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Caffeine does not entrain the circadian clock but improves daytime alertness in blind patients with non-24-hour rhythms.

St Hilaire MA, Lockley SW - Sleep Med. (2015)

Bottom Line: Participants completed daily sleep-wake logs, and rated their alertness and mood using nine-point scales every ~2-4 h while awake on urine sampling days.Non-24-h aMT6s rhythms were confirmed in all three participants (τ range = 24.32-24.57 h).Caffeine treatment significantly improved daytime alertness at adverse circadian phases (p <0.0001) but did not decrease the occurrence of daytime naps compared with placebo.

View Article: PubMed Central - PubMed

Affiliation: Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, MA, USA; Division of Sleep Medicine, Department of Medicine, Harvard Medical School, Boston, MA, USA.

No MeSH data available.


Related in: MedlinePlus

(A–C) Raster double plots of the self-reported sleep times (horizontal black bars), including naps, in totally blind participants S33 (A), S84 (B), and S85 (C). Sequential study days are shown on the ordinate and clock time is double-plotted on the abscissa. Circadian acrophases, which were estimated from cosinor fits to 48-h profiles of aMT6s rhythms, are superimposed (open circles) along with a best-fit regression line (dashed lines) to illustrate the intrinsic non-24-h period. The size of the circle is inversely proportional to the standard error of the circadian phase estimate; the best-fit regression was weighted based on these standard errors. Circadian period was estimated for each condition for each participant. S33: no treatment τ = 24.49 ± 0.21 h; placebo τ = 24.28 ± 0.27 h; caffeine τ = 24.46 ± 0.11 h. S84: no treatment τ = 24.25 ± 0.06 h; caffeine τ = 24.35 ± 0.02 h. S85: no treatment τ = 24.51 ± 0.10 h; placebo t = 24.59 ± 0.03 h; caffeine τ = 24.59 ± 0.03 h. (D–G) Nighttime sleep duration (D), sleep offset (E), and daytime nap duration (F) plotted as a function of beat cycle phase and alert–sleepy scales (G) plotted as a function of circadian phase during the placebo/no treatment (gray circles) and caffeine (black squares) arms of the study across all three participants. Each parameter was normalized in each participant as the deviation from the mean (y-axis; 45° bins), where 0° represents the time at which the midpoint of sleep (for D–F) or the rating assessment (G) coincided with the acrophase of the aMT6s rhythm (x-axis) as a function of the treatment condition (placebo/no treatment vs. caffeine). Significant circadian rhythms are indicated by filled symbols and nonsignificant rhythms by open symbols. Phase bins in which caffeine was significantly different from the placebo/no treatment condition are indicated (*).
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f0010: (A–C) Raster double plots of the self-reported sleep times (horizontal black bars), including naps, in totally blind participants S33 (A), S84 (B), and S85 (C). Sequential study days are shown on the ordinate and clock time is double-plotted on the abscissa. Circadian acrophases, which were estimated from cosinor fits to 48-h profiles of aMT6s rhythms, are superimposed (open circles) along with a best-fit regression line (dashed lines) to illustrate the intrinsic non-24-h period. The size of the circle is inversely proportional to the standard error of the circadian phase estimate; the best-fit regression was weighted based on these standard errors. Circadian period was estimated for each condition for each participant. S33: no treatment τ = 24.49 ± 0.21 h; placebo τ = 24.28 ± 0.27 h; caffeine τ = 24.46 ± 0.11 h. S84: no treatment τ = 24.25 ± 0.06 h; caffeine τ = 24.35 ± 0.02 h. S85: no treatment τ = 24.51 ± 0.10 h; placebo t = 24.59 ± 0.03 h; caffeine τ = 24.59 ± 0.03 h. (D–G) Nighttime sleep duration (D), sleep offset (E), and daytime nap duration (F) plotted as a function of beat cycle phase and alert–sleepy scales (G) plotted as a function of circadian phase during the placebo/no treatment (gray circles) and caffeine (black squares) arms of the study across all three participants. Each parameter was normalized in each participant as the deviation from the mean (y-axis; 45° bins), where 0° represents the time at which the midpoint of sleep (for D–F) or the rating assessment (G) coincided with the acrophase of the aMT6s rhythm (x-axis) as a function of the treatment condition (placebo/no treatment vs. caffeine). Significant circadian rhythms are indicated by filled symbols and nonsignificant rhythms by open symbols. Phase bins in which caffeine was significantly different from the placebo/no treatment condition are indicated (*).

Mentions: Caffeine (150 mg fast-release preparation; Martindale Pharmaceuticals, UK) was administered daily at 10 a.m. uninterrupted for approximately one circadian beat cycle in a single-masked design. Caffeine treatment was scheduled to be initiated at CT1-4 at or just after each participant reached a normal circadian phase (ie, aMT6s peak = 04:30 a.m.). Placebo was also administered in S33 and S85 for approximately one circadian beat cycle split before and after caffeine treatment (see Fig. 1); S84 received caffeine only. The study was approved by the University of Surrey Ethics Committee (EC/2003/144/SBMS). Written informed consent was obtained prior to the study and participants were informed that they were free to withdraw at any time.


