Depression can be clinical (genetic) or based on life experiences. Clinical depression will come and go in one's lifetime. As someone ages they learn to cope with depression, as one does with any other serious illness.
People approach depression in many ways sometimes taking antidepressants often combined with holistic remedies. Electroconvulsive therapy (shock treatments) are having positive affects for many people. It's all about trial and error to find what works and what doesn't. Clinical depression starts at puberty, if not earlier, and accelerates through the teenage years, peaking around age 19, when it becomes full blown. It is at this time that bipolar disorder and other personality disorders emerge. The ability to think, focus and cope is lost, often resulting in substance abuse as a means of self medication.
The brain is a computer - a biochemical machine that process data. Reality is a consciousness hologram set in linear time to experience emotions, depression a prevalent aspect of the journey. In other words, in our bi-polar experiment in linear time, people have always suffered from depression and mental illnesses.
5 Unexpected Signs That You're Depressed Huffington Post - May 8, 2015
You're inexplicably achy.
You're suddenly a slowpoke.
You're ticked off.
Your cravings are out of control.
Depression Makes the Sting of Rejection Linger Epoch Times - March 2, 2015
The pain of social rejection lasts longer for people who are depressed because their brain cells release less natural opioids, a pain and stress-reducing chemical. On the flip side, when someone they're interested in likes them back, depressed people feel relatively better - but only momentarily. Further research could lead to a better understanding of how to boost the opioid response in people who are depressed to reduce the exaggerated effect of social stress, and to increase the benefits of positive social interactions, researchers say.
Obesity and depression often twin ills, study finds PhysOrg - October 16, 2014
Depression and obesity tend to go hand in hand, U.S. health officials reported today. The combination was so common that 43 percent of depressed adults were also obese, according to the report. That association was even more prevalent among those taking antidepressants: 55 percent of those patients were also obese.
Blood test spots adult depression PhysOrg - September 16, 2014
A new blood test is the first objective scientific way to diagnose major depression in adults, a new study claims. The test measures the levels of nine genetic indicators (known as "RNA markers") in the blood. The blood test could also determine who will respond to cognitive behavioral therapy, one of the most common and effective treatments for depression, and could show whether the therapy worked, Northwestern University researchers report. Depression affects nearly 7 percent of U.S. adults each year, but the delay between the start of symptoms and diagnosis can range from two months to 40 months, the study authors pointed out.
Brain networks 'hyper-connected' in young adults who had depression PhysOrg - August 28, 2014
Depression may be better predicted and understood now that University of Illinois at Chicago researchers have discovered that young adults who previously experienced the mental illness have hyper-connected emotional and cognitive networks in the brain.
From Genes to Motherhood: 6 Reasons More Women Get Depressed Live Science - June 23, 2014
Women face almost twice the risk compared to men of having a major depressive disorder during their lifetimes.The reason for this greater risk is unclear, but a combination of biological, hormonal, genetic, psychological and social factors appear to play a role. Women are definitely hit harder by depression, and they are more vulnerable to the illness due to biology. Scientists are beginning to unravel the role of sex differences in the development and functioning of the brain, and how these differences affect psychiatric disorders.
7 Ways Depression Differs in Men and Women Live Science - April 23, 2014
1. Women are more likely to ruminate when feeling depressed.
2. Men with depression are more likely to abuse alcohol and other substances.
3. Women may respond differently to stressful life events.
4. Men's symptoms of depression may be harder for others to recognize.
5. Women are more likely than men to have depression and a co-existing eating disorder.
6. Men and women might respond differently to antidepressants.
7. Men are more likely to commit suicide
Depression 'makes us biologically older' BBC - November 12, 2013
Depression can make us physically older by speeding up the aging process in our cells, according to a study. Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past. These visible differences in a measure of cell aging called telomere length couldn't be explained by other factors, such as whether a person smoked.
