Three
variations of depression: symptoms, causes and treatments review.
Sierra
Corsetti, Amanda Spencer, Kristen Rhode
University
of Alaska Fairbanks
Abstract
Depression is a serious
mental illness that affects a large portion of the world’s population and often
goes unnoticed and untreated due to the wide variety of symptoms it presents.
Although symptoms differ, they all inhibit the function of normal daily life.
This review focuses on three main types of depression: major depressive disorder,
seasonal affective disorder, and postpartum depression. Each type of depression
has a number of treatment methods that have been shown to have varying success.
Overall, the consensus is that the effectiveness of the treatment greatly
depends on the individual and the specific cause of the type of depression that
they suffer from.
Introduction
Mental illnesses affect
people’s ability to function. In 2014, it was recorded that 43.6 million adults
(age 18 and older) in the United States had a mental illness in the previous
year. During that same year, 15.7 million adults had one or more major
depressive episodes. Of those who experienced depression, 65.5% had severe
impairment that interfered with their day to day activities. Also, 2.8
adolescents (ages 12 to 17) experienced at least one major depressive episode
throughout that same year. The percentage of adolescents that also had a severe
impairment was even higher than that of adults at 72.6% (Hedden 2015). Because
mental illness and depression are so prevalent in our society, it is important
to be able to recognize the symptoms and understand the causes to better
receive the necessary treatment for either yourself or someone you may know.
Depression can be broken
down into several depression types, all with various causes and treatments, but
they all create feelings of melancholy, lethargy, and feelings of emptiness or
worthlessness. Depression itself is a spectrum disorder, as well as the types
that fall beneath it. In this review, we will focus on three major depression
types; major depressive disorder (MDD), seasonal affective disorder (SAD), and
postpartum depression.
Major depressive
disorder is a chronic mental disorder. In 75% percent of patients with MDD,
their depressive state is recurrent. MDD patients experience a depressive state
that can last from several weeks to months and years. During remission, the
patient returns to his/her normal state. With MDD, there is no mania phase
present unlike with bipolar disorder.
There are two subgroups
of MDD: melancholic and atypical. Melancholic MDD is found in 25-30% of MDD
patients, while atypical MDD makes up 15-30% of patients. Although these two
subtypes show opposite symptoms, all patients are usually dissatisfied with
life and have an inability to feel pleasure.
MDD is an important
mental illness to study because it affects 8% of men and 15% of women. MDD is
also highly heritable, making it more likely to affect future generations. Of
all MDD patients, 15% commit suicide if left untreated. Patients with MDD
display both mental and biological symptoms. Education about the symptoms,
causes, and treatments of MDD is important because it helps with the diagnosis
and treatment of the mental illness.
SAD is depression that
recurs with seasonal patterns. There are two main types: summer and winter SAD
(Lam 1999). Of the two, winter SAD is the more common with symptoms including
fatigue, decreased motivation, hypersomnia, increased appetite, weight gain,
irritability and reduced sociability. Conversely, summer SAD is much less
common and had opposite symptoms including insomnia and weight loss (Eagles
2003). This review will focus primarily on winter SAD due to the rareness and
lack of study of summer SAD.
SAD has been understood
since the Ancient Greeks as depression related to sun exposure. In a quote by
Aretaeus, “Lethargics are to be laid in the light, and exposed to the rays of
the sun (for the disease is gloom)” (Partonen 1998). SAD does involve
photoperiod but also melatonin, the circadian clock, photobiology, sleep,
weather and is influenced by genetics (Eagles 2003).
Currently SAD is
assessed with SPAQ (seasonal patterns assessment questionnaire). This
questionnaire is particularly useful in determining SAD in patients with two or
more disorders. SAD frequently has comorbidity (multiple chronic diseases) with
panic disorder, social phobia, bulimia nervosa, chronic fatigue and
premenstrual syndrome. Many of these disorder are can be treated with SAD by
using light therapy or serotonergic drugs (Partonen 1998).
