Chronobiology Guide

Circadian rhythm: what it is, how the body clock works, and how to measure it

A circadian rhythm is the roughly 24-hour cycle that an internal biological clock imposes on sleep and wakefulness, hormone release, body temperature and metabolism, and light resets that clock every day.[1][2] This guide, written for researchers and clinicians, explains the biology — the suprachiasmatic nucleus, clock genes, entrainment, melatonin and circadian rhythm sleep-wake disorders. It then explains how the rhythm is measured with DLMO, actigraphy and personal light dosimetry.

By the Condor Research Team · Updated September 2026 · All cited claims link to published sources

What is a circadian rhythm?

A circadian rhythm is an endogenous, approximately 24-hour cycle in physiology and behavior — including the sleep–wake cycle, melatonin secretion and core body temperature — generated by an internal biological clock and synchronized (entrained) to the environment, chiefly by the light–dark cycle.[1][2][3]

The rhythm is generated internally, so it continues when external time cues are removed. In healthy young and older adults studied under carefully controlled lighting, the intrinsic period of the human circadian pacemaker averaged 24.18 hours.[4] In mammals the master clock is the suprachiasmatic nucleus (SCN) of the hypothalamus. It receives light information directly from the retina and coordinates clocks in cells throughout the body.[1][5] Daily light exposure resets the clock so that it stays aligned with the 24-hour day.[3]

Key facts

• The circadian rhythm is endogenous: it persists without time cues and is reset each day by light and other external timing cues.[2][3]
• The master clock is the suprachiasmatic nucleus (SCN). It receives light information from the retina, including from melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs), through the retinohypothalamic tract.[5][6]
• The 2017 Nobel Prize in Physiology or Medicine went to Jeffrey C. Hall, Michael Rosbash and Michael W. Young for discoveries of molecular mechanisms controlling the circadian rhythm.[2]
• The human internal clock tends to run slightly longer than 24 hours. One controlled study measured an average intrinsic period of 24.18 h.[3][4]
• Dim light melatonin onset (DLMO) is the laboratory reference marker of circadian phase. Wearable-based phase estimates are validated against it.[7]
• An expert consensus for healthy, day-active adults recommends ≥ 250 lx melanopic EDI at the eye during the day, ≤ 10 lx from at least 3 hours before bedtime and ≤ 1 lx in the sleep environment.[8]
• The International Classification of Sleep Disorders (ICSD-3) lists seven circadian rhythm sleep-wake disorders. The 2018 AASM guideline gives a conditional recommendation for actigraphy in their assessment.[9][10][11]
• Multi-day actigraphy (most protocols record 1–2 weeks) quantifies the rest–activity rhythm in free-living conditions when analyzed with non-parametric metrics (IS, IV, RA, L5, M10) and cosinor.[12][13]

On this page

• What does circadian mean?
• The SCN master clock
• The molecular clock
• Period, phase, amplitude and acrophase
• A day for the body clock
• Entrainment, zeitgebers and masking
• How light affects the circadian rhythm
• Melatonin and the circadian rhythm
• Sleep timing, sleep duration and the two-process model
• Chronotypes and social jetlag
• Circadian rhythm sleep-wake disorders
• How the circadian rhythm is measured
• Measuring circadian rhythm with Condor instruments
• Frequently asked questions
• References

What does circadian mean?

Circadian means 'about a day'. The word combines the Latin circa ('around') and dies ('day'). It describes biological rhythms that have a period of approximately 24 hours and are generated inside the organism.[2]

Equivalent terms in other European languages: ritmo circadiano (Portuguese, Spanish, Italian), rythme circadien (French), zirkadianer Rhythmus (German).

