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BETA
Benedict, Christian, DocentORCID iD iconorcid.org/000-0002-8911-4068
Publications (10 of 97) Show all publications
Cedernaes, J., Westholm, O. J. & Benedict, C. (2018). Acute Sleep Leads To Tissue-Specific Epigenetic And Transcriptional Responses In Healthy Humans. Paper presented at 32nd Annual Meeting of the Associated-Professional-Sleep-Societies- LLC, JUN 02-06, 2018, Baltimore, MD. Sleep, 41, A5-A5
Open this publication in new window or tab >>Acute Sleep Leads To Tissue-Specific Epigenetic And Transcriptional Responses In Healthy Humans
2018 (English)In: Sleep, ISSN 0161-8105, E-ISSN 1550-9109, Vol. 41, p. A5-A5Article in journal, Meeting abstract (Other academic) Published
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-357656 (URN)000431183400012 ()
Conference
32nd Annual Meeting of the Associated-Professional-Sleep-Societies- LLC, JUN 02-06, 2018, Baltimore, MD
Available from: 2018-08-28 Created: 2018-08-28 Last updated: 2018-08-28Bibliographically approved
Cedernaes, J., Schonke, M., Westholm, J. O., Mi, J., Chibalin, A., Voisin, S., . . . Benedict, C. (2018). Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans. Science Advances, 4(8), Article ID eaar8590.
Open this publication in new window or tab >>Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans
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2018 (English)In: Science Advances, ISSN 0036-8156, E-ISSN 2375-2548, Vol. 4, no 8, article id eaar8590Article in journal (Refereed) Published
Abstract [en]

Curtailed sleep promotes weight gain and loss of lean mass in humans, although the underlying molecular mechanisms are poorly understood. We investigated the genomic and physiological impact of acute sleep loss in peripheral tissues by obtaining adipose tissue and skeletal muscle after one night of sleep loss and after one full night of sleep. We find that acute sleep loss alters genome-wide DNA methylation in adipose tissue, and unbiased transcriptome-, protein-, and metabolite-level analyses also reveal highly tissue-specific changes that are partially reflected by altered metabolite levels in blood. We observe transcriptomic signatures of inflammation in both tissues following acute sleep loss, but changes involving the circadian clock are evident only in skeletal muscle, and we uncover molecular signatures suggestive of muscle breakdown that contrast with an anabolic adipose tissue signature. Our findings provide insight into how disruption of sleep and circadian rhythms may promote weight gain and sarcopenia.

Place, publisher, year, edition, pages
AMER ASSOC ADVANCEMENT SCIENCE, 2018
National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-364473 (URN)10.1126/sciadv.aar8590 (DOI)000443498100025 ()30140739 (PubMedID)
Funder
Swedish Research Council, 2015-03100Knut and Alice Wallenberg FoundationSwedish Research Council, 2014-6888Swedish Research Council, 2016-01088Swedish Research Council, 2016-02195Swedish Research Council, 2015-4870Carl Tryggers foundation Erik, Karin och Gösta Selanders FoundationFredrik och Ingrid Thurings StiftelseLars Hierta Memorial FoundationMagnus Bergvall FoundationNovo NordiskTore Nilsons Stiftelse för medicinsk forskningSwedish Society of Medicine, SLS-694111The Swedish Brain FoundationÅke Wiberg FoundationScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
Available from: 2018-10-31 Created: 2018-10-31 Last updated: 2018-10-31Bibliographically approved
Tan, X., van Egmond, L., Chapman, C. D., Cedernaes, J. & Benedict, C. (2018). Aiding sleep in type 2 diabetes: therapeutic considerations. The Lancet Diabetes and Endocrinology, 6(1), 60-68
Open this publication in new window or tab >>Aiding sleep in type 2 diabetes: therapeutic considerations
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2018 (English)In: The Lancet Diabetes and Endocrinology, ISSN 2213-8587, E-ISSN 2213-8595, Vol. 6, no 1, p. 60-68Article, review/survey (Refereed) Published
Abstract [en]

Insomnia and obstructive sleep apnoea (OSA) are more prevalent in patients with type 2 diabetes than in the general population. Both insomnia and OSA have been linked to cardiometabolic alterations (eg, hypertension, increased activity of the sympathetic nervous system, and systemic insulin resistance) that can exacerbate the pathophysiology of type 2 diabetes. Improvement of sleep in patients with diabetes could therefore aid the treatment of diabetes. To help health practitioners choose the best clinical tool to improve their patients' sleep without detrimentally affecting glucose regulation, this Review critically analyses the effects of common treatments for insomnia and OSA on both sleep and glucose metabolism in patients with type 2 diabetes. These treatments include pharmaceutical sleep aids (eg, benzodiazepine receptor agonists, melatonin) and cognitive behavioural therapy for insomnia, continuous positive airway pressure for OSA, and lifestyle interventions.

