Author
Janet C. Zimmerman
Other affiliations: NewYork–Presbyterian Hospital
Bio: Janet C. Zimmerman is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Circadian rhythm & Sleep Stages. The author has an hindex of 11, co-authored 14 publications receiving 3004 citations. Previous affiliations of Janet C. Zimmerman include NewYork–Presbyterian Hospital.
Papers
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TL;DR: Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues and the duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime.
Abstract: Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues. The duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime and not with the length of prior wakefulness. Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm.
887 citations
TL;DR: A new syndrome called "delayed sleep phase insomnia" is described, which is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.
Abstract: We describe a new syndrome called "delayed sleep phase insomnia." Thirty of 450 patients seen for a primary insomniac complaint had the following characteristics: (1) chronic inability to fall asleep at a desired clock time; (2) when not on a strict schedule, the patients have a normal sleep pattern and after a sleep of normal length awaken spontaneously and feel refreshed; and (3) a long history of unsuccessful attempts to treat the problem. These patients were younger than the general insomniac population and as a group did not have a specific psychiatric disorder. Six patients' histories are described in detail, including the successful nonpharmacological chronotherapy regimen (resetting the patients' biological clock by progressive phase delay). Delayed sleep phase insomnia is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.
473 citations
TL;DR: Studies were carried out on a group of six young and six older normal men who lived under conditions of temporal, but not social isolation, from three to eight weeks, demonstrating a reduction in the period and amplitude of the body temperature rhythms during free-running in the older group.
348 citations
TL;DR: There is an endogenous circadian rhythm of REM sleep propensity which is closely coupled to the body temperature rhythm and is capable of free-running with a period different from both 24 hr and the average period of the sleep-wake cycle.
Abstract: Ten male subjects were studied for a total of 306 days on self-selected schedules Four of them developed bedrest-activity cycle period lengths very different from 24 hr (mean = 368 hr) despite the persistence of near-24-hr oscillations in other physiologic functions, including that of body temperature (mean = 246 hr) The percentage of sleep time spent in REM sleep varied significantly with the phase of that near-24-hr body temperature cycle The peak in REM sleep propensity (RSP) occurred on the rising slope of the average body temperature curve, coincident with the phase of peak sleep tendency This was associated with a significantly increased REM episode duration and shortened REM latency (including sleep-onset REM episodes), but without a significant change in the REM-NREM cycle length We conclude that there is an endogenous circadian rhythm of REM sleep propensity which is closely coupled to the body temperature rhythm and is capable of free-running with a period different from both 24 hr and the average period of the sleep-wake cycle
346 citations
TL;DR: A brief drug-free rescheduling treatment for Delayed Sleep Phase insomnia, a syndrome characterized by sleep-onset insomnia with difficulty in morning awakening, which was designed to reset patients' biological clocks by the phase delay route.
Abstract: We report here the development of a brief drug-free rescheduling treatment ("chronotherapy") for Delayed Sleep Phase (DSP) insomnia, a syndrome characterized by sleep-onset insomnia with difficulty in morning awakening. We postulated that patients with DSP insomnia had an inadequate capacity to achieve phase advance shifts of the circadian pacemaker which times the sleep-wake cycle. Chronotherapy was therefore designed to reset these patients' biological clocks by the phase delay route. This single 5-6 day treatment was tested in 5 patients with a 4-15 year history of DSP insomnia. All 5 patients reported a lasting resolution of their symptoms substantiated by systematic long-term self-reports and objective polygraphic recording before and after treatment (average follow-up of 260 days; range, 42-910 days). The average sleep onset advanced from 4:50 a.m. before treatment to 12:20 a.m. afterwards, and wake times advanced from 1:00 p.m. to 755 a.m. (for both, p less than 0.001), with no reduction in sleep efficiency. As a result, all 5 patients were able to end their chronic dependence on hypnotic medications.
321 citations
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01 Nov 2000
TL;DR: From Neurons to Neighborhoods as discussed by the authors presents the evidence about "brain wiring" and how children learn to learn to speak, think, and regulate their behavior, and examines the effect of the climate-family, child care, community-within which the child grows.
Abstract: How we raise young children is one of today's most highly personalized and sharply politicized issues, in part because each of us can claim some level of "expertise." The debate has intensified as discoveries about our development-in the womb and in the first months and years-have reached the popular media. How can we use our burgeoning knowledge to assure the well-being of all young children, for their own sake as well as for the sake of our nation? Drawing from new findings, this book presents important conclusions about nature-versus-nurture, the impact of being born into a working family, the effect of politics on programs for children, the costs and benefits of intervention, and other issues. The committee issues a series of challenges to decision makers regarding the quality of child care, issues of racial and ethnic diversity, the integration of children's cognitive and emotional development, and more. Authoritative yet accessible, From Neurons to Neighborhoods presents the evidence about "brain wiring" and how kids learn to speak, think, and regulate their behavior. It examines the effect of the climate-family, child care, community-within which the child grows.
5,295 citations
TL;DR: If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis.
Abstract: To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P<0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB—estimated timing confirmed the existence of a circadian rhythm, with a threefold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction ma...
1,797 citations
TL;DR: In this article, the intrinsic period of the human circadian pacemaker averages 24.18 hours in both age groups, with a tight distribution consistent with other species, with important implications for understanding the pathophysiology of disrupted sleep in older people.
Abstract: Regulation of circadian period in humans was thought to differ from that of other species, with the period of the activity rhythm reported to range from 13 to 65 hours (median 25.2 hours) and the period of the body temperature rhythm reported to average 25 hours in adulthood, and to shorten with age. However, those observations were based on studies of humans exposed to light levels sufficient to confound circadian period estimation. Precise estimation of the periods of the endogenous circadian rhythms of melatonin, core body temperature, and cortisol in healthy young and older individuals living in carefully controlled lighting conditions has now revealed that the intrinsic period of the human circadian pacemaker averages 24.18 hours in both age groups, with a tight distribution consistent with other species. These findings have important implications for understanding the pathophysiology of disrupted sleep in older people.
1,483 citations
TL;DR: It is demonstrated that insufficient sleep and irregular sleep-wake patterns, which have been extensively documented in younger adolescents, are also present at alarming levels in the college student population.
1,360 citations
TL;DR: The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans, which has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.
Abstract: A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.
1,303 citations