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Light therapy is increasingly applied in a spectrum of clinical maladies in psychiatry and sleep medicine, including seasonal affective disorder, delirium associated with dementia, and circadian sleep disorders.

This article reviews neural underpinnings of circadian neurobiology crucial for understanding the influence of light therapy upon brain function, common mood and sleep disorders where light therapy may be effectively utilized, and applications of light therapy in clinical practice.

Circadian Neurobiology: Light's Impact Upon the Brain
A circadian rhythm is a self-sustaining biological activity oscillating with a periodicity near 24 hours. Circadian rhythms are universal in mammalian species, governing cyclical homeostatic bodily processes including the sleep-wake cycle, core body temperature and hormonal release.

The endogenous circadian period of humans is slightly longer than the clock day at approximately 25.3 hours, and the light-dark cycle holds key influence over humans in entraining them to the 24-hour day.1

Circadian rhythms are generated within the brain. The suprachiasmatic nucleus (SCN) consists of paired clusters of 50,000 neurons within the anterior hypothalamus, which exert principle neural control over mammalian circadian rhythms as the endogenous pacemaker.

The activity of the SCN is under the control of more than a dozen time-keeping genes that are under the influence of light by a complex feedback loop. Several factors affect the SCN and entrain an individual's circadian rhythms to the environment.

Entrainment is the process by which external stimuli, or so-called zeitgebers (literally, from the German, time-givers), act as time cues to synchronize the timing and periodicity of an organism's biological rhythms with their surrounding environment.

Photic and non-photic cues signal the time of day for humans, thus, internal circadian rhythms may be either in or out of phase with the environment. A significant mismatch may lead to clinical circadian sleep disorders, and circadian imbalances are also associated with a variety of primary mood disorders, giving rise to clinical neurovegetative sleep-wake disturbances such as hypersomnolence and insomnia.

Non-photic cues such as food, social interaction and physical activity exert important influences upon the SCN via inputs from the raphe nucleus, the pineal gland, limbic system and thalamus.

The light-dark cycle is the major synchronizing stimulus for humans. Neurons of the SCN are most active during daylight. Light acts on the central nervous system via both direct and indirect routes. Light is transduced by retinal photoreceptors and melanopsin cells, generating neural activity that is then conveyed to the brain via direct retinohypothalamic and indirect geniculohypothalamic tracts to the SCN.2

Very short light wavelengths (420 to 480 nm) are sufficient to suppress melatonin secretion, differing from the typical scotopic and photopic visual system.3 SCN neurons give rise to widespread projections to other hypothalamic nuclei, the basal forebrain, thalamus and the pineal, where the SCN influences the cyclical release of melatonin.

The function of melatonin is to serve as a signal of darkness by providing inhibitory feedback upon the SCN pacemaker, thereby facilitating and consolidating the nocturnal sleep period.

Clinical Disorders Benefited by Light Therapy
Light therapy can be considered for treatment of several disorders involving misalignment of the sleep-wake cycle and circadian rhythms. Mood disorders, which are highly prevalent in society, usually involve disturbed sleep and other neurovegetative sequelae suggesting disrupted circadian architecture. They're frequently resistant to standard medical therapies, making them desirable targets for adjunctive or primary therapy with bright light.4 The most light responsive mood disorder is seasonal affective disorder (SAD).

SAD is an annually recurring (circannual) disorder, most commonly seen in women and young adults, characterized by atypical, winter depression with features of increased appetite with carbohydrate craving, weight gain, hypersomnia and increased total sleep time.5 By contrast, typical melancholic depression is instead associated with anorexia, weight loss and insomnia.

There's now substantial evidence for the use of light therapy in SAD.6-11 Bright fluorescent light therapy (i.e., >2500 lux) is administered for at least 1.5 to 2 hours each morning, or higher intensity brightness (>10,000 lux) can be given for a briefer exposure of 30 to 40 minutes.11,12

Morning bright light may phase advance delayed circadian rhythms in SAD patients.13 A minority of patients with SAD appear to respond better to evening than morning light administration, but most patients, especially those with hypersomnia, respond best to morning light.14 Interestingly, a recent study suggested that morning light also improved winter sleep quality in a normal community population in the Netherlands.15

There may be potential widespread future commercial uses for light therapy throughout the relatively light-deprived Northern Hemisphere, should further research confirm these benefits.

