Depression has increasingly become a common illness in the world today. It is a major depressive disorder that is described as a common but quite serious mood disorder. According to the behaviourist theory, depression results from the interaction of a person with the environment. The operant conditioning concept suggests that depression is a result of removal of an environment’s positive reinforcement, including a loved one and job. Depression leads to the development of severe symptoms that affect the way one thinks, feels, manages day-to-day activities including working, eating or sleeping. For an individual to be diagnosed as having depression, they must exhibit its symptoms for not less than two weeks (Weiss et al., 1992). Some depression forms are unique or could develop under slightly different circumstances. Persistent depressive disorder, also known as dysthymia, is defined as a depressed mood lasting for more than 24 months. Someone diagnosed with this disorder could have major depression episodes and bouts of less severe symptoms. However, the symptoms should last for the stated period for it to be perceived as dysthymia. Contrarily, postpartum depression is a condition experienced by women after they give birth. Such women report having full-blown serious depression in the course of pregnancy or after they have delivered. Feelings of major anxiety, sadness and exhaustion associated with this condition could make it difficult for them to undertake the daily chores for themselves or their babies (National Institute of Mental Health, 2015). Psychotic depression happens when one exhibits severe depression and psychosis. Psychotic symptoms have a depressive mood or feeling including delusions of illness, poverty or occasionally guilt. The other disorders classified as depression are seasonal affective disorder, disruptive mood dysregulation disorder and bipolar disorder. Depression is among the commonest mental disorders reported in the United States. According to current research, it is caused by an amalgamation of psychological, biological, genetic and environmental factors. In addition, depression may occur at any age, but usually starts during adulthood. Many of the chronic anxiety and mood disorders among adults start as high anxiety levels.
Brain Regions
The Hippocampus and Prefrontal Cortex is a brain region that takes charge of cognitive abnormalities experienced during depression, including guilt, hopelessness, worthlessness as well as memory impairments. Contrarily, the Amygdala plays a role in noting threats and directing attention. This region has a tendency of showing increased activation among individuals with depression. It is also responsible for the fear and anxiety felt in the course of depression and dysphoric emotions. The hypothalamus region plays the role of noticing the neuro-vegetative depression symptoms that include alterations in appetite and sleep (National Institute of Mental Health, 2015). When one is depressed, the Brodmann area 25 often has a tendency of being more active the depressed individuals. On the other hand, locus coeruleus involves itself in physiological responses to panic and stress. It forms a core section or region of the reticular activating system. It acts as the major brain site for synthesis of norepinephrine or noradrenaline. Pleasure pathway is responsible for dysfunction of the dopamine receptors that are associated with depression. The BRS is made up of neural pathways that take part in causing rewarding experiences in both humans and animals. An alteration of the functioning of the BRS could affect one’s feelings. The nucleus accumbens plays the role of anhedonia, which is the inability for one to get pleasure in activities as well as the decreased motivation during depression. Overall, the brain areas described play a crucial role in depression. The next section examines the way drugs impact behavioural outputs associated with depression.