People with depression tend to pursue generalized goals PhysOrg - July 8, 2013
The study found those with clinical depression were more likely to set abstract goals that were difficult to achieve. Researchers from the University of Liverpool have found that people with depression have more generalized personal goals than non-depressed people. A study conducted by Dr Joanne Dickson, in the University's Institute of Psychology, Health and Society, analyzed the lists of personal goals made by people who suffered with depression and those who didn't. The participants were asked to list goals they would like to achieve at any time in the short, medium or long-term. The goals were categorized for their specificity - for example a global or abstract goal such as, 'to be happy' would represent a general goal, whereas, a goal such as 'improve my 5-mile marathon time this summer' would represent a more specific goal. Researchers found that while both groups generated the same number of goals, people with depression listed goals which were more general and more abstract. The study also found that depressed people were far more likely to give non-specific reasons for achieving and not achieving their goals.
Genetic predictors of postpartum depression uncovered PhysOrg - May 21, 2013
The epigenetic modifications, which alter the way genes function without changing the underlying DNA sequence, can apparently be detected in the blood of pregnant women during any trimester, potentially providing a simple way to foretell depression in the weeks after giving birth, and an opportunity to intervene before symptoms become debilitating.
Brain's 'Clock' Disrupted in Depressed People Live Science - May 14, 2013
Disrupted sleep is so commonly a symptom of depression that some of the first things doctors look for in diagnosing depression are insomnia and excessive sleeping. Now, however, scientists have observed for the first time a dysfunctional body clock in the brains of people with depression. People with major depression, also known as clinical depression, show disrupted circadian rhythms across brain regions, according to a new study published today in the journal Proceedings of the National Academy of Sciences. Researchers looked at post-mortem brain samples from mentally healthy donors and compared them with those of people who had major depression at the time of their death. They found that gene activity in the brains of depressed people failed to follow healthy 24-hour cycles.
Depression: Why life can feel out of control PhysOrg - April 18, 2013
People with depression often feel their life is out of control. It can evoke feelings that their life is pointless or by merely existing bad things can happen. Research funded by the Economic and Social Research Council (ESRC) suggests that these feeling may be caused by subtle changes in the way depressed people perceive time and process their surroundings.
Success in patients with major depression: For the first time, physicians stimulated patients' medial forebrain bundles PhysOrg - April 9, 2013
Researchers from the Bonn University Hospital implanted pacemaker electrodes into the medial forebrain bundle in the brains of patients suffering from major depression with amazing results: In six out of seven patients, symptoms improved both considerably and rapidly. The method of Deep Brain Stimulation had already been tested on various structures within the brain, but with clearly lesser effect.
'Obese but happy gene' challenges the common perception of link between depression and obesity PhysOrg - November 20, 2012
McMaster scientists have uncovered evidence that the gene FTO Ð the major genetic contributor to obesity Ð is associated with an eight per cent reduction in the risk of depression. In other words, it's not just an obesity gene but a "happy gene" as well.
How Depression Shrinks the Brain Live Science - August 13, 2012
Certain brain regions in people with major depression are smaller and less dense than those of their healthy counterparts. Now, researchers have traced the genetic reasons for this shrinkage. A series of genes linked to the function of synapses, or the gaps between brain cells crucial for cell-to-cell communication, can be controlled by a single genetic "switch" that appears to be overproduced in the brains of people with depression, a new study finds.
Almost half of depression in adults starts in adolesence PhysOrg - February 29, 2012
A new study by research psychologists at Bangor and Oxford Universities show that half of adults who experience clinical depression had their first episode start in adolescence. In fact, the most common age to see the start of depression is between 13-15 years-old.
Researchers find key genetic trigger of depression PhysOrg - October 18, 2010
Scientists have had a difficult time pinning down the cause of depression, which afflicts almost 16 percent of Americans in any given year and carries an annual economic burden of $100 billion. Symptoms of depression vary widely among individuals. Most now believe that multiple physiological processes are involved in major depressive disorder.
The neural basis of the depressive self PhysOrg - August 31, 2010
Depression is actually defined by specific clinical symptoms such as sadness, difficulty to experience pleasure, sleep problems etc., present for at least two weeks, with impairment of psychosocial functioning. These symptoms guide the physician to make a diagnosis and to select antidepressant treatment such as drugs or psychotherapy.
