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Jefferson Journal of Psychiatry Volume 15 | Issue 1 Article 2 January 2000 Seasonal Affective Disorder and Seasonality: A Review Leo Sher M.D. Section on Biological Rhythms at the National Institute of Mental Health, Bethesda, MD Follow this and additional works at: hps://jdc.jefferson.edu/jepsychiatry Part of the Psychiatry Commons Let us know how access to this document benefits you is Article is brought to you for free and open access by the Jefferson Digital Commons. e Jefferson Digital Commons is a service of omas Jefferson University's Center for Teaching and Learning (CTL). e Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. e Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. is article has been accepted for inclusion in Jefferson Journal of Psychiatry by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: JeffersonDigitalCommons@jefferson.edu. Recommended Citation Sher, Leo M.D. (2000) "Seasonal Affective Disorder and Seasonality: A Review," Jefferson Journal of Psychiatry: Vol. 15 : Iss. 1 , Article 2. DOI: hps://doi.org/10.29046/JJP.015.1.001 Available at: hps://jdc.jefferson.edu/jepsychiatry/vol15/iss1/2

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Page 1: Seasonal Affective Disorder and Seasonality: A Review

Jefferson Journal of Psychiatry

Volume 15 | Issue 1 Article 2

January 2000

Seasonal Affective Disorder and Seasonality: AReviewLeo Sher M.D.Section on Biological Rhythms at the National Institute of Mental Health, Bethesda, MD

Follow this and additional works at: https://jdc.jefferson.edu/jeffjpsychiatryPart of the Psychiatry Commons

Let us know how access to this document benefits you

This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of ThomasJefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarlypublications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers andinterested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion inJefferson Journal of Psychiatry by an authorized administrator of the Jefferson Digital Commons. For more information, please contact:[email protected].

Recommended CitationSher, Leo M.D. (2000) "Seasonal Affective Disorder and Seasonality: A Review," Jefferson Journal of Psychiatry: Vol. 15 : Iss. 1 , Article2.DOI: https://doi.org/10.29046/JJP.015.1.001Available at: https://jdc.jefferson.edu/jeffjpsychiatry/vol15/iss1/2

Page 2: Seasonal Affective Disorder and Seasonality: A Review

Seasonal Affective Disorder and Seasonality:A Review

Leo Sher, M.D .

Abstract

Seasonal ojfective disorder is a condition wheredepressions infall and winter alternate withnondepressedperiods in the spring and summer. The degree to which seasonal changes affict mood,energy, sleep, appetite, .foodpreference, or the wish to socialize with other people has been called"seasonality." The author reviews historical aspects, clinical.features, epidemiology, genetics,pathophy siology, and treatment ofseasonal ojfective disorder and seasonality. Better understandingof the contemporary concept of seasonal affictive disorder, seasonality, and light treatment willimprovepatient careand promote scientific advances in behavioral sciences.

HISTORICAL ASPECTS

Sin ce ancient times people have known about th e seasona l changes in mood andbehavior (I ). The con cept of sea sonal mood disorders da tes to th e dawn of medi cin e( 1,2). Seasonal depressions were described by Hippocr at es circa 400 BC (3). In thesec ond ce ntury Greco-Roman ph ysicians were treating depression a nd lethargy withsunligh t directed towards th e eyes (4,5). About 1500 yea rs ago Posidonius wrot e that" me la nc holy occurs in Autumn, whereas mania in Sum me r" (6). In 1894 Cook link edseasonal loss of sunlight to a mood disorder (7) . Cook described a syndromecha racte rized by loss of sexual desire, fatigue, loss of energy a nd profound ly de­pressed mood. Seas onal cha nge s in mood we re also describ ed by Esq uiro l in 1845 (8)a nd by Kraep elin in 192 I (9).

