Studies show that having greater weight-for-length in infancy and obesity in childhood can lead to obesity in adolescence and adulthood. Reducing obesity risk factors may decrease one’s chance of developing obesity. This longitudinal observational study’s objective was to investigate longitudinal associations of infant nighttime sleep proportion with gut microbiome diversity and taxa abundance (n=30). Fecal samples, sleep diaries and sleep actigraphy were taken at 3 and 8 weeks, and 3, 6, 9, and 12 months during infancy. Diversity analysis was completed in Quantitative Insights Into Microbial Ecology 2 (QIIME 2.0) in conjunction with PERMANOVA tests for group comparisons. QIIME2 diversity plug-ins were used to calculate alpha diversity (Shannon index) and beta diversity (Unweighted UniFrac distance) metrics. Percent abundance values for bifidobacteria and lactobacillus were exported at the genus level for subsequent analyses. Mixed linear models (MLM) and Adonis multiple regression analyses were used to test for significant (alpha = 0.05) effects of nighttime sleep fraction on alpha and beta diversity metrics and abundance of specific microbial taxa. All statistical models accounted for individual effects (baby/subject ID), time, and a time*sleep fraction interaction. For aim 1, the regression model was: Shannon = baby + time + sleep fraction + time*sleep fraction. The overall regression was statistically significant (R2 = 0.518, F = 3.9576, p < 0.0001). Nighttime sleep proportion did not significantly predict gut microbiome richness in infants (β = 0.281, p = 0.8603). For aim 2, when adjusting for covariates in a multiple regression model, sleep fraction was insignificant. The R2= 0.005106, F= 0.810996, p=0.619). For aim 3, the fitted regression models were Bifidobacteria/Lactobacillus= baby + time + sleep fraction + time*sleep fraction. The overall regression for Bifidobacteria was statistically significant (R2 = 0.371944, F = 2.6286, p = 0.0008) but nighttime sleep proportion did not significantly predict Bifidobacteria abundance in infants (β = -54.40518, p = 0.2723). The overall regression for Lactobacillus was statistically significant (R2 = 0.236381, F = 1.8687, p = 0.0208) but sleep fraction was not associated with taxa abundance. Further research is needed to describe associations between sleep, gut microbiome, and the distal outcome of obesity.

This study aimed to investigate the association between active physical comforting strategies during bedtime and autonomy strategies with the relative abundances of Veillonella, Corynebacteria, Prevotella, and Faecalibacterium genera in the gut microbiota of three-month-old infants. We also assessed the impact of mode of delivery (vaginal delivery vs. cesarean section), feeding mode (breastfeeding vs. formula feeding), and sleep patterns on the relative abundances of prespecified bacterial genera. The study also aimed to explore how different nighttime parental interventions influenced gut microbiota composition and identify potential interventions to improve health outcomes in infant growth development and sleep.

The microorganisms that form the gut microbiome begin colonizing the gut at birth. The microorganisms will establish a symbiotic relationship with the host when in a state of eubiosis. However, when there is an imbalance or lack of diversity in the microorganisms present in the gut microbiome, it will shift to a state of dysbiosis, which increases the risk of inflammatory bowel and neurodegenerative diseases. There are known factors that affect the infant intestinal microbiome: mode of delivery, gestational age, and exposures, such as the use of antibiotics and feeding methods. Studies have shown that maternal lifestyle, particularly stress levels and diet, has an association with the infant microbiome diversity. However, there is limited literature that examines how postpartum maternal sleep influences the intestinal microbiome diversity in infants. We hypothesized that sleep efficiency below 85%, total sleep time and nocturnal sleep time below 7 hours, and later nocturnal sleep onset would be associated with decreased gut microbiome diversity within the sample and between samples. 27 Mother-infant pairings were used for this sub-analysis. Postpartum maternal sleep data was obtained via actigraphs and sleep diaries while infant intestinal microbiome data was obtained through fecal samples swabbed from soiled diapers. Actigraphs recorded time, movement, temperature, and light for five 24-hour periods, and sleep diaries were used to supplement the actigraphy and ease the scoring of sleep. DNA samples were extracted and sequenced using next-generation sequences, and QIIME2 was used to analyze these sequences. Alpha- and beta-diversity results following sequencing revealed good postpartum maternal sleep efficiency is associated with increased infant gut microbiome diversity within and between samples. There was a trend for nocturnal sleep onset being associated with beta-diversity measurements which were driven by phylogenetic differences and abundance of bacteria. Nocturnal total sleep time and 24-hour total sleep time were not associated with alpha- and beta-diversity. Our findings as well as the scarcity of the literature illustrate the need for further investigations on the mechanics of maternal sleep efficiency association with infant gut microbiome. Future research is needed to further evaluate the trending nocturnal sleep onset influences on the infant gut microbiome beta-diversity with a larger and more diverse sample.