Bright light also can be applied as adjunctive treatment in non-seasonal cases of depression, given that at least 30 percent of depressed patients have treatment resistance or intolerance toward antidepressant medications.16-20

Light therapy appears promising in both unipolar and bipolar depression, demonstrating a more rapid onset of action than antidepressant medications, and comparable efficacy, although precipitation of mania is possible, and most studies of non-seasonal depression have had limited follow-up.21-23

Elderly institutionalized patients may have severe disturbances of circadian rhythms due to deteriorating SCN function and diminished zeitgebers given decreased social interaction, reduced environmental light, and decreased sensory visual and auditory input.24

Sundowning and medical delirium, especially when associated with underlying dementia, may be benefited by bright light therapy administered during the evening hours. Disruptive nocturnal behaviors such as agitation and wandering may be reduced, and nocturnal sleep improved, by light therapy in both outpatients and hospitalized or institutionalized dementia patients with disrupted sleep-wake cycles.25-29

Evening light administration also may assist in consolidating sleep in elderly with sleep maintenance insomnia or early morning awakening.30-33 However, conflicting evidence regarding the benefit of light therapy in this patient population has been reported. One recent rigorous study failed to demonstrate improvements in nocturnal sleep by light therapy in delirious institutionalized demented patients.34

Additional large prospective clinical trials are warranted to clarify the best role for light therapy in the treatment of behavioral problems accompanying dementia.35

Circadian sleep disorders are misalignments of sleeping patterns with environmental cues for the sleep-wake cycle, resulting in undesirable relative insomnia or hypersomnia relative to the environmental clock time. Circadian disorders may be considered as intrinsic or extrinsic. Extrinsic circadian sleep disorders are most common, such as shift work sleep disorder and jet lag syndrome. Two exemplary intrinsic circadian disorders include advanced sleep phase syndrome (ASPS) and delayed sleep phase syndrome (DSPS).

One extrinsic cause of circadian disturbance is baseline bright light exposure encountered in patients' daily life during their occupation or hobbies. Inquiring about bright light exposure in people with disturbed sleep-wake patterns may assist in helping them to avoid light stimuli that disrupt entrainment to clock time, and inform appropriate prescription of adjunctive light therapy.36

Shift work sleep disorder occurs due to mismatch between the work and sleep-wake cycle schedule and internal circadian rhythms, and can sometimes be aided by light therapy.37,38 Habitual night shift workers demonstrate improved nocturnal alertness under bright light exposure in the workplace, and restriction of morning light.39

Jet lag syndrome occurs due to the mismatch between a previously entrained circadian rhythm and a new external environmental time imposed by transmeridian travel. Humans are capable of resetting their internal clock by only one hour daily.

Eastward travel, when clock time moves forward relative to the traveler's entrained time zone, is particularly difficult for accommodation, while westward travel is somewhat easier given the intrinsic human circadian period that is slightly longer than one day (i.e., westward travelers may "auto-accommodate" as it's somewhat easier to stay up later than to retire unnaturally earlier against a new eastern time zone).

While light therapy can be employed to accelerate and ease the traveler's entrainment to a new time zone, no large controlled studies have yet resolved issues such as optimal timing for light therapy on the first and successive days of treatment, and whether a "one size fits all" or individualized light exposure dosage is best.40

Recent studies have suggested that a preflight program of combined morning light and phase advancement appear feasible, and that even a simpler strategy of scheduled daylight exposure and avoidance may be helpful to minimize jet lag in transmeridian travelers.41-43

ASPS causes an undesirably early onset of sleep in the evening and consequent early morning awakening. Excessive daytime sleepiness results, but most commonly patients with ASPS are plagued by inability to stay awake for social events in evening hours. ASPS is most common in older adults.

DSPS instead is more frequent in adolescents and young adults, and leads to delayed bedtime, and impaired ability to arise early or even to entrain to a usual daytime work schedule. Attempts to realign the sleep cycle without chronotherapy often fail, resulting in sleep-onset insomnia and daytime hypersomnia when patients with DSPS attempt to adhere to an ordinary daytime work schedule.

Appropriately timed bright light exposure can assist in phase shifting patients with ASPS and DSPS back toward an appropriately entrained sleep-wake period for their clock time. Evening light therapy is used in ASPS to phase delay patients toward a later bed time.

Morning light therapy, or light mask treatment administered through closed eyelids during sleep, can be used to phase advance those with DSPS.44,45 One patient with "free-running" circadian rhythms, a young man with non-24 hour sleep-wake syndrome, was entrained to clock time by light therapy alone.46

While adjunctive melatonin dosing also can be considered in circadian disorders, the quality of commercially available melatonin isn't well-regulated, and the quantity of melatonin dosing and best timing of administration remain unclear.