The first experimental hint that such rhythms are internal came in the 18th century. The astronomer Jean Jacques d'Ortous de Mairan placed a mimosa plant in constant darkness and found that its leaves kept opening and closing on a daily schedule.[2] Later work showed that animals and humans have comparable biological clocks, which prepare physiology for the predictable changes of the day.[2]

Circadian vs diurnal

The two words are often used interchangeably, but they mean different things:

• Circadian describes a rhythm that is endogenous, generated by an internal clock. It therefore persists when external time cues are removed, with a period close to but not exactly 24 hours.[3][4]
• Diurnal describes a day–night pattern or a day-active species. A diurnal pattern can be driven by the environment alone, for example activity that simply follows the light. A 24-hour pattern therefore does not by itself prove that a rhythm is circadian.

Humans are a day-active species with circadian rhythms. To show that a particular rhythm is truly circadian, researchers must show that it persists under constant conditions.

Types of biological rhythm

Period boundaries are described qualitatively here. Numeric cutoffs for ultradian and infradian rhythms differ between textbooks.

What controls the circadian rhythm? The SCN master clock

The circadian rhythm is controlled by the suprachiasmatic nucleus (SCN), a small paired cluster of neurons in the hypothalamus that acts as the body's master clock. Light signals from the retina set the SCN; they travel along the retinohypothalamic tract (RHT).[1][5]

The retinal cells that project to the SCN are intrinsically photosensitive retinal ganglion cells (ipRGCs). They contain the photopigment melanopsin and respond to light directly.[5] Their sensitivity, spectral tuning and slow response kinetics match the properties of circadian photoentrainment.[6]

Two companion papers published in Science in February 2002 established this pathway in rodents:

• Hattar and colleagues found that ganglion cells in rat retina that were intrinsically photosensitive always expressed melanopsin. In genetically marked mice, the axons of melanopsin cells projected to the SCN and to other brain areas involved in non-image-forming vision.[5]
• Berson and colleagues recorded from rat retina and showed that ganglion cells projecting to the SCN are intrinsically photosensitive.[6]

The background to this work was the observation that, in rodents, photoentrainment of the SCN persists without functional rods and cones.[5] That finding does not mean rods and cones play no role in the intact human eye. The measurement framework used in circadian research weights light for all five photoreceptor classes of the human retina, because rods and cones can also contribute to non-visual responses.[14]

What does the SCN control?

The SCN translates the light signal into timing outputs:

• Melatonin. The SCN controls melatonin production by the pineal gland according to light, so melatonin rises during the biological night.[1]
• Peripheral clocks. Clock mechanisms operate in cells throughout the body. The SCN keeps these tissue rhythms synchronized with each other and with the external day.[1][2]

Why the melanopsin pathway responds most strongly to short-wavelength light is covered in our guide to ipRGC and melanopsin spectral sensitivity.

How does the molecular clock work?

Inside each clock cell, the circadian rhythm is generated by a transcription–translation feedback loop. Clock genes are transcribed and their protein products accumulate. Those proteins then switch off their own genes, and the cycle restarts roughly once a day.[2]

The mechanism was worked out in fruit flies (Drosophila):[2]

1. In the 1970s, Seymour Benzer and Ronald Konopka showed that mutations in an unknown gene, which they named period, disrupted the flies' circadian clock.
2. In 1984, Jeffrey Hall and Michael Rosbash (Brandeis University) and Michael Young (Rockefeller University) isolated the period gene. Hall and Rosbash then found that its protein, PER, accumulates during the night and is degraded during the day.
3. Hall and Rosbash proposed that PER blocks the activity of its own gene through an inhibitory feedback loop.
4. In 1994, Young discovered a second clock gene, timeless. Its protein, TIM, binds PER, and the pair enters the cell nucleus. There it blocks period gene activity, closing the loop.
5. Young then identified doubletime, whose protein DBT delays PER accumulation. This is one way the oscillation is tuned to a 24-hour cycle.

The laureates also identified proteins required to activate the period gene, and the mechanism by which light synchronizes the clock.[2] The Nobel Committee's scientific background describes the fly transcriptional activators CLOCK and CYCLE as part of this machinery.[15] For these discoveries, Hall, Rosbash and Young received the 2017 Nobel Prize in Physiology or Medicine.[2]

The same principles operate in the cells of other multicellular organisms, including humans, and the biological clock regulates a large proportion of human genes.[2] Mammalian clock genes differ in name and detail from the fly genes shown here.