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Drugs and Depression
Drugs are used by depressed individuals as self-medication for their depression. Weiss, Griffin and Mirin (1992) established that drug abusers use drugs as a way of coping with depression. Basing on the responses made by the patient, the motivation by many of the patients were the depression symptoms as well as elevated alterations within their moods. The abuse is often more common among the male patients that have depression as the study highlights. Despite not all the drug abusers in the study not being diagnosed with serious depression, the study is crucial for diagnosing males who have major depression in case they have a drug abuse history. Substance abuse has increasingly become common among individuals grappling with depressive disorders (National Institute of Mental Health, 2015). Since alcohol is renowned as a central nervous system depressant, usage of drugs has a tendency of triggering depression symptoms including sadness, lethargy as well as hopelessness. Notwithstanding, many of the depressed persons tend to use drugs or alcohol to become happy or take care of their numb painful thoughts. Consequently, depression and substance abuse have a correlation, and one condition will aggravate the other. When someone has an addiction and depression, it is referred to as a Dual Diagnosis. It consists of an amalgamation of a mental disorder and addiction. Whereas people in depression believe that drugs can help them to manage their situations, it only acts to aggravate the problem. This is in tandem with findings that one out of every three adults struggling with drug abuse or alcohol also suffer from depression. Conceptually, clinical depression makes one to become vulnerable to suicide, self-harm as well as accidental injury. Depression may also make the immune system weaker and make people more vulnerable to chronic illness and physical ailments (Weiss et al., 1992). When drugs are added to the problem, there is an exponential increase to the emotional and physical health of the person. In other words, drugs only exacerbate behavioural outputs associated with depression rather than helping people diagnosed with depression to feel better. Drug addiction leads to the creation of physiological changes in the brain of an individual that can imitate and aggravate depression symptoms. Some individuals who abuse drugs find it difficult to realize that they are experiencing depression due to the similarity between depression and addiction symptoms. Underlying depression symptoms may only be diagnosed after the drug has been removed for some time. Consequently, drugs are not beneficial for reducing or eliminating depression as some people may think.
Mechanisms of Action
Feighner (1999) suggests that antidepressants are the commonest drugs prescribed for depression. They aid in reducing the depression symptoms by changing the chemical imbalances of the brain’s neurotransmitters. Chemical imbalance results in the change in behavior and mood. Neurotransmitters, located in vesicles in the nerve cells, connect the neurons found in the brain. Some of the neurotransmitters include serotonin, noradrenaline and dopamine that are often released by one nerve’s exonic end while being received by another nerve. Antidepressants prevent the reuptake of neurotransmitters using selective receptors. Consequently, this increase the concentration of particular neurotransmitters found around brain nerves. Selective serotonin is one of these antidepressants. T ricyclic antidepressants, TCAs, block the reuptake of serotonin and norepinephrine. This is the main mechanism of action of many antidepressants and leads to alterations of neuro-receptors’ physiological behavior. TCAs also block muscarinic, histaminic receptors as well as alpha 1 adrenergic. Contrarily, these molecules could contribute to various side effects among patients. Antidepressants achieve their functions by significantly affecting the concentration of neurotransmitters within the brain and central nervous system.
Furthermore, antidepressants, basing on their mechanism of action, have 17 substances that could be further categorized into subgroups: TCAs, Monoamine oxidase inhibitors, MAOI, non-TCA antidepressants, selective serotonin-reuptake inhibitors and serotonin-norepinephrine reuptake inhibitor. SSRIs have little impact on other neurotransmitters’ reuptake. They do not exhibit any activity that would possibly lead into minute anti-cholinergic as well as sedative impacts. Mechanisms of action of various antidepressants including phenelzine, tranylcypromine and monoamine oxidase inhibitors are linked to enzymatic conversion inhibition. The prescription of MAOIs is often done in the form of drug resistant or atypical depression. They have some level of toxicity that has to be taken into consideration (Weiss et al., 1992). Overall, antidepressants are the commonly prescribed drug for managing depression. However, the exact mechanism of action of these drugs remains uncertain. The major theory is that they increase the concentration of brain chemicals or neurotransmitters used by the brain for communication.
Brain Changes during Behavioral States
As earlier discussed, there are various antidepressants: tricyclic, MAO inhibitors, serotonin-norepinephrine reuptake inhibitors, SNRIs, and selective serotonin reuptake inhibitors, SSRIs. In one’s brain, information often moves from the neuron or brain cell to another through chemical messengers referred to as neurotransmitters. Each neurotransmitter unlocks certain receptors on neurons to allow the messages to continue traveling. Ingestion of the drugs could result in efficient brain functioning or poor reception. The main result is that the intake of these drugs leads to neurotransmitter dysregulation (Dusi et al., 2015). Because the information is not sent to the right neurotransmitters after drug intake, messages are not delivered. Drugs, especially antidepressants, change the way one’s neurotransmitters function and avails more to ensure that when a message is sent, it can be delivered appropriately. It is often achieved through the slow-down of the reuptake process, which is fundamentally a recycling or clean-up process. After messages begin flowing in the appropriate way, the brain often works in a better way, thus diminishing or eliminating symptoms that are related to the slow-down. Notwithstanding, as a complex environment each neurotransmitter in the brain has various roles. Increasing available neurotransmitters could alleviate one’s depression, reducing neuropathic pain and helping victims to think straight. Whereas these appear as great benefits, drugs could also result in all forms of unwanted impacts.
