Saturday, February 9, 2019

Three variations of depression: symptoms, causes and treatments review.


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).
Interestingly vitamin D, a common treatment was found to be ineffective for alleviating the symptoms of patients with SAD (Bertone-Johnson 2009). There are two types or ways to intake vitamin D. The first is by dietary consumption and endogenous production in skin. The endogenous vitamin D from 7-dehydrocholesterol in epidermis and dermis is converted to vitamin D after ultraviolet B radiation. Trials with dietary consumption of vitamin D compared to a placebo showed no changes in symptoms and phototherapy using traditional effective methods did alleviate symptoms, but showed no changes in vitamin D levels (Bertone-Johnson 2009). Tanning additions have comorbidity with SAD, however vitamin D does not appear to play a role in this addition (Nolan 2008).
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.

Figure 1: Mean changes in depression over weeks of treatment (Raymond 2006).
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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Temporal Patterns in Passerine Productivity Index in Fairbanks, Alaska.

12/11/2015
Amanda Spencer

RH: Spencer × Productivity Index from Creamer's Field Migratory Waterfowl Refuge
Temporal Patterns in Passerine Productivity Index in Fairbanks, Alaska.
AMANDA SPENCER University of Alaska Fairbanks
ABSTRACT Passerines, Dark-eyed Juncos (Junco hyemalis), Lincoln Sparrows (Melospiza lincolnii), and Orange-crowned Warblers (Vermivora celata), breed in interior Alaska’s boreal forest. Climate change is dramatically affecting the boreal forest (Hinzman 2005). Bird abundance can indicate changes in vegetation and changes in weather (Tauzer 2013). This study used the Creamer’s Field Migration Station (CFMS) in Fairbanks, Alaska banding bird data from 1992. These data were used to determine temporal patterns for productivity index and relate the productivity index to species first arrival and weather patterns. The annual productivity indices of these passerines, number of juveniles per 100 mist net hours, were related by linear regression to first arrival and weather of the Fairbanks area. This study found the indices’ related over time and have a negative relationship to mean annual temperature. Other explanatory variables’ linear regression relationship had various and magnitudes and directions. The passerine’s productivity various productivity responses are likely due to the diversity of foraging techniques. Understanding passerine’s productivity responses to weather can predict future passerine abundance. This is important for managers in areas where range shift may occur in the future.
KEYWORDS Alaska, boreal forest, climate change, passerine, productivity index.
Climate change is dramatically and disproportionately affecting polar regions globally (Hinzman 2005). The state of Alaska, which is comprised of arctic and sub-arctic regions, is among areas experiencing rapid change, especially in the vegetation composition of habitats, and the bird species that rely on them (Butler 2003, Markus 2004, and Tauzer 2013,). The interior Alaska is primarily composed of boreal forest with massive expanses of spruce (Picea spp.) forest (Boreal 2012). Bird abundance can indicate changes in vegetation and changes in weather (Tauzer 2013). Productivity is an effective indicator of changes in abundance.
As a relatively high proportion of autumn caught birds are juveniles, using a metric consisting of the number of juveniles caught in relation to mist net catch effort can represent a productivity index (Benson 2012). Many variables have been found to affect this productivity index including first arrival of the species (Butler 2003, Huppop 2003, Markus 2004), annual snowfall (DeSante 1987, Dybala 2013), annual mean temperature (Dickey 2008), and annual precipitation (Dickey 2008). This study considers the annual number of juveniles caught to catch effort (mist net hours) as it relates to each of these factors to explain temporal patterns. These relationships can help to understand the productivity index and find likely models to explain temporal patterns. Boreal nesting passerines have a variety of migration patterns and diets. To account for the various life histories, three representative migratory passerine species were chosen from the watch list of the Neotropical Migratory Bird Conservation Act. These species were also chosen because of their various migration patterns, diets and high abundances in Interior Alaska. The species of choice are Dark-eyed Juncos (Junco hyemalis), Lincoln Sparrows (Melospiza lincolnii), and Orange-crowned Warblers (Vermivora celata).
