Insomnia Abstracts 7




Association between insomnia symptoms and hemoglobin A1c level in Japanese men
            (Kachi et al., 2011) Download
BACKGROUND: The evidence for an association between insomnia symptoms and blood hemoglobin A(1c) (HbA(1c)) level has been limited and inconclusive. The aim of this study was to assess whether each symptom of initial, middle, and terminal insomnia influences HbA(1c) level in Japanese men. METHODS: This cross-sectional study examined 1,022 male workers aged 22-69 years with no history of diabetes at a Japanese company's annual health check-up in April 2010. High HbA(1c) was defined as a blood level of HbA(1c) >/=6.0%. Three types of insomnia symptoms (i.e., difficulty in initiating sleep, difficulty in maintaining sleep, and early morning awakening) from the previous month were assessed by 3 responses (i.e., lasting more than 2 weeks, sometimes, and seldom or never [reference group]). RESULTS: The overall prevalence of high HbA(1c) was 5.2%. High HbA(1c) was positively and linearly associated with both difficulty in maintaining sleep (P for trend = .002) and early morning awakening (P for trend = .007). More specifically, after adjusting for potential confounding factors, high HbA(1c) was significantly associated with difficulty in maintaining sleep lasting more than 2 weeks (adjusted odds ratio, 6.79 [95% confidence interval, 1.86-24.85]) or sometimes (2.33 [1.19-4.55]). High HbA(1c) was also significantly associated with early morning awakening lasting more than 2 weeks (3.96 [1.24-12.59]). CONCLUSION: Insomnia symptoms, particularly difficulty in maintaining sleep and early morning awakening, were found to have a close association with high HbA(1c) in a dose-response relationship.

Impaired glucose tolerance in sleep disorders.
            (Keckeis et al., 2010) Download
BACKGROUND:  Recent epidemiological and experimental data suggest a negative influence of shortened or disturbed night sleep on glucose tolerance. Due to the high prevalence of sleep disorders this might be a major health issue. However, no comparative studies of carbohydrate metabolism have been conducted in clinical sleep disorders. METHODOLOGY/PRINCIPAL FINDINGS:  We performed oral glucose tolerance tests (OGTT) and assessed additional parameters of carbohydrate metabolism in patients suffering from obstructive sleep apnea syndrome (OSAS, N = 25), restless legs syndrome (RLS, N = 18) or primary insomnia (N = 21), and in healthy controls (N = 33). Compared to controls, increased rates of impaired glucose tolerance were found in OSAS (OR: 4.9) and RLS (OR: 4.7) patients, but not in primary insomnia patients (OR: 1.6). In addition, HbA1c values were significantly increased in the same two patient groups. Significant positive correlations were found between 2-h plasma glucose values measured during the OGTT and the apnea-arousal-index in OSAS (r = 0.56; p<0.05) and the periodic leg movement-arousal-index in RLS (r = 0.56, p<0.05), respectively. Sleep duration and other quantitative aspects of sleep were similar between patient groups. CONCLUSIONS/SIGNIFICANCE:  Our findings suggest that some, but not all sleep disorders considerably compromise glucose metabolism. Repeated arousals during sleep might be a pivotal causative factor deserving further experimental investigations to reveal potential novel targets for the prevention of metabolic diseases.

Neuroendocrine regulation and metabolism of glucose and lipids in primary chronic insomnia: a prospective case-control study
            (Seelig et al., 2013) Download
OBJECTIVES: To investigate the relation between primary chronic insomnia and insulin sensitivity, visceral adiposity, non alcoholic fatty liver disease and neuroendocrine hormones. MATERIALS AND METHODS: In a case-controlled, prospective clinical trial 13 women with primary chronic insomnia according to DSM-IV criteria were compared to 12 healthy controls matched for age, sex, BMI, body composition and menopausal status. All participants had a sleep assessment including polysomnographic studies and neuropsychiatric evaluation. Insulin sensitivity was evaluated using the euglycaemic hyperinsulinemic clamp. Hepatic fat content, visceral adipose tissue and intramyocellular lipid accumulation were assessed using magnetic resonance imaging and spectroscopy. The hormonal stress axis was evaluated by measurements of midnight and early morning salivary cortisol, urinary catecholamines and plasma metanephrines. Body composition was determined using body impedance analysis and indirect calorimetry. RESULTS: Although the diagnosis of primary chronic insomnia was made by established clinical criteria, standard polysomongraphic studies failed to identify altered sleep continuity and architecture when compared to matched controls. However, women with primary chronic insomnia showed significantly higher midnight salivary cortisol concentrations (1.46 vs. 0.76 nmol/l, p = 0.02), indicating dysregulation of the hypothalamo-pituitary-adrenal (HPA) axis. Plasma glucose and lipid concentrations, insulin sensitivity, hepatic and intramyocellular fat content, visceral adipose tissue mass and body composition did not differ between the two groups. CONCLUSION: Healthy women with clinically diagnosed primary chronic insomnia demonstrate a dysregulation of circadian cortisol secretion despite normal sleep continuity and architecture. Increased midnight cortisol levels, however, were not associated with impaired metabolism of glucose and lipids.

