Depression, or Major Depressive Disorder, is a serious illness which is widely misunderstood. Many people believe that it is a weakness and that people with this illness are just not strong-minded. However, there is strong research to suggest that Major Depressive Disorder is caused by several different aspects of the human mind working incorrectly. In addition to life experiences, learned helplessness, and genetic factors, depression is caused in part by physiological malfunctions in the brain. Physiological problems occurring in the brain result in several problems, including disruptions in behavioral and cognitive processing (Dombeck, M., Nemade, R., & Reiss, N.S. 1995). To truly understand this disease, people must understand the symptoms of depression, possible causes of depression, how the physiological causes create the symptoms, and how treatment helps to correct these problems.
In order to be diagnosed with Major Depressive Disorder, patients must exhibit certain symptoms for a period of time. These symptoms include a depressed mood with overwhelming feelings of sadness or grief, a loss of interest or pleasure in activities once enjoyed, disruptions in sleep patterns, fatigue, changes in appetite and weight, psychomotor agitation or retardation, feelings of worthlessness or guilt, inability to think or concentrate, and thoughts of death or suicide (American Psychiatric Association, 2000). At least five of these symptoms must be present for a period of two weeks or more. In addition, at least one of the symptoms must include either a depressed mood or a loss of interest or pleasure. Many of these symptoms may also be reported either by the patient or by outside observers. Doctors must also rule out a general medical condition or substance abuse as the cause for the mood changes in order to diagnose a patient with Major Depressive Disorder (2000).
Although these symptoms do not seem complicated, the exact cause of depression is vastly misunderstood (Schwartz & Schwartz, 1993). According to Dombeck, Nemade, & Reiss (1995), the Diathesis-Stress Model is often used to explain how depression arises, with biological factors functioning as diatheses, which are predispositions, psychological factors functioning as either diatheses or stressors, and sociological factors functioning as stressors. Therefore, each of these factors work together to cause depression. However, since physiological causes seem to best account for the specific symptoms, these will be the focus of this essay.
In the brain, chemical messengers called neurotransmitters are released and then received by neurons in order for neurons to communicate with each other. According to Dombeck et al., (1995), “one neuron (the sender) sends a neurotransmitter message across the synapse and the next neuron (the receiver) receives that message by way of a receptor embedded on its surface.” When neurotransmitters and matching receptors come into contact, the neurotransmitter activates the receptor. If no matching neurotransmitters come into contact, the receptors stay inactive. Once receptors are activated, they re-release neurotransmitters back into the synapse (1995). These neurotransmitters must then be cleared out in order to avoid over-stimulation (Schwartz & Schwartz, 1993). Some of these may be deactivated by enzymes such as monoamine oxidase. Schwartz & Schwartz (1993) say:
In many cases, the neurotransmitter may be ‘inactivated [by being broken down] into smaller molecules…or [may be]… ‘reuptaken’ [that is,] sponged up into the presynaptic nerve terminal…. processes [which] clear the site for the arrival of the next chemical messenger’ (p. 62).
Receptor cells may also become firing cells if they are stimulated. In this case, the entire process is repeated millions of times over. The firing rate, however, is dependent upon the balance of excitatory signals, which speed up the firing rate, and inhibitory signals, which slow down the firing rate (1993).
Clearly, this is a very complex process with much room for error. It is critical, though, for this process to occur in order for all of the brain’s roles to function properly (Dombeck et al., 1995). Research indicates that when the neurotransmitters serotonin, norepinephrine, and dopamine do not function according to this system or are not present in a normal amount, Major Depression occurs (1995). Serotonin is involved in many functions of the brain. These include sleeping, eating, aggression, sexual behavior, and mood (1995). It makes sense, then, that a lack of serotonin in the brain could trigger depression since some of the symptoms of this illness involve sleep problems, change in appetite, feeling irritable, loss of sexual desire, and depressed mood (American Psychiatric Association, 2000). Norepinephrine is also implicated in depression, and a lack of it creates a depressed mood and an inability to handle stress, which are two effects of depression (Dombeck et al., 1995). Dopamine, the third neurotransmitter that partially causes depression, causes people to obtain pleasure (1995). It makes sense, then, that without normal amounts of this neurotransmitter, people would lose interest in things that once gave them pleasure, which is a symptom of depression mentioned earlier. Research suggests imbalances in these neurotransmitters as partial causes of depression, although, according to Dombeck et al. (1995), “evidence is somewhat indirect on these points because it is very difficult to actually measure the level of neurotransmitter in a person’s brain.”
