Impact of sleep debt on metabolic and endocrine function

ABSTRACT‘How much sleep does one need?’ is a critical question that has been difficult to answer. The long history of sleep research has culminated in population‐derived normative values of 7 to 9 h of sleep per night to avoid dysfunction. Such a wide range is sufficiently large that one cannot know what is required for any given individual. ‘Sleep need’ cannot currently be directly measured, might not be represented by one number (given the multiple functions that sleep subserves), and likely varies from individual‐to‐individual and from day‐to‐day. This said, the concept should be embraced and can be considered alongside more easily operationalised and routinely measured constructs of ‘sleep opportunity’ (e.g., time in bed) and ‘sleep ability’ (i.e., the obtained sleep, such as sleep duration). Considering the dynamics of all three constructs together may drive greater understanding about sleep health, sleep insufficiency, and sleep disorder pathology. In this article, we describe a new theory called Sleep Opportunity, Need, and Ability and provide a rationale for why this theory has both theoretical and clinical value.

Mild and moderate traumatic brain injuries (TBIs) (and concussion) occur frequently as a result of falls, automobile accidents, and sporting activities, and are a major cause of acute and chronic disability. Fatigue and excessive sleepiness are associated with increased risk of accidents, but it is unknown whether prior sleep debt also affects the pathophysiological outcome of concussive injury. Using the “dark neuron” (DN) as a marker of reversible neuronal damage, we tested the hypothesis that acute (48 hours) total sleep deprivation (TSD) and chronic sleep restriction (CSR; 10 days, 6-hour sleep/day) affect DN formation following mild TBI in the rat. TSD and CSR were administered using a walking wheel apparatus. Mild TBI was administered under anesthesia using a weight-drop impact model, and the acute neuronal response was observed without recovery. DNs were detected using standard bright-field microscopy with toluidine blue stain following appropriate tissue fixation. DN density was low under home cage and sleep deprivation control conditions (respective median DN densities, 0.14% and 0.22% of neurons), and this was unaffected by TSD alone (0.1%). Mild TBI caused significantly higher DN densities (0.76%), and this was unchanged by preexisting acute or chronic sleep debt (TSD, 0.23%; CSR, 0.7%). Thus, although sleep debt may be predicted to increase the incidence of concussive injury, the present data suggest that sleep debt does not exacerbate the resulting neuronal damage.

Short sleep duration is a risk factor of chronic kidney disease, along with cardiovascular diseases and all-cause mortality. Several studies reported that many people sleep longer on weekends than on weekdays, suggesting that they should be compensated for their sleep debt on weekdays on the weekends. Few studies have reported the clinical impact of sleep debt on the kidney. This cross-sectional study included 5799 employees of Osaka University who visited its Health Care Center for their annual health examinations and answered ≤ 6h of sleep duration on weekdays. The independent variable was the sleep debt index defined as a gap in self-reported sleep duration (≤ 5, 5-6, 6-7, 7-8, 8-9, and ≥ 9h) between weekdays and weekends, which was categorized into ≤ 0, + 1, + 2, + 3 and ≥+4. An association between the sleep debt index and a prevalence of proteinuria defined as dipstick proteinuria of ≥ 1 + was assessed using logistic regression models adjusting for clinically relevant factors. More than four-fifths of the subjects had a positive sleep debt index (≤ 0, + 1, + 2, + 3, and ≥+4 recorded for 19%, 36%, 28%, 11%, and 6%, respectively). The multivariable-adjusted logistic regression models showed the sleep debt index ≥ 3 + was significantly associated with the prevalence of proteinuria (sleep debt index ≤ 0, adjusted odds ratio 1.13 [0.77, 1.65]; + 1, 1.00 [reference]; + 2, 1.29 [0.93, 1.79]; + 3, 1.54 [1.02, 2.33]; ≥ + 4, 1.87 [1.15, 3.05]). Sleep debt was associated with the prevalence of proteinuria in a dose-dependent manner.

Associations between sleep duration and sleep debt with insulin sensitivity and insulin secretion in the EGIR-RISC Study