Postpartum depression
exhibits three variants that manifest in 10-50% of childbearing women. The
variants, postpartum “blues,” standard postpartum depression, and postpartum
psychotic depression, have symptoms that range from a mild depressive state to
strong urges to harm oneself or the baby (Miller, 2002).
In addition to the
effects on the mother, there is evidence for a paternal postpartum depression.
Paternal postpartum depression occurs in 24-50% of men whose partners develop
maternal postpartum depression (Goodman, 2003).
Our objective in this
review is to closely examine all three of these types of depression, and
compare and contrast their symptoms, causes, and treatments.
Methods
We reviewed primary and
secondary literature on topics relating to major depressive disorder, seasonal
affective disorder, and postpartum depression. We searched for journal articles
using the University of Alaska journal databases. The main topics of interest
were the varying forms of depression and symptoms, causes of, and treatments.
Results
Symptoms
of MDD
The two types of MDD
have opposite symptoms of one another. MDD patients with melancholic MDD
experience hyperarousal and anxiety; they usually have feelings of
worthlessness and hopelessness. Melancholic symptoms include suppression of
reproductive and growth hormone release, loss of appetite, insomnia, and loss
of interest in sexual activity. Melancholic MDD patients have the most severe
depressiveness in the early morning. Atypical MDD patients, however,
experience feelings of disconnectedness and emptiness. The symptoms of an
atypical MDD patient include lethargy, fatigue, weight gain, and an increase in
food intake. Unlike the melancholic MDD patients, the depressive state of
atypical patients worsens as the day progresses (Gold 2015).
Patients with MDD also
show physiological symptoms in the brain. A study from the Molecular
Psychiatry journal found that people with MDD have lower hippocampal
volumes. They found this to be caused by recurrent MDD. They also found having
an earlier age of depression onset caused amygdala volumes to be lower and the
lateral ventricle volumes to be higher. These patients’ brains were compared to
controls who did not have MDD and did not display these changes in brain
morphology. (Schmaal 2015).
A study from The New
England Journal of Medicine observed the somatic symptoms that were present
in MDD patients. These symptoms included: headache, constipation, weakness, and
back pain. 45-95% of patients reported having somatic symptoms. However, 11% of
the patients exhibiting somatic symptoms denied experiencing any of the
psychological symptoms (Simon 1999).
Causes and Treatments of MDD
The causes of MDD are
like a complex network of dominoes. They all tie into one another, and once one
incident occurs, it falls into the next causing a chain reaction of sorts. This
is a positive feedback loop that increases the depression.
The first and most
common cause of depression is low levels of dopamine. Dopamine is a
catecholaminergic neurotransmitter responsible for control of emotion,
motivation, reward, and reinforcement. In a 2012 study, Der-Avakian and Markou
observed the role of dopamine in reward and how it can cause a depressive
state. As the mouse in the study turned a wheel, its brain was stimulated by an
electrical current, which released dopamine and made the mouse feel “good”
causing him to spin the wheel more. Eventually, the amount of energy needed to
spin the wheel to get the larger stimulation was not worth the reward. This was
an increase in the reward threshold, which caused the mouse to experience lower
levels of dopamine. An increase in the reward threshold can be caused by
chronic stress, and then can lead to lower levels of dopamine and a depressive
state (Der-Avakian 2012).
Another way stress
causes depression is through the interactions with the dopaminergic neurons in
the ventral tegmental area. These neurons terminate in two different places:
the medial prefrontal cortex and the nucleus accumbens. Chronic stress causes a
reduction of firing of the dopamine neurons found in the medial prefrontal
cortex. However, chronic stress causes an increase in firing of those neurons
in the nucleus accumbens. Both of these reactions lead to the anhedonia, lack
of pleasure, that is the main characteristic of MDD. When the neurons in the
medial prefrontal cortex and the nucleus accumbens were stimulated and
depressed, respectively, the anhedonia subsided (Russo and Nestler 2013).
