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Publications (10 of 36) Show all publications
Rångtell, F. H., Karamchedu, S., Andersson, P., Liethof, L., Bucaro, M. O., Lampola, L., . . . Benedict, C. (2019). A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner. Journal of Sleep Research, 28(1), Article ID e12651.
Open this publication in new window or tab >>A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner
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2019 (English)In: Journal of Sleep Research, ISSN 0962-1105, E-ISSN 1365-2869, Vol. 28, no 1, article id e12651Article in journal (Refereed) Published
Abstract [en]

Acute sleep deprivation can lead to judgement errors and thereby increases the risk of accidents, possibly due to an impaired working memory. However, whether the adverse effects of acute sleep loss on working memory are modulated by auditory distraction in women and men are not known. Additionally, it is unknown whether sleep loss alters the way in which men and women perceive their working memory performance. Thus, 24 young adults (12 women using oral contraceptives at the time of investigation) participated in two experimental conditions: nocturnal sleep (scheduled between 22:30 and 06:30 hours) versus one night of total sleep loss. Participants were administered a digital working memory test in which eight-digit sequences were learned and retrieved in the morning after each condition. Learning of digital sequences was accompanied by either silence or auditory distraction (equal distribution among trials). After sequence retrieval, each trial ended with a question regarding how certain participants were of the correctness of their response, as a self-estimate of working memory performance. We found that sleep loss impaired objective but not self-estimated working memory performance in women. In contrast, both measures remained unaffected by sleep loss in men. Auditory distraction impaired working memory performance, without modulation by sleep loss or sex. Being unaware of cognitive limitations when sleep-deprived, as seen in our study, could lead to undesirable consequences in, for example, an occupational context. Our findings suggest that sleep-deprived young women are at particular risk for overestimating their working memory performance.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
sound distraction, women and men, nocturnal wakefulness, subjective performance, cognition
National Category
Applied Psychology
Identifiers
urn:nbn:se:uu:diva-376724 (URN)10.1111/jsr.12651 (DOI)000456255400005 ()29383809 (PubMedID)
Funder
Fredrik och Ingrid Thurings StiftelseSwedish Research Council, 2015-03100Åke Wiberg FoundationThe Swedish Brain Foundation, FO2016-0092Swedish Society of MedicineTore Nilsons Stiftelse för medicinsk forskningNovo Nordisk, NNF14OC0009349Erik, Karin och Gösta Selanders FoundationAFA Insurance, 140006Swedish Research Council
Available from: 2019-02-11 Created: 2019-02-11 Last updated: 2019-04-23Bibliographically approved
Tan, X., Cedernaes, J., Risérus, U. & Benedict, C. (2019). Lack of association between self-reported insomnia symptoms and clamp-derived insulin sensitivity in elderly men. Psychoneuroendocrinology, 102, 256-260
Open this publication in new window or tab >>Lack of association between self-reported insomnia symptoms and clamp-derived insulin sensitivity in elderly men
2019 (English)In: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 102, p. 256-260Article in journal (Refereed) Published
Abstract [en]

Insomnia-related sleep disruptions, such as short and disturbed sleep, have been tied to systemic insulin resistance in young adult populations. We therefore sought to confirm these findings in a cohort of elderly men. To this aim, we utilized variables from 980 men who participated in the investigation at age 70 of the Uppsala Longitudinal Study of Adult Men. Self-reported insomnia symptoms were assessed by questions about difficulty initiating sleep, early final awakening, and regular use of hypnotics. All participants also underwent the gold standard hyperinsulinemic-euglycemic clamp technique to assess the insulin sensitivity index (M/I). Finally, fasting blood was collected to measure free fatty acids (FFAs) and adiponectin. Differences in blood parameters between men with and those without insomnia were determined by ANCOVA, and were adjusted for lifestyle and cardio-metabolic risk factors. Our analysis yielded no differences in M/I, FFAs, and adiponectin between men with and those without insomnia symptoms. Analyses in non-diabetic and diabetic subsamples confirmed these negative findings. Our cross-sectional results therefore suggest that insomnia symptoms may have a minimal effect, if any, on measures of insulin sensitivity in elderly men. Given the observational design of our study, future studies are needed to determine whether experimental sleep manipulations influence systemic insulin sensitivity in elderly humans, as has previously been shown in young adult populations.