Depression Leads to Weight Gain, Study Confirms Live Science - June 11, 2010
A new study at the University of Alabama at Birmingham (UAB) confirms the relationship between depression and abdominal obesity, which has been linked to an increased risk for cancer and cardiovascular disease.
Half of Depressed Americans Get No Treatment Live Science - January 4, 2010
About half of Americans with major depression do not receive treatment for the condition, and in many cases the therapies are not consistent with the standard of care, according to a new study. The study also showed that ethnicity and race were important factors in determining who received treatment, with Mexican Americans and African Americans the least likely to have depression care. While many people can feel sad from time to time, a depressive disorder occurs when these feelings start to interfere with everyday life, preventing someone from functioning normally, according to the National Institutes of Health (NIH). The condition can be debilitating, hindering a person's ability to work, sleep and eat. A combination of factors likely contributes to the disorder, including imbalances in brain chemicals, genetics, and stressful situations, the NIH says. Pervious research has indicated that many Americans with depression go untreated, but the current study was the first to break down large ethnic and racial groups into subgroups to look at disparities in treatment.
New brain stimulation treatment may offer hope for those with treatment resistant depression PhysOrg - October 13, 2009
A new neurosurgical procedure may prove helpful for patients with treatment-resistant depression. Bilateral epidural prefrontal cortical stimulation (EpCS) was found generally safe and provided significant improvement of depressive symptoms in a small group of patients, according to lead researcher Ziad Nahas, M.D. at the Medical University of South Carolina. The data are reported in the on-line issue of Biological Psychiatry.
Fine-tuning treatments for depression PhysOrg - October 18, 2009
New research clarifies how neurotransmitters like norepinephrine, serotonin, and dopamine, are regulated - a finding that may help fine-tune therapies for depression. Current drugs for depression target the regulatory process for neurotransmitters, and while effective in some cases, do not appear to work in other cases. Recent findings suggest that synucleins, a family of small proteins in the brain, are key players in the management of neurotransmitters -- specifically, alpha- and gamma-synuclein. Additionally, researchers have found elevated levels of gamma-synuclein in the brains of both depressed animals and humans.
Using Brain Waves to Help Treat Depression PhysOrg - September 24, 2009
Researchers conducted a study at 9 sites in the U.S. with 375 people suffering from major depression. The testing takes about 15 minutes and could help people suffering from depression find fast relief. In the study researchers used a customized version of quantitative electroencephalography (QEEG) to study brainwave patterns.Brain waves are measured by a few electrodes attached to a strap that is placed around a patient's forehead. The electrodes plugs into a device that digitizes and filters the EEG signals from the brain. The device is then plugged into a computer for analysis.
The Science (and Art) of Depression Medication Live Science - September 22, 2009
In the study researchers used a customized version of quantitative electroencephalography (QEEG) to study brainwave patterns. Brain waves are measured by a few electrodes attached to a strap that is placed around a patient's forehead. The electrodes plugs into a device that digitizes and filters the EEG signals from the brain. The device is then plugged into a computer for analysis.
Children seriously affected when a parent suffers from depression PhysOrg - March 6, 2009
Life is hard for the children of a parent suffering from depression. Children take on an enormous amount of responsibility for the ill parent and for other family members. It is therefore important for the health services to be aware of this and have support functions in place for the whole family, and not just for the person who is ill. This is the conclusion of a thesis from the Sahlgrenska Academy, University of Gothenburg, Sweden.
Genes 'play key happiness role' BBC - March 2008
Our level of happiness throughout life is strongly influenced by the genes with which we were born, say experts. An Edinburgh University study of identical and non-identical twins suggests genes may control half the personality traits keeping us happy. The other half is linked to lifestyle, career and relationships. However, another expert said despite the research in the journal Psychological Science, we can still train ourselves to be more content.