The next cause of MDD is
through the hypothalamic-pituitary axis. When stressed, the hypothalamus releases
corticotropin-releasing factors, which trigger the release of stress hormones
such as cortisol. Under normal circumstances, glucocorticoid receptors detect
these levels and cause a negative feedback to the hypothalamus to stop
producing the corticotropin releasing factor. During chronic stress, there are
malfunctions with the glucocorticoid receptors which impair this negative
feedback. This results in a build-up of the stress hormones; large amounts of
these hormones impair neurogenesis and the size of the hippocampus is reduced
(Rot 2009).
Another side effect of
the large amounts of stress hormones is inflammation in the brain. The
inflammation decreases monoamines, which includes serotonin. Brain inflammation
also increases the amount of tryptophan catabolites, which, in large
quantities, are toxic to the brain (Rot 2009).
Another factor, which
can either be independent to the other causes or independent of them, is the
level of brain-derived neurotrophic factor (BDNF). This protein is involved in
the creation of new neurons. In MDD patients, the levels of BDNF are low. There
are two types of the neurotrophic factor: Val and Met. People with the Met type
A hypersensitivity in the hippocampus to stress. This hypersensitivity make the
patient more prone to developing MDD (Rot 2009).
Genetics also plays a
role in determining whether or not a person is more likely to develop MDD. The
serotonin transporter gene has two different alleles: long and short. People
either homozygous or heterozygous for the short allele are more sensitive to
stress. Therefore, the more stress they are exposed to, the higher risk they
have of developing MDD (Rot 2009).
As the levels of stress
an individual experiences increases, the amount of glutamate in the brain also
increases. The excess glutamate causes activations of N-methyl-D-aspartic acid
type glutamate receptors. This process increases the intracellular calcium,
which causes a decrease in the brain-derived neurotrophic factor. The glial
cells also begin to degenerate with the decrease in the neurotrophic factor
(Rot 2009).
A study by Verduijn et
al. (2015) looked at the stages of MDD and the following causes:
Hypothalamic-pituitary axis, brain inflammation, brain-derived neurotrophic
factor, and vitamin D. He found that HPA, inflammation, and vitamin D
deficiency were the most involved in causing MDD. However, they did not seem to
be the cause of the progression of MDD, just the initial onset of the disorder
(Verduijn 2015).
There is a specific set
of criteria for the diagnosis of MDD. The criteria are listed in the Diagnostic
and Statistical Manual of Mental Disorders. The patient must have at least
five of the following symptoms for two or more weeks: depressed mood for the
majority of the day, significant decrease in interest or pleasure in all
activities for most of the day, significant weight loss, insomnia or
hypersomnia, psychomotor agitation, fatigue, feelings of worthlessness,
diminished ability to concentrate, and recurrent thoughts of death. One of the
five symptoms must include either the depressed mood or the significant
decrease in interest. There are also four other requirements that must be met
in order to be diagnosed with MDD: the patient cannot show any signs of mania,
the symptoms must significantly affect the patient’s functioning, the symptoms
cannot be due to substances, and the symptoms are not accounted for by
bereavement (Monroe and Reid 2009).
The first step to
treatment of a MDD patient is the assessment of the patient. The physician will
first determine the psychiatric state of the patient. Then the safety of the
patient is evaluated. This determines how likely the patient is to commit
suicide. Based on the state of the patient, a treatment setting will then be
established. If the patient is in a severe state of MDD with a high risk of
suicide, the patient will be sent to a hospital and be treated there. The
patient’s impairments and quality of life will also be evaluated to determine
exactly which aspects of their life are being affected by MDD. Lastly,
education about MDD symptoms as well as the treatments will be given to the
patient and the patient’s family where applicable (Gelenberg 2010). This
assessment allows the physician to know what severity of MDD the patient has
and what treatment would be best.
The different severities
of MDD require different treatments. Unfortunately, each treatment has its own
varieties of side effects. If the side effects are troublesome enough, a
corresponding treatment to deal with the side effects would be prescribed
(Gelenberg 2010).
There are several
different types of treatments for MDD. These include antidepressant drugs,
behavioral therapy, and a widely varying assortment of miscellaneous
treatments.
Antidepressant drugs
come in different varieties and have different effects on the patient.