Applying Light Therapy in Clinical Practice
Light stimuli capable of influencing the neural circadian pacemaker need to be extraordinarily bright, comparable to outdoor daylight intensity, which typically ranges from 5,000 to 20,000 lux. Light therapy must be administered regularly for approximately 5,000 lux-hours daily (i.e., 10,000 lux over a half-hour, 5,000 lux over one hour, or 2,500 lux over two hours would all be equivalent to 5,000 lux-hours).

Therefore, standard indoor lighting (typically 100 to 500 lux) or homemade light sources are usually ineffective. Several commercially available light sources are available.

Adherence to light therapy takes a dedicated patient. The light source should be placed about 16 inches from the patient. Variation in the position of the light source relative to the patient's visual field appears to make little difference, as either upper or middle visual field illumination produces comparable melatonin suppression.47

Recent evidence has suggested that spectral properties of light therapy may be important; short to medium wavelengths, especially blue light, as well as green and yellow, appear necessary for efficacy in SAD, while red and ultraviolet wavelengths aren't essential and may be blocked. Other studies have shown that white light has greater therapeutic benefit.48-50

Administration of light therapy has greatest impact when administered at two chief times. Phase shifting influences by light therapy are related to the time of administration in relationship to the minimum core body temperature, which occurs in most healthy young adults in the hour or two before habitual awakening; phase delays occur when light is given before this time, and phase advances when light is given afterward.1

Thus, the two main times where light is used in clinical practice are early morning administration, which causes phase advances in patients with circadian disorders, and evening administration, which causes phase delays.

In SAD, morning administration, generally prior to 0800 hours, is most effective, throughout the fall and winter months. In delirious demented patients with undesired sundowning behaviors, early evening administration is most beneficial.

Bright lights can pose dangers in patients with retinal pathology and in those utilizing photosensitizing medications. Ophthalmologic evaluation every few years is a reasonable precaution, although no long-term complications of light therapy have been firmly established.

Side effects of light therapy overdose may include agitation, headache or nausea. Insomnia, particularly initial insomnia, also has been seen. Side effects can be obviated by reducing light intensity, increasing distance from the light source, limiting duration of exposure, or by moving morning therapy sessions to a later time or evening treatments to an earlier time.

Continued Expansion
The main clinical applications of light therapy are in mood and circadian sleep disorders, and delirium associated with dementia. About 5,000 lux hours daily administered in the morning or evening for several weeks is usual. Baseline and occasional ophthalmological assessments are a reasonable safety precaution to protect against retinal damage with chronic use.

Given the widespread influences of light upon circadian brain functions, the spectrum of clinical disorders where light therapy is used is likely to continue to expand, with early evidence pointing toward potential efficacy in non-seasonal, premenstrual, and peripartum mood disorders, seasonal bulimia and adult attention deficit disorder.51

Large randomized, controlled clinical trials in non-seasonal mood and circadian sleep disorders would help refine future clinical applications for light therapy.

Erik K. St. Louis, MD, is an assistant professor of neurology, University of Iowa Carver College of Medicine, and co-director of the Iowa Comprehensive Epilepsy Program, University of Iowa Hospitals and Clinics, Iowa City. Dr. St. Louis is a diplomate of the American Boards of Psychiatry and Neurology, Clinical Neurophysiology and Sleep Medicine. His research interests include the relationship between sleep and epilepsy.


1. Dijk DJ, Boulos Z, Eastman CI, et al. Light treatment for sleep disorders: consensus report. II. Basic properties of circadian physiology and sleep regulation. J Biol Rhythms. 1995;10(2):113-25.

2. Brainard GC, Hanifin JP, Greeson JM, et al. Action spectrum for melatonin regulation in humans: evidence for a novel circadian photoreceptor. J Neurosci. 2001;21(16):6405-12.

3. Thapan K, Arendt J, Skene DJ. An action spectrum for melatonin suppression: evidence for a novel, non-rod, non-cone photoreceptor system in humans. J Physiol. 2001;535(Pt 1):261-7.

4. Healy D. Rhythm and blues. Neurochemical, neuropharmacological and neuropsychological implications of a hypothesis of circadian rhythm dysfunction in the affective disorders. Psychopharmacology (Berl). 1987;93(3):271-85.