Depression more harmful than angina, says study Guardian - September 7, 2007
Depression can do more physical damage to a person's health than several long-term diseases, according to a study. Saba Moussavi of the World Health Organization led the largest population-based study on the physical effects of several illnesses by analyzing data from more than 245,000 people in 60 countries. His results, published today in the Lancet, showed that depression had more impact on sufferers than angina, arthritis, asthma, and diabetes.
What was previously known as melancholia and is now known as clinical depression, major depression, or simply depression and commonly referred to as major depressive disorder by many health care professionals, has a long history, with similar conditions being described at least as far back as classical times.
In Ancient Greece, disease was thought due to an imbalance in the four basic bodily fluids, or humors. Personality types were similarly thought to be determined by the dominant humor in a particular person. Derived from the Ancient Greek melas, "black", and kohl, "bile", melancholia was described as a distinct disease with particular mental and physical symptoms by Hippocrates in his Aphorisms, where he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.
Aretaeus of Cappadocia later noted that were "dull or stern; dejected or unreasonably torpid, without any manifest cause". The humoral theory fell out of favor but was revived in Rome by Galen. Melancholia was a far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.
Influenced by Greek and Roman texts, physicians in the Persian and then the Muslim world developed ideas about melancholia during the Islamic Golden Age. Ishaq ibn Imran (d. 908) combined the concepts of melancholia and phrenitis. The 11th century Persian physician Avicenna described melancholia as a depressive type of mood disorder in which the person may become suspicious and develop certain types of phobias.
His work, The Canon of Medicine, became the standard of medical thinking in Europe alongside those of Hippocrates and Galen. Moral and spiritual theories also prevailed, and in the Christian environment of medieval Europe, a malaise called acedia (sloth or absence of caring) was identified, involving low spirits and lethargy typically linked to isolation.
The term depression itself was derived from the Latin verb deprimere, "to press down". From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.
The term also came in to use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.
Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.
Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised. The patient's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor.
Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual's life, and argued that the term depression should be used instead of melancholia. The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.
In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.
The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria), and was incorporated in to the DSM-III in 1980. To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes. The ancient idea of melancholia still survives in the notion of a melancholic subtype.
The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia. There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.
Major depressive disorder (MDD) (also known as recurrent depressive disorder, clinical depression, major depression, unipolar depression, or unipolar disorder) is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and by loss of interest or pleasure in normally enjoyable activities. This cluster of symptoms (syndrome) was named, described and classified as one of the mood disorders in the 1980 edition of the American Psychiatric Association's diagnostic manual. The term "depression" is ambiguous. It is often used to denote this syndrome but may refer to other mood disorders or to lower mood states lacking clinical significance. Major depressive disorder is a disabling condition that adversely affects a person's family, work or school life, sleeping and eating habits, and general health. In the United States, around 3.4% of people with major depression commit suicide, and up to 60% of people who commit suicide had depression or another mood disorder.
The diagnosis of major depressive disorder is based on the patient's self-reported experiences, behavior reported by relatives or friends, and a mental status examination. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. The most common time of onset is between the ages of 20 and 30 years, with a later peak between 30 and 40 years.
Typically, patients are treated with antidepressant medication and, in many cases, also receive psychotherapy or counseling, although the effectiveness of medication for mild or moderate cases is questionable. Hospitalization may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. A minority are treated with electroconvulsive therapy (ECT). The course of the disorder varies widely, from one episode lasting weeks to a lifelong disorder with recurrent major depressive episodes. Depressed individuals have shorter life expectancies than those without depression, in part because of greater susceptibility to medical illnesses and suicide. It is unclear whether or not medications affect the risk of suicide. Current and former patients may be stigmatized.
The understanding of the nature and causes of depression has evolved over the centuries, though this understanding is incomplete and has left many aspects of depression as the subject of discussion and research. Proposed causes include psychological, psycho-social, hereditary, evolutionary and biological factors. Certain types of long-term drug use can both cause and worsen depressive symptoms. Psychological treatments are based on theories of personality, interpersonal communication, and learning. Most biological theories focus on the monoamine chemicals serotonin, norepinephrine and dopamine, which are naturally present in the brain and assist communication between nerve cells.