Differences in insulin secretion and sensitivity in short-sleep insomnia
            (Vasisht et al., 2013) Download
OBJECTIVE: Short-sleep insomnia is associated with increased risk of diabetes. The role of altered insulin secretion and action in this association is poorly understood. DESIGN: Observational study. SETTING: Academic clinical research center. PARTICIPANTS: Nondiabetic individuals with insomnia (mean [standard deviation] age 48 [9] y, body mass index 25.6 [3.9] kg/m(2)) with </= 6 h (short sleep, n = 14) and > 6 h of sleep (n = 14) during overnight laboratory polysomnography. MEASUREMENTS AND RESULTS: Standard oral glucose testing was used to assess glucose tolerance, beta-cell function (homeostasis model assessment [HOMA-B]; second-phase insulin secretion) and insulin resistance (HOMA-IR; insulin sensitivity index). There was no significant difference in hemoglobin A1C and fasting or 2-h blood glucose concentrations between sleep groups. Short-sleep insomnia sufferers had lower fasting and postchallenge serum insulin concentrations associated with lower estimates of fasting and glucose-stimulated insulin secretion, and increased insulin sensitivity. CONCLUSIONS: Individuals with short-sleep insomnia appear to have higher indices of systemic insulin sensitivity and secrete less insulin without changes in overall glucose tolerance.

Insomnia with objective short sleep duration is associated with type 2 diabetes: A population-based study
            (Vgontzas et al., 2009) Download
OBJECTIVE: We examined the joint effects of insomnia and objective short sleep duration, the combination of which is associated with higher morbidity, on diabetes risk. RESEARCH DESIGN AND METHODS: A total of 1,741 men and women randomly selected from Central Pennsylvania were studied in the sleep laboratory. Insomnia was defined by a complaint of insomnia with duration of >or=1 year, whereas poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, or early final awakening. Polysomnographic sleep duration was classified into three categories: >or=6 h of sleep (top 50% of the sample); 5-6 h (approximately third quartile of the sample); and <or=5 h (approximately the bottom quartile of the sample). Diabetes was defined either based on a fasting blood glucose >126 mg/dl or use of medication. In the logistic regression model, we simultaneously adjusted for age, race, sex, BMI, smoking, alcohol use, depression, sleep-disordered breathing, and periodic limb movement. RESULTS: Chronic insomnia but not poor sleep was associated with a higher risk for diabetes. Compared with the normal sleeping and >or=6 h sleep duration group, the highest risk of diabetes was in individuals with insomnia and <or=5 h sleep duration group (odds ratio [95% CI] 2.95 [1.2-7.0]) and in insomniacs who slept 5-6 h (2.07 [0.68-6.4]). CONCLUSIONS: Insomnia with short sleep duration is associated with increased odds of diabetes. Objective sleep duration may predict cardiometabolic morbidity of chronic insomnia, the medical impact of which has been underestimated.

Insomnia increases insulin resistance and insulin secretion in elderly people
            (Yamamoto et al., 2010) Download
To the Editor: Elderly people with insomnia showed high insulin resistance and high insulin secretion after an oral glucose tolerance test (OGTT). Decreased insulin secretion is not a cause of diabets but rather a consequence of insulin resistance in elderly people with insomnia. In August 2006 and 2007 at the healthcare center of Tosa Town, 402 subjects aged 75 and older were recruited. The main finding of this study was that insomnia was associated with high insulin resistance and high insulin secretion.



Child's Sleep-Effect of Certain Foods and Beverages on Sleep Motility.
            (Giddings, 1934) Download
We have attempted a study of a very homely problem. What is the effect of various foods and beverages on sleep? We have used 42 children. The drinking of 6 oz. of warm milk at bedtime seems to produce quiet sleep in normal children. The eating of a heavy evening meal produces marked restlessness. The eating of a very light evening meal differs in no respect from the sleep seen after a child has eaten its normal supper.