There are numerous side-effects of drugs, and could range from debilitating, life-threatening and mildly annoying. In addition, there is the problem of antidepressants increasingly becoming ineffective after some time as the body gets used to them. Since antidepressants and other drugs become less effective with time as one becomes tolerant, symptoms may re-emerge. This is not the case for all people who have worse depression while on drugs. The hypothesis is that drugs could alter the brain and cause depression (Dusi et al., 2015). The term tardive dysphoria is used for describing an increase in depression symptoms. The meaning of ‘tardive’ is that it emerges later during the treatment whereas dysphoria means a state of restlessness, depression, discomfort and dissatisfaction. Tardive dysphoria is a major side effect associated with the use of drugs and is a probable factor in studies examining treatment-resistant depression. Reuptake inhibitors affect the brain by reabsorbing neurotransmitters into the brain’s nerve cells after being released to send messages. Rather than being absorbed, a reuptake inhibitor makes the neurotransmitter to stay temporarily in the synapse or gap between the nerves. SSRI affect the functioning of the serotonin transporter and other serotonin receptors to get rid of major depression (Dusi et al., 2015). Contrarily, tetracyclic affects neurotransmitters but does not deter reuptake in a similar way. Rather, it appears to refrain neurotransmitters from binding onto specific receptors on nerves. Since serotonin and norepinephrine do not bind to receptors, they appear to accumulate in areas found between nerve cells. Consequently, the levels of neurotransmitters rise.
Empirical Studies vs. Paper Arguments
Kandel (1982) used a self-reported scale to measure depressive mood among public high school students. He established that adolescents who were diagnosed with major depressive disorder had a higher score compared to the ones with other psychiatric diagnoses. The sex differences in the adolescent sample were similar to some of the arguments made in this paper, with girls recording higher scores than boys. Adolescents had higher depressive moods compared to their parents and the differences were higher in the relationship between daughters and their mothers than sons and their fathers. Judging from the mood differences, one could infer that adolescence was the most stressful period. Lowest levels of depressive mood among adolescents were in tandem with high attachment levels to parents and peers. The sex differences in adolescents contributed to the varying depressive moods and masked depression and higher delinquency account for this relationship. Despite the study having some similarities, the discussion presented in it differs with many of the arguments made in this paper. Whereas it examined the sexual differences in depressive moods, this paper largely examined the effect of drugs on the brain, especially the various brain parts.
Van, den Oord, Pickles and Waldman (2003) carried out a similar study by focusing on adolescents. The findings resonate with those of the previous study, but do not correlate with many of the discussions in this paper. The emphasis of this study is on delinquency, adolescents and depressive mood. The main similarity is the concept of depression, discussed earlier in the paper, and depressive mood that has been explored by the authors appear in both discussions. Finally, Weiss et al (1992) findings are the most relevant for the discussions in this paper. The study revolved around drug abuse as a way of self-medication for relieving depression. Basing on the findings, it is clear that depressed persons get motivated to use drugs because of the symptoms they have and the need to change their moods. Substance abuse becomes common among the male patients diagnosed with major depression. The findings are similar to the discussion and none of them differs in any way to this paper’s arguments. Overall, the first two studies significantly differed with the paper’s arguments while the final study provides a clear image of the discussions made in this paper. This does not mean, however, that the first two studies do not provide any similar information to that presented in this paper.
