SAD
is a seasonal disease that affects about 6 percent of the population in temperate
zones and and to a lesser degree about 14 percent of the population. Approximately
75 percent are women. The most common age of onset is in the thirties. Some
of the symptoms are craving for carbohydrates and thus weight gain(which
can add to the depression), depressed mood, irritability, some thought and
motor retardation-general malaise, tendency to sleep too much, difficulty
concentrating, and tendency to withdraw and isolate from social activities.
Selective Serotonin Reuptake Inhibitors such as Paxil,
Zoloft are often prescribed as antidepressants..
The Food and Mood Handbook:
Find Relief at Last from Depression, Anxiety,
Pms, Cravings and Mood Swings
Psychiatry Clin Neurosci 2001 Feb;55(1):27-30
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Open study of effects of alprazolam on seasonal affective
disorder .
Yamadera H, Okawa M, Takahashi K.
Department of Neuropsychiatry, Nippon Medical School, Tama Nagayama
Hospital, Tokyo, Japan. yamadera@nms.ac.jp Seasonal affective disorder (SAD) differs from depression with melancholic
features in atypical symptoms, such as hyperphagia, hypersomnia and weight gain.
Moreover, SAD is confined to a certain season of the year. We examined the
pharmacological efficacy of alprazolam for treatment of patients with SAD. Six
patients with SAD were treated with alprazolam at doses of 1.2 mg/day or 1.2
mg/day first and then 2.4 mg/day for 2 weeks. The improvement was evaluated by
the change of total score of the SIGH-SAD (with both 21 items HAMD and eight
items atypical symptoms) and the clinical global impression (CGI). Although only
two patients showed a remarkable improvement by SIGH-SAD, all patients showed
a higher than moderate improvement with CGI. Our findings suggest that
alprazolam might be efficacious for certain SAD patients. J Biol Rhythms 2000 Aug;15(4):344-50
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Seasonal variation of depression and other moods: a longitudinal
approach.
Harmatz MG, Well AD, Overtree CE, Kawamura KY, Rosal M, Ockene IS.
Department of Psychology, University of Massachusetts at Amherst, 01003, USA. The present study examined the effect of season of the year on depression and
other moods. Previous work, primarily cross sectional or retrospective in design
and involving clinically depressed or seasonally affective disordered samples, has
suggested that mood changes as a function of season. However, the literature also
shows conflicting and/or inconsistent findings about the extent and nature of this
relationship. Importantly, these prior studies have not adequately answered the
question of whether there is a seasonal effect in nondepressed people. The
present study employed a longitudinal design and a large sample drawn from a
normal population. The results, based on those participants for whom mood
measures were collected in each season, demonstrated strong seasonal effects.
Beck Depression Inventory (BDI) scores were highest in winter and lowest in
summer. Ratings on scales of hostility, anger, irritability, and anxiety also showed
very strong seasonal effects. Further analyses revealed that seasonal variation in
BDI scores differed for females and males. Females had higher BDI scores that
showed strong seasonal variation, whereas males had lower BDI scores that did
not vary significantly across season of the year. Med Hypotheses 2000 Jul;55(1):56-9
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The role of brain thyroid hormones in the mechanisms of
seasonal changes in mood and behavior.
Sher L. Many individuals experience seasonal changes in mood and behavior. Various
theories have been suggested to explain the mechanisms of these changes.
However, the mechanisms of seasonal mood and behavioral changes remain unclear.
The author suggests that brain thyroid hormones may play an important role in
seasonal changes in mood and behavior. This suggestion is based on the facts that
seasonal changes in light and temperature may affect the metabolism of brain
thyroid hormones and that small alterations of the brain thyroid economy,
independent of peripheral changes in thyroid status, may produce significant
behavioral effects. The author further suggests that there may be a fault in the
thyroid metabolism in the brain in seasonal affective disorder patients, and that
fault cannot be identified by studying the peripheral thyroid hormone metabolism.
Seasonal mood and behavioral changes may also be related to the interaction
between thyroid hormones and different neurotransmitter systems in the brain. Med Hypotheses 2000 May;54(5):704-7
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The role of genetic factors in the etiology of seasonality and
seasonal affective disorder: an evolutionary approach.
Sher L.
Rockville, Maryland, USA. The degree to which seasonal changes affect mood, energy, sleep, appetite, food
preference, or the wish to socialize with other people has been called seasonality.
Seasonal affective disorder (SAD), a condition where depressions in fall and
winter alternate with non-depressed periods in spring and summer, is the most
marked form of seasonality. Several lines of evidence suggest that genetic
factors play an important role in the etiology of seasonality and SAD. Millions of
years of evolution and adaptation have optimized human biochemical and
physiological systems for function and survival under equatorial environmental
conditions. Modern humans began their migration out of Africa only about 150 000
years ago. Little change in our 'equatorial' systems might have been expected over
this relatively short evolutionary time-span. The author suggests that a genetic
susceptibility to seasonal changes in mood and behavior is a genetic predisposition
to an insufficient adaptation to temperate and high latitudes. J Affect Disord 1999 Dec;56(2-3):163-9
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Winter and summer outdoor light exposure in women with and
without seasonal affective disorder.
Graw P, Recker S, Sand L, Krauchi K, Wirz-Justice A.