DIAG NOSIS

In 1984 Rosentha l and associates described th e syndrome of "seasona l a ffectivedisorder" (SAD), a condit ion where depressions in fall a nd winter alte rna te withnondepressed periods in th e spring a nd sum me r ( 10). Rosen th al a nd colleaguessugges te d that in orde r to be diagn osed as having SAD a patient mu st meet th efollowing crite ria : a hist ory of major a ffec t ive disorder; a t least two consec ut ivepr evious yea rs in whi ch th e dep ressions developed during fall or winter a nd remitt edby th e following spring and summe r; abse nce of any ot he r Ax is I psychia tric d isorders ;a nd absen ce of a ny clear-cut seasona lly chang ing psych osocial variab les that wou ldaccount for th e se aso na l variability in mood a nd beh avior ( 10). Lat er, an op pos itepatt ern, depressions in th e summer a nd non-depressed periods in th e win ter ("su rn-

3

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4 JEFFERSON JOURNAL OF PSYCHIATRY

mer SAD" ), has been described ( I I). These two typ es of SAD probably represent asubse t of a variet y of seasona l behavioral dis orders. SAD has bee n included in th eRevised Third Edition a nd in th e Fourth Edition of th e " Diagnostic and Sta t istica lManual of Mental Disorders" of th e Am erican Psychiat r ic Associat ion as "seasona lpattern," an adject ival modifier of a ny form of seasonally rec urren t mood diso rders(12,13) .

The onse t of winter SAD occurs usu all y between ag e 20 yea rs an d 30 yea rs, bu ta ffec te d peopl e oft en do not see k psychi atric help for some years (2,14). Manypatients report disliking winter since th eir teenage yea rs, though the problem usuallybecom es severe only in adulthood. Sadness , a nxiety, ir r itabil ity, decreased activity,diffi cu lti es at work, socia l withdrawal, cha nges in appe t ite , decreased libido, a ndcha nges in slee p are cha rac te rist ic symptoms of wint er dep ression (10) . Most win terSAD patients hav e " a typical" depressive symptoms such as increased sleep duration ,increased appet it e a nd weight, a nd carbohydra te crav ing . Depressive episodes aregen erally mi ld to modera te but some patients need hospitali zation. The neurovegeta­tive symptoms of " subsyndromal SAD" are sim ilar to th ose of SAD but majordepression is ab sent (15) . Patients with winter SAD may ex pe rience a reve rsal of th eirwint er symptoms in sum me r: mild hypomania, elevate d moo d, increased libido, socia lactivity a nd ene rgy, and decr ea sed sleep requir em ents, a ppe ti te and weigh t (2) . Mostepisodes of SAD occ ur within unipolar major depressive disorder, a substantialminority hav e accompanying hypom anic episodes (bipo lar II di sorder) , and very fewa re associated with manic episodes. Patients with summer depression usua lly rep ort" typ ica l" vege tat ive sympto ms , suc h as insomnia and loss of app eti te and weight ( I I) .

The degree to whi ch seasonal cha nges a ffec t mood , ene rgy, sleep, appetite, foodpreferen ce, or th e wish to socia lize with ot he r peopl e has be en ca lled "seasona lity"( 15). Season ality ca n manifest to different degr ees in di fferent ind ividuals. Som epeopl e ex pe rience only very mild seasonal changes while others are severely affect ed.

SAD in child re n usu all y pr esents with fa t igue , irritabilit y, d ifficu lty getting outof bed in th e morning a nd problems in schoo l ( 16). Sadness a nd changes in a ppe titehave also been observed in child re n with SAD. C hi ld re n with win ter SAD tend toblame th e exte rnal world (pa re n ts, tea ch ers, etc .) for treating th em poorl y.

Identifica tion of a seasona l pattern ca n only be mad e if both patient andph ysician act ively look for it (2,17). Clinicians should as k: "W he n th e seasons change ,do you I) Feel down or depressed? 2) Have less ene rgy th an usu al? 3) Feel lessproductiv e or cre a tive? 4) Need more sleep ? 5) Have less contro l ove r your appeti te?"If physicians fail to ask th ese qu estions many patients with seasonal depression ma ybe diagnosed as " non-seasona ls."

