Seasonal Affective Disorder: SAD or Fad?

Seasonal Affective Disorder: SAD or Fad?
J. Thomas Pichot, M.D.
Peter S. Jensen, M.D .
Seasonal affective d isorder (SAD) and phototherapy ha ve recentl y been th e
su bject of a great dea l of interest in the psychiatri c literature. First d escribed in
1984 (I), SA D is now defined as " a cyclic illn ess c ha rac te r ized by recurre n t
episodes of fal l/winter depression alternating with peri ods o f spring/summ e r
euthymia (no r ma l mood) or hypomania (mild elation and beha vioral ac t iva tion) "
(2). Rece n t findings indicate that th ere ma y be at least two additi onal patterns of
seasonal d e p ressio ns, one characterized by annual summer depressions with
euthyrnic, hypomanic or manic symptoms in the winter, and th e other characterize d by depressive episodes occurring in both winter and summer (3-6).
As defined b y Rose n thal e t al. (3), SAD d iagnostic cr ite r ia include :
I) a hi story of at least one major depressive e p isode, accordin g to RD C (7)
criteria;
2) regu larly occurring fall-winter depressions (a t least two oc currin g
during consecutive winters) alternating with nondepressed pe r iod s
during spring and summer;
3) no other major psychiatric disorders; and,
4) no psychosoc ial variables acco u n t in g for the regular cha nges in mood .
SAD has ga ined increased acceptance with the inclusion of " seasonal
pattern" criter ia for a n umber of different diagnoses within th e Mood Disorder
section of DSM lll-R (8).
Recently a n umber of reports of additiona l "seaso na l" diagnostic e nt ities
have appeared in the scientific literature , including, " reverse seaso na l a ffec tive
disorder" (3), "seasonal affective disorder in ch ild re n and ad ol escents" (9),
"seasonal premenstrual syndrom e" ( 10), seasonal batterin g of wom en ( I I) a nd a
h ypothesized seasona l obesity di sorder (12). Furthermore , th e lay press has
reported extensivel y on SAD and phototherapy (13- 19), with photothe rap y
currentl y being touted as potentiall y beneficial for d epression , multiple sclerosis, A IDS, premenstrua l syndrome, school absenteei sm , low work produ ct ivit y,
poor morale , j e t lag , a nd denta l cavities ( 13-20).
Whi le others h a ve written to express concern about th e validity of th ese
diagnoses and there proposed etiologies (21 -23), the validity o f th e di agnosis of
SAD is the focus of this paper.
LITERAT URE SUP PORT FOR SAD
Although numerous papers have been published o ve r th e yea rs th a t
support the existence of seasonal differences in psychiatri c disorde rs (24-39),
41
42
JEFFERSON JOURNAL OF PSYCHI ATR Y
many of these early papers do not seem readily applicable to support cu r rent
notions of the entity of SAD . Although, Rosentha l et al. briefly allude to t he
numerous discrepancies in these early studies (40), Christensen et al. in th e
"Myths of Mid-Winter Depression," present a detailed literature r e view of t he
conflicting nature of the empirical data that relates to se aso na l peaks of
psychiatric disorders (41). On closer review many of these seaso nal st udy
populations do not appear to relate to the current populations being described
as having the SAD diagnosis. For example, the early research was don e almost
exclusively with psychiatric inpatients and with few exceptions (42), SAD is
described as a mi ld disorder found primarily in outpatient populations (13,43-45). Many of the early studies did not differentiate the specific "s easonal "
diagnoses, or if diagnoses were provided, they did not discuss th e specific
symptomatology. In addition, although not specifically stated , one must assume
from the current clinical descriptions of SAD that most patients do not di spl ay
suicidal thoughts or suicidal behavior, therefore, excluding many of th e subject
populations reported on in the papers on seasonality of suicides.
A related issue is the lack of current epidemiologic evidence fo r SAD and
the absence of literature support for determining its reliability, validity or
prevalence as a psychiatric diagnosis. The patient population upon whi ch the
SAD diagnosis was developed was a partly self-selected research population at
NIMH, which was included in what appears to be a non-controlled phototherapy
trial (I). Unfortunately, the majority of the follow-up studies, by NIMH a nd
other groups, have used this same method of subject selection to d evelop th ei r
study populations, to test the effects of phototherapy and to establish th ei r
demographic data . An exception to this approach was a recent co m pa r iso n of
seasonal and nonseasonal affective disorders (46) . This study used a psychiatry
clinic population as its source of subjects, did not incorporate a phototherap y
protocol, and used a control population to test their h ypothesis. They repo rted a
"prevalence of seasonal depression" of 38 % in their study population (46 ),
whereas the most frequently quoted prevalence estimate for SAD ha s bee n
"about 4-5 % of manic-depressive patients" (47). Unfortunately, Garve y et al.
use their own idiosyncratic criteria to diagnosis SAD (46). In fa ct, this type of
diagnostic variance is a common problem throughout the SAD literature . Th e
significance of this variability in describing psychiatric syndromes has bee n
discussed by Spitzer (49). He stated that "criterion variance " o ccurs wh en th e re
are differences in the criteria that are used to make a certain diagnosi s and this is
one of the major sources of difficulty with reliability in psychiatric diagn oses.