5. Magnusson A, Partonen T. The diagnosis, symptomatology, and epidemiology of seasonal affective disorder. CNS Spectr. 2005;10(8):625-34.

6. Partonen T, Lonnqvist J. Seasonal affective disorder. Lancet. 1998;352(9137):1369-74.

7. Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective disorder: A description of the syndrome and preliminary findings with light therapy. Arch Gen Psychiatry. 1984;41(1):72-80.

8. Eastman C, Young MA, Fogg LF, et al. Bright light treatment of winter depression: a placebo-controlled trial. Arch Gen Psychiatry. 1998;55(10):883-9.

9. Eastman CI, Boulos Z, Terman M, et al. Light treatment for sleep disorders: consensus report. VI. Shift work. J Biol Rhythms. 1995;10(2):157-64.

10. Terman M, Terman JS, Quitkin FM, et al. Light therapy for seasonal affective disorder: A review of efficacy. Neuropsychopharmacology. 1989;2(1):1-22.

11. Terman M, Terman JS. Light therapy. In: Kryger M, et al., editors. Principles and practice of sleep medicine. 3rd ed. Philadelphia: WB Saunders and Co.; 2000. p. 1258-74.

12. Yerevanian BI, Anderson JL, Grota LJ, et al. Effects of bright incandescent light on seasonal and nonseasonal major depressive disorder. Psychiatry Res. 1986;18(4):355-64.

13. Avery DH, Dahl K, Savage MV, et al. Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression. Biol Psychiatry. 1997;41(11):1109-23.

14. Avery DH, Khan A, Dager SR, et al. Morning or evening bright light treatment of winter depression? The significance of hypersomnia. Biol Psychiatry. 1991;29(2):117-26.

15. Leppamaki S, Meesters Y, Haukka J, et al. Effects of simulated dawn on quality of sleep - a community-based trial. BMC Psychiatry. 2003;3:14.

16. Eisenberg DM, Kessler RC, Foster C, et al. Unconventional medicine in the United States: Prevalence, costs, and patterns of use. N Engl J Med. 1993;328(4):246-52.

17. Elkin I, Shea T, Watkins JT, et al. National Institute of Mental Health Treatment of Depression Collaborative Research Program: General effectiveness of treatment. Arch Gen Psychiatry. 1989;46(11):971-82.

18. Manber R, Allen JJ, Morris MM. Alternative treatments for depression: empirical support and relevance to women. J Clin Psychiatry. 2002;63(7):628-40.

19. Keller MB, McCullogh JP, Klein DN, et al. A comparison of nefazodone, cognitive behavioral-analysis system of psychotherapy, and their combination for the treatment of chronic depression. N Engl J Med. 2000;342(20):1462-70.

20. Keller MB, Gelenberg AJ, Hirschfield RM, et al. The treatment of chronic depression, part 2: a double-blind randomized trial of sertraline and imipramine. J Clin Psychiatry. 1998;59(11):598-607.

21. Kripke DF. Light treatment for nonseasonal depression: speed, efficacy, and combined treatment. J Affect Disord. 1998;49(2):109-17.

22. Martiny K. Adjunctive bright light in non-seasonal major depression. Acta Psychiatr Scand Suppl. 2004;(425):7-28.

23. McEnany GW, Lee KA. Effects of light therapy on sleep, mood, and temperature in women with nonseasonal major depression. Issues Ment Health Nurs. 2005;26(7):781-94.

24. Mishima K, Okawa M, Hozumi S, et al. Supplementary administration of artificial bright light as potent treatment for disorganized circadian rest-activity and dysfunctional autonomic and neuroendocrine systems in institutionalized demented elderly persons. Chronobiol Int. 2000;17(3):419-32.

25. Lyketsos CG, Lindell Veiel L, Baker A, et al. A randomized, controlled trial of bright light therapy in dementia patients residing in long-term care. Int J Geriatr Psychiatry. 1999;14(7):520-5.

26. Satlin A, Volicer L, Ross V, et al. Bright light treatment of behavioral and sleep disturbances in patients with Alzheimer's disease. Am J Psychiatry. 1992;149(8):1028-32.

27. Skjerve A, Holsten F, Aarsland D, et al. Improvement in behavioral symptoms and advance of activity acrophase after short-term bright light treatment in severe dementia. Psychiatry Clin Neurosci. 2004;58(4):343-7.

28. Skjerve A, Bjorvatn B, Holsten F. Light therapy for behavioural and psychological symptoms of dementia. Int J Geriatr Psychiatry. 2004;19(6):516-22.