What is depression? PhysOrg - March 11, 2013
Many people know what it's like to feel sad or down from time to time. We can experience negative emotions due to many things - a bad day at work, a relationship break-up, a sad film, or just getting out of bed on the "wrong side". Sometimes we even say that we're feeling a bit "depressed". But what does that mean, and how can we tell when it's more than just a feeling? Depression is more than the experience of sadness or stress. A depressive episode is defined as a period of two weeks or longer where the individual experiences persistent feelings of sadness or loss of pleasure, coupled with a range of other physical and psychological symptoms including fatigue, changes in sleep or appetite, feelings of guilt or worthlessness, difficulty concentrating or thoughts of death. To be diagnosed with major depressive disorder, individuals must experience at least one depressive episode that disrupts their work, social or home life.
Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health. Its impact on functioning and well-being has been compared to that of chronic medical conditions such as diabetes.
A person having a major depressive episode usually exhibits a very low mood, which pervades all aspects of life, and an inability to experience pleasure in activities that were formerly enjoyed. Depressed people may be preoccupied with, or ruminate over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self-hatred.
In severe cases, depressed people may have symptoms of psychosis. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. Other symptoms of depression include poor concentration and memory (especially in those with melancholic or psychotic features), withdrawal from social situations and activities, reduced sex drive, and thoughts of death or suicide. Insomnia is common among the depressed. In the typical pattern, a person wakes very early and cannot get back to sleep. Insomnia affects at least 80% of depressed people. Hypersomnia, or oversleeping, can also happen. Some antidepressants may also cause insomnia due to their stimulating effect.
A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression. Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.
Family and friends may notice that the person's behavior is either agitated or lethargic. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements. Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.
Depressed children may often display an irritable mood rather than a depressed mood, and show varying symptoms depending on age and situation. Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure. Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness. Depression may also coexist with attention-deficit hyperactivity disorder (ADHD), complicating the diagnosis and treatment of both.
Major depression frequently co-occurs with other psychiatric problems. The 1990-92 National Comorbidity Survey (US) reports that 51% of those with major depression also suffer from lifetime anxiety. Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts. American neuroendocrinologist Robert Sapolsky similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically. There are increased rates of alcohol and drug abuse and particularly dependence, and around a third of individuals diagnosed with ADHD develop comorbid depression. Post-traumatic stress disorder and depression often co-occur.
Depression and pain often co-occur. This conforms with Seligman's theory of learned helplessness. One or more pain symptoms is present in 65% of depressed patients, and anywhere from five to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome worsens. The outcome can also obviously worsen if the depression is noticed but completely misunderstood
Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating cardiovascular disorders, which further increases their risk. In addition, cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.
The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis-stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.
These interactive models have gained empirical support. For example, researchers in New Zealand took a prospective approach to studying depression, by documenting over time how depression emerged among an initially normal cohort of people. The researchers concluded that variation among the serotonin transporter (5-HTT) gene affects the chances that people who have dealt with very stressful life events will go on to experience depression. To be specific, depression may follow such events, but seems more likely to appear in people with one or two short alleles of the 5-HTT gene.
In addition, a Swedish study estimated the heritability of depression the degree to which individual differences in occurrence are associated with genetic differences to be around 40% for women and 30% for men, and evolutionary psychologists have proposed that the genetic basis for depression lies deep in the history of naturally selected adaptations. A substance-induced mood disorder resembling major depression has been causally linked to long-term drug use or drug abuse, or to withdrawal from certain sedative and hypnotic drugs.
MRI scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Recent meta-analyses of neuroimaging studies in major depression, reported that compared to controls, depressed patients had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus). Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.
There may be a link between depression and neurogenesis of the hippocampus, a center for both mood and memory. Loss of hippocampal neurons is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Drugs may increase serotonin levels in the brain, stimulating neurogenesis and thus increasing the total mass of the hippocampus. This increase may help to restore mood and memory.
