Thursday, February 16, 2017

The Social Construction of the Chemical Imbalance Theory: Part II

Also of significance in the 1950s was reserpine, which is an alkaloid contained in the root of Rauwolfia serpentina. Prior to being introduced in the United States, this herbal medicine was used in India as a treatment for both psychosis and hypertension. This drug was found to have neuroleptic effects, meaning it operates as a depressant (France et al. 412). What is fascinating about this is that nearly 70 years ago, herbal medicine was intersecting with the pharmaceutical industry. Through animal studies, it was first found that serotonin was present in the CNS and affected behavior. Reserpine was found to decrease serotonin levels, and so, a hypothesis was developed that low serotonin levels caused depression (France et al. 412).

Notice here though that this study was performed on animals and not humans. As Michael B. Bracken, an epidemiologist at Yale University, mentions in an article from 2009, this has been a controversial subject for a long time. For instance, the Persian polymath Ibn Sina was writing about this topic a thousand years ago, not to mention that one of 18th century poet Alexander Pope’s most quoted statements is “The proper study of mankind is a man” (Bracken 120). For my purposes here, the most important implication is the similarity between the CNS of human and non-human animals, particularly the brain, since the CNS simply refers to the brain and spinal cord (Colman). The spinal cord is only of peripheral importance (if any at all) since antidepressants are used to treat the brain. Of course, it is common sense that human brains are more complex than non-human animal brains. 

Robert O. Duncan, a behavioral scientist from York College, offers some interesting insight on the topic. Focusing on the sub-topic of self-awareness (sometimes called metacognition), Duncan writes that this is what distinguishes humans from a majority of other animal species. He notes that the prefrontal cortex is generally regarded as the source of self-awareness, though there is no certainty in the matter. There are other factors that could have a part in this ability, such as the size of the brain, a more robust cognitive ability, as well as a greater degree of connection between brain areas (Duncan). Now, I should like to note here that self-awareness has massive implications for antidepressant usage and their effect on the body. Depression and anxiety are difficult mental states to manage precisely because of self-awareness. This is not to say that a lack of self-awareness would cause the burdensome effects of anxiety and depression for its sufferers to simply vanish into thin air. What I am saying is that self-awareness multiplies the mental pain. For instance, suppose that someone struggles with pessimism and worry, two symptoms of depression and anxiety. In particular, this person is concerned about going to a certain location where people they know are. This person does not want to go there because they have bad past experiences and are sure those experiences will happen again if they go. The person in this example could not have any of those concerns without self-reflection because it is, in part, themselves they are worried about. In addition to this, people who are concerned about their mental health, at least some of them, will go to see someone who might be able to help them, such as a doctor or a therapist. To say to oneself “I need help” is contingent upon self-reflection.

The next monumental moment in the process happened in the early 1980s, when the first SSRI, zimelidine, appeared on the market. The efficacy zimelidine had at the time not only caused other pharmaceutical companies to follow suit and add SSRIs to their repertoire of products, but also caused a re-evaluation of the serotonin hypothesis of the 1950s. The new hypothesis added that in addition to insufficient serotonin levels in the brain, depression was caused by other chemical insufficiencies, particularly, in monoamines norepinephrine and dopamine (Owens 6).

Works Cited

Bracken, Michael B. “Why animal studies are often poor predictors of human reactions to exposure.” Journal of the Royal Society of Medicine, vol. 101, 2008, pp. 120-122. DOI: 10.1258/jrsm.2008.08k033.

Colman, Andrew M. "central nervous system." A Dictionary of Psychology. Oxford University Press, 2015, Oxford Reference,  www.oxfordreference.com/view/10.1093/
acref/9780199657681.001.0001/acref-9780199657681-e-1346>.


Duncan, Robert O. “What Are the Structural Differences in the Brain between Animals That Are Self-Aware (Humans, Apes) and Other Vertebrates?” Scientific American. 2012. www.scientificamerican.com/article/what-are-the-structural-differences/.

France, Christopher M. et al. “The 'chemical imbalance' explanation for depression: Origins, lay    endorsement, and clinical implications.” Professional Psychology: Research and Practice, vol. 38, no. 4, 2007, pp. 411-420. DOI: 10.1037/0735-7028.38.4.411.

Owens, Michael J. “Selectivity of Antidepressants: From the Monoamine Hypothesis of Depression to the SSRI Revolution and Beyond.” The Journal of Clinical Psychology, vol. 65, 2004, pp. 5-10. www.psychiatrist.com.cyber.usask.ca/JCP/article/
_layouts/ppp.psych.controls/BinaryViewer.ashx?Article=/JCP/article/Pages/2004/
v65s04/v65s0402.aspx&Type=Article.

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