Period, phase, amplitude and acrophase: how a rhythm is described

A circadian rhythm is described by five parameters:[12]

• period: how long one cycle lasts
• phase: when a reference point in the cycle occurs
• MESOR: the rhythm-adjusted mean
• amplitude: half the predictable change within a cycle
• acrophase: the timing of the fitted peak

The standard way to estimate these parameters is cosinor analysis, which fits a cosine curve of known period to a time series. The single-component cosinor model is:[12]

Y(t) = M + A·cos(2πt/τ + φ) + e(t)

where M is the MESOR, A the amplitude, τ the period, φ the acrophase expressed as an angle, and e(t) the error term. In this form the fitted peak occurs at clock time t = −φ·τ/(2π) (modulo τ). This is why acrophase is often reported as a negative angle and then converted to clock time.

Two cautions apply when comparing studies. First, some texts define amplitude as the whole peak-to-trough difference, which the cosinor convention calls the double amplitude. Second, software packages use different sign conventions for acrophase, such as negative degrees versus positive clock time. Check the convention before comparing acrophases.[12]

Phase can be expressed with several markers: the acrophase of a fitted activity or temperature curve, the midpoint of sleep, or a physiological marker such as DLMO. These markers are related but not interchangeable. Activity timing, for instance, can shift with behavior without a corresponding shift in melatonin timing (see How is the circadian rhythm measured?).

What does a day look like for the body clock?

Over 24 hours, the body clock produces a predictable sequence of physiological events. Melatonin begins to rise in the evening and sleep follows. Core body temperature reaches its minimum during the biological night, and melatonin declines toward morning, before waking.[4][16]

For a day-active adult living on a regular schedule, the main markers occur in this order:

1. Dim light melatonin onset (DLMO): the evening rise of melatonin, measured under dim light. It is the most widely used anchor for circadian phase.[7]
2. Sleep onset: in entrained sleepers, after the evening melatonin rise.
3. Core body temperature (CBT) minimum: during the biological night. In the cited laboratory studies, light seen before this point tended to delay the clock and light seen after it tended to advance it.[16]
4. Melatonin offset: the decline of melatonin toward the end of the biological night.
5. Wake: followed by the active day, when melatonin remains low.

The intervals between these markers vary between individuals and with chronotype. This guide therefore gives the order of events rather than fixed clock times or offsets. Individual timing should be measured, not assumed.

Internal and external temporal organization

Chronobiologists distinguish two kinds of temporal order:

• Internal temporal organization is the stable phase relationship between rhythms inside the body, for example between melatonin, core body temperature, cortisol and the sleep–wake cycle.[4]
• External temporal organization is the relationship between those internal rhythms and the environment, above all the light–dark cycle.

Healthy entrainment preserves both. Circadian misalignment disturbs one or both (see What happens when the circadian rhythm is disrupted?).

How is the circadian rhythm synchronized? Entrainment, zeitgebers and masking

The circadian rhythm is synchronized by entrainment. The human clock tends to run slightly longer than 24 hours, so external timing cues (zeitgebers) have to reset it every day, and light is the dominant zeitgeber.[3][4]

Why the clock needs daily resetting

Under carefully controlled lighting, the intrinsic period of the human circadian pacemaker averaged 24.18 hours in both young and older adults, with a tight distribution between individuals.[4] Left alone, a clock with a period longer than 24 hours would drift later each day. NIOSH describes the practical consequence: the internal rhythm tends to run longer than 24 hours, but the sun's light–dark cycle resets it every day.[3]

Zeitgebers

Light reaching the eye is the strongest zeitgeber for the human SCN (see How does light affect the circadian rhythm?). Non-photic cues also carry time information and are studied as secondary synchronizers: the timing of meals, physical activity, social schedules and ambient temperature.