Reduced time in bed relative to biological sleep need is common. The impact of habitual short sleep on auditory attention has not been studied to date. In the current study, we utilized novelty oddball tasks to evaluate the effect of habitual short sleep on brain function underlying attention control processes measured by the mismatch negativity (MMN, index of pre-attentive stage), P3a (attention-dependent), and P3b (memory-dependent) event related brain potentials (ERPs). An extended time in bed in a separate study was used to evaluate the possible reversal of the impairments of these processes in habitual short sleepers. Ten self-defined short sleepers (total sleep time [TST] ≤ 6 h) and 9 normal-sleeping subjects with TST 7-8 h, participated. ERPs were recorded via a 64-channel EEG system. Two test conditions: "ignore" and "attend" were implemented. The ERPs were analyzed and compared between groups on the 2 task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data were compared between groups by t-test. Sleep was recorded by the Zeo sleep monitoring system for a week in both habitual and extended sleep conditions at home. The main findings of the present study show that short sleeping individuals had deficiency in activity of the MMN and P3a brain responses over frontal areas compared to normal-sleeping subjects. The P3b amplitude was increased over frontal areas and decreased over parietal with respect to the control group. Extension of time in bed for one week increased TST (from 5.7 h to 7.4 h), and concomitantly MMN amplitude increased from -0.1 μV up to -1.25 μV over frontal areas. Reduced time in bed is associated with deficiency of the neuronal process associated with change detection, which may recover after one week of sleep extension, whereas attention-dependent neural processes do not normalize after this period of time in habitually short sleeping individuals and may require longer recovery periods.

Obesity has increased rapidly among children and adolescents during the last 30 years. Paediatric patients with a BMI above the 85th centile are more often diagnosed with increased TSH levels than are children with proper body weight. The data of 961 overweight and obese children, aged 13 years, recruited in four cities in Poland as part of PoZdro!, a two-year prophylactic program, were analysed to observe the relationship between serum TSH and fT4 concentration and carbohydrate and lipid metabolism parameters, as well as anthropometric parameters. TSH concentration in the study group was positively correlated, whereas fT4 concentration was negatively correlated with WHR and WHtR values, fasting serum glucose concentrations and one-hour glucose concentration, fasting serum insulin concentrations, one-hour and two-hour insulin concentration, ALT serum activity, as well as total cholesterol, LDL cholesterol, and triglyceride serum concentrations. An increased risk of metabolic syndrome was diagnosed previously in patients with TSH concentrations > 2.5 mUI/L. TSH concentration in the upper half of the current reference range (> 2.50 mIU/L) is associated with an increased risk of lipid and carbohydrate metabolism disorders and therefore increased chances of developing metabolic syndrome. It seems advisable to regularly monitor thyroid function in overweight and obese paediatric patients.

The aim of this study was to examine the effect of total parenteral nutrition (TPN) on the endocrine and exocine function of the pancreas. Endocrine function was investigated using an intravenous glucose tolerance test (IGTT) in rats with TPN for 7 or 14 days. Exocrine function was evaluated by measuring amylase secretion from isolated acini as well as pancreatic weight, water content, protein, and enzymes after 7 days of TPN. When the TPN rats were compared with the controls, the glucose tolerance curve after an IGTT was unchanged, the basal plasma insulin levels were slightly lower and the insulin secretory response to intravenous glucose was markedly impaired. No differences could be seen between the insulin response after 7 days and that after 14 days of TPN. The weight of pancreas, the total content and concentration of pancreatic protein, and the total amylase content of the pancreas were lower, whereas the total content of both chymotrypsin and trypsin was higher. The concentration of DNA remained intact, whereas the total DNA content decreased. The levels of lipolytic enzymes, except for carboxylesterlipase, were unaffected. After TPN treatment, the insulin secretory response to glucose is impaired, the exocrine pancreas is hypoplastic and the storage pattern of pancreatic exocrine enzymes is altered.

Central neuropeptide Y infusion and melanocortin 4 receptor antagonism inhibit thyrotropic function by divergent pathways

BackgroundThere is growing evidence that patients with Essential Tremor (ET) are at higher risk for Mild Cognitive Impairment (MCI) and dementia than controls. ET is a quite heterogeneous disorder, including not only motor symptoms, but sleep deficits as some of its non‐motor characteristics. The aim of the current research was to investigate the extent to which sleep problems predict cognitive change over time in patients with ET.MethodTwo hundred and one patients enrolled in a longitudinal, observational study of cognitive function in ET (COGNET) were included in the current analyses. Sleep was examined used the Pittsburg Sleep Quality Index (PSQI). Five cognitive domains were extracted from an extensive neuropsychological assessment: memory, executive function, attention, language, and visuo‐spatial ability. Generalized estimated equations were used to examine the association between sleep problems at baseline and cognitive changes over four‐intervals follow‐up spanning of 4 years.ResultOur sample was mostly women (60%), with 78 mean years of age, and 16 mean education years. Habitual sleep efficiency (dividing the amount of time spent asleep divided by the total amount of time in bed) was significantly associated with attention performance longitudinally, so that poorer efficiency was associated with more rapid decline in attentional abilities over the years. No other sleep problem was associated with change in any cognitive domain.ConclusionPeople with ET have increased chance for decline in attentional abilities when having sleep problems and more specifically, less habitual sleep efficiency. Early detection of, and intervention for, difficulty with sleep efficiency may protect against aspects of cognitive decline in people with ET.

