Seasonal Affective Disorder

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Coming off Antidepressants written for patients

Synonyms: SAD, seasonal adjustment disorder, winter depression, winter blues

Low mood during winter months has been noted as far back as 1845; however, it was not formally recognised as a disorder until the 1980s.

Seasonal affective disorder (SAD) is now classified as a variant of depression, characterised by depressive episodes that recur annually at the same time each year, usually during the winter months. It can be very disabling for patients, and 6-35% of patients require hospitalisation for SAD at some point.

SAD patients spend over 40% of the year struggling with substantial depressive symptoms during most years, beginning in young adulthood.

  • 2% of the population in Northern Europe have severe depression resulting from SAD.
  • In the UK, up to 6% of adults have 'recurrent major depressive episodes with seasonal pattern'.[1]
  • The mean age at presentation of SAD is 27 years.
  • During the reproductive years, it is four times more common in women than in men.
  • Children can also be affected and rates in boys and girls are similar.
  • The prevalence rates reduce in older age and the genders are affected equally.
  • Vulnerability to SAD is increased the further away you live from the equator.
  • There is also a genetic component in that you are more likely to suffer from SAD if a close relative is affected.
  • A seasonal pattern has been observed in 15% of patients with recurrent mood disorders, including unipolar and bipolar forms.

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Light and darkness are thought to affect mood and behaviour via the complex interaction between circadian rhythms and the biological clocks which control them.

Circadian rhythms are innate physiological, mental and behavioural changes which follow a roughly 24- to 25-hour cycle. Biological clocks are groups of interacting molecules in cells throughout the body. A master biological clock is located in the supra-chiasmic nucleus (SCN) which sits within the hypothalamus. This co-ordinates all the body clocks so that they are synchronised.

The master clock in the SCN is affected by light and darkness via the retino-hypothalamic tract. The retino-hypothalamic tract is a neurological pathway connecting the retinal ganglion cells (RGCs) of the retinae to the SCN in the hypothalamus. This connects with the pineal gland via the superior cervical ganglion (SCG).

RGCs → melanopsin → SCN → SCG → pineal gland → supression of melatonin

Sunlight (or light at 480 nm) stimulates the RGCs to produce the photoreceptor melanopsin. Melanopsin 'signals' daytime to the SCN which in turn induces the pineal gland to suppress melatonin production.

Melatonin is produced by the pineal gland. Its primary function is to signal day length to the SCN, acting as a cue for innate nighttime behaviour. Via the activation of melatonin receptors, it affects sleep propensity and the sleep/wake rhythm, circadian rhythms; it induces heat loss, reduces arousal, and delays cortisone production. Melatonin is synthesised from serotonin, which is in turn synthesised from L-tryptophan. Large increases in melatonin production at night are due to a concomitant increase in the activity of the penultimate enzyme in melatonin synthesis, arylalkylamine N-acetyltransferase (serotonin N-acetyltransferase, AANAT). Serotonin levels have a major role in mood modulation.

Light can also affect mood by affecting 'alertness'. Light can affect alertness via non-circadian pathways.[4]

Despite ardent research, the cause of SAD is not yet fully understood. One prevailing theory is that patients with SAD are phase-delayed.[7] This suggests that most patients with SAD become depressed in the winter, at least in part because of a phase delay in circadian rhythms relative to the sleep/wake cycle.  The cause of this 'phase delay' and why it has such a pronounced effect on mood and behaviour, is likely to be multifactorial, involving abnormalities at various levels along the retino-hypothalamic tract, its links with the pineal gland, and the metabolism of melatonin and serotonin. Familial studies suggest a higher incidence of SAD among first-degree relatives, with genetic factors accounting for between 29-69% of variance in seasonal mood symptoms.[2] This suggests that genetic aberrations may underlie the various abnormalities which cause SAD symptoms.

Melatonin secretion occurs later in the night, and for longer periods during the early morning compared to healthy individuals.

Sensitivity to light and melanopsin in SAD patients

  • Recent studies have shown that the retinal sensitivity to light is decreased in SAD patients compared to controls, and that this reduced sensitivity is more frequent among those with a mutated variant of the melanopsin gene.[8]  .
  • Preliminary investigations have found that individuals with a mutated variant of the melanopsin gene (TT) were 5.6 times more likely to have SAD than those without this variant.[2]
  • Sleep onset among those with the TT genotype was later in the day when individuals were assessed on longer days and earlier in the day on shorter days, whereas individuals in the other genotype groups (ie CC and CT) did not show this interaction effect.[9] 

Light and melatonin[10] 

  • Light therapy clearly improves depressive symptoms.
  • Melatonin levels rise later in the night in those with SAD compared with those who do not have SAD. 
  • SAD patients have a longer duration of nocturnal melatonin secretion in winter than in summer months, while healthy controls do not.