Entrainment vs masking

• Entrainment is a genuine adjustment of the clock's phase and period, so that the internal rhythm keeps a stable relationship with the external cycle. The adjustment persists after the cue is removed.
• Masking is a direct effect of an event on a measured variable, with no change in the underlying clock. Examples are activity suppressed by darkness, or a rise in temperature caused by exercise. The rhythm appears shifted only while the event lasts.

Masking matters for measurement. Rest–activity data collected in daily life mix clock-driven and behavior-driven components. This is one reason activity timing cannot directly substitute for a physiological phase marker.

Free-running rhythms and laboratory protocols

When a person is removed from time cues, the clock free-runs at its intrinsic period, and sleep and other rhythms drift progressively later relative to clock time. Laboratories use two classic designs to separate clock-driven variation from masking:

• Constant routine. Participants stay awake under constant dim light and posture, with food given in small, evenly spaced portions. The remaining variation in melatonin, core body temperature or cortisol then reflects the clock.
• Forced desynchrony. Participants live on an imposed 'day' that is too long or too short for the clock to follow. Sleep and wake then occur at all circadian phases, so the intrinsic period and circadian effects can be estimated separately from sleep–wake effects.

The 24.18-hour estimate above came from melatonin, core body temperature and cortisol rhythms measured under carefully controlled lighting.[4]

For study-design considerations, see our guide to light exposure and circadian entrainment with integrated wearable sensors.

How does light affect the circadian rhythm?

Light resets the SCN clock through the melanopsin-based ipRGC pathway. The direction of the shift depends on when the light is seen, and its size depends on the light's intensity, spectrum and duration.[14][16][17]

Melanopic EDI: measuring light as the clock sees it

ipRGCs are most sensitive to shorter wavelengths than the visual system is. Photopic lux weights light by visual sensitivity, so it is not the right measure for circadian research. The international standard CIE S 026:2018 defines the spectral sensitivities of the five photoreceptor classes of the human eye and a set of metrics for ipRGC-influenced responses.[17]

The standard's most practical metric is melanopic equivalent daylight illuminance (melanopic EDI). It is the illuminance, in lux, of standard D65 daylight that would produce the same melanopsin-weighted stimulus as the light being measured.[17] Computing it requires spectral information. The step-by-step method is in our guide on how to calculate melanopic EDI.

Timing: the phase response curve

The phase response curve (PRC) describes how a light pulse shifts the clock, depending on the circadian time at which it is seen. In the constant-routine studies cited below, light before the core body temperature minimum (in the evening and early biological night) generally delayed the clock, and light after the minimum generally advanced it.[16] Three constant-routine laboratory studies quantified this:

• A 6.7-hour pulse of about 10,000 lx white light produced a fitted peak-to-trough PRC amplitude of 5.02 h.[16]
• A single 1-hour pulse of about 8,000 lx produced an amplitude of 2.20 h.[18]
• A 6.5-hour pulse of 480 nm blue light at only about 11 photopic lux produced a maximum delay of −2.6 h and a maximum advance of +1.3 h.[19]

These are laboratory results obtained with controlled gaze, intensity and timing. Shifts in everyday life are smaller and more variable. A full PRC figure is in our circadian light guide.

How much light, and when? The 2022 expert consensus

Brown and colleagues published consensus recommendations for indoor light exposure in healthy adults on regular, day-active schedules. All are expressed as melanopic EDI:[8]

• Daytime: at least 250 lx melanopic EDI at the eye, measured in the vertical plane at about 1.2 m height. Daylight is preferred; where electric light is used, a short-wavelength-enriched spectrum is recommended.
• Evening: no more than 10 lx melanopic EDI, starting at least 3 hours before bedtime.
• Sleep environment: as dark as possible, with no more than 1 lx melanopic EDI.

