Developmental dyslexia is a genetic condition that has been proven to make it difficult for otherwise normal children to learn how to read. An individual having this condition finds it hard to learn to read despite the fact that they are highly intelligent. This condition of slow and ponderous reading process might progress into adulthood, and it is referred to as developmental dyslexia. The research paper titled “ The Interface between Genetics and Psychology: Lessons from Developmental Dyslexia” by D.V. M. Bishop seeks to understand the causes of developmental dyslexia. This article states that dyslexia results from certain genetic mutations, and it is hoped that soon it will be possible to screen children for this condition. If developmental dyslexia is detected early, then there will be potential chances of providing some special assistance that could help resolve the reading problem before it becomes evident ( Boder, 1973).
According to the Diagnostic and Statistical Manual of the American Psychiatric Association (DSM5) and the International Classification of Diseases (ICD-10), dyslexia results when there is an apparent mismatch between an individual’s measured intelligence and reading achievement. However, the IQ-discrepancy criterion is yet to be proven. Better definitions view dyslexia as a condition whereby one tends to reverse letters while reading or have an unusual perception of words. Now that genes can be looked into through molecular methods, it is evident that it is not very easy to discover the genes for dyslexia. However, it is good to note that some families display clear-cut patterns of dyslexia inheritance. The complexity of developmental dyslexia becomes even more apparent by the fact that the condition is not Mendelian. Dyslexia results from the mutation of multiple genes, making its study rather complicated ( Ramus, 2003).
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This genetic condition is researched using two approaches, the family approach and molecular approach. The family approach looks for any present phenotypic similarities between individuals. The molecular approach, on the other hand, looks for any presence variations in the DNA. The twin study is also used to get an understanding of whether identical (MZ) twins exhibit more similarity and connection to one another compared to fraternal (DZ) twins. When considering the polymorphic DNA (a genetic material that results in differences in people), we can conclude that MZ twins have a 100% genetic relatedness, while in DZ twins it is 50%.
The twin approach is rather striking because it completely deviates from the previous argument of developmental dyslexia being hereditary. The approach argues that if the effect of poor reading in one twin is due to a completely random event, then we do not expect the other twin to have the same problem ( Boder, 1973). If the problem results from the environment to which one twin is subjected to, then we would expect that the other twin would also have problems when it comes to reading. However, if the cause is purely genetic, then it is expected that twins would have a similar performance when they read. The contribution of all these three potential causes of dyslexia is measured and estimated ( Ramus, 2003).
One can see the evident distinction in hereditability when using the twin approach and the molecular approach. In the twin approach, we see that in places where there is the education of excellent quality, hereditability is low. However, if the quality of education is poor, then hereditability is high. Therefore, when using this approach, we would say that developmental dyslexia is not a hereditary condition. Rather, it has so much to do with the environment of the child. However, molecular approach seeks to understand the genome component of individuals with dyslexia, and it proves that the condition is hereditary. It has been proven that there is the potential of there being some genetic variation depending on the environment. For this reason, we can conclude that these two approaches can be merged in that dyslexia is a genetic condition, but there is a possibility of some genetic modifications being depending on the subjected environment ( Ramus, 2003).
The article should have made an effort to give a clear-cut cause of developmental dyslexia. One is left wondering if the heredity issues affect the condition. Imagine a scenario where there is a constant high-quality education for the young people. Then this would mean that the condition would not exist in any way. However, if anything changes and the quality of education declines, then the condition would surface, and it would be blamed on hereditary causes. For this reason, we can see that this article is not clear on what causes developmental dyslexia.
The second article titled “ Implications of Oxytocin in Human Linguistic Cognition: from Genome to Phenome” served as a supplemental review of the genome to phenome conversion by the study of the neurohormone oxytocin (OXT) which regulates complex socioemotional cognition in both humans and animals. The article sheds light on how OXT affects heredity based on the individual’s environment. Depending on the environment, the levels of OXT released will vary, and this in return will affect the extent to which a condition will be viewed as hereditary. It is worth noting that the hormone in question (OXT) is greatly involved in multiple pathophysiological and physiological processes including sexual activity, milk ejection, pain modulation, uterine and pregnancy contractions, social interactions and bonding, and parental care, among others. However, OXT has a major role when it comes to our linguistic capabilities, and it affects both our abilities to speak and also what motivates our speech.
There are multiple potential interactions of OXT in the body, and all these are proven to affect the linguistic capabilities through molecular means. It is striking to note that this single OXT hormone has major effects on the body ranging from affecting normal language development, regulation of facial expressions, while other reactions affect specific language endophenotypes.
The second article has made a clear effort to bring out how the OXT hormone affects many processes in the body, and especially the linguistic aspect. The article has supplemented the questions and lack of clarity that we found in the first article, making it easier to understand the whole concept of the heredity of developmental dyslexia. We get a clear understanding that the hormone which controls an individual’s reading and linguistic capabilities could be affected by the environment to which one is subjected to. As such, there is a direct connection between the environment and hereditary aspects.
The two articles are connected in that, the first one talks of developmental dyslexia as a partially hereditary condition depending on the environment, while the second one comes in to explain why these differences happen. The second article explains this issue of partial heredity that is brought up in the first article by stating that the levels of OXT hormone released vary depending on the environment, and this is what impact the heredity aspect of the condition. These articles can be used to explain the disparity that exists in real-life situations whereby kids that come from modern and developed homes tend to be relatively better linguists compared to kids coming from poor backgrounds.
References
Boder, E. (1973). Developmental dyslexia: A diagnostic approach based on three atypical reading ‐ spelling patterns. Developmental Medicine & Child Neurology , 15 (5), 663-687.
Ramus, F. (2003). Developmental dyslexia: specific phonological deficit or general sensorimotor dysfunction?. Current opinion in neurobiology , 13 (2), 212-218.