Direct and indirect cellular effects of aspartame on the brain.
            (Humphries et al., 2008) Download
The use of the artificial sweetener, aspartame, has long been contemplated and studied by various researchers, and people are concerned about its negative effects. Aspartame is composed of phenylalanine (50%), aspartic acid (40%) and methanol (10%). Phenylalanine plays an important role in neurotransmitter regulation, whereas aspartic acid is also thought to play a role as an excitatory neurotransmitter in the central nervous system. Glutamate, asparagines and glutamine are formed from their precursor, aspartic acid. Methanol, which forms 10% of the broken down product, is converted in the body to formate, which can either be excreted or can give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives. Previously, it has been reported that consumption of aspartame could cause neurological and behavioural disturbances in sensitive individuals. Headaches, insomnia and seizures are also some of the neurological effects that have been encountered, and these may be accredited to changes in regional brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine. The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders (DSM-IV-TR 2000) and also in compromised learning and emotional functioning.

Milk intolerance in children with persistent sleeplessness: a prospective double-blind crossover evaluation.
            (Kahn et al., 1989)  Download
From July 1986 to July 1988, 146 children less than 5 years of age were referred by their physicians to our university sleep clinic for continual waking and crying during sleep hours. For 85 children (58.2%), the sleeplessness was attributed to inappropriate sleep habits. For 17 children (11.6%), no explanation was found for the sleep difficulties in spite of an extensive workup. Their median age at referral was 13.5 months (range 2.5 to 29 months). Their persistent sleeplessness was tentatively attributed to an undiagnosed intolerance to cow's milk. Cow's milk was excluded from their diet. In 15 children sleep normalized after 5 weeks (range 4 to 6 weeks). As seen from the parents' logs, the median time needed by the children to fall asleep decreased from 15 minutes (range 15 to 60 minutes) to 10 minutes (range 10 to 15 minutes, P = .001). The number of complete arousals decreased from 5 (range 1 to 12) to less than 1 per night (range 0 to 2) (P = .001). Total sleep time per 24 hours increased from 5.5 hours (range 3 to 8.5 hours) to 13.0 hours (range 10 to 14.5 hours, P = .001). Sleep normalized in one child who continued to receive no cow's milk only after the hydrolyzed hypoallergenic diet was discontinued. In every child, a double-blind crossover challenge was conducted involving a control diet containing no cow's milk and a diet containing cow's milk. The challenge induced the reappearance of insomnia and agitated behavior in all except one child. The child's initial sleep difficulties were retrospectively attributed to inappropriate sleep habits.(ABSTRACT TRUNCATED AT 250 WORDS)

Fiber and Saturated Fat Are Associated with Sleep Arousals and Slow Wave Sleep.
            (St-Onge et al., 2016) Download
STUDY OBJECTIVES:  Sleep restriction alters food intake, but less is known about how dietary patterns affect sleep. Current goals were to determine whether: (1) sleep is different after consumption of a controlled diet vs. an ad libitum diet, and (2) dietary intake during ad libitum feeding is related to nocturnal sleep. METHODS:  Twenty-six normal weight adults (30-45 y), habitually sleeping 7-9 h/night, participated in a randomized-crossover inpatient study with 2 phases of 5 nights: short (4 h in bed) or habitual (9 h in bed) sleep. Only data from the habitual sleep phase were used for the present analyses. During the first 4 days, participants consumed a controlled diet; on day 5, food intake was self-selected. Linear regression was used to determine relations between daytime food intake and nighttime sleep on day 5. RESULTS:  Sleep duration did not differ after 3 days of controlled feeding vs. a day of ad libitum intake. However, sleep after ad libitum eating had less slow wave sleep (SWS, P = 0.0430) and longer onset latency (P = 0.0085). Greater fiber intake predicted less stage 1 (P = 0.0198) and more SWS (P = 0.0286). Percent of energy from saturated fat predicted less SWS (P = 0.0422). Higher percent of energy from sugar and other carbohydrates not considered sugar or fiber was associated with arousals (P = 0.0320 and 0.0481, respectively). CONCLUSIONS:  Low fiber and high saturated fat and sugar intake is associated with lighter, less restorative sleep with more arousals. Diet could be useful in the management of sleep disorders but this needs to be tested. CLINICAL TRIAL REGISTRATION:, #NCT00935402.