POOR RELIABILITY DUE TO CRITERION VARIANCE
Development of diagnostic criteria would provide a means to ve rify
reliability of SAD as a diagnosis and possibly establish its d escriptive val id ity.
However, while most researchers have attempted to describe the di agnosis of
SAD based on the Research Diagnostic Criteria (RDC) for major depression (7),
SEASONAL AFFECTIVE DISORDER
43
there is a recurring problem with various authors changing th e SA D cr ite ria
they report in their individual studies. While Rosenthal e t al. h ave report ed th at
other researchers have used similar criteria (3), a review shows th a t the current
SAD criteria differ significantl y from those initially presented in 1984 (1) and
those presented by other groups (2,47,48). Sometimes the cha nge s are qui te
extensive, such as, diagnosing SAD without a major affective di agnosis as a
cr ite r ia (47), leaving out criteria pertaining to ps ychosocial influ ences (1), or not
ruling out other psychiatric disorders (48). Therefore, failure to specifica lly
define how these individuals are being diagnosed could decrease the reliab ility
of SAD . Perhaps this accounts for Yerevan ian et al. reporting that SAD pat ie n ts
usuall y have unipolar disorder (50), Rosenthal et al. reporting that SAD pati e nt s
usually have bipo lar disorder (1,3), and Wirz-J ustice et al. reporting that SAD
patients usually give a history consistent with bipolar disorder , but actuall y fai l to
show an y evidence of mania or h ypomania on longitudinal fo llo w-up in to the
spring/summer (47).
ETIOLOGIC HYPOTHESES
Rosenthal and Fishman (51) recently revi ewed current th eories of the
reported antidepressant effect of light on SAD patients and di scu ssed fo ur:
THE MELATONI
THEORY: Melatonin is se creted in a circadian
pattern with nocturnal release from the pineal gland in response to e n vironmental light input to the retinas. The pathway of information flow is reported
as ; light input to the retinas is passed along the retino-h ypothalamic tract to the
suprachiasmatic nuclei of the hypothalamus, which in turn st im u lates the
specific pattern of melatonin release from the pineal gland. In SAD it is
postulated that "the symptoms of SAD are due to an abnormality in mela to ni n
secretion or, perhaps, an abnormal brain response to melatonin" (5 1). While not
being totally excluded, this theory se ems less plausible now that report d ata
indicates that melatonin suppression is not necessary to dem onstrate beneficial
effects of light treatment (48).
THE PHASE-SHIFT HYPOTHESIS: A theory dis cu ssed by nume rous
authors (51-56), who postulate that "light corrects an abnorm ality of circad ian
phase either relative to real clock time or intern all y (between different circad ian
rhythms)" (51). These authors have also speculated that exposure to light in th e
morning brings the SAD patient's rhythms back to normal , thus stabilizing their
mood. Conversely they suggest that phototherapy in the e ve n ings should d ela y
circadian rh ythms, thus exacerbating the patient's symptoms. Th e mo st important arguments against this theory are the more recent reports th at the tim e of
day of phototherapy application does not alter th e antidepressant e ffec t of
phototherapy (9,48,57).
THE DIRECT PHOTO-CHEMICAL HYPOTHESIS: This is a general
theory that postulates an abnormality existing in the brain , perhaps in th e
hypothalamus, that is probably genetic and which produces the sym p to ms of
44
J EFFER SO N JO UR A L OF PSYC HIATRY
SAD in the absence of su fficie n t light. Phototherapy fun cti ons by reversing this
brain deficiency (51).
THE PLACEBO THEORY: A major co ncern with all of the SAD lite rature lies in the difficulty of controlling for placebo and p ositi ve expectancy
effects. This is particularly important because most of th e literature that bears
on the biologic theories seems to a rgue b y inference that response to photo th e rapy treatment constitutes reasonable eviden ce of the validity of th e SAD
diagnosis (1-5,47 ,52). Further, a number of SAD papers d o not consider the
placebo effect at all (3-5 ,42,55), while papers that d o , p r o vid e a one-sided
argument against it (1-2 ,44-45 ,47-48 ,51,5 3,5 8).