Serotonin and SAD[11] 

  • It is well established that serotonin has a major role in suppressing various aspects of feeding behaviour. SAD patients report distinct subjective responses to high-carbohydrate meals, which can enhance serotonin turnover via increased tryptophan uptake into the brain.
  • Serotonin levels in human postmortem samples are found to be at minimum levels during the winter months.
  • Depletion of L-tryptophan, which is a precursor of serotonin, is associated with a relapse of depressive symptoms in patients who are in remission due to light therapy.
  • Although treatment with melatonin itself is not helpful for people with SAD, the novel drug agomelatine, which acts as a melatonin receptor agonist, but also as a 5HT2C antagonist (and so increases serotonin availability at the synapse), has been found to have good results in treating SAD.
  • Exercise, which activates the serotoninergic system potentiates light-induced delays of circadian rhythms.

SAD with autumn- or winter-onset depression, with symptoms remitting or hypomanic or manic symptoms during the spring or summer, is the most common.

Sub-syndromal SAD is characterised by seasonal mood disruptions with milder functional impairments. Symptom changes may not be as severe. Patients may not meet Diagnostic and Statistical Manual of Mental Disorders - Fourth Edition Text Revision (DSM-IV-TR) or International Classification of Diseases Tenth Revision (ICD-10) criteria for a clinical mood disorder. However, the mood disruption and impairments may still be significant.

SAD with summer onset of depressive symptoms, with remission or hypomanic or manic symptoms during the winter months (less common than autumn- or winter-onset depression).

Patients may develop the following symptoms in a step-wise fashion, beginning in September and culminating with depression and anxiety in December. SAD symptoms persist until springtime in April.

  • Difficulty waking
  • Decreased energy/lethargy
  • Carbohydrate craving
  • Increased appetite
  • Increased sleep
  • Weight gain
  • Difficulty concentrating
  • Decreased libido
  • Withdrawal from family and friends
  • Depression/anxiety/irritability

Other symptoms include

  • Family problems
  • Tearfulness
  • Physical symptoms - eg, headache, palpitations, and generalised aches and pains

The patient should be assessed for other psychological conditions including:

  • Major depressive disorder.
  • Bipolar I and ll disorders (all patients with autumn- or winter-onset depression should be screened for spring or summer hypomania or mania symptoms. An estimated 20% of people with SAD may present with a bipolar disorder).
  • Dysthymic disorder. 
  • Cyclothymic disorder.
  • Premenstrual dysphoric disorder (associated with bloating and breast tenderness with onset during the later part of the luteal phase of the menstrual cycle and remission of symptoms during the follicular phase).
  • Chronic fatigue syndrome.
  • Hypothyroidism.
  • Substance misuse.
  • Alcohol misuse.

Many of these disorders do not have a seasonal pattern. The seasonality of symptoms may be determined by asking the patient to record symptoms in a diary or using the seasonal pattern assessment questionnaire (SPAQ).[12] 

TFTs and urine and blood tests for illicit substances and alcohol will help to rule out some of the above conditions.

SAD is categorised as a form of depressive disorder in the DSM-IV. The gold standard for diagnosis is a structured interview to determine whether patients fulfil the DSM-IV criteria. The SIGH-SAD clinical assessment tool is commonly used.[13] 

Using this tool, the diagnosis of SAD is based on:

  • Depression cycles on a regular basis during autumn/winter.
  • Full remission of symptoms in spring/summer.
  • Seasonal symptoms for at least two consecutive years.
  • Atypical features, which may or may not be present.

During the psychological examination, it is also important to assess:

  • Suicidal ideation.
  • Abnormal mechanisms of coping - eg, social isolation, alcohol use.

The most current National Institute for Health and Care Excellence (NICE) guidelines for depression state that depression in SAD patients should be managed in the same way as non-seasonal depression.[14] 

Cognitive behavioural therapy (CBT), light therapy and prescribed medications have all been found to help to induce remission of SAD symptoms during winter months. In patients with SAD, or symptoms that are highly suspicious of it, it is important not to wait until they are showing signs of depression, but to start nondrug treatment while they have early symptoms such as lethargy and carbohydrate cravings around September.


