Intermittent fasting (IF) refers to various dietary regimens that cycle between a period of non-fasting and a period of total fasting. This study aimed to determine the effects of IF on cognitive function among elderly individuals who practice IF who have mild cognitive impairment (MCI). A total of 99 elderly subjects with MCI of Malay ethnicity without any terminal illness were recruited from a larger cohort study, LRGS TUA. The subjects were divided into three groups, comprising those who were regularly practicing IF (r-IF), irregularly practicing IF (i-IF), and non-fasters (n-IF). Upon 36 months of follow-up, more MCI subjects in the r-IF group reverted to successful aging with no cognitive impairment and diseases (24.3%) compared to those in i-IF (14.2%) and n-IF groups (3.7%). The r-IF group’s subjects exhibited significant increment in superoxide dismutase (SOD) activity and reduction in body weight, levels of insulin, fasting blood glucose, malondialdehyde (MDA), C-reactive protein (CRP), and DNA damage. Moreover, metabolomics analysis showed that IF may modulate cognitive function via various metabolite pathways, including the synthesis and degradation of ketone bodies, butanoate metabolism, pyruvate metabolism, and glycolysis and gluconeogenesis pathways. Overall, the MCI-afflicted older adults who practiced IF regularly had better cognitive scores and reverted to better cognitive function at 36 months follow-up.

Background A cross sectional study was conducted in a group of 317 subjects older than 60 in Malaysia, aimed to determine risk factors associated with cognitive impairment in older adults, focusing on trace elements and DNA damage. Method Cognitive decline was determined by Montreal Cognitive Assessment (MoCA). Oxidative stress markers (malondialdehyde-MDA and superoxide dismutase-SOD) were determined and DNA damage was assayed using Alkaline Comet Assay. Toenail samples were taken and analyzed using ICP-MS to determine trace element levels. Results A total of 62.1 % of subjects had cognitive impairment. Subjects with cognitive impairment had significantly higher levels of MDA and DNA damage as compared to the group with normal cognitive function; MDA (2.07 ± 0.05 nmol/L vs 1.85 ± 0.06 nmol/L) (p<0.05) and DNA damage (% Tail Density, 14.52 ± 0.32 vs 10.31 ± 0.42; Tail Moment, 1.79 ± 0.06 vs 1.28 ± 0.06) (p<0.05 for all parameters). However, the level of SOD among subjects with cognitive impairment (6.67 ± 0.33 u.e/min/mg protein) was lower than the level among those with normal cognitive functions (11.36 ± 0.65 u.e/min/mg protein) (p<0.05). Multiple logistic regression revealed the predictors for cognitive impairment among the subjects were DNA damage (Adjusted odd ratio [OR], 1.37; 95% confidence interval [CI], 1.18-1.59), level of trace elements in toenails namely, lead (OR, 2.471; CI, 1.535-3.980) and copper (OR, 1.275; CI, 1.047-1.552) (p<0.05). Conclusion High levels of lead and copper can lead to increase in oxidative stress levels and are associated with DNA damage that eventually could be associated with cognitive decline.

Cognitive impairments are often related to aging and micronutrient deficiencies. Various essential micronutrients in the diet are involved in age-altered biological functions such as, zinc, copper, iron, and selenium that play pivotal roles either in maintaining and reinforcing the antioxidant performances or in affecting the complex network of genes (nutrigenomic approach) involved in encoding proteins for biological functions. Genomic stability is one of the leading causes of cognitive decline and deficiencies or excess in trace elements are two of the factors relating to it. In this review, we report and discuss the role of micronutrients in cognitive impairment in relation to genomic stability in an aging population. Telomere integrity will also be discussed in relation to aging and cognitive impairment, as well as, the micronutrients related to these events. This review will provide an understanding on how these three aspects can relate with each other and why it is important to keep a homeostasis of micronutrients in relation to healthy aging. Micronutrient deficiencies and aging process can lead to genomic instability.