The recommendations were developed for healthy adults. Applying them to shift workers, children, older adults or clinical groups requires caution, and they are consensus values, not individual dose–response guarantees.[8]

Checking whether a participant actually receives these exposures requires a wearable spectral light dosimeter. Our related guides cover:

• why melanopic light measurement matters in lighting design
• quantifying circadian light exposure in real-world research
• wearable placement strategies for circadian research

How is melatonin related to the circadian rhythm?

Melatonin is the hormone through which the SCN signals biological night. The pineal gland secretes it during the night under SCN control, and light at night suppresses it.[1][14]

Melatonin is therefore both an output of the clock and a way to read it. Its evening rise, dim light melatonin onset (DLMO), is the most widely used marker of circadian phase in humans. DLMO must be sampled under dim light, because light suppresses melatonin and would mask the onset. In the validation study by Cheng and colleagues, participants provided hourly saliva samples in dim light below 10 lux.[7] DLMO is measured in saliva or plasma. A urinary melatonin metabolite (6-sulfatoxymelatonin, aMT6s) is also used to characterize the overall melatonin rhythm.

DLMO requires timed sampling under controlled light, which makes it burdensome outside the laboratory. Home-based saliva protocols and model-based estimates from wearable data are therefore active research areas (see How is the circadian rhythm measured?).

This guide does not give melatonin dosing or treatment advice; clinical questions belong with a sleep medicine specialist. For more on the hormone's physiology, see our article on melatonin and its relationship with sleep and biological rhythms.

Does sleep timing matter as much as sleep duration? The two-process model

Both matter, and they are complementary. The two-process model of sleep regulation describes sleep as the product of two processes:[20]

• a homeostatic process (Process S) that depends on how long one has been awake and asleep
• a circadian process (Process C) that depends on the time of day

Alexander Borbély proposed the model in 1982. It was reappraised in 2016 as evidence accumulated and revisited in a 2022 retrospective.[20][21][22] In its classic form:

• Process S, or sleep pressure, builds up during wakefulness and dissipates, roughly exponentially, during sleep.[22]
• Process C, the circadian process, sets the thresholds at which sleep begins and ends. The same level of sleep pressure therefore has different consequences at different circadian times.[22]

For research, the implication is that sleep duration and sleep timing answer different questions. Duration reflects how much homeostatic recovery occurred. Timing relative to the circadian clock determines whether sleep falls within the circadian window that favors sleep. Neither replaces the other, so well-designed protocols measure both: sleep duration from actigraphy or polysomnography, and circadian timing from phase markers or rest–activity rhythm metrics.

What are chronotypes and social jetlag?

A chronotype is a person's characteristic timing of sleep and activity within the 24-hour day, from early (morning) types to late (evening) types. Social jetlag is the mismatch between that biological timing and the timing imposed by work or school schedules.[23][24][25]

Measuring chronotype

• Morningness–Eveningness Questionnaire (MEQ). Horne and Östberg's 1976 self-assessment has 19 items, with total scores from 16 to 86. Higher scores indicate a stronger morning preference, and scores fall into five categories from definite evening type to definite morning type. In the original study, the self-reported time of peak alertness matched the time of peak body temperature.[23]
• Munich ChronoType Questionnaire (MCTQ). Introduced by Roenneberg and colleagues in 2003, it asks about sleep times separately for work days and free days.[24] Chronotype is expressed as mid-sleep on free days, usually corrected for the extra sleep people obtain on free days (MSF_sc).[25]

Chronotype questionnaires measure preference or behavior, not circadian phase itself. In research they complement physiological markers such as DLMO.

Social jetlag

Wittmann and colleagues introduced the term social jetlag in 2006 to describe the misalignment between biological and social time. It shows up as the difference between sleep timing on work days and on free days.[25] Later studies usually compute it as the absolute difference between mid-sleep on free days (MSF) and mid-sleep on work days (MSW):

Social jetlag = |MSF − MSW|

Mid-sleep is sleep onset plus half the sleep duration. A worked example with hypothetical sleep times:

The example is hypothetical, not participant data or a study result. Published studies may also use a signed version or the corrected MSF_sc. Travel jet lag and social jetlag share the same underlying problem, a clock out of step with the schedule; our article on jet lag and social jetlag discusses both.

