Due to SAD’s variety of causes and manifestations, study of the disease is extremely difficult. According to HealthLine.com, a medical research website that is partnered with the Food and Drug Administration, the exact cause of SAD is unknown and the cause is most likely a combination of genetic and environmental factors. This is where the disorder becomes complex. Just as every person is different, so too is their experience with SAD. Every person’s genes are different and the genetic code that causes SAD has not been discovered. Every one’s life experiences are different and therefore the contributions to their SAD are vastly different compared to other victims. This makes testing difficult because there is no definitive cause that can be …show more content…
WHile a chemical imbalance may be responsible for an SAD patient’s symptoms, often times a conclusion is never drawn by a medical professional. The only way to determine whether or not a patient has a chemical imbalance is to have a brain scan of the patient and analyze the chemicals in their brain and how they relate to their symptoms. The problem with this is that according to Bernard Healthcare, a brain scan of a patient costs a minimum of $1,200. This is far out of the price range for the majority of SAD patients. This means that most SAD patients do not where their disorder came from! Likewise, treatment for a person with SAD becomes extremely difficult when they do not even know the cause of their disorder! The lack of reasonably priced brain scans makes the disease even harder to understand in ordinary people. If the Affordable Care Act is replaced, the price of these scans would go up even higher making it even more difficult to scan and analyze the causes of millions of people’s mental disorders. If that was not enough, there is no single test to determine if someone has SAD. This astonishing lack of testing to diagnose SAD makes it even harder to track. Due to the lack of a test, medical misunderstandings and misdiagnoses are …show more content…
According to Medical News Today, no direct link between any genetic makeup and SAD has been discovered, but there are other factors that cause SAD inside a person’s genes. Heredity is the major factor in this instance. According to the Mayo Clinic, if a person has a first degree relative who has SAD, they are 2 to 3 times more likely to develop SAD in their lifetime. According to the University of Maryland Health, the genetic component of the disorder has been proven to be the cause of 35-40% of cases of SAD. While no particular gene sequence has been found to cause SAD, there are chromosomes that cause other social disorders. These chromosomes could also be responsible for SAD as well. Chemicals in the brain known as neurotransmitters are responsible for sending signals from your brain to different parts of the body. For example, neurotransmitters tell your heart to beat, lungs to breathe, and your eyes to blink. These neurotransmitters relay signals from the brain to nerve centers throughout the body. According to the Mayo Clinic, the major neurotransmitters associated with mood are dopamine, norepinephrine, serotonin, and gamma-aminobutyric acid. An imbalance of these chemicals in the brain directly cause mood swings and depression. It is very possible that these chemicals cause SAD. According
Information about age of onset and duration of SAD, subtypes of SAD, psychiatric comorbidity and medication use were also obtained. The patients were assessed with an extensive questionnaire battery using observer-rated assessments and self report questionnaires at baseline, post-treatment and at 3 and 12-month follow-ups.
210). This creates difficulty with understanding the possible consequences or rewards of an action. According to Dolan, (2010), certain cues can be missed due to the deficits within the brain, creating a difficulty for that person to empathize. It has also been found that there are possible genetic links involving dopamine and serotonin, although these genes may be affected by the environment as well, which complicates the research (Rosenberg & Kosslyn, 2011).
Persons who are depressed have feelings of sadness, loneliness, irritability, worthlessness, hopelessness, agitation, and guilt that may be accompanied by an array of physical symptoms. A diagnosis of major depression requires that symptoms be present for two weeks or longer…Targeted screening in high-risk patients such as those with chronic diseases, pain, unexplained symptoms, stressful home environments, or social isolation, and those who are postnatal or elderly may provide an alternative approach to identifying patients with depression”
Experts believe bipolar disorder is caused by an underlying problem with specific brain circuits and the balance of brain chemicals called neurotransmitters (WebMD). There are five brain chemicals noradrenaline (norepinephrine), serotonin, dopamine, oxytocin, and endorphin. Noradrenaline and serotonin are the most common chemicals linked to psychiatric mood disorders such as depression and bipolar (WebMD). Dopamine is linked to the pleasure system in the brain (WebMD). When a disruption happens to the dopamine system connects to psychosis and schizophrenia (WebMD). If there is too much dopamine in one place, it can cause psychosis. Dopamine motivates us (Deans, 2011). Dopamine is linked to everything, metabolism, evolution, and the brain (Dean, 2011). Serotonin is connected to many different body functions including sleep, wakefulness, eating and impulsivity (WebMD). Researchers believe that abnormal brain functioning of brain circuits that involve serotonin as a chemical messenger contributes to mood disorders (WebMD). Oxytocin is a hormone commonly associated with childbirth and breastfeeding. Oxytocin plays a critical role in social and emotional behavior. Oxytocin increases the susceptibility to feeling fearful and anxious during stressful events (NWU, 2013).