The main objective of this study is to determine the association of various trace elements’ status with the 5-year mortality rate among community-dwelling older adults in Malaysia. This study was part of the Long-term Research Grant Scheme—Towards Useful Ageing (LRGS-TUA). The participants were followed up for five years, and their mortality status was identified through the Mortality Data Matching Service provided by the National Registration Department, Malaysia. Of the 303 participants included in this study, 34 (11.2%) participants had died within five years after baseline data collection. As compared to the survivors, participants who died earlier were more likely (p < 0.05) to be men, smokers, have a lower intake of total dietary fiber and molybdenum, higher intake of manganese, lower zinc levels in toenail samples, lower calcium and higher lead levels in hair samples during baseline. Following the multivariate Cox proportional hazard analysis, lower total dietary fiber intake (HR: 0.681; 0.532–0.871), lower calcium (HR: 0.999; 95% CI: 0.999–1.000) and higher lead (HR: 1.309; 95% CI: 1.061–1.616) levels in hair samples appeared as the predictors of mortality. In conclusion, higher lead and lower calcium levels are associated with higher risk of mortality among community-dwelling older adults in Malaysia. Our current findings provide a better understanding of how the trace elements’ status may affect older populations’ well-being and mortality rate.

Despite being acknowledged globally as one of the primary environmental pollutants, pesticides appear as one of the toxic compounds that are available purposefully to be used in controlling pests and vectors, especially in agricultural areas ^[1]. Nevertheless, pesticides have been discovered to be associated with a broad scope of pathologies, especially with Parkinson’s disease (PD) Most previous studies could not determine a significant positive relationship due to the discrepancies in their methodologies. Based on data published by the Department of Statistics Malaysia, the proportion of citizens with PD in Malaysia is anticipated to grow five-fold by 2040, from an estimated 20,000 to 120,000 cases ^[2]. Hence, this study is employed to deliver an up-to-date systematic review and meta-analysis regarding pesticide exposure and PD which will be based on the highest quality of evidence along with a broader extent of study designs that encompass cohort, case-control and cross-sectional studies to identify the significant link between them. The objective of this study was to find out whether there is an increased risk of PD among adults with occupational exposure to pesticides and to determine the pesticides that are associated with PD. In formulating the research question, the P (population) E (exposure) C (control) O (outcome) model was used. The search was done from databases such as Google Scholar, Pubmed and Science Direct. The key points used were as followed: “occupational” OR “professional” OR “work-related” OR “job-related” OR/AND “pesticidal” OR “pesticide's” OR “pesticides” OR “pesticide” AND “Parkinson disease” OR “Parkinsons disease” OR “Parkinson's disease” OR “Parkinson” OR “Parkinsons” OR “Parkinson’s”. Meta-analysis was directed by utilizing the Review Manager 5 software to inspect the data regarding work-related pesticide acquaintance and the development of Parkinson’s disease based on all included studies of selected characteristics. The systematic review encompassed 26 studies where 23 of them displayed a significant association between occupational exposures to pesticides that increased the risk of developing PD. The meta-analysis also supported the hypothesis of this study where work-related pesticide acquaintance showed 89% higher odds to develop PD [OR = 1.89, 95% CI (1.63 to 2.20)]. For specific types of pesticides, organophosphorus contact revealed the strongest association with 89% higher odds [OR = 1.89, 95% CI (1.35 to 2.64)] followed by insecticides contact with 86% higher odds [OR = 1.57, 95% CI (1.58 to 1.92)], organochlorine exposure with 71% higher odds [OR = 1.71, 95% CI (1.21 to 2.41)], fungicides acquaintance at 42% higher odds [OR = 1.42, 95% CI (1.33 to 1.51)] and herbicides contact with 23% higher odds [OR = 1.23, 95% CI (1.03 to 1.46)] to establish PD (Table 1). Overall, occupational pesticide contact exhibited an increased risk of PD with organophosphorus displaying the strongest association among other specific types of pesticide. The theory concerning the specific kind of pesticides that can lead to PD is inconsistent where it is immensely dependent upon their mechanism of toxicity and chemical composition as well as its explicit biochemical passageways which up until this moment is not yet being fully understood. Hence, the result of this study can supplement advanced knowledge in the literature where it can be utilized to govern further studies and implementations in the future to improve the safety and health of the workers who are involved with pesticides’ application day to day as well as the health of the public. Therefore, a safer class of pesticides may also be invented consequently. On the other hand, it may also aid in future studies to find out the specific biomarkers or reliable tools which can measure the causal relationship between pesticides’ acquaintance and PD more accurately. Thus, the forthcoming studies that can count on more unbiased and quantifiable approaches regarding the evaluation of pesticides’ acquaintance and PD must be fostered.