This study aims to improve understanding of the major factors impacting productivity of passerines in the boreal forest. The results of this study will benefit Alaska Department of Fish and Game, Creamer’s Field Waterfowl Migration Refuge, land managers of boreal forest (Department of Natural Resources, Borough of Land Management, US Fish and Wildlife Service), ornithologists, and fellow volunteer bird banders.
Using the proportion of juveniles captured in autumn at CFMS, the objectives of this study are to 1) determine temporal patterns for productivity index and 2) relate the productivity index to species first arrival and local weather.
STUDY AREA
This study took place in interior Alaska’s Creamer’s Field Migratory Waterfowl Refuge, located in Fairbanks, Alaska (Fig. 1, 2).  The 1,800 acre land functioned as a dairy during the Alaska gold rush in the early 1900s. It was purchased by the community in 1966 to preserve the migratory birds to create Creamer’s Migratory Waterfowl Refuge managed by Alaska Department of Fish and Game for human use and recreation (Creamer’s 2015).  The long-term migration bird banding station started in the autumn of 1992 at Creamer’s Field Migration Station (CFMS), the farthest north migration station (64 50’N, 147 50’W). Bird banding takes place in the spring and autumn to catch migrating passerines.
Fairbanks has an annual temperature of -2.45C with variation from 3.3C to -8.2C. The average precipitation is 275mm with 112 rain days. The average annual snowfall is 165mm (U.S. Climate Data 2015).
CFMS consistently maintained mist nets in the same locations beginning in 1992 with little variation. These mist nets are in old growth spruce forest, deciduous birch forests, shrub lands dominated by willow and alder, edge habitats and seasonal wetlands (Fig. 3).
The refuge is used and managed for human experiences with wild spaces. There are numerous dog walking trails, dog mushing trails, hiking and snow machining trails. Hunting and trapping is permitted in the area.
METHODS
To determine temporal patterns for productivity index, juveniles were captured at CFMS for 24 years. This study used years 1992-2004, 2006-2011. Methods for banding the songbirds were established for CFMS and are written in the Creamers Field Migration Station Operations Manual (Guers 2002). CFMS adheres to this manual to reduce variability among observers over many years. All nets are open for six hours each day from approximately sunrise or 5:30 am (whichever is later). Many nets in the seasonal wetlands are not opened if the flooding is above 1.5 meters which occurs in spring. Nets are closed early in heavy or constant rain, snow, intense wind or excessively hot or cold weather. Daily records of open net duration are used to calculate total net hours for each season. Nets are checked at 45 minute intervals to collect birds from the nets and the following information is recorded: species, age, date, and morphometric data are collected.
Age is determined by ‘skulling’ (determining ossification of skull) and by plumages, and presence of breeding characteristics (i.e. brooding patches and cloacal protuberances). In this study young of the year and fledglings are considered juveniles. The productivity index is calculated using the number of juveniles caught divided by 100 mist net hours of effort.
To relate the productivity index to species first arrival and weather patterns, the average annual productivity is compared to weather data collected from Fairbanks International Airport.  The productivity can be related using linear regression to first arrival of the species, annual snowfall, annual mean temperature, annual brooding season temperature and annual precipitation to find relationships between arrival, local weather and productivity.
Weather data was collected the Fairbanks International Airport. The maximum daily temperature, minimum daily temperature, amount of snowfall and amount of precipitation was recorded each day. The mean annual temperature was an average of daily maximum and minimums averaged over the course of the year. The annual brooding season temperature was an average of daily maximums and minimums for June through August. The total annual snowfall was the total sum of all fallen snow for the calendar year. The total annual precipitation was the total sum of all rainfall and snowfall over the course of a calendar year (Fairbanks 2015).