EPIDEMIOLOGY

Seasonality of mood and beh avior is commo n throughout th e pop ulation (15,17­19). Surveys suggest th at th e pr evalen ce of SAD in th e USA increases with incr easinglatitude and ranges from 1.4% in Florida to 9.7% in New Ha mpshi re (18) . A survey inth e Washingt on area found th at approximate ly 4% of the popul ation hav e winter

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SEASO AL AFFECTIVE DISORDER REVIEW 5

seasonal affective disorder and over 10% more hav e sub-syndrornal SAD ( 15).Twenty-seven percent of respondents rep orted that changes with t he seasons were aproblem for t hem, 66% reported sea son al cha nges in ene rgy level, 64% re ported som eseasonal cha nges in mood, an d 49% reported season a l cha nges in weight. Anothersurvey, in New York Ci ty, ind icated approximately 6% with pot ential clinica l severity ,18% report ing mi lder symptoms that are bothersome, a nd 35% noting symptoms butwithout compla int (19).

Many clinical studies re port th at winter SAD mainly affec ts wom en (2,14).However, th e high pr oportion of women see n in research clinics may result fromse lect ion bias. Blazer et al. suggest th at SAD with major depressive episode s is mor efre que nt a mo ng men , whereas wom en more com mo nly experience minor depressionwith a seasonal pattern (20) .

GENETICS

The study of th e ge ne tic basi s of SAD has recently rece ived a cons iderab leattention (2 1). The data on th e ge ne t ics of seasona l affect ive disorders a re of threetypes:

I. Famil iality: st udies on th e pr evalen ce of psychi a tric d isorders among relativesof patients with SAD suggeste d a fa milia l contribut ion to the deve lopment ofSAD (22- 26);

2. H erit ability: th e surveys of two coho rts of twins showed that genet ic sus cepti­bi lit y to se ns it ivity to se asonal change s runs in famili es (27,28);

3. Molecu lar gen et ic research: two ge ne t ic variants relat ed to se ro to nergictransmission, th e 5-HT f LPR and th e 5-HT2A, - 1438G/A, gene promoterpolymorphisms, are associat ed with SAD; th e for me r but not the la tt erpolymorphism is relat ed to seasonality (29-3 1).

Future research may clarify th e role of different genes in the development of SAD.The purpose of molecul ar ge ne t ic stud ies on SAD inclu des th e development ofpredi cti ve testing for SAD th at ca n help to establish the correct diagnosis a nd th eidentification of target for th erap eutic drugs.

PATHOPHYSIOLOGY

Several lin es of evide nce sugges t th at disturbed se ro to nin fun cti onin g plays a nimportant role in th e development of SAD. Many SAD sympto ms such as overeating,ca rbohydrate craving , we ight ga in, and ove rs lee ping ca n be related to seroton ergicdysfun ction. It has been sugges te d th at dieta ry ca rbohyd ra tes increase brain seroto­nin (32,33) . Carbohydra te crav ing in patients with SAD may be a "s elf-m edi cation "procedure by whi ch brain seroto nin level is incr eased . In a post-mortem study wint erdecr ease in serotonin conce nt ra t ions was observed in human hypothala mus (34).Se lec t ive se ro tonin reuptake inhibitors have a ben efi cia l effec t in pa ti en ts with SAD(35,36) . St udi es on th e effec t of adminis te ring of se ro to ne rgic ago nist rn-chlorophenyl-

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6 JEFFERSON JO URNAL OF PSYCHIATRY

piperazin e in patients with SAD have shown that the infusion of this subst an ce ca nact ivate patients a nd mak e th em eupho ric (37-39) . Another serotonergic agon ist,d-fenflura rnine, has been foun d to be effect ive in rev ersing symptoms of SAD (40). Asnot ed above, polymorphism in two seroto nin system gen es has been found to beassociated wit h win te r SAD (2 1,29,30).

