Iron plays a crucial role in many physiological processes, including oxygen transport, bioenergetics, and immune function. Iron is assimilated from food and also recycled from senescent red blood cells. Iron exists in two dietary forms: heme (animal based) and non-heme (mostly plant based). The body uses iron for metabolic purposes, and stores the excess mainly in splenic and hepatic macrophages. Physiologically, iron excretion in humans is inefficient and not highly regulated, so regulation of intestinal absorption maintains iron homeostasis. Iron losses occur at a steady rate via turnover of the intestinal epithelium, blood loss, and exfoliation of dead skin cells, but overall iron homeostasis is tightly controlled at cellular and systemic levels. Aging can have a profound impact on iron homeostasis and induce a dyshomeostasis where iron deficiency or overload (sometimes both simultaneously) can occur, potentially leading to several disorders and pathologies. To maintain physiologically balanced iron levels, reduce risk of disease, and promote healthy aging, it is advisable for older adults to follow recommended daily intake guidelines and periodically assess iron levels. Clinicians can evaluate body iron status using different techniques but selecting an assessment method primarily depends on the condition being examined. This review provides a comprehensive overview of the forms, sources, and metabolism of dietary iron, associated disorders of iron dyshomeostasis, assessment of iron levels in older adults, and nutritional guidelines and strategies to maintain iron balance in older adults.

According to the United Nations, by 2050, one in six individuals will be over age 65 globally, and one in four people would be aged 65 and older in western countries. The unprecedented growth of the aging population is associated with increased age-related disorders like Alzheimer's disease (AD) and Mild cognitive impairment (MCI). To date, no cure is known for AD, thus lifestyle interventions including calorie restriction (CR) and time-restricted eating (TRE) are proposed as potential approach to delay the onset and progression of the disease. Sleep disturbances are common in people with MCI and AD. Moreover, accumulating data indicates that pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-6, IL-8 and IL-10 increase in individuals with AD and MCI versus healthy subjects. Thus, the purpose of the present review is to describe the potential effects of TRE on sleep, cognition decline, and neuroinflammatory markers in humans. Preliminary evidence suggests that TRE may produce neuroprotective effects on cognition and reduce neuroinflammatory markers related to AD in humans. To date, no studies investigated the effects of TRE on sleep disturbances and patients with AD. Thereby, the impact of TRE on cognition in individuals with cognitive decline and AD needs to be investigated further in randomized controlled trials (RCTs).

Introduction: Time-restricted eating (TRE), a dietary pattern reducing the duration of daily food consumption, has recently gained popularity. Existing studies show the potential benefits of TRE for cardiometabolic health. Uncertainty remains about whether these benefits are solely from altered meal timing or influences on other health behaviors, including sleep. Despite growing scientific interest in the effects of TRE on sleep parameters, the topic has not been systematically explored.Methods: This review examined the effects of TRE interventions (daily fasting duration ≥14 h) lasting at least 8 weeks on objective and subjective sleep parameters. Six randomized control trials were identified through Pubmed, Embase, Google Scholar, and Scopus through September 2023.Results: Of the included studies, three employed objective sleep measures using wearables and five studies assessed sleep subjectively through self-report questionnaires. Only one study reported significant improvements in subjective sleep quality following a TRE intervention. Additionally, one study found significant decreases in sleep duration, two studies found significant decreases in sleep efficiency, and one found significant increases in sleep onset latency.Discussion: Current evidence indicates that short to mid-term TRE does not typically worsen sleep parameters. However, some populations may experience reduced sleep disturbances, while others may experience reductions in sleep efficiency. Longer duration studies with objective sleep assessments are needed to better understand the effects of TRE on sleep parameters.

Background/Objectives: Time-restricted eating (TRE) has been associated with beneficial effects for inflammation and oxidative stress; however, the effects of TRE on inflammation and oxidative stress in the aging population have not been explored. Methods: This secondary analysis tested the effects of TRE on pro-inflammatory (hs-CRP [high-sensitivity C-reactive protein], IL-1β [interleukin 1 beta], IL-6 [interleukin 6], TNF-α [tumor necrosis factor alpha]) and oxidative stress (8-isoprostane) biomarkers in ten overweight older adults (mean age = 77.1 ± 6.1 years; six women and four men), who followed a TRE protocol of 16 h of fasting per day and consumed food ad libitum during an 8 h window for 4 weeks. Results: TNF-α levels decreased from 43.2 (11.2) pg/mL to 39.7 (10.0) pg/mL with a Cohen’s d effect size of 0.33, and IL-1β levels decreased from 1.4 (0.8) pg/mL to 1.3 (0.6) pg/mL with a Cohen’s d effect size of 0.23, suggesting potential anti-inflammatory benefits. IL-6 and hs-CRP levels showed no substantial changes (Cohen’s d ≤ 0.03). The oxidative stress marker 8-isoprostane levels decreased slightly with a Cohen’s d effect size of 0.07. Conclusions: The findings of this pilot study provide initial insights into the potential effects of TRE on inflammatory and oxidative stress markers in older adults. Given the small sample size and short-term intervention, well-powered studies of longer duration are needed to better understand the effects of TRE on inflammation and oxidative stress in aging populations.