Associations of testosterone and cortisol concentrations with sleep quality in Japanese male workers

While daytime napping could support recovery in athletes, poorly timed or prolonged naps may interfere with nighttime sleep. Therefore, this study aimed to explore the effect of two different, well-timed nap opportunity durations, 25 and 90 min, on subsequent objectively measured nighttime sleep in student athletes. Fourteen student athletes (7 females, 7 males; age: 23 ± 2 years) completed three in-lab conditions using a randomised, counterbalanced, crossover design: no nap (NN), a 25-min nap opportunity (N25, 14:35-15:00) and a 90-min nap opportunity (N90, 13:30-15:00). Nighttime sleep following each condition was assessed at home via wrist actigraphy measuring bedtime, wake time, total sleep time, time in bed, wake after sleep onset (WASO) and sleep stages. Neither N25 nor N90 opportunity negatively affected the following night's sleep compared to the NN condition, including bedtime, wake time, WASO, total sleep time, light sleep, deep sleep and rapid eye movement (REM) sleep (p > 0.05 for all). Mean total sleep time was 7 h 13 min after NN, 7 h 5 min after N25 and 7 h 1 min after N90. In student athletes, afternoon nap opportunities of either 25 or 90 min, when ending at 15:00, did not disrupt subsequent nighttime sleep. These findings suggest that a strategically timed early afternoon nap may be a viable recovery option for this population. While individual differences in sleep need and academic demands should be considered, these results highlight the potential of well-timed naps to support athlete recovery. Future research is needed to determine whether these effects generalise to other populations or nap timings.

To examine the sleep habits of 3-year-old children, we questioned guardians during a routine health examination for 3-year-old children at a public health center. According to the 1105 questionnaires analyzed, the proportion of children who fell asleep at 10 p.m. or later was 49.6%. The nocturnal sleep onset time was significantly correlated with the wake-up time in the morning and was significantly negatively correlated with the nocturnal sleep duration. The average daily total sleep duration (nocturnal sleep duration + nap duration) of regular nap-takers showed a significant negative correlation with the nocturnal sleep onset time. The average values for height, weight, and body mass index (BMI) were not correlated with the nocturnal sleep onset time. Children who went to sleep later got less sleep than those who went to sleep earlier. Because sleep debt has a harmful impact on older children and adults, late sleep onset may have adverse health consequences in young children.

Clinical study on acute pancreatitis associated with pancreatectomy in 10 cases

AimDiabetes is associated with altered endogenous hydrogen sulfide levels, which plays an important role in regulating glucose homeostasis. Here we report on the long‐term effects of sodium hydrosulfide (NaSH) administration on carbohydrate metabolism in obese type 2 diabetic rats.MethodType‐2 diabetes was established using high fat‐low dose streptozotocin. Rats were treated for 9 weeks with intraperitoneal injections of NaSH (0.28, 0.56, 1.6, 2.8, and 5.6 mg/kg) or vehicle. Serum fasting glucose was measured weekly for one month and then at the end of the study. Fasting serum insulin was measured before and after the treatment. At the end of the study, glucose tolerance, pyruvate tolerance, and insulin secretion were determined and blood pressure was measured.ResultsIn diabetic rats, NaSH at 1.6–5.6 mg/kg increased serum glucose and decreased serum insulin; NaSH at 0.28 and 0.56 mg/kg had no effect on these parameters. High doses of NaSH in diabetic rats decreased glucose and pyruvate tolerance as well as insulin secretion; 0.28 mg/kg had no effect, 0.56 mg/kg improved glucose tolerance but not pyruvate tolerance and insulin secretion. Diabetic rats had higher BP than controls; all doses of NaSH decreased blood pressure in these cohorts. In controls, NaSH (5.6 mg/kg) decreased insulin secretion as well as glucose and pyruvate tolerance, while increased serum glucose. NaSH at 1.6–5.6 mg/kg decreased blood pressure in controls.ConclusionIn diabetic rats high doses of NaSH increased serum glucose level, decreased serum insulin and impaired glucose and pyruvate tolerance, a low dose decreased serum glucose during glucose tolerance. NaSH decreased blood pressure at all doses.Support or Funding InformationKK: Supported in part by the National Institutes of Health [R24DA018055; R01GM123508]. SG, SJ, AG: Supported in part by Shahid Beheshti University of Medical Sciences[grant No. 1396/D/93065], Tehran, Iran.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Excerpt The old dictum that every diabetic has a high prolonged glucose tolerance curve, but that every high prolonged curve is not indicative of diabetes, still holds true. The lack of specificity...