  • Give information about the disorder and self-help groups.
  • Simple advice should include the following:
    • Spend more time out of doors
    • Work in bright conditions
    • Exercise outside regularly
    • Eat a healthy diet

Light therapy or phototherapy[5][15] 

  • Light therapy, or phototherapy, has been associated with a reduction in depression fatigue, sleepiness and health-related quality of life.
  • It may be carried out using various devices such as a light box, LED screen and a light room; however, the light box is the most commonly used.
  • Light therapy with a light box that meets evidence-based guidelines from a reputable vendor, is recommended for first-line treatment of SAD. Self-reported reductions in depression scores have been demonstrated after one hour of light therapy exposure[16] .

General instructions for light therapy

  • Sit for 30-60 minutes daily in an area with bright light.  The light is much stronger than regular light sources, of the order of 2,500-10,000 lux (the greater the lux, the less time of exposure required).
  • Light therapy helps approximately two thirds of patients.[17] 
  • Although randomised trials are difficult to perform, attempts at comparisons of light therapy show that light therapy is as effective as drug therapy.[18] 
  • Light therapy can take several weeks to produce and effect; if it takes longer than six weeks, extra help should be sought. However, it is not available on the NHS, although some hospitals may have facilities available on site.
  • Common side-effects include headache, irritability and fatigue.
  • Dawn simulators are also available.
  • Despite all of these, more lux is available from natural sunlight.

Relative contra-indications for light therapy

  • Retinal disease.
  • Macular degeneration.
  • Current use of photosensitising medicines (such as some antihypertensives, antibiotics and oncology drugs).

Compliance with light therapy is difficult and relapses occur rapidly if treatment is discontinues.


  • There are little good-quality data supporting the use of antidepressants (citalopram, paroxetine, and escitalopram and duloxetine) for the treatment of SAD.
  • Up to 27% of participants treated with second-generation antidepressants for SAD withdrew from the studies early due to adverse effects.
  • Fluoxetine has been found to have a non-statistically significant improvement compared with placebo, and has been found to be at least as effective as light therapy. Light therapy, however, has fewer side-effects.
  • Combined light therapy and antidepressant therapy can be initiated in many SAD patients. More severe and functionally impairing depressive symptoms may warrant combined treatments. Depressive symptoms that do not fully remit during the spring or summer months may also warrant combined treatments.

Psychological - CBT[17] 

Despite its efficacy, light therapy is associated with poor compliance. A small trial has found CBT to be associated with significantly lower interviewer- and patient-related depression severity at one year, as compared to light therapy alone.[19] This persisted after adjustment for ongoing treatment with light therapy, antidepressants, and psychotherapy. A more robust randomised control trial comparing CBT and light therapy is underway.

Herbal treatments

St John's wort has been found to be effective in the treatment of mild-to-moderate depression. There is some evidence that it is at least as effective as light therapy in the treatment of SAD.[20] 

Experimental treatments

  • Use of blue light instead of bright white light.
  • Use of a combination of light therapy and CBT.
  • Bupropion has been researched in a randomised controlled trial to review the possible prevention of SAD. Bupropion was administered by mouth from autumn to winter and was associated with a reduction in the rates of recurrence of depression. It may have a role to play in prevention of SAD.[21] 
  • Agomelatine is a new antidepressant which acts as a melatonin agonist and a 5HT2C antagonist. It may have potential benefits in the treatment os SAD.[22] 

