@article{18f8bf9b3f2c4df5aeb764aa8a310217,
title = "Rapid suppression of bone formation marker in response to sleep restriction and circadian disruption in men",
abstract = "Summary: We describe the time course of bone formation marker (P1NP) decline in men exposed to ~ 3 weeks of sleep restriction with concurrent circadian disruption. P1NP declined within 10 days and remained lower with ongoing exposure. These data suggest even brief exposure to sleep and circadian disruptions may disrupt bone metabolism. Introduction: A serum bone formation marker (procollagen type 1 N-terminal, P1NP) was lower after ~ 3 weeks of sleep restriction combined with circadian disruption. We now describe the time course of decline. Methods: The ~ 3-week protocol included two segments: “baseline,” ≥ 10-h sleep opportunity/day × 5 days; “forced desynchrony” (FD), recurring 28 h day (circadian disruption) with sleep restriction (~ 5.6-h sleep per 24 h). Fasted plasma P1NP was measured throughout the protocol in nine men (20–59 years old). We tested the hypothesis that PINP would steadily decline across the FD intervention because the magnitude of sleep loss and circadian misalignment accrued as the protocol progressed. A piecewise linear regression model was used to estimate the slope (β) as ΔP1NP per 24 h with a change point mid-protocol to estimate the initial vs. prolonged effects of FD exposure. Results: Plasma P1NP levels declined significantly within the first 10 days of FD (β^ = − 1.33 μg/L per 24 h, p < 0.0001) and remained lower than baseline with prolonged exposure out to 3 weeks (β^ = − 0.18 μg/L per 24 h, p = 0.67). As previously reported, levels of a bone resorption marker (C-telopeptide (CTX)) were unchanged. Conclusion: Sleep restriction with concurrent circadian disruption induced a relatively rapid decline in P1NP (despite no change in CTX) and levels remained lower with ongoing exposure. These data suggest (1) even brief sleep restriction and circadian disruption can adversely affect bone metabolism, and (2) there is no P1NP recovery with ongoing exposure that, taken together, could lead to lower bone density over time.",
keywords = "Bone formation, Bone loss, Circadian disruption, P1NP, Sleep restriction",
author = "Swanson, {C. M.} and Kohrt, {W. M.} and P. Wolfe and Wright, {K. P.} and Shea, {S. A.} and Cain, {S. W.} and M. Munch and N. Vujovi{\'c} and Czeisler, {C. A.} and Orwoll, {E. S.} and Buxton, {O. M.}",
note = "Funding Information: OMB was supported in part by the NHLBI (R01HL107240). Funding Information: NV was supported by the following NIH grants: F32AG051325, R01DK099512, R01HL118601, and R01DK105072. Funding Information: SAS received support from The Oregon Institute of Occupational Health Sciences at Oregon Health & Science University via funds from the Division of Consumer and Business Services of the State of Oregon, and NIH grants R01 HL142064, R01 HL125893, HL125893-03A1, and R01 HL140577 (to SA Shea); DoD grant PT150133 (to L Hammer); and CDC grant U19 OH010154 (to WK Anger). Funding Information: ESO as overall PI for the Osteoporotic Fractures in Men (MrOS) Study is supported by NIH funding via the following institutes: the National Institute on Aging, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Center for Advancing Translational Sciences, and NIH Roadmap for Medical Research, under the following grant numbers: U01AG027810, U01AG042124, U01AG042139, U01AG042140, U01 AG042143, U01 AG042145, U01 AG042168, and U01 AR066160. Funding Information: KPW reports research support from the NIH, Office of Naval Research, Pac-12, Philips Inc., CurAegis Technologies (formerly known as Torvec Inc.), Somalogics; Financial relationships: consulting fees from or served as a paid member of scientific advisory boards for NIH (Sleep Disorders Research Advisory Board - National Heart, Lung and Blood Institute), CurAegis Technologies, Circadian Therapeutics, LTD, Kellogg Company; Board of Directors: Sleep Research Society; Speaker/educational consultant honorarium fees: American Academy of Sleep Medicine, American College of Chest Physicians, American Diabetes Association. Funding Information: SAS received support from The Oregon Institute of Occupational Health Sciences at Oregon Health & Science University via funds from the Division of Consumer and Business Services of the State of Oregon, and NIH grants R01 HL142064, R01 HL125893, HL125893-03A1, and R01 HL140577 (to SA Shea); DoD grant PT150133 (to L Hammer); and CDC grant U19 OH010154 (To WK Anger). Funding Information: This work was further supported by K23AR070275 (Swanson), P50 HD073063 (Kohrt), and the National Center for Advancing Translational Sciences of the NIH under award number UL1TR000128 . Funding Information: Data collection was supported by NIA (P01 AG009975), NHLBI (K24 HL76446), and NSBRI through NASA NCC 9-58 (HFP01601), and was conducted in the BWH{\textquoteright}s General Clinical Research Center supported by the NCRR (M01 RR02635), and the CCI of the Harvard Clinical and Translational Science Center (1 UL1 RR025758-01). Publisher Copyright: {\textcopyright} 2019, International Osteoporosis Foundation and National Osteoporosis Foundation.",
year = "2019",
month = dec,
day = "1",
doi = "10.1007/s00198-019-05135-y",
language = "English (US)",
volume = "30",
pages = "2485--2493",
journal = "Osteoporosis International",
issn = "0937-941X",
publisher = "Springer London",
number = "12",
}