Similar relationships have been observed between depression and an area of the anterior cingulate cortex implicated in the modulation of emotional behavior. One of the neurotrophins responsible for neurogenesis is brain-derived neurotrophic factor (BDNF). The level of BDNF in the blood plasma of depressed subjects is drastically reduced (more than threefold) as compared to the norm. Antidepressant treatment increases the blood level of BDNF. Although decreased plasma BDNF levels have been found in many other disorders, there is some evidence that BDNF is involved in the cause of depression and the mechanism of action of antidepressants.
There is some evidence that major depression may be caused in part by an overactive hypothalamic-pituitary-adrenal axis (HPA axis) that results in an effect similar to the neuro-endocrine response to stress. Investigations reveal increased levels of the hormone cortisol and enlarged pituitary and adrenal glands, suggesting disturbances of the endocrine system may play a role in some psychiatric disorders, including major depression. Oversecretion of corticotropin-releasing hormone from the hypothalamus is thought to drive this, and is implicated in the cognitive and arousal symptoms.
The hormone estrogen has been implicated in depressive disorders due to the increase in risk of depressive episodes after puberty, the antenatal period, and reduced rates after menopause. On the converse, the premenstrual and postpartum periods of low estrogen levels are also associated with increased risk. Sudden withdrawal of, fluctuations in or periods of sustained low levels of estrogen have been linked to significant mood lowering. Clinical recovery from depression postpartum, perimenopause, and postmenopause was shown to be effective after levels of estrogen were stabilized or restored.
Other research has explored potential roles of molecules necessary for overall cellular functioning: cytokines. The symptoms of major depressive disorder are nearly identical to those of sickness behavior, the response of the body when the immune system is fighting an infection. This raises the possibility that depression can result from a maladaptive manifestation of sickness behavior as a result of abnormalities in circulating cytokines.
Some relationships have been reported between specific subtypes of depression and climatic conditions. Thus, the incidence of psychotic depression has been found to increase when the barometric pressure is low, while the incidence of melancholic depression has been found to increase when the temperature and/or sunlight are low.
Various aspects of personality and its development appear to be integral to the occurrence and persistence of depression, with negative emotionality as a common precursor. Although depressive episodes are strongly correlated with adverse events, a person's characteristic style of coping may be correlated with his or her resilience. In addition, low self-esteem and self-defeating or distorted thinking are related to depression. Depression is less likely to occur, as well as quicker to remit, among those who are religious. It is not always clear which factors are causes and which are effects of depression; however, depressed persons who are able to reflect upon and challenge their thinking patterns often show improved mood and self-esteem.
American psychiatrist Aaron T. Beck, following on from the earlier work of George Kelly and Albert Ellis, developed what is now known as a cognitive model of depression in the early 1960s. He proposed that three concepts underlie depression: a triad of negative thoughts composed of cognitive errors about oneself, one's world, and one's future; recurrent patterns of depressive thinking, or schemas; and distorted information processing. From these principles, he developed the structured technique of cognitive behavioral therapy (CBT). According to American psychologist Martin Seligman, depression in humans is similar to learned helplessness in laboratory animals, who remain in unpleasant situations when they are able to escape, but do not because they initially learned they had no control.
Attachment theory, which was developed by English psychiatrist John Bowlby in the 1960s, predicts a relationship between depressive disorder in adulthood and the quality of the earlier bond between the infant and the adult caregiver. In particular, it is thought that "the experiences of early loss, separation and rejection by the parent or caregiver (conveying the message that the child is unlovable) may all lead to insecure internal working models ... Internal cognitive representations of the self as unlovable and of attachment figures as unloving or untrustworthy would be consistent with parts of Beck's cognitive triad". While a wide variety of studies has upheld the basic tenets of attachment theory, research has been inconclusive as to whether self-reported early attachment and later depression are demonstrably related.
