Yes....Scientific research supports seasonal relationships with changes in mood....changes that can cause depressive episodes. As described by the Mayo Clinic .....
Seasonal affective disorder is a
cyclic, seasonal condition. This means
that signs and symptoms come back and
go away at the same time every year.
Usually, seasonal affective disorder
symptoms appear during late fall or
early winter and go away during the
sunnier days of spring and summer.
Some people have the opposite pattern
and become depressed with the onset of
spring or summer. In either case,
problems may start out mild and become
more severe as the season progresses.
I found the following bits on the research helpful for a start (there is a lot of research...these are really small bits).....
From: Re-Examining Seasonal Affective Disorder. Psychiatric Times. Vol. 19 No. 10. 2002.
The initial focus of the
pathophysiology of SAD was on
circadian rhythm theories, but
research interest has expanded to
include hypotheses related to
abnormalities in monoamine
neurotransmitters, personality and
genetics (Lam and Levitan, 2000;
Partonen and Magnusson, 2001)....
.....Neurotransmitters and genetics. A
robust body of research also supports
the role of neurotransmitters such as
serotonin in the pathophysiology of
SAD (Neumeister et al., 2001a). For
example, neuroendocrine studies have
shown evidence for serotonergic
dysregulation in SAD.
From: Seasonal effects on human striatal presynaptic dopamine synthesis. 2010
Sorry this is a bit long. I tried cutting it down....and failed.
Past studies in rodents have
demonstrated circannual variation in
central dopaminergic activity as well
as a host of compelling interactions
between melatonin--a
scotoperiod-responsive neurohormone
closely tied to seasonal
adaptation--and dopamine in the
striatum and in midbrain neuronal
populations with striatal projections.
In humans, seasonal effects have been
described for dopaminergic markers in
CSF and postmortem brain, and there
exists a range of affective,
psychotic, and substance abuse
disorders that have been associated
with both seasonal symptomatic
fluctuations and dopamine
neurotransmission abnormalities.
Together, these data indirectly
suggest a potentially crucial link
between circannual biorhythms and
central dopamine systems. However,
seasonal effects on dopamine function
in the living, healthy human brain
have never been tested. For this
study, 86 healthy adults underwent
(18)F-DOPA positron emission
tomography (PET) scanning, each at a
different time throughout the year.
Striatal regions of interest (ROIs)
were evaluated for differences in
presynaptic dopamine synthesis,
measured by the kinetic rate constant,
K(i), between fall-winter and
spring-summer scans. Analyses
comparing ROI average K(i) values
showed significantly greater putamen
(18)F-DOPA K(i) in the fall-winter
relative to the spring-summer group (p
= 0.038). Analyses comparing voxelwise K(i) values confirmed this finding and
evidenced intrastriatal localization
of seasonal effects to the caudal
putamen (p < 0.05, false-discovery
rate corrected), a region that
receives dopaminergic input
predominantly from the substantia
nigra. These data are the first to
directly demonstrate a seasonal effect
on striatal presynaptic dopamine
synthesis and merit future research
aimed at elucidating underlying
mechanisms and implications for
neuropsychiatric disease and new
treatment approaches.
Spectral quality of light modulates emotional brain responses in humans.
Light therapy can be an effective
treatment for mood disorders,
suggesting that light is able to
affect mood state in the long term. As
a first step to understand this
effect, we hypothesized that light
might also acutely influence emotion
and tested whether short exposures to
light modulate emotional brain
responses. During functional magnetic
resonance imaging, 17 healthy
volunteers listened to emotional and
neutral vocal stimuli while being
exposed to alternating 40-s periods of
blue or green ambient light. Blue
(relative to green) light increased
responses to emotional stimuli in the
voice area of the temporal cortex and
in the hippocampus. During emotional
processing, the functional
connectivity between the voice area,
the amygdala, and the hypothalamus was
selectively enhanced in the context of
blue illumination, which shows that
responses to emotional stimulation in
the hypothalamus and amygdala are
influenced by both the decoding of
vocal information in the voice area
and the spectral quality of ambient
light. These results demonstrate the
acute influence of light and its
spectral quality on emotional brain
processing and identify a unique
network merging affective and ambient
light information.