Further reading & references

  1. Management of seasonal affective disorder; Management of seasonal affective disorder. BMJ. 2010 May 21;340:c2135. doi: 10.1136/bmj.c2135.
  2. Roecklein KA, Rohan KJ, Duncan WC, et al; A missense variant (P10L) of the melanopsin (OPN4) gene in seasonal affective disorder. J Affect Disord. 2009 Apr;114(1-3):279-85. doi: 10.1016/j.jad.2008.08.005. Epub 2008 Sep 18.
  3. Pandi-Perumal SR, Srinivasan V, Maestroni GJ, et al; Melatonin: Nature's most versatile biological signal? FEBS J. 2006 Jul;273(13):2813-38.
  4. Stephenson KM, Schroder CM, Bertschy G, et al; Complex interaction of circadian and non-circadian effects of light on mood: shedding new light on an old story. Sleep Med Rev. 2012 Oct;16(5):445-54. doi: 10.1016/j.smrv.2011.09.002. Epub 2012 Jan 14.
  5. Pail G, Huf W, Pjrek E, et al; Bright-light therapy in the treatment of mood disorders. Neuropsychobiology. 2011;64(3):152-62. doi: 10.1159/000328950. Epub 2011 Jul 29.
  6. Srinivasan V, De Berardis D, Shillcutt SD, et al; Role of melatonin in mood disorders and the antidepressant effects of agomelatine. Expert Opin Investig Drugs. 2012 Oct;21(10):1503-22. Epub 2012 Aug 9.
  7. Lewy AJ, Rough JN, Songer JB, et al; The phase shift hypothesis for the circadian component of winter depression. Dialogues Clin Neurosci. 2007;9(3):291-300.
  8. Roecklein K, Wong P, Ernecoff N, et al; The post illumination pupil response is reduced in seasonal affective disorder. Psychiatry Res. 2013 Jun 25. pii: S0165-1781(13)00282-5. doi: 10.1016/j.psychres.2013.05.023.
  9. Roecklein KA, Wong PM, Franzen PL, et al; Melanopsin gene variations interact with season to predict sleep onset and chronotype. Chronobiol Int. 2012 Oct;29(8):1036-47. doi: 10.3109/07420528.2012.706766. Epub 2012 Aug 10.
  10. Levitan RD; The chronobiology and neurobiology of winter seasonal affective disorder. Dialogues Clin Neurosci. 2007;9(3):315-24.
  11. Gupta A, Sharma PK, Garg VK, et al; Role of serotonin in seasonal affective disorder. Eur Rev Med Pharmacol Sci. 2013 Jan;17(1):49-55.
  12. Lam RW; Seasonal Pattern Assessment Questionnaire (SPAQ), 1998
  13. SIGH-SAD (Ham-D) Summary Score Sheet
  14. Depression in adults: recognition and management; NICE Clinical Guideline (October 2009)
  15. Rastad C, Ulfberg J, Lindberg P; Improvement in Fatigue, Sleepiness, and Health-Related Quality of Life with Bright Light Treatment in Persons with Seasonal Affective Disorder and Subsyndromal SAD. Depress Res Treat. 2011;2011:543906. doi: 10.1155/2011/543906. Epub 2011 Jun 13.
  16. Reeves GM, Nijjar GV, Langenberg P, et al; Improvement in depression scores after 1 hour of light therapy treatment in patients with seasonal affective disorder. J Nerv Ment Dis. 2012 Jan;200(1):51-5. doi: 10.1097/NMD.0b013e31823e56ca.
  17. Rohan KJ, Evans M, Mahon JN, et al; Cognitive-behavioral therapy vs. light therapy for preventing winter depression recurrence: study protocol for a randomized controlled trial. Trials. 2013 Mar 21;14:82. doi: 10.1186/1745-6215-14-82.
  18. Thaler K, Delivuk M, Chapman A, et al; Second-generation antidepressants for seasonal affective disorder. Cochrane Database Syst Rev. 2011 Dec 7;(12):CD008591. doi: 10.1002/14651858.CD008591.pub2.
  19. Rohan KJ, Roecklein KA, Lacy TJ, et al; Winter depression recurrence one year after cognitive-behavioral therapy, light therapy, or combination treatment. Behav Ther. 2009 Sep;40(3):225-38. doi: 10.1016/j.beth.2008.06.004. Epub 2008 Nov 3.
  20. Miller AL; Epidemiology, etiology, and natural treatment of seasonal affective disorder. Altern Med Rev. 2005 Mar;10(1):5-13.
  21. Niemegeers P, Dumont GJ, Patteet L, et al; Bupropion for the treatment of seasonal affective disorder. Expert Opin Drug Metab Toxicol. 2013 Sep;9(9):1229-40. doi: 10.1517/17425255.2013.804062. Epub 2013 May 27.
  22. Kasper S, Hajak G, Wulff K, et al; Efficacy of the novel antidepressant agomelatine on the circadian rest-activity cycle and depressive and anxiety symptoms in patients with major depressive disorder: a randomized, double-blind comparison with sertraline. J Clin Psychiatry. 2010 Feb;71(2):109-20. doi: 10.4088/JCP.09m05347blu.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Gurvinder Rull
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
547 (v25)
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