The relationship between sleep and physical activity is an area of growing scientific interest, particularly in the context of older adults. The importance of examining long sleep duration and its influence on physical activity in this demographic becomes increasingly relevant given rising healthcare costs. This dissertation aims to investigate this intricate relationship via secondary analysis by examining the effects of moderate time-in-bed (TIB) restriction (60 minutes per night)) on various intensities of physical activity (sedentary, light, moderate, vigorous, moderate-vigorous physical activity) in older adults classified as long sleepers and average duration sleepers. It was hypothesized that moderate TIB restriction would result in differential changes in physical activity levels across various intensities, with long sleepers exhibiting increased physical activity and average sleepers displaying decreased activity, potentially influenced by alterations in TST (total sleep time) and SE (sleep efficiency). Utilizing a randomized controlled trial design, this study examined the effect of treatment changes in objectively measures activity (waist actigraphy) and subjects physical activity levels as measured by the Godin Leisure-Time Exercise Questionnaire . Eligible participants were long sleepers (sleeping > 9 hours per night) and average sleepers (sleeping 7-9 hours per night). Both types of sleepers were either randomized to TIB restriction or asked to maintain their average sleep patterns. Mean TIB restriction compared with baseline was 39.5 minutes in average sleepers and 52.9 minutes in long sleepers randomized to TIB restriction . Contrary to the original hypothesis, no significant effect of TIB restriction was observed across all physical activity levels in either long sleepers or average sleepers. However, a notable association was found between increased sleep efficiency (+0.09% [SD = ± 4.64%]) and light physical activity (±31 minutes [SD = ± 104.81, R=0.445, P < 0.007]) in long sleepers undergoing TIB restriction. While this study presents several methodological limitations, including its nature as a secondary analysis and the less-than-intended achievement of TIB restriction, it adds a valuable layer to the existing body of research on sleep and physical activity in older adults. The findings suggest that moderate TIB restriction may not be sufficiently impactful to change behavior in physical activity levels, thus highlighting the need for more nuanced, targeted research in this domain.

Food insecurity affects more than 10 million households in the United States and has been shown to impact what and how a child is fed. Additionally, there is some evidence to suggest that food insecurity may affect how an infant is soothed (either with food or another mechanism), but no study has examined the possible relationship between soothing techniques and the incidence of food insecurity. To evaluate whether food security status and nighttime soothing techniques have a relationship, surveys were administered to a sample of mothers from various racial and socioeconomic backgrounds at 3-weeks, 8-weeks, and 3-months postpartum. Of the 69 participants sampled, 61 had data that could contribute to evaluations of food security status and soothing techniques used at night. A chi-square model was utilized to determine what, if any, relationship existed between the two variables. The chi-square model did not yield statistically significant results (Pearson Chi-Square= .506, p=.477) and descriptive statistics showed that just six of the 61 participants sampled did not use food to soothe at the time their baby was 3-weeks-old. Further examination of descriptive statistics revealed that, between breastfeeding and bottle-feeding as a means to soothe an infant, breastfeeding was used twice as much as bottle-feeding. For participants enrolled in the Special Supplemental Nutrition Program for Women, Infants, Children (WIC), the use of food to soothe increased at each of the three time points. Among participants found to be food-insecure, the use of breastfeeding and bottle-feeding as means to soothe varied from time point to time point. The physical and mental toll of the postpartum period may contribute to the high use of food-to-soothe among mothers seen in this study. Future research efforts in this area should examine whether the observations reported in this study are similar among larger samples, and if more mental health support for mothers has any effect on whether food is used to soothe.