Tricyclic antidepressants are effective in cases of severe MDD. Of the MDD
patients, 50-75% respond favorably to this treatment. However, side effects and
overdoses are possible with tricyclic antidepressants. Another class of
antidepressant includes the monoamine oxidase inhibitors. These are as
effective as tricyclics, but they can have severe interactions with other
substances, such as tyramine which is found in foods and other medications.
Overdoses are also possible with this drug, which also has undesirable side
effects. The third type of antidepressant is selective serotonin reuptake
inhibitors (SSRIs). They are a new class of medication and are just as
effective as other antidepressants. Beneficially, SSRIs have fewer side
effects. The last type of antidepressant is N-methyl-D-aspartate receptor
antagonists. These drugs are not new, but are seldom prescribed for treating
depression. This type has a rapid effect, but has a relatively low
effectiveness overall. The side effects are mild and well-characterized. Unlike
the other antidepressants, these exploit a different biochemical pathway to
reduce the depression symptoms (Ladarola 2015).
There are two types of
behavioral therapy: cognitive behavioral therapy and interpersonal therapy.
Cognitive behavioral therapy theory states that thoughts, feelings, and
behaviors are connected. With this theory, the depression results from the
individual’s distorted thinking. Cognitive behavioral therapy practitioners
collaborate with the patient in a scientific approach by working to alter the
way the patient thinks. This behavioral therapy is more effective than having
no treatment at all. However, data is scarce about this particular therapy and
how it compares with drug treatments. Interpersonal therapy theory states that
depression results from a combination of symptoms, social dysfunction, and
personality. Clinician that perform this therapy focus on specific areas of
weakness in a patient’s interpersonal functioning. In general, it is as
effective as cognitive behavioral therapy. However, interpersonal therapy may
be even more effective when combined with medication, yet it could be less
effective if the patient also has a personality disorder (Valdivia 2004,
Pradhan 2015).
Miscellaneous treatments
for MDD include atypical antidepressants, electroconvulsive therapy, repetitive
transcranial magnetic stimulation, and yoga and mindfulness based cognitive
therapy. Atypical antidepressants were recently introduced as a treatment for
depression. They are dissimilar to other chemical categories. However, research
has yet to be conclusive on the efficacy of this type of treatment.
Electroconvulsive therapy is an invasive procedure where certain parts of the
brain are given an electric shock. This form of treatment can be effective in
cases of MDD that are not otherwise treatable. The results from
electroconvulsive therapy can be superior to drug treatments alone. Side
effects are generally mild, but can at time be more serious, such as extended
periods of memory loss. Repetitive transcranial magnetic stimulation is a
non-invasive treatment using magnetic fields to stimulate the brain. This form
is potentially useful for treatment resistant depression. The long term
effectiveness has been insufficiently researched. It has milder side effects
than electroconvulsive therapy, but the range of patient profiles is restricted
due to the use of magnetic fields. Lastly, yoga and mindfulness based cognitive
therapy is a form of complementary and alternative medicine. It is similar in
some ways to cognitive behavioral therapy. Clinicians in this therapy require
intensive training in the philosophical system. Reported results in a limited
trial were positive, however, substantial research in the efficacy of this
therapy is needed (Pradhan 2015).
Symptoms
of SAD
SAD has classic
depression symptoms that occur with seasonal patterns. These symptoms include
fatigue, decreased motivation, hypersomnia, increased appetite, weight gain,
irritability and reduced sociability (Eagles 2003).
SAD does exhibit unique
symptoms including decreased night body temperature (Schwartz 1998). This is
caused by melatonin and serotonin 1A receptor activation abnormalities of
internal thermostat control during sleep. The serotonin receptor activates
hypothermia. This is governed by a central nervous system control thermostat
that is modulated by both melatonin and the core temperature. The night body
temperature is proportional to the severity of the depression (Schwartz 1998).
Causes
and Treatments of SAD
SAD is caused by
circadian phase delay (Lewy 1998). This has been shown in patients with SAD
getting well faster in rooms with bright windows, particularly with morning
light (Beauchemin 1996). In a workplace study in Norway, people with low SAD
severity had increased mood and vitality when the lights were changed to full
spectrum lighting (Partonen 2000).