Place, publisher, year, edition, pages
PERGAMON-ELSEVIER SCIENCE LTD, 2019
Keywords
Male cohort, Insomnia symptoms, Clamp-derived insulin sensitivity, Adiponectin, Free fatty acids
National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-382522 (URN)10.1016/j.psyneuen.2018.12.227 (DOI)000462800900032 ()30594818 (PubMedID)
Funder
Swedish Research Council, 2015-03100Novo Nordisk, NNF14OC0009349The Swedish Brain FoundationÅke Wiberg Foundation, M17-0088Fredrik och Ingrid Thurings Stiftelse, 2017-00313
Available from: 2019-04-29 Created: 2019-04-29 Last updated: 2019-04-29Bibliographically approved
Cedernaes, J., Huang, W., Ramsey, K. M., Waldeck, N., Cheng, L., Marcheva, B., . . . Bass, J. (2019). Transcriptional Basis for Rhythmic Control of Hunger and Metabolism within the AgRP Neuron. Cell Metabolism, 29(5), 1078-1091.e5
Open this publication in new window or tab >>Transcriptional Basis for Rhythmic Control of Hunger and Metabolism within the AgRP Neuron
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2019 (English)In: Cell Metabolism, ISSN 1550-4131, E-ISSN 1932-7420, Vol. 29, no 5, p. 1078-1091.e5Article in journal (Refereed) Published
Abstract [en]

The alignment of fasting and feeding with the sleep/ wake cycle is coordinated by hypothalamic neurons, though the underlying molecular programs remain incompletely understood. Here, we demonstrate that the clock transcription pathway maximizes eating during wakefulness and glucose production during sleep through autonomous circadian regulation of NPY/AgRP neurons. Tandem profiling of whole-cell and ribosome-bound mRNAs in morning and evening under dynamic fasting and fed conditions identified temporal control of activity-dependent gene repertoires in AgRP neurons central to synaptogenesis, bioenergetics, and neurotransmitter and peptidergic signaling. Synaptic and circadian pathways were specific to whole-cell RNA analyses, while bioenergetic pathways were selectively enriched in the ribosome-bound transcriptome. Finally, we demonstrate that the AgRP clock mediates the transcriptional response to leptin. Our results reveal that time-of-day restriction in transcriptional control of energy-sensing neurons underlies the alignment of hunger and food acquisition with the sleep/wake state.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-384072 (URN)10.1016/j.cmet.2019.01.023 (DOI)000467054100010 ()30827863 (PubMedID)
Funder
Swedish Research Council, 2014-6888
Note

De 2 första författarna delar förstaförfattarskapet.

Available from: 2019-05-28 Created: 2019-05-28 Last updated: 2019-05-28Bibliographically approved
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, 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: 2019-03-15Bibliographically 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., 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
Tan, X., Cedernaes, J., Forsberg, L. A., Schiöth, H. B. & Benedict, C. (2018). Self-reported sleep disturbances and prostate cancer morbidity and mortality in Swedish men: A longitudinal study over 40 years. Journal of Sleep Research, 27(6), Article ID e12708.
Open this publication in new window or tab >>Self-reported sleep disturbances and prostate cancer morbidity and mortality in Swedish men: A longitudinal study over 40 years
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2018 (English)In: Journal of Sleep Research, ISSN 0962-1105, E-ISSN 1365-2869, Vol. 27, no 6, article id e12708Article in journal (Refereed) Published
Abstract [en]

The present study, with an observational period of about 40 years, examined the association between self-reported sleep disturbances (i.e. problems with falling and staying asleep; use of hypnotics) and prostate cancer morbidity and mortality in initially 2322 men (all 50 years old at baseline). Self-reported sleep disturbances and established risk factors (e.g. age, lower urinary tract symptoms, smoking and family history of cancer) were measured at ages 50 and 70 years. Information about prostate cancer diagnosis and deaths as a result of prostate cancer was available from the National Cancer Registry and the Swedish Civil Registry of Morbidity. During the observational period, 263 participants developed prostate cancer (11% of the total cohort); 146 of them died as a result of prostate cancer. There was no association between sleep disturbances and prostate cancer morbidity or mortality (hazard ratio 1.09, 95% confidence interval (CI) 0.79, 1.52, and hazard ratio 1.21, 95% CI 0.77, 1.91, respectively). Similar findings were observed when examining associations between single sleep disturbance parameters and prostate cancer morbidity and mortality. Our study does not provide evidence that reports of sleep disturbances increase the risk of prostate cancer morbidity or mortality in middle to older-aged men. Therefore, assessing subjective sleep problems may not meaningfully help to identify men at risk of developing prostate cancer or dying of this devastating condition.