National Category
Endocrinology and Diabetes Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-342756 (URN)10.1016/S2213-8587(17)30233-4 (DOI)000423799900020 ()28844889 (PubMedID)
Funder
Novo NordiskSwedish Research CouncilAFA InsuranceSwedish Society of MedicineThe Swedish Brain FoundationÅke Wiberg FoundationLars Hierta Memorial Foundation
Available from: 2018-02-23 Created: 2018-02-23 Last updated: 2018-05-08Bibliographically approved
Tan, X. & Benedict, C. (2018). Association between high-glycemic diet and cerebral amyloid burden: a possible role for sleep [Letter to the editor]. American Journal of Clinical Nutrition, 107(3), 480-480
Open this publication in new window or tab >>Association between high-glycemic diet and cerebral amyloid burden: a possible role for sleep
2018 (English)In: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 107, no 3, p. 480-480Article in journal, Letter (Other academic) Published
National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:uu:diva-356236 (URN)10.1093/ajcn/nqx073 (DOI)000427882800018 ()29566198 (PubMedID)
Available from: 2018-07-27 Created: 2018-07-27 Last updated: 2018-07-27Bibliographically approved
Tan, X., Chapman, C. D., Cedernaes, J. & Benedict, C. (2018). Association between long sleep duration and increased risk of obesity and type 2 diabetes: A review of possible mechanisms. Sleep Medicine Reviews, 40, 127-134
Open this publication in new window or tab >>Association between long sleep duration and increased risk of obesity and type 2 diabetes: A review of possible mechanisms
2018 (English)In: Sleep Medicine Reviews, ISSN 1087-0792, E-ISSN 1532-2955, Vol. 40, p. 127-134Article, review/survey (Refereed) Published
Abstract [en]

For the last two decades research has revealed an alarming association between short sleep duration and metabolic disorders. In tandem, the hormonal, behavioral, and genetic mechanisms underlying this relationship have been extensively investigated and reviewed. However, emerging evidence is revealing that excessive sleep duration has remarkably similar deleterious effects. Unfortunately, to date there has been little attention to what drives this connection. This narrative review therefore aims to summarize existing epidemiological findings, experimental work, and most importantly putative molecular and behavioral mechanisms connecting excessive sleep duration with both obesity and type 2 diabetes mellitus. It will also address recent findings suggesting a worrisome bidirectional effect such that metabolic disorders create a positive feedback loop which further perpetuates excessive sleep.

Keywords
Chronotype, Long sleep duration, Obesity, Positive feedback loop, Putative mechanisms, Type 2 diabetes mellitus
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-342958 (URN)10.1016/j.smrv.2017.11.001 (DOI)000438201300012 ()29233612 (PubMedID)
Funder
Novo Nordisk, NNF14OC0009349The Swedish Brain Foundation, FO2016-0092Swedish Research Council, 2015-03100
Available from: 2018-02-23 Created: 2018-02-23 Last updated: 2018-11-12Bibliographically approved
Titova, O. E., Lindberg, E., Elmstahl, S., Lind, L., Schiöth, H. B. & Benedict, C. (2018). Associations Between the Prevalence of Metabolic Syndrome and Sleep Parameters Vary by Age. Frontiers in Endocrinology, 9, Article ID 234.
Open this publication in new window or tab >>Associations Between the Prevalence of Metabolic Syndrome and Sleep Parameters Vary by Age
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2018 (English)In: Frontiers in Endocrinology, ISSN 1664-2392, E-ISSN 1664-2392, Vol. 9, article id 234Article in journal (Refereed) Published
Abstract [en]