Proponents of SAD and light treatment ac cept th at th e consistent two- to
four-da y time lag for improvement with phototherapy a nd the likel ih o od of
relapse occurring over a similar tim e spa n whe n the lights a re wit hdrawn
mitigate against th e placebo hypothesis. Also , SAD research ers re port that the
beneficial effects of phototherapy persist throughout th e t reat ment co urse and
reliably return with subsequent treatments during r elapses. Furthe rmo re , a fair
degree of consistent findings in phototherapy responses from year to year and
between different in vestigative groups (1 ,47 ,59) ha s been cla im ed , as well as a
dose-response relationship. To bolster argum ents agains t th e placeb o theory,
proponents also cit e the evidence o f a circad ian rh ythm in response se nsi tivity to
treatment (i.e . " so me stud ies have shown a great er efficacy of light t reatment in
the morning than in the evening") (6 1- 6 2). Additionall y, SA D p r o po ne nt s
invoke the notions about light's multiple biologi cal e ffects (6 1-68) and the
superiority of light therapy co m pa red to sham light co n trol treatments
(1 ,47 ,53,69,70) as evidence to refute the placebo effect.
However, accumulating evidence seems to refute a number of these
arguments: In regard to the reported co nsiste n t time lag until sym p tom relapse
when lights are withdrawn, at least one group rep o rts th at sym ptom relapse is
not co ns iste nt and ma y oc cur within o ne da y of th e withdra wal of ligh ts or not
occu r a t a ll (4 7). Al so , recent data suggests that a circad ia n sensiti vity to response
to timing o f phototherapy is not present, as the timing o f th e pho toth e rap y is not
critical for producing th e a n t idep ressa n t effect (i.e . applicati ons a t var ious times
throughout the da y and e ve n in g have resulted in b enefi cial effec ts) (48,57,6970).
Th e theory behind dim (250-300 lux) light as a co ntrol vers us bri g h t
(2,500 lux) light as the active treatment was initiall y based on th e findin g th a t at
500 lux, light suppresses production of melatonin in normal vo lu n teers (61).
Howev er, a subsequent st ud y demonstrated that the suppression of mel a ton in is
not necessary for phototherapy to produce its antidepressant effec t in SA D
patients (48) . This finding casts d oubt not onl y o n the melatonin hypo th esis, but
a lso on the use of dim light as a " no nac t ive" co ntro l and bright ligh t as an
" ac t ive " treatment. Wehr et al. have reported th at dim "control" ligh ts have
repeatedl y not shown sign ifica n t antidepressant e ffects (48) a nd tha t other
SEASONAL AFFECTIVE DISORD ER
45
studies have confirmed these findings (47 ,59). Howev er, a review of the other
studies they reference reveals that Wirz-Justice e t aI. , reports antidepressant
effects with dim light, at levels as low as 250 lux , in 8 3% of th e ir SAD population
(47 ,71) . One of the other papers, b y Hellekson et aI., was a non-co ntro lled
treatment trial of six SAD patients that used onl y bright light (2500 lu x) (59) .
Furthermore, Wirz-J ustice et al. (47) note that 30 to 40 % of SA 0 pat ien ts in
previous phototherapy trials have responded to dim light ( 1,57,58). T hese
authors sp ecu la te that with th e sma ll number o f su bjects in a ll of t hese SAD
studies, such differences in response may be related to the se lec t io n cr iteria (47).
Doubts are further increased by reports that, in addition to less light in tensity ,
antidepressant responses are seen with less time of e xp os ure to ph oto th erap y
(9 ,47).
SAD advocates note that " pa t ie n ts become d epressed in a regular and
predictable way" (3), ye t almost 40 % of Rosenthal e t al. 's in itial group of SAD
patients failed to develop an y eviden ce of d epression wh en foll owed d uring th e
fal l/winter of 1984 (1). Further Ros enthal e t a l. report th at > 90% of SAD
patients have a bipolar di sorder (3), yet two o t her g roups h ave reported th a t
non e of th eir SAD patients di spl a yed e vid e nce o f man ia o r h ypoma nia on foll ow
up (4 7 ,50). Furthermore , whil e "winter depression " is the term that is used with
the diagnosis, th e actual onset of th e reported d epressions ca n occu r a nyti me
between July and January (5).