National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-352162 (URN)10.1111/jsr.12708 (DOI)000450273000016 ()29740901 (PubMedID)
Funder
Novo Nordisk, NNF14OC0009349The Swedish Brain FoundationSwedish Research Council, 2015-03100
Available from: 2018-06-01 Created: 2018-06-01 Last updated: 2019-03-14Bibliographically approved
Cedernaes, J., Osorio, R. S., Varga, A. W., Kam, K., Schiöth, H. B. & Benedict, C. (2017). Candidate mechanisms underlying the association between sleep-wake disruptions and Alzheimer's disease. Sleep Medicine Reviews, 31, 102-111
Open this publication in new window or tab >>Candidate mechanisms underlying the association between sleep-wake disruptions and Alzheimer's disease
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2017 (English)In: Sleep Medicine Reviews, ISSN 1087-0792, E-ISSN 1532-2955, Vol. 31, p. 102-111Article, review/survey (Refereed) Published
Abstract [en]

During wakefulness, extracellular levels of metabolites in the brain increase. These include amyloid beta (Aβ), which contributes to the pathogenesis of Alzheimer's disease (AD). Counterbalancing their accumulation in the brain, sleep facilitates the removal of these metabolites from the extracellular space by convective flow of the interstitial fluid from the para-arterial to the para-venous space. However, when the sleep-wake cycle is disrupted (characterized by increased brain levels of the wake-promoting neuropeptide orexin and increased neural activity), the central nervous system (CNS) clearance of extracellular metabolites is diminished. Disruptions to the sleep-wake cycle have furthermore been linked to increased neuronal oxidative stress and impaired blood-brain barrier function - conditions that have also been proposed to play a role in the development and progression of AD. Notably, recent human and transgenic animal studies have demonstrated that AD-related pathophysiological processes that occur long before the clinical onset of AD, such as Aβ deposition in the brain, disrupt sleep and circadian rhythms. Collectively, as proposed in this review, these findings suggest the existence of a mechanistic interplay between AD pathogenesis and disrupted sleep-wake cycles, which is able to accelerate the development and progression of this disease.

Place, publisher, year, edition, pages
Saunders Elsevier, 2017
Keywords
Aging, Amyloid beta, Blood brain barrier, Circadian misalignment, Neurodegeneration, Orexin, Oxidative stress, Sleep disruption, Slow-wave sleep, Tau
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-318575 (URN)10.1016/j.smrv.2016.02.002 (DOI)000393936700012 ()26996255 (PubMedID)
Funder
The Swedish Brain FoundationFredrik och Ingrid Thurings StiftelseNovo Nordisk, NNF14OC0009349AFA InsuranceSwedish Society for Medical Research (SSMF)Swedish Research CouncilNovo Nordisk
Available from: 2017-03-26 Created: 2017-03-26 Last updated: 2019-02-26Bibliographically approved
Rångtell, F. H., Karamchedu, S., Andersson, P., van Egmond, L., Hultgren, T., Broman, J.-E., . . . Benedict, C. (2017). Learning performance is linked to procedural memory consolidation across both sleep and wakefulness. Scientific Reports, 7, Article ID 10234.
Open this publication in new window or tab >>Learning performance is linked to procedural memory consolidation across both sleep and wakefulness
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2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 10234Article in journal (Refereed) Published
Abstract [en]

We investigated whether learning performance in a procedural finger tapping task before nocturnal sleep would predict performance gains after sleep in 60 young adults. Gains were defined as change in correctly tapped digit sequences between learning (12 trials administered in the evening) and retesting (3 trials administered in the morning after sleep). The same task was also administered to a separate wake group (N = 54 young adults), which learned in the morning and was retested in the evening. Learning performance was determined by either using the average performance on the last three learning trials or the average performance on the best three learning trials. Our results demonstrated an inverse association between learning performance and gains in procedural skill, i.e., good learners exhibited smaller performance gains across both wakefulness and sleep than poor learners. Regardless of learning performance, gains in finger tapping skills were greater after sleep than daytime wakefulness. Importantly, some of our findings were influenced by how learning performance was estimated. Collectively, these results suggest that learning performance and the method through which it is estimated may influence performance gains in finger tapping skills across both sleep and wakefulness.

National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-334935 (URN)10.1038/s41598-017-09263-5 (DOI)000408781200093 ()28860592 (PubMedID)
Funder
AFA InsuranceLars Hierta Memorial FoundationNovo NordiskSwedish Society for Medical Research (SSMF)Swedish Society of MedicineThe Swedish Brain FoundationSwedish Research CouncilÅke Wiberg Foundation
Available from: 2017-12-01 Created: 2017-12-01 Last updated: 2019-04-23Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-9052-8372

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