Objective: To examine whether the relationship between the metabolic syndrome (MetS) and various sleep parameters [sleep duration, symptoms of sleep-disordered breathing (SDB), and sleep disturbances] varies by age. Methods: Waist circumference, blood pressure, triglycerides, high-density lipoprotein cholesterol, and fasting glucose were used to determine MetS status in a cohort (N = 19,691) of middle-aged (aged 45-64 years) and older (aged >= 65 years) subjects. Habitual sleep duration (short, <= 6 h/day; normal, 7-8 h/day; and long >= 9 h/day), sleep disturbances (such as problems with falling and staying asleep), and symptoms of sleep-disordered breathing (SDB, such as snoring and sleep apneas) were measured by questionnaires. Results: Among the participants, 4,941 subjects (25.1%) fulfilled the criteria for MetS. In the entire sample, both short and long sleep durations were associated with higher prevalence of MetS as compared to normal sleep duration. When stratified by age, a similar pattern was observed for middle-aged subjects (<65 years old; prevalence ratio (PR) [95% CI], 1.13 [1.06-1.22] for short sleep and 1.26 [1.06-1.50] for long sleep duration). In contrast, in older individuals (>= 65 years old), only long sleep duration was linked to a higher prevalence of MetS (1.26 [1.12-1.42]; P < 0.01 for sleep duration x age). In the entire cohort, having at least one SDB symptom >= 4 times per week was linked to an increased prevalence of MetS; however, the PR was higher in middle-aged subjects compared with older subjects (1.50 [1.38-1.63] vs. 1.36 [1.26-1.47], respectively; P < 0.001 for SDB x age). Finally, independent of subjects' age, reports of sleep disturbances (i.e., at least one symptom >= 4 times per week) were associated with a higher likelihood of having MetS (1.12 [1.06-1.18]; P > 0.05 for sleep disturbance x age). Conclusion: Our results suggest that age may modify the associations between some sleep parameters and the prevalence of MetS.

Keywords
sleep duration, sleep disturbance, sleep-disordered breathing, metabolic syndrome, age
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:uu:diva-356873 (URN)10.3389/fendo.2018.00234 (DOI)000431867800001 ()29867766 (PubMedID)
Funder
Swedish Research Council, 2015-03100The Swedish Brain FoundationNovo Nordisk, NNF14OC0009349
Available from: 2018-08-09 Created: 2018-08-09 Last updated: 2018-08-09Bibliographically approved
Cai, G.-H., Janson, C., Theorell-Haglöw, J., Benedict, C., Elmståhl, S., Lind, L. & Lindberg, E. (2018). Both Weight at Age 20 and Weight Gain Have an Impact on Sleep Disturbances Later in Life: Results of the EpiHealth Study. Sleep, 41(1), Article ID zsx176.
Open this publication in new window or tab >>Both Weight at Age 20 and Weight Gain Have an Impact on Sleep Disturbances Later in Life: Results of the EpiHealth Study
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2018 (English)In: Sleep, ISSN 0161-8105, E-ISSN 1550-9109, Vol. 41, no 1, article id zsx176Article in journal (Refereed) Published
Abstract [en]

Study Objectives: Obesity is often associated with impaired sleep, whereas the impact of body mass index (BMI) at younger age and previous weight gain on sleep problems remains unknown.

Methods: The present study utilized data from the Swedish EpiHealth cohort study. A total of 15 845 participants (45-75 years) filled out an internet-based questionnaire. BMI was calculated from both measured data at study time and self-reported data at age 20 from the questionnaire.

Results: Sleep-related symptoms were most common among obese individuals (BMI >30 kg/m(2)). An association between weight gain and sleep problems was found and those with a low BMI at age 20 were most vulnerable to weight gain when it came to risk of sleep problems. Among those who were underweight (BMI <18.5 kg/m(2)) at age 20, weight gain (kg/year) was associated with difficulties initiating sleep with an adjusted OR of 2.64 (95% CI: 1.51-4.62) after adjusting for age, sex, smoking, alcohol consumption, physical activity, education, and civil status. The corresponding adjusted OR's among those who had been normal weight (BMI 18.5-24.99) and overweight (BMI 25-29.99 kg/m(2)) at age 20 were 1.89 (1.47-2.45) and 1.02 (0.48-2.13), respectively. Also difficulties maintaining sleep and snoring were most strongly related to weight gain among those who were underweight at age 20 with decreasing odds with increasing BMI at that age.

Conclusions: Sleep problems are related to weight gain and obesity. The impact of weight is most pronounced among those who had a low BMI when young.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS INC, 2018
Keywords
epidemiology, insomnia, obesity, aging, weight gain, EpiHealth study, body mass index (BMI), Epworth Sleepiness Scale (ESS), sleep problems, snoring
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-342460 (URN)10.1093/sleep/zsx176 (DOI)000422879100012 ()
Funder
Swedish Research Council
Available from: 2018-02-26 Created: 2018-02-26 Last updated: 2018-02-26Bibliographically approved
Chapman, C. D., Benedict, C. & Schiöth, H. B. (2018). Experimenter gender and replicability in science. Science Advances, 4(1), Article ID e1701427.
Open this publication in new window or tab >>Experimenter gender and replicability in science
2018 (English)In: Science Advances, ISSN 0036-8156, E-ISSN 2375-2548, Vol. 4, no 1, article id e1701427Article, review/survey (Refereed) Published
Abstract [en]

There is a replication crisis spreading through the annals of scientific inquiry. Although some work has been carried out to uncover the roots of this issue, much remains unanswered. With this in mind, this paper investigates how the gender of the experimenter may affect experimental findings. Clinical trials are regularly carried out without any report of the experimenter's gender and with dubious knowledge of its influence. Consequently, significant biases caused by the experimenter's gender may lead researchers to conclude that therapeutics or other interventions are either overtreating or undertreating a variety of conditions. Bearing this in mind, this policy paper emphasizes the importance of reporting and controlling for experimenter gender in future research. As backdrop, it explores what we know about the role of experimenter gender in influencing laboratory results, suggests possible mechanisms, and suggests future areas of inquiry.