The circadian rhythm and
sleep-awake cycle usies length of day signaling with more dim light the more
melatonin is secreted in SAD patients (Wehr 2001). This increase in serotonin
during winter leads to the abnormalities with the circadian rhythm and
sleep-awake cycles in SAD patients. Neural circuits that mediate the effects of
seasonal changes in day length on mammalian behavior mediate effects of season
and light treatment on seasonal affective disorder (Wehr 2001). The levels of
serotonin change in the hypothalamus seasonally in SAD patients which supports
this (Neumeister 2000).
The probability of
having SAD increases with latitude in North America with residents of
Fairbanks, Alaska having nearly 40% chance of having SAD compared to 4% in
Florida (Brooker 1992). Interestingly this correlation was not found in Europe
(Mersch 1999).
The increased appetite
and weight gain can be attributed to low doses of serotonin in the medial
hypothalamic nuclei (Leibowitz 1998). Serotonin in this nuclei inhibits the
cravings of carbohydrates, fats, and proteins. Eating carbohydrates increases
the levels of serotonin in the medial hypothalamic nuclei. However, when the
dose of serotonin is low, the serotonin cannot inhibit the craving for
carbohydrates after it has been consumed, which is to say the negative feedback
loop fails. This leads to an unregulated carbohydrate craving (Leibowitz 1998).
Serotonin plays a role
in hormonal and behavioral responses (Garcia-Borreguero 1995). Tryptophan’s
(the predecessor to serotonin) depletion in SAD patients produced depression
(Neumeister 1997). SAD patients had reduced abundance of serotonin transporters
(Willeit 2000). The pathophysiology of SAD is thought to involve altered
Serotonin neurotransmission (Neumeister 1997). Because of these studies, SSRIs
were studied to alleviate SAD symptoms.
Various SSRIs are
currently on the market. To discuss their usefulness this review will focus on
sertraline, a potent SSRI with little or no affinity for other neurotransmitter
receptors (Moscovitch 2003). Sertraline was used in a placebo controlled study
taking into account multi cultural and ethnic diversity and found a significant
result with Sertraline alleviating the symptoms of SAD and anxiety. However
there were side effects including nausea, diarrhea, insomnia and dry mouth
(Moscovitch 2003). Other successful SSRI studies used citalopram and fluoxetine
(Lam 1999).
Unlike MMD, heterocyclic
antidepressants tend to be poorly tolerated by SAD patients (Neumeister 1997).
Bright, full spectrum artificial light has been demonstrated to ameliorate SAD
symptoms (Terman 1998), but many patients find this type of treatment time
consuming, tedious and with headaches, eye and visual problems a common side
effects (Krogan 1998).
Since Ancient Greece,
the primary method of alleviating the symptoms of SAD was the use of light
(Eagle 2003). Currently the most practiced method is a daily morning use of 30
minute, 10,000 lux light during the winter months. This was established through
a series of studies including Terman’s 1998 study which successfully showed
that light therapy had significant results compared to a ion placebo. He
used variations in his study including morning light and evening light and
found that morning light with 10,000 lux for 30 min worked best. This quickly
became adapted as the standard and became part of the Canadian Consensus
Guidelines for the Treatment of Seasonal Affective Disorder (Lam 1999).
Raymond et al. in 2006
studied the effects of light therapy and the SSRI fluoxetine in SAD patients.
He divided 96 SAD patients into 2 groups for the 8 week long study. One group
got light therapy (10,000-lux for 30 minutes) and a placebo pill and the other
group for fluoxetine and an ion placebo for the light therapy portion. They
were assessed at weeks 1,2,4, and 8 over three winter seasons. The results of
this study are in figure 1. The light therapy group had more effect in the
first week, otherwise the two groups had similar improvements over the course
of the study and had the same number of adverse side effects.