Accord ing to th e "mela to nin hypothesis," SAD may be a result of a bnormalsecret ion of or sensitiv ity to mela tonin , a nd pho totherapy may modify melatoni nsec ret ion (2, I0) . However, oral ad minist rat ion of mela ton in to SAD patients who hadrespond ed to light th erapy did not indu ce return of th e depression, a nd a te no lol (thebeta-adren ergic receptor blocking drug which suppresses production of melaton in)fail ed to induce remission in SAD (4 1). These observat ions raised qu esti ons as towhe ther mela tonin plays a n importa n t ro le in th e develop me nt of SAD and seasona l­ity.

The " phase-shift" hypothesis sugges ts th at th e sympto ms of SAD may resultfrom abnormally delayed circadian rh ythms (42) . This th eory is based on th e fact sth at bright light in th e eve ning delays th e nocturnal rise of melatonin, a nd that bri ghtlight in t he morning adva nces th e melatoni n rhyt hm. T hr ee controlled clinical t rial sreported rece nt ly support th e phase-shift hypothesis by demonstrating th erap euticsuperior ity of ea rly mo rning ligh t exposure over eve ning exposure or placebo cont rols(43-45) . However, in two trials a minority of pa t ie nts responded pr eferentiall y toevening light (43,44) .

Depu e a nd colleagues proposed that the do paminerg ic syst em might be involvedin the pathogen esis of SAD (46,47) . It has been suggested th at a hypodopaminergics ta te in the nigrostriata l syst em may be associated with up -regu lation of dopaminereceptors in th e pr efrontal corte x. However, a double-blind study showed that th eadministrat ion of a combinat ion of levodopa plu s ca rbidopa was not supe rior toplac ebo in patien ts with SAD (48) .

The study of th yroid funct ion in patien ts wit h SAD is of cons ide rable int erest ,beca use symptoms of SAD incl ude decr eased energy a nd weight gain (2,10), wh ichare also com mo n in hypothyroid ism (49). It is possible tha t persons with SAD have asubtle decr ease in th yroid fun cti on simila r to th at which has been descri bed in somepati ents with non-seasonal depression (50,5 1). Results of studi es of thyroid fun cti onin SAD, however, a re inconsist ent. Thyroid abnorm ali ties in SAD patients wererep orted by Kasper et a l. (15) , Ra iti ere (52) , Coiro et a l. (53), a nd Sher et al. (54) butnot by Rosenthal et a l. (10), Bau er et al. (55) , a nd Lingjaerd e et al. (56) . We stud iedblood levels of free th yroxin e (T4) a nd th yroid-sti mulating hormon e (TS H) in SADpatients a nd mat ch ed contro ls in th e winter (54) . We foun d th at free T4 blood levelswe re slight ly but significa nt ly lower in pat ien ts th an in heal th y volu nt eers but th erewas no diff eren ce in TSH levels bet ween patien ts a nd normal volun teers. Fu tureresearch will be need ed to det ermine whether th e di fferen ce in th yroid fun ctionbetween SAD pa ti ents a nd controls is a n epiphe nome non or is related to th ebiological mech anisms that ca use sym ptoms of SAD.

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SEASOI AL AFFECTIVE DISORD ER REVIEW

TREATMENT

7

Man y SAD patients seek profession al treatmen t for dep ression but th ey are notdiagnosed as having SAD. This may be related to th e ph ysicia n's insuffi cientknowl edge about SAD a nd seasonality and/or th e ph ysician 's inability to gather th eappropria te history because of th e patient 's un coop erativeness or the ph ysician 'sfailure to conduc t th e appropriate di agn ostic intervi ew. Treat ment s generally effec­tive for depression including com bine d psychotherapy a nd a n tid epressant medica­tion s ofte n do not work un til spr ing time .