The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in
They are popularly referred to as being part of a continuum, the ability to successfully perform in productive activities and relationships, as opposed to the inability to do such things (Mental Illness Overview). Ever since the first edition of the DSM was published in 1952, scientists have studied how a person’s mind relates to their brain and whether the disorders they listed were organic or purely in the mind (Arben). Science has made extraordinary leaps in this aspect, as they have come to discover not only the biological change that causes mental illnesses, but they are also able to pin down even specific chromosomes linked to them. One in particular that has been heavily studied is depression, which is known to be related to a lack of the neurotransmitter serotonin in the brain. Some of the more recently developed medications, known as SSRIs, block the receptors that recycle serotonin from taking in too much and allowing enough to carry proper signals throughout the brain (Johnson). While some people insist on the opinion that drugs such as these are overprescribed (Medications for Mental Illness Are Overprescribed), professionals use tested algorithms when determining whether a patient is in need of medication, and if so what medication to use (Restricting Medications for Mental Illness Harms Patients). These methods have been fine-tuned over the past few decades and are used treat a patient to their own personal needs, and to aid
The general public increasingly attributes mental disorders to biological causes such as a chemical imbalance or inherited genes (Schnittker, 2008; Schomerus et al., 2012).
After Meesters modified Rosenthal’s definition, it was possible to diagnose correctly many more patients under the umbrella of SAD. Thus, as greater numbers of people were diagnosed, observed trends began to develop. Three in particular were noticed early on, and continue to prove true today. They included an overall lower rate of SAD in children compared to the general population, an increasing diagnosis rate in adolescents, and a much higher rate in adult females versus males. One study that became instrumental in establishing concrete evidence for the rates in children and adolescents was conducted after the inherent trends were noticed throughout the general population.
There really have only been studies conducted on people with possible SAD since 1984 when a man named Norman E. Rosenthal actually defined the psychological disorder (Lam). Since Rosenthal defined SAD as a syndrome characterized by recurrent depressions that occur annually at the same time each year characterized by hypersomnia, overeating, and carbohydrate craving (Newsome), there have been several studies conducted and published on people with possible SAD. Many of the studies that have been published for the general public focus mainly on the different forms of treatment for SAD, such as light therapy and different forms of Phototherapy, rather than focusing on the cause. Discovering the main causes of SAD would help to clearly identify who is actually in need of treatment related to light therapy compared to anti depressants. In my situation I had symptoms that were both characteristic of what identified SAD patients and patients suffering from mild forms of depression. When symptoms of one disorder are so closely related to symptoms of
The leading theory explaining the biology of depression is the monoamine hypothesis of depression. (Stahl, 3) This theory suggests that depression is caused by a deficiency in one or another of the three neurotransmitters: serotonin, norepinephrine and dopamine. The theory was formulated after the accidental discovery of the original drugs for depression and psychosis, much in the same way Fleming discovered penicilin.
The causes of this disorder, like the majority of psychiatric diseases, explain the different theories. Biochemical rely on changes in the level of serotonin and norepinephrine, and the sensitivity of their receptors. A psycho-social causes explain the loss of
(3) While successful drug therapies which act on neurotransmitters in the brain imply that depression is a neurobiological condition (4), the fact that such medications do not help about 20 percent of depression-sufferers seems to show that not all depression is due to such imbalances. Rather, depression is not caused by one single factor; it is most often caused by many different things. Genetics, biochemical factors, medicines and alcohol, developmental and other external factors, and relationships, marriage and children all have effect on the development of clinical depression. (5) The strongest hypotheses on the pathways to depression are in decreases in the activity of specific neurotransmitters, or the overactivity of certain hormonal systems. (3)
Another possibility is that depression is a secondary development in cardiac patients, whereby patients with more
Although there are known, effective treatments for mood-disorders, fewer than half of those affected in the world (in many countries, fewer than 10%) receive such treatments, and most seek attention only after mounting symptomology forces intervention2, 3. Significant global barriers include that mood-disorders are not routinely screened, the incidence of inaccurate diagnosis is high and the absence of ongoing mood-level change assessment rests upon the evaluation of the patient, who is ill. Currently, a major obstacle in the field of mood-disorder diagnostics is that current diagnostics focus on post-symptom self-reports3 which occur after the symptomology has progressed to life-disrupting levels, and breakthroughs focus on expensive, time-consuming equipment4, 5 which do not realistically allow medical professionals access for every patient (i.e., Functional Magnetic Resonance Imaging, or fMRI, which costs approx. $2600 per scan6, and requires a time commitment of approximately 1.5 hours per scan). Early and accurate assessment via a widely accessible model is vital toward the future of mood-disorder diagnostics and treatment.
Neurotransmitters involved in depression include norepinephrine, dopamine, and serotonin. An imbalance of hormones may also play a role in depression. Many depressed people have higher than normal levels of hydrocortisone, a hormone secreted by the adrenal gland in response to stress. In addition, an underactive or overactive thyroid gland can lead to depression.4