Caffeine does not entrain the circadian clock but improves daytime alertness in blind patients with non-24-hour rhythms.

St Hilaire MA, Lockley SW - Sleep Med. (2015)

(A–C) Raster double plots of the self-reported sleep times (horizontal black bars), including naps, in totally blind participants S33 (A), S84 (B), and S85 (C). Sequential study days are shown on the ordinate and clock time is double-plotted on the abscissa. Circadian acrophases, which were estimated from cosinor fits to 48-h profiles of aMT6s rhythms, are superimposed (open circles) along with a best-fit regression line (dashed lines) to illustrate the intrinsic non-24-h period. The size of the circle is inversely proportional to the standard error of the circadian phase estimate; the best-fit regression was weighted based on these standard errors. Circadian period was estimated for each condition for each participant. S33: no treatment τ = 24.49 ± 0.21 h; placebo τ = 24.28 ± 0.27 h; caffeine τ = 24.46 ± 0.11 h. S84: no treatment τ = 24.25 ± 0.06 h; caffeine τ = 24.35 ± 0.02 h. S85: no treatment τ = 24.51 ± 0.10 h; placebo t = 24.59 ± 0.03 h; caffeine τ = 24.59 ± 0.03 h. (D–G) Nighttime sleep duration (D), sleep offset (E), and daytime nap duration (F) plotted as a function of beat cycle phase and alert–sleepy scales (G) plotted as a function of circadian phase during the placebo/no treatment (gray circles) and caffeine (black squares) arms of the study across all three participants. Each parameter was normalized in each participant as the deviation from the mean (y-axis; 45° bins), where 0° represents the time at which the midpoint of sleep (for D–F) or the rating assessment (G) coincided with the acrophase of the aMT6s rhythm (x-axis) as a function of the treatment condition (placebo/no treatment vs. caffeine). Significant circadian rhythms are indicated by filled symbols and nonsignificant rhythms by open symbols. Phase bins in which caffeine was significantly different from the placebo/no treatment condition are indicated (*).
© Copyright Policy - CC BY
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4465963&req=5

f0010: (A–C) Raster double plots of the self-reported sleep times (horizontal black bars), including naps, in totally blind participants S33 (A), S84 (B), and S85 (C). Sequential study days are shown on the ordinate and clock time is double-plotted on the abscissa. Circadian acrophases, which were estimated from cosinor fits to 48-h profiles of aMT6s rhythms, are superimposed (open circles) along with a best-fit regression line (dashed lines) to illustrate the intrinsic non-24-h period. The size of the circle is inversely proportional to the standard error of the circadian phase estimate; the best-fit regression was weighted based on these standard errors. Circadian period was estimated for each condition for each participant. S33: no treatment τ = 24.49 ± 0.21 h; placebo τ = 24.28 ± 0.27 h; caffeine τ = 24.46 ± 0.11 h. S84: no treatment τ = 24.25 ± 0.06 h; caffeine τ = 24.35 ± 0.02 h. S85: no treatment τ = 24.51 ± 0.10 h; placebo t = 24.59 ± 0.03 h; caffeine τ = 24.59 ± 0.03 h. (D–G) Nighttime sleep duration (D), sleep offset (E), and daytime nap duration (F) plotted as a function of beat cycle phase and alert–sleepy scales (G) plotted as a function of circadian phase during the placebo/no treatment (gray circles) and caffeine (black squares) arms of the study across all three participants. Each parameter was normalized in each participant as the deviation from the mean (y-axis; 45° bins), where 0° represents the time at which the midpoint of sleep (for D–F) or the rating assessment (G) coincided with the acrophase of the aMT6s rhythm (x-axis) as a function of the treatment condition (placebo/no treatment vs. caffeine). Significant circadian rhythms are indicated by filled symbols and nonsignificant rhythms by open symbols. Phase bins in which caffeine was significantly different from the placebo/no treatment condition are indicated (*).
Mentions: Caffeine (150 mg fast-release preparation; Martindale Pharmaceuticals, UK) was administered daily at 10 a.m. uninterrupted for approximately one circadian beat cycle in a single-masked design. Caffeine treatment was scheduled to be initiated at CT1-4 at or just after each participant reached a normal circadian phase (ie, aMT6s peak = 04:30 a.m.). Placebo was also administered in S33 and S85 for approximately one circadian beat cycle split before and after caffeine treatment (see Fig. 1); S84 received caffeine only. The study was approved by the University of Surrey Ethics Committee (EC/2003/144/SBMS). Written informed consent was obtained prior to the study and participants were informed that they were free to withdraw at any time.

Bottom Line: Participants completed daily sleep-wake logs, and rated their alertness and mood using nine-point scales every ~2-4 h while awake on urine sampling days.Non-24-h aMT6s rhythms were confirmed in all three participants (τ range = 24.32-24.57 h).Caffeine treatment significantly improved daytime alertness at adverse circadian phases (p <0.0001) but did not decrease the occurrence of daytime naps compared with placebo.

View Article: PubMed Central - PubMed

Affiliation: Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, MA, USA; Division of Sleep Medicine, Department of Medicine, Harvard Medical School, Boston, MA, USA.

No MeSH data available.


Related in: MedlinePlus