How early life is experienced and perceived can greatly affect mental and physical health outcomes. An individual is greatly influenced by their first models of what social relationships look and feel like, and with time also learn how to survive when less favorable social experiences occur. The lessons learned may lead to healthy problem solving and resilience, or it may lead to unhealthy problem-solving habits that hinder well-being. Anxious thoughts and other mental health symptoms may accompany an individual long-term and hinder an essential need for a healthy life. The first main purpose of this thesis is to examine the impact of Adverse Childhood Experiences (ACEs) on mental health (anxiety symptoms), and on sleep quality (an essential need). The second purpose of my thesis is to investigate the impact of genetics on resilience, specifically, the mu-opioid receptor gene. The first hypothesis proposed ACEs that were perceived as more traumatic and occurred more frequently would be associated with more poor sleep quality symptoms. The second hypothesis predicted that anxiety symptoms would mediate the association. The third hypothesis (exploratory) suggested that an individual’s alleles for the mu-opioid receptor gene would moderate the mediation pathway. The study was conducted with 318 participants between the ages of 18 and 35 years old. The study demonstrated a direct effect for ACEs and sleep. Anxiety mediated the association between ACEs (exposure and severity) and sleep (insomnia, quality, sleepiness), suggesting that ACEs possibly increase feelings of anxiety which, in turn, lead to worse sleep outcomes. Finally, the moderated-mediation model with OPRM1 as the moderator, was not significant for the mediation pathway A; however, there was a significant interaction with anxiety and sleep symptoms.

Sleep paralysis is when a person finds themselves in a state of conscious paralysis as they are falling asleep or waking up. It is often accompanied by shallowing breathing, visual and auditory hallucinations, and a sense of terror. Sleep paralysis has a rich folklore consisting of sleep demons, spirits, and curses some of which are still told to children today. This thesis will explore a timeline of this folklore that involves modern day sleep paralysis, a history of sleep science, and how they collided resulting in the official diagnosis of sleep paralysis as a sleep disorder.

Older adults tend to learn at a lesser extent and slower rate than younger individuals. This is especially problematic for older adults at risk to injury or neurological disease who require therapy to learn and relearn motor skills. There is evidence that the reticulospinal system is critical to motor learning and that deficits in the reticulospinal system may be responsible, at least in part, for learning deficits in older adults. Specifically, delays in the reticulospinal system (measured via the startle reflex) are related to poor motor learning and retention in older adults. However, the mechanism underlying these delays in the reticulospinal system is currently unknown.

Along with aging, sleep deprivation is correlated with learning deficits. Research has shown that a lack of sleep negatively impacts motor skill learning and consolidation. Since there is a link between sleep and learning, as well as learning and the reticulospinal system, these observations raise the question: does sleep deprivation underlie reticulospinal delays? We hypothesized that sleep deprivation was correlated to a slower startle response, indicating a delayed reticulospinal system. Our objectives were to observe the impact of sleep deprivation on 1) the startle response (characterized by muscle onset latency and percentage of startle responses elicited) and 2) functional performance (to determine whether subjects were sufficiently sleep deprived).

21 young adults participated in two experimental sessions: one control session (8-10 hour time in bed opportunity for at least 3 nights prior) and one sleep deprivation session (0 hour time in bed opportunity for one night prior). The same protocol was conducted during each session. First, subjects were randomly exposed to 15 loud, startling acoustic stimuli of 120 dB. Electromyography (EMG) data measured muscle activity from the left and right sternocleidomastoid (LSCM and RSCM), biceps brachii, and triceps brachii. To assess functional performance, cognitive, balance, and motor tests were also administered. The EMG data were analyzed in MATLAB. A generalized linear mixed model was performed on LSCM and RSCM onset latencies. Paired t-tests were performed on the percentage of startle responses elicited and functional performance metrics. A p-value of less than 0.05 indicated significance.

Thirteen out of 21 participants displayed at least one startle response during their control and sleep deprived sessions and were further analyzed. No differences were found in onset latency (RSCM: control = 75.87 ± 21.94ms, sleep deprived = 82.06 ± 27.47ms; LSCM: control = 79.53 ± 17.85ms, sleep deprived = 78.48 ± 20.75ms) and percentage of startle responses elicited (control = 84.10 ± 15.53%; sleep deprived = 83.59 ± 18.58%) between the two sessions. However, significant differences were observed in reaction time, TUG with Dual time, and average balance time with the right leg up. Our data did not support our hypothesis; no significant differences were seen between subjects’ startle responses during the control and sleep deprived sessions. However, sleep deprivation was indicated with declines were observed in functional performance. Therefore, we concluded that sleep deprivation may not affect the startle response and underlie delays in the reticulospinal system.