Light therapy is
currently evolving to other more effective methods including blue-light and
transcranial light using the ear channel. Gordijn 2012 studied the effects of
blue-enriched light treatment compared to standard light treatment methods and
found that 20 minutes of blue light had a 71% patient increase which was
comparable to 30 minutes of full spectrum light’s success rate of 75%. This is
possibly due to the circadian rhythm sensors being sensitive to blue light.
Timonen 2012 created an earplug with an LED light for relieving SAD. He found
that transcranial brain-targeted bright light treatment via ear canals can be
effective in relieving symptoms in seasonal affective disorder. However he did
not have a placebo for this study, but he had a 92% success rate with norway
office workers who wore the ear peice of twelve minutes five times per week for
four weeks.
Symptoms
of Postpartum Depression
There are three main
categories used to define the symptoms of postpartum depression. All of the
categories share similarities, but the degrees of severity of the symptoms
vary.
Postpartum blues, or
“baby blues,” is the mildest form of postpartum depression and occurs in
approximately 50% of women who give birth. Symptoms appear 3-5 days after
giving birth and can from a few days or several weeks. The term “blues” is a
misnomer, since women with this condition often appear to be happy, but are
more emotional than usual and can cry easily or become irritated quickly
(Miller 2002).
Postpartum depression
occurs in approximately 10-20% of women in the postpartum period, and manifests
within six months of giving birth. Symptoms are often consistent with major
depression disorder, and include feelings of inadequacy as a parent, impaired
concentration, despondency, and changes in sleep patterns and appetite. When
left untreated, this condition can become chronic depression (Miller 2002).
A history of mental
illness such as bipolar disorder or schizophrenia can lead to postpartum
psychotic depression. Women with postpartum psychotic depression can pass
initial psychiatric evaluations and develop symptoms within three weeks of
giving birth. Postpartum psychotic depression often presents with
hallucinations and delusions. Women with this disorder who have thoughts of
harming themselves or their child are often much more likely to act on these
impulses than women with other forms of postpartum depression (Miller 2002).
Causes
and Treatments of Postpartum Depression
It is not
well-understood what exactly causes postpartum depression. There are a few
biochemical factors that contribute to the symptoms of postpartum depression,
as well as many risk factors that influence the development of the condition.
Early studies of
postpartum depression determined that the mental illness was associated with
changes in the pelvic organs (Bloch 2003). The symptoms of postpartum
depression were described as atypical, which included labile mood with
prominent anxiety, inability to cope, confusion, and early insomnia (Pitt
1968).
Postpartum blues are
thought to be mainly caused by the activation of a mammalian biological system
that is regulated by oxytocin (Miller 2002). Early studies assumed that
postpartum depression was simply a withdrawal effect from the sudden decline in
gonadal hormones (Stowe 1995). A study done at the University of Helsinki
treated postpartum depressive women with 17β-estradiol for 8 weeks, and
observed that after only 2 weeks of treatment, 83% of the women in the study
had clinically recovered from their symptoms. Before beginning the study, the
women who participated all showed a level of 17β-estradiol level that was lower
than the threshold for gonadal failure. They also exhibited major depressive
symptoms with postpartum onset, indicating that there may be a correlation
between the level of sex hormones such as 17β-estradiol and the onset of
postpartum depression (Ahokas 2001).
Other biochemical
factors shown to be associated with postpartum depression were low levels of
free-serum tryptophan (Stowe 1995), and elevated levels of dopamine (Weick
1991). Both of these factors have been associated with major depressive
disorder.
In addition to
biochemical factors, there are many risk factors that can lead to the
development of postpartum depression. The two major risk factors are a personal
history of depression, and a family history of depression. A personal history
of mental illness, or a family history of depression greatly increases the
likelihood of developing postpartum depression (Stowe 1995).
A study in Sweden
demonstrated a number of other risk factors that were seen in women who later
developed postpartum depression. This study showed that a high level of
antenatal care and sick leave during pregnancy, as well as a greater number of
clinical visits during pregnancy showed a strong correlation with the
development of postpartum depression. Complications during pregnancy, such as
premature contractions and hyperemesis gravidarum, and previous obstetric
issues such as abortions and Cesarean sections were also contributing risk
factors (Josefsson 2002).
