Objective but not subjective sleep predicts memory in community‐dwelling older adults

Research on the relationship between habitual sleep patterns and memory performance in older adults is limited. No previous study has used objective and subjective memory measures in a large, older‐aged sample to examine the association between sleep and various domains of memory. The aim of this study was to examine the association between objective and subjective measures of sleep with memory performance in older adults, controlling for the effects of potential confounds. One‐hundred and seventy‐three community‐dwelling older adults aged 65–89 years in Victoria, Australia completed the study. Objective sleep quality and length were ascertained using the Actiwatch 2 Mini‐Mitter, while subjective sleep was measured using the Pittsburgh Sleep Quality Index. Memory was indexed by tests of retrospective memory (Hopkins Verbal Learning Test – Revised), working memory (n‐back, 2‐back accuracy) and prospective memory (a habitual button pressing task). Compared with normative data, overall performance on retrospective memory function was within the average range. Hierarchical regression was used to determine whether objective or subjective measures of sleep predicted memory performances after controlling for demographics, health and mood. After controlling for confounds, actigraphic sleep indices (greater wake after sleep onset, longer sleep‐onset latency and longer total sleep time) predicted poorer retrospective (?R² = 0.05, P = 0.016) and working memory (?R² = 0.05, P = 0.047). In contrast, subjective sleep indices did not significantly predict memory performances. In community‐based older adults, objectively‐measured, habitual sleep indices predict poorer memory performances. It will be important to follow the sample longitudinally to determine trajectories of change over time.     

A single night of partial sleep loss impairs fasting insulin sensitivity but does not affect cephalic phase insulin release in young men

The present study sought to investigate whether a single night of partial sleep deprivation (PSD) would alter fasting insulin sensitivity and cephalic phase insulin release (CPIR) in humans. A rise in circulating insulin in response to food‐related sensory stimulation may prepare tissues to break down ingested glucose, e.g. by stimulating rate‐limiting glycolytic enzymes. In addition, given insulin's anorexigenic properties once it reaches the brain, the CPIR may serve as an early peripheral satiety signal. Against this background, in the present study 16 men participated in two separate sessions: one night of PSD (4.25 h sleep) versus one night of full sleep (8.5 h sleep). In the morning following each sleep condition, subjects’ oral cavities were rinsed with a 1‐molar sucrose solution for 45 s, preceded and followed by blood sampling for repeated determination of plasma glucose and serum insulin concentrations (?3, +3, +5, +7, +10 and +20 min). Our main result was that PSD, compared with full sleep, was associated with significantly higher peripheral insulin resistance, as indicated by a higher fasting homeostasis model assessment of insulin resistance index (+16%, P = 0.025). In contrast, no CPIR was observed in any of the two sleep conditions. Our findings indicate that a single night of PSD is already sufficient to impair fasting insulin sensitivity in healthy men. In contrast, brief oral cavity rinsing with sucrose solution did not change serum insulin concentrations, suggesting that a blunted CPIR is an unlikely mechanism through which acute sleep loss causes metabolic perturbations during morning hours in humans.     

Anticipated next‐day demand affects the magnitude of the cortisol awakening response,but not subjective or objective sleep

Whilst the association between sleep and stress is well established, few studies have examined the effects of an anticipated stressor upon sleep and relevant physiological markers. The aim of the present study was to examine whether an anticipated stressor in the form of next‐day demand affects subjective and objective sleep, and multiple indices of the cortisol awakening response. Subjective and objective sleep and the cortisol awakening response were measured over three consecutive nights in 40 healthy adults in a sleep laboratory. During their second night, participants were informed that they would either be required to complete a series of demanding cognitive tasks, in a competition format, during the next day (anticipation condition; n = 22), or were given no instruction (sedentary condition; n = 18). Sleep was measured subjectively using sleep diaries, objectively using polysomnography, and saliva was measured at awakening, +15, +30, +45 and +60 min each morning, from which cortisol awakening response measurement indices were derived: awakening cortisol levels, the mean increase in cortisol levels and total cortisol secretion. There were no between‐group differences in subjective or objective sleep in the night preceding the anticipated demand; however, compared with the sedentary condition, those in the anticipation group displayed a larger mean increase in cortisol levels, representing the cortisol awakening response magnitude, on the morning of the anticipated demand. Overall, the results suggest that whilst anticipated stress affected the subsequent cortisol awakening response, subjective and objective sleep remained undisturbed. It is possible that the timing of an anticipated stressor, rather than its expected duration, may influence subsequent sleep disruption.     

Vitamin A or E and a catechin synergize as vaccine adjuvant to enhance immune responses in mice by induction of early interleukin‐15 but not interleukin‐1β responses

Vitamins A and E and select flavonoids in the family of catechins are well‐defined small molecules that, if proven to possess immunomodulatory properties, hold promise as vaccine adjuvants and various therapies. In an effort to determine the in vivo immunomodulatory properties of these molecules, we found that although mucosal and systemic vaccinations with a recombinant HIV‐1_BaLgp120 with either a catechin, epigallo catechin gallate (EGCG) or pro‐vitamin A (retinyl palmitate) alone in a vegetable‐oil‐in‐water emulsion (OWE) suppressed antigen‐specific responses, the combination of EGCG and vitamin A or E in OWE (Nutritive Immune‐enhancing Delivery System, NIDS) synergistically enhanced adaptive B‐cell, and CD4⁺ and CD8⁺ T‐cell responses, following induction of relatively low local and systemic innate tumour necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6) and IL‐17, but relatively high levels of early systemic IL‐15 responses. For induction of adaptive interferon‐γ and TNF‐α responses by CD4⁺ and CD8⁺ T cells, the adjuvant effect of NIDS was dependent on both IL‐15 and its receptor. In addition, the anti‐oxidant activity of NIDS correlated positively with higher expression of the superoxide dismutase 1, an enzyme involved in reactive oxygen species elimination but negatively with secretion of IL‐1β. This suggests that the mechanism of action of NIDS is dependent on anti‐oxidant activity and IL‐15, but independent of IL‐1β and inflammasome formation. These data show that this approach in nutritive vaccine adjuvant design holds promise for the development of potentially safer effective vaccines.     

The damage‐associated molecular pattern HMGB1 is elevated in human alcoholic hepatitis,but does not seem to be a primary driver of inflammation

The role of sterile inflammation caused by release of damage‐associated molecular patterns (DAMP) remains unclear in human alcoholic hepatitis (AH). The DAMP, high mobility group box‐1 protein (HMGB1) is released by tissue damage and inflammation. We aimed to investigate whether HMGB1 is a primary inflammatory driver in AH by determining HMGB1 serum levels and effects on inflammatory cells from AH patients. We measured serum HMGB1 in 34 AH patients and 10 healthy controls using ELISA. Toll‐like receptor 4 (TLR4) and CD14 expressions were assessed by flow cytometry on HMGB1‐stimulated peripheral blood mononuclear cells (PBMC) and ELISA was used to measure TNF‐α and IL‐1β in the supernatants. We observed 5‐fold higher serum levels of HMGB1 in AH patients at the day of diagnosis and day 30, but no associations to clinical outcome. HMGB1 stimulation increased the expression of TLR4 on CD14+‐monocytes compared with unstimulated cells in the AH patients. The TNF‐α and IL‐1β production in response to HMGB1 was diminished in AH patients. In conclusion, AH patients have increased levels of HMGB1 in their blood. This combined with an increased TLR4 expression, but an unaffected cytokine response to HMGB1 suggest that HMGB1 is not the primary driver of inflammation in AH.