (NCDs) globally. The objective of this paper was to describe the role of dietary practices and physical activity in the interaction of the social determinants of NCDs in Nepal, a developing economy. The study was a qualitative study design involving two districts in Nepal, whereby data was collected via key informant interviews (n = 63) and focus group discussions (n = 12). Thematic analysis of the qualitative data was performed, and a causal loop diagram was built to illustrate the dynamic interactions of the social determinants of NCDs based on the themes. The study also involved sense-making sessions with policy level and local stakeholders. Four key interacting themes emerged from the study describing current dietary and physical activity practices, influence of junk food, role of health system and socio-economic factors as root causes. While the current dietary and physical activity-related practices within communities were unhealthy, the broader determinants such as socio-economic circumstances and gender further fuelled such practices. The health system has potential to play a more effective role in the prevention of the behavioural and social determinants of NCDs.
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    Potent inhibition of human monoamine oxidase A and B by phenolic compounds and polyunsaturated fatty acids in tobacco smoke
    (Elsevier B V, 2025-05-25) Hong SW; Heydari A; Watson PR; Teesdale-Spittle PH; Page R; Northcote PT; Keyzers RA; Vyssotski M; Truman P
    Smoking is a main cause of premature death and preventable disease in the world. Interestingly, animal studies indicate that inhibition of monoamine oxidase (MAO), key enzymes for the degradation of neurotransmitters, increased self-administration of nicotine. The purpose of this study was to identify and characterize the potential MAO inhibitors in tobacco smoke responsible for MAO inhibition in smokers. A bioassay-guided isolation from an extract of tobacco smoke showed that catechol, 4-methylcatechol, hydroquinone, α-linolenic acid, and linoleic acid all displayed potent human MAO inhibitory activity. Additionally, the tobacco catechols 4-ethylcatechol and 4-vinylcatechol were included to test their inhibitory potencies. Catechol, 4-methylcatechol, 4-ethylcatechol, and hydroquinone are potent and irreversible MAO inhibitors. Among the phenolic compounds tested, 4-methylcatechol and 4-ethylcatechol inhibited MAO A with IC50 values of 10.0 and 12.6 μM, respectively, reducing to 0.27 and 0.43 μM after 1 h preincubation. In addition, α-linolenic acid and linoleic acid competitively inhibited MAO A with Ki values of 10.50 and 6.95 μM, respectively. These results suggest that MAO inhibition by phenolics and polyunsaturated fatty acids in tobacco smoke may be important contributors to the MAO inhibition experienced by smokers and to the enhancement of nicotine dependence this MAO inhibition is believed to cause.
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    Smoking, coffee intake, and Parkinson's disease: Potential protective mechanisms and components.
    (Elsevier B.V., 2024-12-20) Hong SW; Page R; Truman P
    Parkinson's disease (PD) is a common progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Environmental and lifestyle factors, such as smoking and coffee drinking, have been associated with a decreased risk for PD. However, the biological mechanisms underlying protective effects on PD are still not fully understood. It has been suggested that non-nicotine components in cigarette smoke and non-caffeine components in coffee may contribute to this protective effect. The aim of this review was to explore candidate molecules and mechanisms behind the effects of smoking and coffee drinking on PD by integrating findings from previous studies. By cross-referencing an index of tobacco constituents and a list of coffee constituents with existing literature on natural compounds and their structural analogs that show inhibitory activities against monoamine oxidase B, catechol O-methyltransferase, and α-synuclein fibrillation, we have identified tobacco and coffee components that inhibit these targets. Furthermore, tobacco and coffee components potentially play roles in suppressing neuroinflammation, activating the Nrf2 pathway as natural activators, and altering the gut microbiome. This review suggests that the phenolic compounds from tobacco and coffee investigated may contribute to the low incidence of PD in smokers and coffee drinkers, showing moderate to strong potential as therapeutic interventions. The current review suggests that multifunctional molecules found in coffee and cigarette smoke may have potential neuroprotective effects, but none of the data indicates that multifunctionality is required for these effects. This review will deepen our understanding of how smoking and coffee drinking are linked to a reduced risk of PD and will also be important in elucidating the mechanisms underlying the protective effects of smoking and coffee drinking on PD.