Depressed individuals often blame themselves for negative events, and, as shown in a 1993 study of hospitalized adolescents with self-reported depression, those who blame themselves for negative occurrences may not take credit for positive outcomes. This tendency is characteristic of a depressive attributional, or pessimistic explanatory style. According to Albert Bandura, a Canadian social psychologist associated with social cognitive theory, depressed individuals have negative beliefs about themselves, based on experiences of failure, observing the failure of social models, a lack of social persuasion that they can succeed, and their own somatic and emotional states including tension and stress. These influences may result in a negative self-concept and a lack of self-efficacy; that is, they do not believe they can influence events or achieve personal goals.
An examination of depression in women indicates that vulnerability factors such as early maternal loss, lack of a confiding relationship, responsibility for the care of several young children at home, and unemployment can interact with life stressors to increase the risk of depression. For older adults, the factors are often health problems, changes in relationships with a spouse or adult children due to the transition to a care-giving or care-needing role, the death of a significant other, or a change in the availability or quality of social relationships with older friends because of their own health-related life changes.
The understanding of depression has also received contributions from the psychoanalytic and humanistic branches of psychology. From the classical psychoanalytic perspective of Austrian psychiatrist Sigmund Freud, depression, or melancholia, may be related to interpersonal loss and early life experiences. Existential therapists have connected depression to the lack of both meaning in the present and a vision of the future. The founder of humanistic psychology, American psychologist Abraham Maslow, suggested that depression could arise when people are unable to attain their needs or to self-actualize (to realize their full potential).
Poverty and social isolation are associated with increased risk of mental health problems in general. Child abuse (physical, emotional, sexual, or neglect) is also associated with increased risk of developing depressive disorders later in life. Such a link has good face validity given that it is during the years of development that a child is learning how to become a social being.
Abuse of the child by the caregiver is bound to distort the developing personality and create a much greater risk for depression and many other debilitating mental and emotional states. Disturbances in family functioning, such as parental (particularly maternal) depression, severe marital conflict or divorce, death of a parent, or other disturbances in parenting are additional risk factors.
In adulthood, stressful life events are strongly associated with the onset of major depressive episodes. In this context, life events connected to social rejection appear to be particularly related to depression.Evidence that a first episode of depression is more likely to be immediately preceded by stressful life events than are recurrent ones is consistent with the hypothesis that people may become increasingly sensitized to life stress over successive recurrences of depression.
The relationship between stressful life events and social support has been a matter of some debate; the lack of social support may increase the likelihood that life stress will lead to depression, or the absence of social support may constitute a form of strain that leads to depression directly. There is evidence that neighborhood social disorder, for example, due to crime or illicit drugs, is a risk factor, and that a high neighborhood socioeconomic status, with better amenities, is a protective factor. Adverse conditions at work, particularly demanding jobs with little scope for decision-making, are associated with depression, although diversity and confounding factors make it difficult to confirm that the relationship is causal.
To confer major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression).
Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.
Bipolar disorder, also known as manic-depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.
Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a substance abused including a drug of abuse, a medication, or exposure to a toxin, it is then diagnosed as a substance-induced mood disorder. In such cases, a substance is judged to be etiologically related to the mood disturbance.
Schizoaffective disorder is different from major depressive disorder with psychotic features because in the schizoaffective disorder at least two weeks of delusions or hallucinations must occur in the absence of prominent mood symptoms.
Depressive symptoms may be identified during schizophrenia, delusional disorder, and psychotic disorder not otherwise specified, and in such cases those symptoms are considered associated features of these disorders, therefore, a separate diagnosis is not deemed necessary unless the depressive symptoms meet full criteria for a major depressive episode. In that case, a diagnosis of depressive disorder not otherwise specified may be made as well as a diagnosis of schizophrenia.
Some cognitive symptoms of dementia such as disorientation, apathy, difficulty concentrating and memory loss may get confused with a major depressive episode in major depressive disorder. They are especially difficult to determine in elderly patients. In such cases, the premorbid state of the patient may be helpful to differentiate both disorders. In the case of dementia, there tends to be a premorbid history of declining cognitive function. In the case of a major depressive disorder patients tend to exhibit a relatively normal premorbid state and abrupt cognitive decline associated with the depression. Read more ...
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