Additional arguments for light being a n " ac tive" agent, a nd not a p lacebo
effect were presented by Wirz-Justice e t al. (4 7). Th e a ut hors stated th a t placebo
e ffec ts are more ev iden t in mild or neurotic depressions a nd report that th eir
SAD patients were severely d epressed. This argument is problemat ic for two
reasons: First, th ere is little empirical e vid e nce to support this assertion because
placebo reactions are commonly demonstrat ed in norm al , neu r oti c and psych o t ic indi viduals (62 ). Se cond, as stated before most SAD patients a re reported
to have "mild" depressions (1-2 ,4 3-45). Further, the y argu e th at th e "use of
lights under self-selected conditions led to repeated improv em ent in th e sam e
individual." While we would agree this probabl y suggests th e individual is
deriving so me type of benefit from phototherapy, it is n ot clear if it serves to
diffe rentiate " active" from "placebo " origins o f that benefit, particularly in
light of th e reports of co nd itio ned placebo effec ts (72-73) . Lastl y, they assert
that "relapse after withdrawal is considered a criterion for a n active agent." The
authors did not provide a reference for this statement, howev er th ere are
reports that individuals have displayed several yea rs of ch ro n ic d ependence with
withdrawal sym p to ms on placebo al one (74) . Further, dru g withdrawal symptom s may occur as a psychologicall y co nd it io ned responses, rath e r tha n as
biologicall y induced sym p tom s (72-7 3).
The placebo effect has been th e subject of extensive research and the re is
little doubt that it occurs in both experimental and clinical stu d ies (75). So me of
the findings about placebo responses that are appli cable to the cur rent discus-
46
J EFF ERSO N JO UR N A L OF PSYCHIATRY
sion o f SAD include: A positive th erapeutic resp onse of almost 10 0 % has be en
reported with placebo a lo ne (72- 75), this co u ld accou n t for the 80 % positive
response rate most fr equentl y reported for phototherapy (3) . In addition, the
most fr equently cite d sym p to ms associated with the placebo reaction a re
" dep ressio n , anxiety and e motio nality" (75), whereas Rose nthal et al. report th e
three affects associated with SA D a re "sad ness, a nx ie ty a nd irritability." Nausea ,
h eadach es, and nervousn ess are side e ffec ts th at a re freq uentl y seen with
placebos (75) . Wirz-] usti ce e t al. report phototherapy side effects consist o f
nausea, headach es, " hy po ma n ic ac tiva tio n ," a nd /or irritabili ty (42).
Experimenter bias e xp la ins why uncontrolled stu d ies report success more
frequ entl y than co ntro lle d stud ies (7 5). While it has bee n demonstra ted that th e
transfer o f research er bias to patients can occu r sub t le ty (75) , in th e phototherapy trials written presentation of th e research ers' SA D t heories and past
" successfu l" use o f light treatments are used as pre-cond itions for subject
selection (1,9,44,4 5,49 ,59).
DISCUSSIO N
We hav e been unabl e to find an y clinical , d em ogra ph ic, fami ly histor y,
laboratory stu dy, o r co ntro lled light th erapy research th a t h as va lidated SAD as
a distinct synd rome. Yet d espite th is lack of support we now see a Aurry of
additional "seasonal" di agn osti c e n t ities a p peari ng in t he scientific literature
(3,9- 12, 2 0) and the la y press ( 13- 19) . One must quest ion whether seasonal
variation in mood is a characte r istic found in t he genera l pop ula t io n , including
psychiatric patients ge nera lly, or if th ere is actua lly a d ist inct subgroup with
ex treme seasona l differences in psyc hia tric sym p toms .
Furthermore, if SAD represents some typ e o f spec ific b iol og ic mechanism ,
sim ilar to hibernation in a n ima ls (3), wh y is th e re so much variabilit y in the
onset, presentation , and response to treatment? T hese di ffe ren ces occur within
indi vidual patients and wh en co m pa r ing different SA D pa t ients.
As recently pointed o ut by Winokur e t aI., " ma king up ne w sets of
diagnostic cr ite r ia in Am erican psychiatry has beco me a cottage industr y with
littl e attempt at quality co ntro l" (76) . Th e hi st ory of psychiat r y a nd med icin e is
marked with clinicians a nd resea rchers a like e m bracing ne w di sord ers and
uncontrolled treatments, whi ch for a while, se em to provide dram a tic progress.
Only after fu rth e r clinical e xpe r ie nce and judicious application of the scientific
method, do these breakthroughs assume a more modest position in th e unde rsta nd in g of psychiatric di sorders and their treatments. A lt hough face va lidity
ma y b e th e fir st step toward id enti fying a psychiatric di sorder (77), we must be
a b le to es ta b lish more powerful ty pes of diagnostic va lidi ty , such as d escr ip t ive
a n d predicti ve validity. Only if suc h co nd itio ns ca n be met can we justify
presenting SAD as a di stinct behavioral syn drome, rather tha n a random
co llec t io n of clinical features com mo n ly seen in indi vidual s with other types of
mental disorders a nd in individuals wit hou t mental di sorders.
47
SEASONAL AFFECTIVE DISORDER
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