What happens when the circadian rhythm is disrupted?

When the circadian rhythm is disrupted, the internal clock falls out of step with the timing of sleep, work or light exposure. This is circadian misalignment. When it causes persistent insomnia or excessive sleepiness with significant distress or impairment, it may constitute one of the circadian rhythm sleep-wake disorders (CRSWD) in the International Classification of Sleep Disorders.[9][10]

Misalignment can arise from the clock itself, as with an unusually early or late phase or a weak rhythm, or from the environment, as with shift work or transmeridian travel. Even a temporary mismatch, such as jet lag after crossing several time zones, affects wellbeing.[2]

Circadian rhythm sleep-wake disorders in ICSD-3

The American Academy of Sleep Medicine publishes the third edition of the International Classification of Sleep Disorders (ICSD-3) and its text revision (ICSD-3-TR), which list seven CRSWD.[9][10] Reviews summarizing ICSD-3 describe general criteria shared by all seven:[9][10]

• a chronic or recurrent disturbance of the sleep–wake pattern, due to an alteration of the circadian system or a misalignment between the internal rhythm and the desired or required schedule
• insomnia, excessive sleepiness or both
• clinically significant distress or impairment

The disturbance is generally required to persist for at least three months; jet lag disorder is the exception.[10]

The table summarizes categories and core features for orientation. It is not a diagnostic instrument: diagnosis requires clinical evaluation against the full ICSD-3-TR criteria.

Circadian rhythm disorder vs insomnia

A circadian rhythm sleep-wake disorder can look like insomnia, but the cause differs. In a CRSWD, the complaint of insomnia or sleepiness arises mainly because the required sleep schedule conflicts with circadian timing. In phase disorders, sleep is typically less disturbed when it can occur at the time the clock favors.[9] Because the symptoms can overlap, a clinician evaluates their timing and history and considers other possible causes.

Telling the two apart requires clinical evaluation, commonly with multi-week sleep diaries and actigraphy. The 2018 American Academy of Sleep Medicine clinical practice guideline gives a conditional recommendation ('we suggest') for the use of actigraphy in the assessment of circadian rhythm sleep-wake disorders.[11]

Research on these populations is covered in our articles on actigraphy in shift-work research and actigraphy in psychiatric practice for circadian rhythm sleep-wake disorders.

Educational note: this section is educational and is not medical advice. Persistent sleep or sleepiness complaints should be evaluated by a qualified sleep medicine clinician.

How is the circadian rhythm measured?

Researchers measure the circadian rhythm by combining several methods:[4][7][12][13]

• physiological phase markers: DLMO, core body temperature, cortisol
• rest–activity actigraphy, analyzed with non-parametric metrics and cosinor
• personal light dosimetry in melanopic EDI
• sleep diaries and questionnaires

Model-based methods can also estimate phase from wearable data.

No single method captures everything. Phase markers give the most direct estimate of clock timing but are burdensome. Actigraphy and light dosimetry capture weeks of free-living behavior and exposure. Questionnaires capture preference and schedule.

Comparison of methods

Rest–activity rhythm metrics: NPCRA and cosinor

Non-parametric circadian rhythm analysis (NPCRA), as applied to actigraphy by Van Someren and colleagues, summarizes the rest–activity rhythm without assuming a sinusoidal shape:[13]

Cosinor analysis adds the MESOR, amplitude and acrophase of a fitted 24-hour curve (see Period, phase, amplitude and acrophase).[12] Most actigraphy protocols record 7–14 consecutive days, 24 hours per day, so that day-to-day stability and both work and free days are represented. See actigraphy: how it works and when to use it.