Microsoft Excel was used to make linear regressions of the annual productivity index to weather data and arrival data for each year and for each species to best explain productivity temporal patterns. Each explanatory variable was graphed against each species productivity index. A linear regression, best supported by the data, gave the change in the explanatory variable for each unit of productivity, one juvenile per 100 mist net hours. This linear regression also supplied the multiple correlation (R2) to determine how close the data correlated. This was done for each explanatory variable for each passerine species.
RESULTS
Our sample determined temporal patterns for productivity index using 23,245 juveniles of the three species caught over a series 189,099.2 mist net hours from 1992-2004 and 2006-2011 (Fig. 4). The data for year 2005 was not available for analysis at this time of the study. The Dark-eyed Juncos’, Orange-crowned Warbler’s and Lincoln Sparrow’s productivity indices were related by linear regression to first arrival and weather patterns. Linear regression compares one dependent variable, productivity, to one explanatory variable. Due to the single explanatory variable, no result was statistically significant, however some trends were observed.
Our survey included 11,671 juvenile Dark-eyed Junco. The first arrival of Dark-eyed Juncos at CFMS had a slight positive relationship of 0.062 Julian days per productivity with a multiple correlation (R2) value of 0.0025. The annual mean temperature had a negative effect on productivity with -0.673 degrees Celsius per productivity with a R2 of 0.3328 (Fig. 5). The annual brooding season temperature had a slightly negative impact in productivity with -0.0136 degrees Celsius per productivity with an R2 of 0.026. Total annual precipitation had a slight negative relationship with productivity with a relationship of -0.0468 centimeters of precipitation per productivity with a R2 of 0.0132. Total annual snowfall had a negative effect on productivity with -1.1688 centimeters of snowfall per productivity with a R2 of 0.0332.
Our survey included 7,309 juvenile Orange-crowned Warblers. The first arrival of Orange-crowned Warblers at CFMS had a negative relationship of -0.4545 Julian days per productivity with a R2 value of 0.0779 (Fig. 6). The annual mean temperature had a negative effect on productivity with -0.5226 degrees Celsius per productivity with a R2 of 0.1406. The annual brooding season temperature had a slightly positive impact in productivity with .0449 degrees Celsius per productivity with an R2 of 0.016. Total annual precipitation had a slight negative relationship with productivity with a relationship of -0.0017 inches of precipitation per productivity with a R2 of 0.000001. Total annual snowfall had a negative effect on productivity with -1.9743 centimeters of snowfall per productivity with a R2 of 0.2122.
Our survey included 4,265 juvenile Lincoln Sparrows. The first arrival of Lincoln Sparrows at CFMS had a positive relationship of 2.1291 Julian days per productivity with a R2 value of 0.0084 (Fig. 7). The annual mean temperature had a negative effect on productivity with -1.6123 degrees Celsius per productivity with a R2 of 0.1246. The annual brooding season temperature had a slightly negative impact in productivity with -0.0042 degrees Celsius per productivity with an R2 of 0.00001. Total annual precipitation had a slight negative relationship with productivity with a relationship of -0.1057 centimeters of precipitation per productivity with a R2 of 0.0036. Total annual snowfall had a slightly negative effect on productivity with -3.7836 centimeters of snowfall per productivity with a R2 of 0.0185.
DISCUSSION
In determining the temporal patterns of the productivity index, there is a visual relationship between the three species productivity each year. While the productivity of each species is different than the others and reacts differently to environmental factors, all the species have joint peaks of productivity at 1994-1995, 1997-1998 and 2009. They all have productivity crashes at 1996, 2002-2003 and 2008 (Fig. 4).
While the peaks and crashes in productivity appear to be related, each species has a different relationship to first arrival and weather patterns. These different relationships vary in magnitude and direction. All species in this study have lower numbers of juveniles during fall migration when the annual mean temperatures are high. As temperatures are expected to increase in interior Alaska due to climate change (Dybala 2013), these species may experience reduced productivity. This negative relationship between passerine productivity with temperature could be attributed to a variety of factors including food abundance, heat affects or the increased abundance of parasites. Interestingly, the annual brooding season temperature had little effect on the productivity index compared to annual mean temperature. This possibly could be because the forage available each summer is dependent on the over-wintering conditions or other in-direct affects.