National Category
Neurosciences Psychology (excluding Applied Psychology)
Identifiers
urn:nbn:se:uu:diva-352930 (URN)10.1126/sciadv.1701427 (DOI)000426694200010 ()
Funder
Swedish Research Council
Available from: 2018-06-08 Created: 2018-06-08 Last updated: 2018-06-08Bibliographically approved
Benedict, C. & Grillo, C. A. (2018). Insulin Resistance as a Therapeutic Target in the Treatment of Alzheimer's Disease: A State-of-the-Art Review. Frontiers in Neuroscience, 12, Article ID 215.
Open this publication in new window or tab >>Insulin Resistance as a Therapeutic Target in the Treatment of Alzheimer's Disease: A State-of-the-Art Review
2018 (English)In: Frontiers in Neuroscience, ISSN 1662-4548, E-ISSN 1662-453X, Vol. 12, article id 215Article, review/survey (Refereed) Published
Abstract [en]

Research in animals and humans has shown that type 2 diabetes and its prodromal state, insulin resistance, promote major pathological hallmarks of Alzheimer's disease (AD), such as the formation of amyloid plaques and neurofibrillary tangles (NFT). Worrisomely, dysregulated amyloid beta (A beta) metabolism has also been shown to promote central nervous system insulin resistance; although the role of tau metabolism remains controversial. Collectively, as proposed in this review, these findings suggest the existence of a mechanistic interplay between AD pathogenesis and disrupted insulin signaling. They also provide strong support for the hypothesis that pharmacologically restoring brain insulin signaling could represent a promising strategy to curb the development and progression of AD. In this context, great hopes have been attached to the use of intranasal insulin. This drug delivery method increases cerebrospinal fluid concentrations of insulin in the absence of peripheral side effects, such as hypoglycemia. With this in mind, the present review will also summarize current knowledge on the efficacy of intranasal insulin to mitigate major pathological symptoms of AD, i.e., cognitive impairment and deregulation of A beta and tau metabolism.

Place, publisher, year, edition, pages
FRONTIERS MEDIA SA, 2018
Keywords
intranasal insulin, diabetes, mild cognitive impairment, amyloid beta, neurofibrillary tangles
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-357169 (URN)10.3389/fnins.2018.00215 (DOI)000429596300001 ()
Funder
Swedish Research Council, 2015-03100
Available from: 2018-08-14 Created: 2018-08-14 Last updated: 2018-08-14Bibliographically approved
Chapman, C. D., Schiöth, H. B., Grillo, C. A. & Benedict, C. (2018). Intranasal insulin in Alzheimer's disease: food for thought. Neuropharmacology, 136, 196-201
Open this publication in new window or tab >>Intranasal insulin in Alzheimer's disease: food for thought
2018 (English)In: Neuropharmacology, ISSN 0028-3908, E-ISSN 1873-7064, Vol. 136, p. 196-201Article in journal (Refereed) Published
Abstract [en]

Accumulating evidence suggests that disrupted brain insulin signaling promotes the development and progression of Alzheimer's disease (AD), driving clinicians to target this circuitry. While both traditional and more modern antidiabetics show promise in combating insulin resistance, intranasal insulin appears to be the most efficient method of boosting brain insulin. Furthermore, intranasal delivery elegantly avoids adverse effects from peripheral insulin administration. However, there remain significant open questions regarding intranasal insulin's efficacy, safety, and potential as an adjunct or mono-therapy. Thus, this review aims to critically evaluate the present evidence and future potential of intranasal insulin as a meaningful treatment for AD.

Place, publisher, year, edition, pages
Elsevier, 2018
Keywords
Alzheimer's disease, Brain insulin resistance, Cognition, Intranasal insulin, Neurodegeneration
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-342186 (URN)10.1016/j.neuropharm.2017.11.037 (DOI)000440121600006 ()29180222 (PubMedID)
Funder
Novo Nordisk, NNF14OC0009349The Swedish Brain Foundation, FO2016-0092Swedish Research Council, 2015-03100
Available from: 2018-02-19 Created: 2018-02-19 Last updated: 2018-11-20Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/000-0002-8911-4068

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