Josiane L. Broussard

Elevated ghrelin predicts food intake during experimental sleep restriction

Sleep curtailment has been linked to obesity, but underlying mechanisms remain to be elucidated. This study assessed whether sleep restriction alters 24‐h profiles of appetite‐regulating hormones ghrelin, leptin, and pancreatic polypeptide during a standardized diet and whether these hormonal alterations predict food intake during ad libitum feeding.

The changing microbial landscape of Western society: Diet, dwellings and discordance

Background The last 50–100 years has been marked by a sharp rise in so-called “Western-diseases” in those countries that have experienced major industrial advances and shifts towards urbanized living. These diseases include obesity, type 2 diabetes, inflammatory bowel diseases, and food allergies in which chronic dysregulation of metabolic and/or immune processes appear to be involved, and are likely a byproduct of new environmental influences on our ancient genome. What we now appreciate is that this genome consists of both human and co-evolved microbial genes of the trillions of microbes residing in our body. Together, host–microbe interactions may be determined by the changing diets and behaviors of the Western lifestyle, influencing the etiopathogenesis of “new-age” diseases. Scope of review This review takes an anthropological approach to the potential interplay of the host and its gut microbiome in the post-industrialization rise in chronic inflammatory and metabolic diseases. The discussion highlights both the changes in diet and the physical environment that have co-occurred with these diseases and the latest evidence demonstrating the role of host–microbe interactions in understanding biological responses to the changing environment. Major conclusions Technological advances that have led to changes in agriculture and engineering have altered our eating and living behaviors in ways never before possible in human history. These changes also have altered the bacterial communities within the human body in ways that are seemingly linked with the rise of many intestinal and systemic metabolic and inflammatory diseases. Insights into the mechanisms of this reciprocal exchange between the environment and the human gut microbiome may offer potential to attenuate the chronic health conditions that derail quality of life. This article is part of a special issue on microbiota.

Two Nights of Recovery Sleep Reverses the Effects of Short-term Sleep Restriction on Diabetes Risk

Sleep restriction is associated with insulin resistance and an increased risk for type 2 diabetes (1–3). Here, we investigated whether only 2 nights of recovery sleep, as may occur on weekends, reverses the negative effects of short-term sleep restriction on glucose homeostasis. Nineteen healthy young lean men were studied under controlled laboratory conditions during normal sleep and sleep restriction in a randomized order, as previously reported (1,2,4). The institutional review board of The University of Chicago approved the protocol, and all participants gave written informed consent. During normal sleep, participants were allowed 8.5 h in bed (2300–0700) for 4 consecutive nights. During sleep restriction, participants were allowed 4.5 h in bed (0100–0530) for 4 consecutive nights, immediately followed by recovery sleep for 2 consecutive nights with 12 h in bed on the first night (2200–1000) and 10 h in bed on the second night (2200–0800). A frequently sampled intravenous glucose tolerance test (ivGTT) was performed at 1000 after 4 nights of normal sleep, 4 nights of sleep restriction, and 2 nights …

Diagnosis, cause, and treatment approaches for delayed sleep-wake phase disorder

Delayed sleep-wake phase disorder (DSWPD) is commonly defined as an inability to fall asleep and wake at societal times resulting in excessive daytime sleepiness. Although the cause is multifaceted, delays in sleep time are largely driven by misalignment between the circadian pacemaker and the desired sleep-wake timing schedule. Current treatment approaches focus on correcting the circadian delay; however, there is a lack of data investigating combined therapies for treatment of DSWPD.

