Low socio-economic status (SES) is often associated with various health-related problems. Therefore, the present paper aims to review the available literature to identify the prevalence of malnutrition, prevalence of poor diet quality and its associated risk factors among older adults with low SES. A literature search was performed using four databases, namely PubMed, Google Scholar, Springer and Science Direct. The search terms used were 'diet quality', 'nutritional status', 'dietary intake', 'overweight', 'obesity', 'underweight', 'older people' and 'low socioeconomic status (SES)'. The overall prevalence of undernutrition among older adults with low SES worldwide was in the range of 28·9 to 48 %, while overnutrition was reported to be between 8·1 to 28·2 %. In Asia, the prevalence of undernourished older adults ranged from 3 to 64·9 %, while 2·5 to 32·8 % were overnourished. Most of the studies (60 %) included in the present review used BMI as the tool to identify malnutrition, but none of the nutritional screening tools were considered to be the 'gold standard'. For dietary assessment, FFQ and multiple 24 h dietary recall improved the estimation of individual dietary intake. Risk factors for poor diet quality included financial hardship, functional limitation, sex, place of residence, smoking and oral health. Poor nutritional status, especially lack of good-quality diet, and thinness are prevalent among older adults with low SES. Hence, it is important to establish nutrition-related programmes and intervention studies among this group of individuals for improving their health status and quality of life.
A six-month survey of 828 patients admitted to the Coronary Care Unit (CCU) of the General Hospital, Kuala Lumpur was carried out to ascertain whether the smoking habits of the patients predisposed them to definite coronary events and its immediate outcome i.e. early mortality (within seven days). The various ethnic groups were also screened to determine if they were at increased risk to coronary events in relation to other known risk factors. Three hundred and eleven patients - 239 males, and 72 females - had confirmed acute myocardial infarctions of whom 190 were smokers (172 males, and 18 females). Sixty-nine infarct patients died within the first seven days post-Ml: 35 were smokers (50.7%). Two-hundred and eighty other patients had non-infarct coronary events. Of these, 167 were smokers. In contrast, only 99 out of 237 patients admitted for non-coronary events, were smokers. It thus appeared that patients admitted to the CCU for suspected cardiac events had a greater incidence of confirmed acute myocardial infarction or acute coronary events if they were smokers (p < 0.001). Mortality from these coronary events was not seen to increase among smokers in this population sample. Women who smoked as a whole, were not found to be at increased risk to coronary events, but women smokers 60 years and older were shown to be at increased risk to developing confirmed coronary events (p < 0.01).
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.