In order to correct these problems with neurotransmitters, antidepressants can be used. Three of the most common antidepressants are the Tricyclic Antidepressants, Monoamine Oxidase Inhibitors, and Selective Serotonin Reuptake Inhibitors. Each of these drugs works to correct the lack of neurotransmitters in the brain. It is important to note, however, that it may take two weeks or more for these drugs to begin to correct symptoms. They also often cause unpleasant side-effects, and are therefore not a perfect choice for many patients with depression. They may reduce symptoms, but are by no means a cure for depression (Weissman, 2001).
One of the oldest forms of antidepressants on the market is the Tricyclic Antidepressants. These antidepressants work by inhibiting the reuptake of norepinephrine and serotonin (2001). As discussed earlier, reuptake involves the presynaptic nerve terminal reabsorbing the neurotransmitter where it can be broken down. If this process in inhibited, the neurotransmitters will stay in the synapse for a longer period of time, allowing them to continue to communicate with other neurons. This therefore would help to increase the effects of these neurotransmitters. By inhibiting the reuptake of key neurotransmitters that play a role in depression, symptoms can be decreased. However, Tricyclics cause several severe side effects, including drowsiness, weight gain, constipation, dry mouth, blurred vision, postural hypotension, and dizziness. They also pose a high risk for overdose (2001).
A second form of antidepressants is the Monoamine Oxidase Inhibitors. Monoamine oxidase is a naturally-occurring enzyme in the brain. It comes in two forms: MAO-A and MAO-B. MAO-A metabolizes serotonin, and MAO-B oxidizes dopamine. Both forms also oxidize other neurotransmitters as well (Weissman, 2001). Monoamine Oxidase Inhibitors, then, keep this enzyme from working properly. If the enzyme is kept from oxidizing neurotransmitters that play a role in depression, then these neurotransmitters, specifically serotonin and dopamine, would not be broken down as quickly. They then would be able to communicate with neurons for a longer period of time. This helps to decrease symptoms of depression because the neurotransmitters would be able to perform their proper functions in this situation. However, these drugs interact poorly with many foods and cold medicines, and patients wishing to take these drugs must follow a strict diet. Therefore, these are not a safe choice for many people (2001).
One of the most popular forms of antidepressants is the Selective Serotonin Reuptake Inhibitors. These drugs work by blocking the reuptake of serotonin in the brain. This allows serotonin to perform its functions for a longer period of time in the brain (Carey, 2007). According to Myrna M. Weissman (2001), these antidepressants are as effect as the Tricyclics and Monoamine Oxidase Inhibitors, but have a “much more benign side effect profile, which made them more palatable to patients” (p. 124). Building on the Selective Serotonin Reuptake Inhibitors, newer drugs have come onto the market such as Effexor and Cymbalta, which prolong activity of norepinephrine in addition to serotonin (Carey, 2007). Benedict Carey (2007) says that “experts consider these drugs to be essentially an extension of SSRI therapy, not a real departure.
Although these drugs are effective at reducing some symptoms of Major Depressive Disorder, they are not a cure (Weissman, 2001). This has caused researchers to search for new treatments of depression and to look for further causes. For example, researchers are beginning to look at the role of the hippocampus in depression. They are also using brain imaging to see what areas of the brain are activated when people feel depressed. Brodman’s area 25 is an area of the brain which was not suspected for causing depression, but due to brain imaging, is now being looked at more closely (Carey, 2007). Ketamine is another drug that is being looked at for the treatment of depression. However, many patients may be more likely to recover through talk therapy such as cognitive behavior therapy (2007).
As complex a process as depression seems; there is hope for the future of this devastating illness. The severe, debilitating symptoms of depression are a result of many factors, both physiological and social. Many drugs are on the market to treat these symptoms. The future of depression is unknown, but research is being conducted to further understand the causes of depression. Once the causes are better understood, treatment will hopefully become much more effective. In the meantime, patients suffering from this illness can take advantage of the current treatments available and remain hopeful of a future with a cure for depression.
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