29. Van Someren EJ, Kessler A, Mirmiran M, et al. Indirect bright light improves circadian rest-activity disturbances in demented patients. Biol Psychiatry. 1997;41(9):955-63.

30. Campbell SS, Eastman CI, Terman M, et al. Light treatment for sleep disorders: consensus report. I. Chronology of seminal studies in humans. J Biol Rhythms. 1995;10(2):105-9.

31. Campbell SS, Terman M, Lewy AJ, et al. Light treatment for sleep disorders: consensus report. V. Age-related disturbances. J Biol Rhythms. 1995;10(2):151-4.

32. Campbell SS, Dawson D, Anderson MW. Alleviation of sleep maintenance insomnia with timed exposure to bright light. J Am Geriatr Soc. 1993;41(8):829-36.

33. Lack L, Wright J. The effect of evening bright light in delaying the circadian rhythms and lengthening the sleep of early morning awakening insomniacs. Sleep. 1993;16(5):436-43.

34. Dowling GA, Hubbard EM, Mastick J, et al. Effect of morning bright light treatment for rest-activity disruption in institutionalized patients with severe Alzheimer's disease. Int Psychgeriatr. 2005;17(2):221-36.

35. Forbes D, Morgan DG, Bangma J, et al. Light therapy for managing sleep, behaviour, and mood disturbances in dementia. Cochrane Database Syst Rev. 2004;(2):CD003946.

36. Doljansky JT, Kannety H, Dagan Y. Working under daylight intensity lamp: an occupational risk for developing circadian rhythm sleep disorder? Chronobiol Int. 2005;22(3):597-605.

37. Boivin DB, James FO. Light treatment and circadian adaptation to shift work. Ind Health. 2005;43(1):34-48.

38. Stewart KT, Hayes BC, Eastman CI. Light treatment for NASA shiftworkers. Chronobiol Int. 1995;12(2):141-51.

39. Yoon IY, Jeong DU, Kwon KB, et al. Bright light exposure at night and light attenuation in the morning improve adaptation of night shift workers. Sleep. 2002;25(3):351-6.

40. Boulos Z, Campbell SS, Lewy AJ, et al. Light treatment for sleep disorders: consensus report. VII. Jet lag. J Biol Rhythms. 1995;10(2):167-76.

41. Burgess HJ, Crowley SJ, Gazda CJ, et al. Preflight adjustment to eastward travel: 3 days of advancing sleep with and without morning bright light. J Biol Rhythms. 2003;18(4):318-28.

42. Eastman CI, Gazda CJ, Burgess HJ, et al. Advancing circadian rhythms before eastward flight: a strategy to prevent or reduce jet lag. Sleep. 2005;28(1):33-44.

43. Lieberman DZ. An automated treatment for jet lag delivered through the internet. Psychiatr Serv. 2003;54(3):394-6.

44. Cole RJ, Smith JS, Alcala YC, et al. Bright-light mask treatment of delayed sleep phase syndrome. J Biol Rhythms. 2002;17(1):89-101.

45. Rosenthal NE, Joseph-Vanderpool JR, Levendosky AA, et al. Phase-shifting effects of bright morning light as treatment for delayed sleep phase syndrome. Sleep. 1990;13(4):354-61.

46. Watanabe T, Kajimura N, Kato M, et al. Case of a non-24 h sleep-wake syndrome patient improved by phototherapy. Psychiatry Clin Neurosci. 2000;54(3):369-70.

47. Smith JS, Kripke DF, Elliott JA, et al. Illumination of upper and middle visual fields produces equivalent suppression of melatonin in older volunteers. Chronobiol Int. 2002;19(5):883-91.

48. Brainerd GC, Sherry D, Skwerer RG, et al. Effects of different wavelengths in seasonal affective disorder. J Affect Disord. 1990;20(4):209-16.

49. Glickman G, Byrne B, Pineda C, et al. Light therapy for seasonal affective disorder with blue narrow-band light-emitting diodes (LEDs). Biol Psychiatry. 2005 Sep 13.

50. Lee TM, Chan CC, Paterson JG, et al. Spectral properties of phototherapy for seasonal affective disorder: a meta-analysis. Acta Psychiatr Scan. 1997;96(2):117-21.

51. Terman M, Terman JS. Light therapy for seasonal and nonseasonal depression: efficacy, protocol, safety, and side effects. CNS Spectr. 2005;10(8):647-63.

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