Effect of Six-Month Diet Intervention on Sleep among Overweight and Obese Men with Chronic Insomnia Symptoms: A Randomized Controlled Trial.
            (Tan et al., 2016) Download
Growing evidence suggests that diet alteration affects sleep, but this has not yet been studied in adults with insomnia symptoms. We aimed to determine the effect of a six-month diet intervention on sleep among overweight and obese (Body mass index, BMI ≥ 25 kg/m²) men with chronic insomnia symptoms. Forty-nine men aged 30-65 years with chronic insomnia symptoms were randomized into diet (n = 28) or control (n = 21) groups. The diet group underwent a six-month individualized diet intervention with three face-to-face counseling sessions and online supervision 1-3 times per week; 300-500 kcal/day less energy intake and optimized nutrient composition were recommended. Controls were instructed to maintain their habitual lifestyle. Sleep parameters were determined by piezoelectric bed sensors, a sleep diary, and a Basic Nordic sleep questionnaire. Compared to the controls, the diet group had shorter objective sleep onset latency after intervention. Within the diet group, prolonged objective total sleep time, improved objective sleep efficiency, lower depression score, less subjective nocturnal awakenings, and nocturia were found after intervention. In conclusion, modest energy restriction and optimized nutrient composition shorten sleep onset latency in overweight and obese men with insomnia symptoms.

Dietary Patterns and Insomnia Symptoms in Chinese Adults: The China Kadoorie Biobank.
            (Yu et al., 2017) Download
Limited attention has been paid to the effect of dietary patterns on sleep problems. In the present study, we analyzed the cross-sectional data of 481,242 adults aged 30-79 years from the China Kadoorie Biobank. A laptop-based questionnaire was administered to collect information on food intakes and insomnia symptoms. Logistic regression was used to estimate the odds ratios of each insomnia symptom according to quartiles of each dietary pattern, with adjustment for potential confounders. Two major dietary patterns were derived by factor analysis. The traditional northern dietary pattern was characterized by high intakes of wheat and other staple food, whereas the modern dietary pattern was characterized by high intakes of meat, poultry, fish, eggs, fresh fruit, and dairy products. Both dietary patterns were associated with a decreased prevalence of insomnia symptoms (p for trend < 0.001); after adjustment for potential confounders, individuals who had the highest quartile score of traditional northern dietary pattern were 12%-19% less likely to have insomnia symptoms compared to those in the lowest quartile (odds ratio: 0.81-0.88), and the corresponding values for the modern dietary pattern were 0.89-1.01. Furthermore, interactions of these two dietary patterns on insomnia symptoms were observed. Further prospective studies are needed to elucidate the relationship between diet and insomnia.



Giddings, G (1934), ‘Child’s Sleep-Effect of Certain Foods and Beverages on Sleep Motility.’, Am J Public Health Nations Health, 24 (6 Pt 1), 609-14. PubMed: 18014113
Humphries, P, E Pretorius, and H Naudé (2008), ‘Direct and indirect cellular effects of aspartame on the brain.’, Eur J Clin Nutr, 62 (4), 451-62. PubMed: 17684524
Kachi, Y., et al. (2011), ‘Association between insomnia symptoms and hemoglobin A1c level in Japanese men’, PLoS ONE, 6 (7), e21420. PubMed: 21747936
Kahn, A, et al. (1989), ‘Milk intolerance in children with persistent sleeplessness: a prospective double-blind crossover evaluation.’, Pediatrics, 84 (4), 595-603. PubMed: 2780120
Keckeis, M, et al. (2010), ‘Impaired glucose tolerance in sleep disorders.’, PLoS One, 5 (3), e9444. PubMed: 20209158
Seelig, E., et al. (2013), ‘Neuroendocrine regulation and metabolism of glucose and lipids in primary chronic insomnia: a prospective case-control study’, PLoS ONE, 8 (4), e61780. PubMed: 23593497
St-Onge, MP, et al. (2016), ‘Fiber and Saturated Fat Are Associated with Sleep Arousals and Slow Wave Sleep.’, J Clin Sleep Med, 12 (1), 19-24. PubMed: 26156950
Tan, X, et al. (2016), ‘Effect of Six-Month Diet Intervention on Sleep among Overweight and Obese Men with Chronic Insomnia Symptoms: A Randomized Controlled Trial.’, Nutrients, 8 (11), PubMed: 27886073
Vasisht, K. P., et al. (2013), ‘Differences in insulin secretion and sensitivity in short-sleep insomnia’, Sleep, 36 (6), 955-57. PubMed: 23729940
Vgontzas, A. N., et al. (2009), ‘Insomnia with objective short sleep duration is associated with type 2 diabetes: A population-based study’, Diabetes Care, 32 (11), 1980-85. PubMed: 19641160
Yamamoto, N., et al. (2010), ‘Insomnia increases insulin resistance and insulin secretion in elderly people’, J Am Geriatr Soc, 58 (4), 801-4. PubMed: 20398173
Yu, C, et al. (2017), ‘Dietary Patterns and Insomnia Symptoms in Chinese Adults: The China Kadoorie Biobank.’, Nutrients, 9 (3), PubMed: 28335373