Circadian Rhythms Versus Daily Patterns in Human Physiology and Behavior

The endogenous circadian timekeeping system modulates human physiology and behavior with a near 24 h periodicity conferring adaptation to the ~24 h solar light-dark cycle. Thus, the circadian timekeeping system times physiology and behavior so that it is prepared for environmental changes. The term circadian implies an endogenous “clock-driven” process. However, not all observed daily patterns in physiology and behavior are clock driven and instead may be due to environmental or behavioral factors. For example, the barren rock on the top of a mountain shows a daily temperature oscillation that is not endogenous to the rock but instead is caused by the sun heating the rock during the day and radiative heat loss after sunset. Other factors such as wind, rain, and cloud cover impact the observed daily temperature oscillation of the rock. Similarly, some of the daily patterns observed in physiology and behavior are driven by external factors, while others arise from the interaction between circadian and behavioral processes (e.g., sleep-wake, fasting-feeding). To improve understanding of the mechanisms underlying observed daily patterns in physiology and behavior in humans, a variety of circadian protocols have been implemented (Tables 13.1 and 13.2). These protocols will be reviewed in the following pages, and the strengths and limitations of each will be discussed. First, we review markers of the endogenous clock in humans. Table 13.1 Comparison of common experimental procedures for circadian protocols Constant routine Ultrashort sleep-wake schedule Forced desynchrony Shift of sleep to daytime Ambient light Constant dim light (e.g., 1.5 lx in the angle of gaze) Alternating rapid LD cycle (e.g., 20 min, 60 min, or 90 min day) Alternating dim LD cycle (e.g., 20 h, 28 h, or 42.85 h days) Shift of LD cycle on a 24 h day Ambient temperature Constant thermoneutral Controlled yet alternating due to changes in activity and bed microclimate during sleep opportunity Controlled yet alternating due to changes in activity and bed microclimate during sleep opportunity Controlled yet alternating due to changes in activity and bed microclimate during sleep opportunity Food intake/meals Continuous IV feeding or miniature meals divided into isocaloric hourly snacks Snacks Typical BLDS Typical BLDS Posture Bed rest with head of bed raised to 35–45° Alternating ambulatory during wakefulness and supine during sleep Alternating ambulatory during wakefulness and supine during sleep Alternating ambulatory during wakefulness and supine during sleep Wakefulness-sleep Continuous wakefulness Alternating wakefulness and sleep Alternating wakefulness and sleep Alternating wakefulness and sleep Duration Day to days Days Days to weeks Days LD light-dark, BLDS breakfast, lunch, dinner, snack, IV intravenous Table 13.2 Outcomes derived from circadian protocols Constant routine Ultrashort sleep-wake schedule Forced desynchrony Shift of sleep to the daytime Circadian phase Yes, gold standard No, except for melatonin phase Not ideal, except for melatonin phase Not ideal, except for melatonin phase Circadian amplitude Yes No Yes No Circadian period No Yes Yes, gold standard No Circadian oscillations in physiology and behavior Yes Yes Yes Yes Circadian versus sleep-wake modulation of physiology and behavior and interactions No No Yes, gold standard Yes

Insulin Access to Skeletal Muscle is Preserved in Obesity Induced by Polyunsaturated Diet: Insulin Access to Muscle in Diet-Induced Obesity

Diets high in saturated fat induce obesity and insulin resistance and impair insulin access to skeletal muscle, leading to reduced insulin levels at the muscle cell surface available to bind insulin receptors and induce glucose uptake. In contrast, diets supplemented with polyunsaturated fat improve insulin sensitivity (SI) and reduce the risk for type 2 diabetes. It was hypothesized that a diet high in polyunsaturated fat would preserve SI and insulin access to muscle, as compared with a diet high in saturated fat.

Sleepy, circadian disrupted and sick: Could intestinal microbiota play an important role in shift worker health?

A sizable percentage of the population stands to benefit from importance of sufficient, consolidated sleep to maintain a diverse and elucidating mechanisms linking sleep loss, circadian misalignment, and metabolic disease. In particular, shift work is associated with increased risk for metabolic diseases, including type 2 diabetes, obesity, and metabolic syndrome [1]. These workers also report less sleep per day, and often outside of the biological night. While a reflexive instinct to these discoveries is to encourage more sleep, this may not always be practical for shift working individuals. In light of inevitable sleep loss and circadian misalignment associated with these work patterns comes a need for suitable therapeutic targets to support better long-term health outcomes. In a recent issue of Molecular Metabolism, Benedict and colleagues [2] provide the first published insights into the relationship between sleep and gut microbiota in human subjects. Their study provides a novel consideration of acute sleep restriction and the gut microbiota and opens an important discussion of future investigations of the gut microbiota in human sleep research. The last twenty years have seen a proliferation of rodent and human sleep studies investigating health consequences associated with sleep loss and circadian misalignment. However, the foundations for the more recent research investigating sleep, gut microbiota, and health can be traced to seminal work in the sleep field by Rechtschaffen and colleagues [3] who identified systemic demise in rats exposed to prolonged sleep deprivation. The possibility that this was at least in part a function of negative impacts on the community of microbes in the intestinal tract (collectively known as the intestinal microbiota) and subsequent bacterial translocation was then reflected in the work of Everson and Toth [4]. Proliferation of intestinal bacteria and movement of bacteria into what was thought to be previously sterile tissue (particularly in mesenteric lymph nodes, where bacteria correlated with those identified in intestinal overgrowth) and negative energy balance are facilitated by immune suppression in rats. More recent research has shown that sleep and circadian disruption, via clock gene mutation or weekly shifts of the light-dark cycle, can negatively impact gastrointestinal tract function and produce dysbiosis, especially when combined with alcohol induced colitis or a high-fat high-sugar diet (see [5] for review). With the increasing accessibility of high-throughput sequencing technology for quantifying microbiota, support for the