Estimating circadian phase from wearable data

Mathematical models of the human circadian clock can estimate phase, usually expressed as predicted DLMO, from longitudinal activity, sleep and light data. Results depend strongly on the population and the reference method:

• Cheng et al. 2021 studied 45 fixed night-shift workers who wore wrist actigraphs before an in-laboratory DLMO assessment. Model predictions agreed with laboratory DLMO with a Lin's concordance coefficient of 0.70, about twice the agreement obtained when average sleep timing was used as a proxy. The mean absolute error was 2.88 h; 76% of predictions fell within 2 h of laboratory DLMO and 91% within 4 h.[7]
• Huang et al. 2021 compared several mathematical models and wearable devices for predicting circadian phase across populations with different degrees of circadian disruption.[26]

These results show agreement that is useful for research applications. They also show that individual estimates can differ from the reference by hours. Our guide to circadian phase estimation using wearables covers initialization, recording duration and validation design.

Illustrative image.

Building a multimodal protocol

In practice, circadian studies combine several data streams:

• actigraphy for rest–activity rhythms
• a spectral light dosimeter for exposure
• a digital sleep diary for rest intervals and context
• a phase marker such as DLMO, where the research question requires it

Related methods articles cover circadian biomarker discovery from integrated wearable sensor data and wearable sensor fusion for circadian health studies. Publications are listed in our bibliography.

Measuring circadian rhythm with Condor instruments

Condor Instruments product information: Condor Instruments manufactures the devices described in this section.

ActLumus combines a 10-channel spectral light sensor with melanopic EDI (CIE S 026) and photopic lux reporting in a research actigraph. The sensor combines its 10 channels to estimate melanopic EDI and photopic illuminance. Light exposure is therefore recorded, alongside activity, in the metric used by the 2022 consensus recommendations.

ActLumus also includes:

• an accelerometer
• wrist and ambient temperature sensors
• off-wrist detection
• an event button
• Bluetooth connection, Condor Cloud integration and an API for third-party systems

Explore ActLumus

Independent benchmark. NIH-affiliated investigators tested four wearable light sensor models (eight units each) against a criterion spectrometer under cool and warm LED white light and sunlight; ActLumus was one of the four. The abstract reports:[27]

• the lowest inter-device variability of the four models for ActLumus
• melanopic illuminance that was less accurate for one comparator device than for ActLumus, particularly under warm indoor light

ActTrust 2 is a research actigraph with:

• an RGB light sensor that measures red, green and blue intensity independently
• temperature sensors
• an event marker
• an LCD time display

In a prospective study, 9 adults wore ActTrust 2 and the discontinued Actiwatch 2 simultaneously for 7 days. Interdaily stability, intradaily variability, relative amplitude and L5 did not differ significantly between the devices, while M10 was lower with ActTrust 2. The authors concluded that the devices gave equivalent results for rest–activity rhythm and sleep, and advised caution when interpreting MESOR, amplitude, sleep onset latency, awakenings and M10.[28] Explore ActTrust 2

ActStudio is Condor's analysis software. It provides cosinor, non-parametric (NPCRA), periodogram and actogram analyses, reports light as melanopic EDI and photopic lux, and generates customizable reports. Explore ActStudio

Frequently asked questions

What is a circadian rhythm in simple terms?

A circadian rhythm is the body's internal daily cycle. An internal clock times sleep and wakefulness, hormone release and body temperature over roughly 24 hours, and light resets that clock every day.[1][3]

What does circadian mean?

Circadian means 'about a day', from the Latin circa ('around') and dies ('day'). It describes rhythms of approximately 24 hours that the organism generates internally rather than simply following the environment.[2]

How long is the human circadian rhythm?

The human circadian clock runs slightly longer than 24 hours. Under carefully controlled lighting, its intrinsic period averaged 24.18 hours in both young and older adults, and daily light exposure keeps it aligned to 24 hours.[3][4]

What controls your circadian rhythm?

The suprachiasmatic nucleus (SCN) in the hypothalamus is the master clock. It receives light information from melanopsin-containing retinal ganglion cells through the retinohypothalamic tract, and it coordinates clocks in cells throughout the body.[1][5][6]

What is the difference between circadian and diurnal rhythms?