The development of
paternal postpartum depression is greatly affected by risk factors, as opposed
to biochemical factors. Paternal postpartum depression is evaluated the same
way as maternal postpartum depression and both forms exhibit the same symptoms
(Goodman 2003). The main risk factors for paternal postpartum depression are a
personal history of depression, social functioning ability, belonging to the
working class, and the dynamics of the relationship with the mother of the
child (Goodman, 2003).
The effects of
antidepressants on postpartum depression have been studied, but are not a
popular treatment method because of the possible developmental issues that the
baby could suffer as a result of the mother using antidepressant drugs
(Hendrick 2000).
Since some of the major
risk factors involved in postpartum depression are a lack of social support and
relationship dynamics, interpersonal psychotherapy has been shown to be an
effective method of treating postpartum depression. Interpersonal psychotherapy
focuses on regaining control of mood and function, as well as reestablishing
healthy relationships, which are critical when dealing with both postpartum
depression and major depressive disorder (O’Hara 2000).
Discussion
MDD is a very complex
mental disorder. Like the other disorders examined in this paper, it presents
with a wide variety of symptoms, causes, and potential treatments. In fact, it
overlaps in a number of ways with the other forms of mental illness we have
studied. What sets MDD apart from the others is that it does not show a
seasonal relationship, nor does it follow a particular life event, but rather
represents a persistent depressive state.
Treatment for MDD
generally takes one of two forms: either it is treated through some form of
therapy or it is dealt with via some method that physically alters the brain,
usually in the form of an antidepressant drug regimen, but including techniques
such as electroshock therapy or even transcranial magnetic stimulation. This
highlights one of the most confusing and interesting questions about MDD: is it
a glitch in a neurochemical reward pathway that produces depressive behavior,
or does some harmful life experience such as stress affect a victim's behavior
in such a way that the reward pathways in the brain become dysfunctional? A
third possibility is that certain individuals are susceptible to depression,
but the disorder itself requires some sort of external stimulus to manifest. A
relationship between depression and genetics has been demonstrated (Rot 2009).
Another place to look for links could be in the realm of epigenetics, still a
fairly new field of study.
In typical cases of
depression, either therapy or antidepressants are prescribed as treatment.
Little benefit is generally seen from applying both methods, save for atypical
cases of depression. Generally speaking, all treatments for depression show
some degree of effectiveness, although the effectiveness varies widely for all
treatments, and each treatment method has different characteristics over the
short and long term. Antidepressant drugs are the standard method of treatment.
Some of the major categories include monoamine oxidase inhibitors (MAOIs),
tricyclic antidepressants (TCAs), and SSRIs. MAOIs were the first
antidepressant drug developed. While effective, they have severe side effects.
TCAs are also an older type of drug, also with significant side effects. SSRIs
are newer and represent the most prescribed antidepressant drugs, because they
have relatively few and milder side effects than the older drugs. Drug regimens
in general show a 50-75% favorable response rate. However, there is a
significant chance of relapse after a drug regimen is concluded, and they don't
seem to provide any protection against developing MDD in the future (DeRubeis
2008).
Therapy is a common
alternative to antidepressant drugs. Therapy shows a similar degree of success
to drug regimens, with some additional benefits and drawbacks. Obviously,
therapy does not cause physical side effects. However, it requires an
experienced practitioner. Therapy does not show the immediate results that
drugs can. However, there is some evidence to indicate that therapy has a lower
relapse rate and does a better job of helping patients cope with future
situations. The neurological mechanisms by which therapy works are not well
understood. In addition to conventional drugs and therapy, there are a wide
variety of miscellaneous treatments, including electroconvulsive therapy (ECT),
transcranial magnetic stimulation (TMS), and several drugs that don't fall into
the usual classes of antidepressant drugs. These methods are often prescribed
for patients for whom traditional methods are ineffective. While they all show
some potential effectiveness in the treatment of MDD, they are not as
well-characterized in terms of success rates, long-term results, and method of
action as the other methods (DeRubeis 2008).