Comparison of the Empirical Studies
The first and second studies are similar because they focus on adolescents. In the first study, adolescents had higher depressive moods compared to their parents, with many of the adolescent girls having the higher level. The two studies also explore the concept of delinquency with the first study concluding that increased delinquency could mask depression among adolescent boys. The other similarity is that both are inconclusive on the aspect of depression. The results can be generalized to depression among the youth, but the impact of delinquency masking or negating the truth remains unidentifiable. Weiss et al (1992) study is different because it does not analyze delinquency. The three papers are comparable since they all focus on delinquency. They are only different in the way they approach the concept of depression, but the findings remain largely comparable. The three studies are also complementary because of using varying approaches but the findings point to a unique aspect of depression. The aspect of gender differences among adolescents has also been incorporated to ascertain the level of differences regarding depressive moods. The studies also supplement each other by ensuring that aspects not covered in one study are covered in another study. By combining the three, one gets valuable information on depression and major insight on depression, delinquency, substance abuse and effects of drugs on depressed individuals. With this in mind, it could be inferred that the three studies are largely comparable than different because of their findings on the concept of depression. The contradiction is mainly on the way the studies were carried out, study samples and individual topics studied.
New Questions
As Kandel and Davies (1982) provided findings on a gender basis, one of the questions would be whether the distinction and inclusion of sexes within the Den Oord et al (2003) could make it easier to understand the role of delinquency. It is interesting because of the fact that both Kandel and Davies (1982) and Den Oord et al (2003) studies embed the child-parent relationship. A new question that arises from this is whether the familial aspect in the studies influences the answers received. The other question is whether there will be more likelihood of children reporting that they are depressed in case they think their parents perceive that they are depressed. The fourth issue is whether the children will refrain from reporting because of the incorporation of their families. The fifth question is whether, apart from parent questioning and self-reporting, there is another way that can be used for measuring delinquency rates in relation to depression.
Answered and Unanswered Questions
The unanswered question is whether the study findings in the Weiss et al (1992) study would have been different if the range of ages would have been incorporated rather than using only males and females. The other unanswered question is about the period that self-medication can be used by persons suffering from depression. However, the studies have addressed numerous questions that I sought to find answers to prior to analysing them. They have mainly addressed the issues of how depression can be analyzed, observed and managed. The self-medication content has been particularly critical as it provides pertinent information for people suffering from depression.
References
Dusi, N., Barlati, S., Vita, A., & Brambilla, P. (2015). Brain structural effects of antidepressant treatment in major depression. Current neuropharmacology , 13 (4), 458-465.
Feighner, J. P. (1999). Mechanism of action of antidepressant medications. In Assessing Antidepressant Efficacy: A Re-examination., Jan, 1998, Phoenix, AZ, US . Physicians Postgraduate Press.
Kandel, D. B., & Davies, M. (1982). Epidemiology of depressive mood in adolescents: An empirical study. Archives of general psychiatry , 39 (10), 1205-1212. doi:10.1001/archpsyc.1982.04290100065011
Weiss, R. D., Griffin, M. L., & Mirin, S. M. (1992). Drug abuse as self-medication for depression: An empirical study. The American journal of drug and alcohol abuse , 18 (2), 121-129.
U.S. Department of Health and Human Services, National Institutes of Health, National Institute of Mental Health. (2015). Depression. What You Need to Know. (NIH Publication No. 15-3561). Bethesda, MD: U.S. Government Printing Office. Accessed on August 13, 2018 from https://www.nimh.nih.gov/health/publications/depression-what-you-need-to-know/depression-what-you-need-to-know-pdf_151827.pdf
Van, den Oord, E. J., Pickles, A., & Waldman, I. D. (2003). Normal variation and abnormality: an empirical study of the liability distributions underlying depression and delinquency. Journal of Child Psychology and Psychiatry , 44 (2), 180-192.