Chronobiology and Sleep Laboratory, Psychiatric University Clinic, Basel,
Switzerland. BACKGROUND: The annual decrease of daylight duration initiates a depressive
phase in patients with seasonal affective disorder (SAD), and light therapy treats
it. How much bright light exposure in winter and summer these patients actually
receive may help understand the pathogenetic factors initiating SAD. METHODS:
During a week in winter and summer, women with and without SAD kept daily logs
of the time spent outdoors, subjective sleep, and self-ratings of mood and
alertness. RESULTS: Compared with the winter depressive state, mood, alertness,
and sleep of SAD patients improved in summer to control values, but did not
correlate with the amount of light exposure. In summer, patients with SAD spent
more time outdoors than controls. LIMITATION: Light logs--in comparison with
light monitor measurements--may overestimate light exposure outdoors.
CONCLUSION: Women with SAD do not spend less time outdoors in winter than
controls, but spend more time outdoors in summer. CLINICAL RELEVANCE:
Patients with SAD show a high amplitude seasonal difference in outdoor light
exposure. The susceptibility to winter depression may arise not from
behaviourally-related lack of sufficient light exposure, but an increased
vulnerability to the amount of light received. They may require more light than
controls to remain euthymic (higher light exposure in summer, light therapy in
winter). J Affect Disord 1999 Nov;56(1):27-35
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Monorhinal odor identification and depression scores in patients
with seasonal affective disorder.
Postolache TT, Doty RL, Wehr TA, Jimma LA, Han L, Turner EH,
Matthews JR, Neumeister A, No C, Kroger H, Bruder GE, Rosenthal NE.
Section on Biological Rhythms/NIMH, Bethesda, MD 20892-1390, USA.
postolache@nih.gov BACKGROUND: Visual and olfactory pathways are interconnected. Olfactory
deafferentation unmasks photoperiodic responsiveness in some nonphotoperiodic
animals such as laboratory rats. By analogy, we hypothesized that olfactory
deficits may unmask seasonal rhythms in certain individuals, namely those with
seasonal affective disorder (SAD). Since previous studies suggest lateralized
hemispheric dysfunction in SAD, and since olfactory neurons' primary projections
are largely ipsilateral, we assessed olfactory identification performance on both
the right and left side of the nose. METHODS: Twenty-four patients with SAD
and 24 matched controls were studied using a phenyl ethyl alcohol detection
threshold test bilaterally and the University of Pennsylvania Smell Identification
Test unilaterally. Subjects rated their mood using the Self Assessment Mood
Scale for SAD. Patients' testing was done in both 'depressed' and 'improved on
light' states. RESULTS: No difference in olfactory performance was found
between patients and controls or between patients before and after light
treatment. However, right-side identification scores were negatively correlated
with 'typical' depression scores (r = -0.56, P = 0.006), while left-side olfactory
scores were not. Atypical depression scores were unrelated to olfactory
performance. Similar correlations emerged between the olfactory identification
laterality quotient (Right - Left)/(Right + Left) and typical depressive scores (r = -
0.64, P < 0.001) and total depression scores (r = - 0.59, P < 0.004). LIMITATIONS:
We studied a demographically heterogeneous sample and did not control for
menstrual factors. DISCUSSION: Our results add to previous evidence of
lateralized hemispheric involvement in SAD and suggest that olfaction may be
related to seasonal emotional rhythms in humans. Behavioral effects of tryptophan depletion in seasonal affective
disorder associated with the serotonin transporter gene?
Lenzinger E, Neumeister A, Praschak-Rieder N, Fuchs K, Gerhard E, Willeit
M, Sieghart W, Kasper SF, Hornik K, Aschauer HN.
Department of General Psychiatry, University Hospital for Psychiatry, Vienna,
Austria. here is some evidence that the neurotransmitter serotonin
(5-hydroxytryptamine; 5-HT) may be involved in the pathogenesis of seasonal
affective disorder (SAD). Short-term tryptophan (TRP) depletion was carried out
in 18 drug-free remitted patients who met DSM-IV criteria for SAD. Behavioral
effects were measured with the Hamilton Depression Rating Scale (HDRS) both
24 h before and 24 h after TRP depletion. Some of the patients showed behavioral
responses such as lowered mood, feelings of guilt, loss of interest, agitation, loss
of energy, fatigue, social withdrawal, increased appetite, and carbohydrate
craving. It was the aim of our study to investigate whether the genotypes of the
serotonin transporter gene were associated with symptoms of transient
depressive relapse after TRP depletion. In addition, we matched the SAD patients
with healthy control subjects to see if alleles and genotypes of the serotonin
transporter gene were associated with SAD. High molecular weight DNA was
isolated from peripheral blood leukocytes using standard methods. For the 5-HTT
receptor gene, a 17-bp repetitive element of intron 2 was genotyped (variable
number tandem repeat, VNTR). Alterations in HDRS scores after TRP depletion
showed no significant association with alleles or genotypes of the 5-HTT gene,
although heterozygotes showed a trend toward increased HDRS scores. The
serotonin transporter is known to play a critical role in the termination of
serotonergic neurotransmission by sodium-dependent uptake of 5-HT into the
presynaptic neuron. The present study in a small group of SAD patients was unable
to demonstrate that the 5-HTT gene plays a role in the pathogenesis of SAD or in
short-term depressive relapse after TRP depletion.