One could look at MDD
from an evolutionary perspective. Consider that human beings become physically
capable of reproducing in their teens and reach their physical peak in their
early 20's, then start to deteriorate. In primitive cultures, living longer
than 30 years or so is a gift, not an expectation. That gives the average monogamous
pair of human beings time to produce a dozen or so offspring and raise a few of
them to breeding age before at least one of the pair dies. Consider that the
rate of developing appendicitis is one in fifteen individuals. That's a cause
of death for 7% of the population right there, not even considering illness and
injury. We have already determined that MDD affects 8% of men and 15% of women,
or better than 10% of the population. Of those victims, 15% commit suicide
without treatment. That's roughly an additional 1-2% of the population dying
prematurely. Could humanity as a species bear so many fatal burdens and thrive
in the way that it has? Or does this say something about the conditions under
which modern humans live, that depression is so severe a disorder? These
questions are difficult to answer, although applying a study of history or
anthropology to epidemiology might shed some light on the subject.
SAD patents at the low
end of the spectrum benefit immensely from better lighting as seen in Beauchemin
1996. As such, a greater effort should be put forth in areas with prevalent SAD
to better lighting conditions to increase the health and vitality of people.
For the people who seek help with SAD, there is a large variety of options
available to help combat the depression. Because each treatment option has side
effects and has it’s own inconveniences, the patients can choose which
treatment option is best given their lifestyle.
A large issue with SAD
is the comorbidity. Many patients are not aware that SAD is also affecting them
because of a larger issue. When the issues can be separated and treated the
secondary issues can be alleviated and overall help with wellbeing. However it
is very difficult to determine if someone has underlying SAD unless that are
aware of their seasonal patterns and can report that into the questionnaire.
Most of the comorbid disorders also involve serotonin, melatonin and the
circadian clock. As such, effectively reducing SAD symptoms can also remove the
other disorder.
SAD treatments have a
high placebo effect with 50% of placebo patients met response criteria of
having alleviated the SAD symptoms. This makes studies difficult to filter out
the placebo effect from the effect of the treatment.
Out of all the studies
we found on successful treatments for postpartum depression, treatment with
17β-estradiol seemed to be the fastest treatment method. Antidepressants were
not as effective. One study used antidepressants to treat women with postpartum
depression and women with major depressive disorder, and found that 60% of the
postpartum women required more than one antidepressant to see results,
whereas only 4% of the women with major depression needed more than one
antidepressant. Additionally, postpartum depressive women were slower to
respond to the treatment than women with major depression (Hendrick 2000).
In postpartum
depression, the most important factor to consider when attempting to prevent
the onset or treat symptoms, is social support. A lack of or decreased level of
emotional support has been linked to more severe symptoms in both paternal and
maternal postpartum depression (Goodman 2004).
Similarities between the
depression types in that all three exhibit the same symptoms of emptiness and
lack of interest. MDD and postpartum depression share few of the same
treatments, including interpersonal behavioral therapy. Treatments for SAD and
MDD patients are the same in respect to SSRIs. Although some of the types share
similar treatments, the treatments may not be as effective in one type of
patient versus a patient with the other type of depression. For example, MDD
and postpartum depression both use antidepressants, though it seems
antidepressants work better for MDD patients than postpartum depression
patients.
The major difference
between these types of depression is when they occur. MDD can occur at any time
and last from weeks to years. There is no pattern to the recurrence of the
depressive state. However, SAD patients experience the depressive state in
cycle with the seasons. Usually winter is the opportune time for depression to
strike; then by summer, the depression has lifted, and the patient resumes
his/her normal state. Postpartum depression occurs after a woman has given
birth, which sets it completely apart from MDD and SAD. MDD and SAD can affect
any age or sex; postpartum depression seems to mainly affect women with
newborns. The treatments between the types of depression mainly just differ
between SAD and the other two types. Light therapy is a treatment for SAD, but
does not work, or has not been studied to work in MDD and postpartum depression
patients.
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