An internal clock generates a circadian rhythm, which persists with a period close to 24 hours when time cues are removed. A diurnal rhythm is any day–night pattern and may simply follow the environment, so a 24-hour pattern alone does not prove that a rhythm is circadian.[4]

How does light affect the circadian rhythm?

Light resets the clock through the melanopsin-based ipRGC pathway, and its effect depends on timing. In laboratory studies, light before the core body temperature minimum generally delays the clock, and light after it generally advances the clock.[16] For healthy day-active adults, expert consensus recommends at least 250 lx melanopic EDI during the day and no more than 10 lx in the 3 hours before bedtime.[8]

How is melatonin related to the circadian rhythm?

The pineal gland secretes melatonin during the biological night under the control of the SCN, and light at night suppresses it.[1] Its evening rise, dim light melatonin onset (DLMO), is the reference marker used to measure circadian phase.[7]

Is a circadian rhythm disorder the same as insomnia?

No. In a circadian rhythm sleep-wake disorder, insomnia or sleepiness arises mainly from a mismatch between circadian timing and the required schedule.[9] Telling the two apart requires clinical evaluation, commonly with sleep diaries and actigraphy.[11]

Does sleep timing matter more than sleep duration?

Both matter, and they are complementary. The two-process model describes sleep as the combined result of homeostatic sleep pressure (Process S), which relates to duration, and circadian timing (Process C), so neither can replace the other.[20][21]

Can the circadian rhythm be shifted or reset?

Yes. Light resets the clock every day. Laboratory studies show that light before the core body temperature minimum generally delays the clock, while light after the minimum generally advances it.[16][18] Deliberately shifting the rhythm to treat a sleep problem should be planned and supervised by a sleep medicine clinician.

What is social jetlag?

Social jetlag is the misalignment between biological and social time, seen as a difference between sleep timing on work days and free days.[25] It is usually calculated as the absolute difference between mid-sleep on free days and mid-sleep on work days, |MSF − MSW|.

How do researchers measure circadian rhythm?

They combine phase markers such as DLMO and core body temperature with multi-week actigraphy, analyzed with non-parametric metrics (IS, IV, RA, L5, M10) and cosinor. They add personal light dosimetry in melanopic EDI and sleep diaries or chronotype questionnaires.[7][12][13]

Planning a circadian rhythm study?

Tell us your protocol — population, duration, and whether light exposure is an outcome. We will send device specifications, validation references and sample data so you can evaluate fit.

Talk to our team · Explore ActLumus

Related research resources

• Melanopic EDI and how to measure circadian light
• Actigraphy: how it works, what it measures, and when to use it
• Circadian phase estimation using wearables: methods, limitations and validation
• Light exposure and circadian entrainment with integrated wearable sensors
• Why melanopic light measurement matters in today's lighting design
• Bibliography

References

1. National Institute of General Medical Sciences (NIGMS). Circadian rhythms [fact sheet]. National Institutes of Health. nigms.nih.gov
2. Nobel Assembly at Karolinska Institutet. The 2017 Nobel Prize in Physiology or Medicine: press release. 2 October 2017. nobelprize.org
3. National Institute for Occupational Safety and Health (NIOSH). Circadian rhythms and circadian clock. Centers for Disease Control and Prevention; archived training module. archive.cdc.gov
4. Czeisler CA, Duffy JF, Shanahan TL, et al. Stability, precision, and near-24-hour period of the human circadian pacemaker. Science. 1999;284(5423):2177–2181. doi:10.1126/science.284.5423.2177
5. Hattar S, Liao HW, Takao M, Berson DM, Yau KW. Melanopsin-containing retinal ganglion cells: architecture, projections, and intrinsic photosensitivity. Science. 2002;295(5557):1065–1070. doi:10.1126/science.1069609
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Last reviewed September 2026 by the Condor Research Team. Condor Instruments manufactures the ActLumus and ActTrust actigraphs; product mentions are identified as such. This guide is educational and is not medical advice.