Interestingly the Lincoln Sparrow productivity remained more consistent than the other species’ productivity indices. This shows that Lincoln Sparrows are less affected by positive or negative changes. This may be because of the foraging behavior or nesting behavior of Lincoln Sparrows being different than the other species. This may also be because the Lincoln Sparrows are able to use more alternatives to use available forage. More research exploring Lincoln Sparrows resilience should be explored.
The Dark-eyed Junco and Orange-crowned Warbler have higher productivity indexes in years with less snowfall. This may be a direct cause of decreasing available forage or nest sites, but it maybe indirect with snowfall decreasing early spring forage by other methods or it could be a correlation. More research exploring snowfall depth’s impacts on passerines should be explored. Doing a productivity study for a wider range of passerines with stratification by foraging behaviors would allow more insight on particular weather’s effects of various foraging behaviors.
Orange-crowned Warblers’ and Lincoln Sparrows’ productivity indices have opposite relations to arrival dates. Orange-crowned Warblers have lower productivity when they arrive late (Fig. 6). Conversely, Lincoln Sparrows benefit from earlier arrivals (Fig. 7). Arrival timing is expected to continue to alter with climate changes (Butler 2013). Arrival dates have not been correlated to breeding dates, therefore arrival does not necessarily mean the birds are beginning the breeding season. A more definitive way to find the beginning of the breeding season is checking cloacal protrusions on males and brooding patches on females to note active breeding behaviors.
Annual precipitation had little relation to productivity for any of the species possibly because the annual precipitation is not as important as precipitation during the brooding season itself (DeSante 1987). A further study looking at consecutive rain days during the brood season may have a larger effect on nest survival.
Juveniles of most passerine species depart their breeding grounds in Alaska significantly earlier than adults (Benson 2012). The juvenile to mist net hours is not accounting for departure of juveniles, this biases the data because an early autumn migration will reduce the total juveniles caught. This will lead to underestimating the productivity index in those years. To correct for this, the last date of juvenile capture should mark the end of the season.
This study likely consistently underestimates productivity. However, because this index is used with explanatory variables to find influential factors of productivity, the question is if the productivity index a good representation of actual productivity and not biased by detection probability variation. In this study, detection bias is not considered an issue because the same methods for detection with the same nets were used each year. The variation of detection probability between years would be minimal. A future passerine study of productivity could be coupled with juvenile mist net effort to determine if indeed there is a detection bias.
MANAGEMENT IMPLICATIONS
Modeling passerine productivity index’s response to various weather, allows predictions of passerine recruitment due to weather. The correlation between annual mean temperature and productivity index shows a decrease in productivity during warmer years. This can be used to predict passerine abundance changes due to potential annual temperatures. As recruitment to a population declines, the population abundance will decline. To stabilize recruitment into the population, passerines may nest in more northern latitudes or high altitudes to avoid this ecological trap.
Acknowledgments
I thank T. J. Brinkman, J. A. Curl, A. Harding Scurr for review comments and contributions to this manuscript.
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Figure 1. Location of Creamer’s Field Migratory Waterfowl Refuge in Interior Alaska.


Figure 2. Creamer’s Field Migratory Waterfowl Refuge in Fairbanks, Alaska.


Figure 3. Mist net locations of the Creamer’s Field Migration Station.

Figure 4. Relationships between annual productivity indices of Dark-eyed Juncos, Orange-crowned Warblers, and Lincoln Sparrows and time in years.

Figure 5. Relationship between annual mean temperature in Celsius and productivity index of Dark-eyed Juncos.

Figure 6. Relationship between date of first arrival and productivity index of Orange-crowned Warblers.


Figure 7. Relationship between date of first arrival and productivity index of Lincoln Sparrows.