Light is th e mainst ay of t reatment for win ter depression (2,10 , 14,17 ,57). Theefficacy of light treat ment has been show n in many controlled studies in differentcount r ies. Light th erapy ca uses improvement in mos t SAD patient s. For exa mple,Oren a nd Rosenthal rep orted th at significa n t improvement in depressive symptomsoccurred in at least three-quarters of SAD patients treated wit h lig ht (2) . Manyresearch ers reported th at morning is th e mo st effec t ive ti me for ligh t th erapy(2,43-45) wh ereas others have found patients to respond well to light at oth er tim esof th e day (58-6 1) . Treatment wit h 10,000 lux for 30 minutes in th e morning appearsto be as successful as 2500 lux for 120 minutes (62) . Lately, the higher levels of lightinte ns ity have been pr eferred beca use th ey allow for sho rter daily treatments. Lightt re atme n t is easy to ad ministe r in ou tpa tient se ttings, lacks major sid e effec ts, and iscos t-effective. Caution is recommend ed whe n light th erapy is used in patients with atendency toward mania or with ph otosensi tive skin.

Patients initially sho uld be give n mo rn ing light sho r t ly after awakening a t th edose of 10,000 lux for 30 minutes ( 14,57) . If this treatme nt fai ls to elicit anant ide pressan t response within several days th e treatment ti me sho uld be exte nde dand/or eve ning treatment should be added . O ren and Rosenth al sugges te d that mostSAD patients require a t least 45 minutes a day of light therapy at th e 10,000 luxilluminance (2) .

Sertraline and flu oxetine appeared to be effect ive in SAD but less effec t ive thanligh t the ra py (57,63) . For exam ple, Ruh rma nn et a l. rec ent ly conduct ed a study th atdi rectl y com pa re d br ight light a nd fluoxetine in the treatment of SAD (63). Theremission effec t for light was supe rior to Iluoxet ine (50% vs. 25%), and ligh t th erapyimproved H amilton Depression Ra ting Scale scores faster than the administration offluoxetine. Se ro to nin-agonis t d-fenfluramine is effective in t rea tmen t of overweightpatients with SAD (40). Antidepressive drugs a rc ofte n combined wi th light th erapy.Lithium, va lp ro ic ac id, ca rba mazepine, and ga ba pe nti n ca n be used to con tro l th ehypom anic sym ptoms th at affect some SAD patient s in spring an d sum me r (17).

Light t reatmen t a nd me d ica tio ns ca nnot so lve a ll psychologica l problem s in allcases of SAD. Psych oth erapy inclu d ing cognitive, behavioral , and insi ght-ori entedth erapy may be useful for some SAD patients ( 14,17).

A recent con trolled stu dy suggested that high-de nsity negative ai r ioni za tio nmay ac t as a n a nt ide pressant in pa tient s wi th SAD (43). Subj ect s were random lyassigne d to a 3-4 wee k t reat me nt period with 30 mi nute negative ion expos uresessions every day, a t low and high ion concent ra t ion. The reduction in depression

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8 J EFFERSON J OURNAL OF PSYCHIATRY

rating scale scores was significa nt ly greate r at the high er dose th an at the lower dos e.The resu lts of this study support previous reports th at exposure to negative ions mayhave a mood -enhancing effec t (64-66).

Diet a nd exe rc ise are important conside ra tions in SAD and should be part of th eSAD patient 's health mainten ance plan ( 14, 17) . Possibly, St. John's wort has a nantidepressive effec t on pat ients with SAD ( 17).

CONCLUS IO N

Sea son al changes in mood , ene rgy, slee p, appe tite, food preference, or th e wishto socia lize with other people are com mon in the ge neral popu la tion. In th e past 15yea rs scie nt ists have established a firm definition of th e win ter SAD an d seasonality,a nd the efficacy of light th erapy for winter SAD . In th e past several years resea rchershave found that ge ne tic factors play a n important ro le in th e et iology of SAD andseasonality. We ca n expect that our knowl ed ge about the et iology a nd pathogen esis ofSAD and seasonality will grow in th e yea rs to come.

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