Deer momee and dadee
I bo not wont to do to shool eny more becouse the children ar lafing at me. I canot reed pleese help me
your sun david
David is not a slow learner. In fact, according to the evaluations of a few professionals he is quite intelligent. Yet, he certainly has a problem, and he shares it with millions of other children and adults. David has dyslexia.
The word “dyslexia” comes from Greek and means “difficulty with words or language.” Perhaps the simplest modern definition of dyslexia is that it is a difficulty in learning to read and write, particularly in learning to spell correctly and to express one’s thoughts on paper.
Dyslexia is a subject that belongs to the study field of learning disabilities, and its cause is widely accepted to be neurological or genetic. Some researchers blame a supposed neurological dysfunction on brain damage incurred before, during, or after birth. Others hold that the neurological dysfunction is genetically determined and inherited from generation to generation.
They support this view by referring to many studies indicating that there is frequently a family history of learning disabilities.
DeFries and colleagues (1978) initiated a large family study of dyslexia. They recruited a sample of 133 children who were identified by teachers as having significant reading difficulty. The researchers tested them in the laboratory with an extensive battery to confirm their reading problems and related cognitive disabilities. A matched group of 125 children with no reading problems was also identified and tested, as well as the parents and siblings of both groups. The main result of the DeFries family study was clear: there was strong evidence for the familial transmission of dyslexia. The relatives of the children ascertained with dyslexia were significantly more likely to also have reading problems, compared to the relatives of children with normal-range reading abilities.
The relative contributions of genetic influences and shared family environment can be dissected in twin studies. It has been shown robustly that concordance for a qualitative diagnosis of dyslexia is significantly higher in identical twins, who have a virtually identical genetic makeup, than it is in non-identical twins who (like ordinary siblings) share about half of their segregating alleles. A large-scale study of twins with dyslexia yielded a concordance rate of 68% in identical twins, as compared with 38% in non-identical twins, indicating a substantial genetic component (DeFries & Alarcón, 1996).
The way in which discoveries in molecular genetics are reported can be misleading, encouraging us to think that there are specific genes that might be used to screen for dyslexia, says Bishop (2015). Dyslexia, she says, is not a classic Mendelian disorder that is caused by a mutation in a single gene. Rather, like many other common disorders, it appears to involve combined effects of many genes and environmental factors, each of which has a small influence, possibly supplemented by rare variants that have larger effects but apply to only a minority of cases.
One should also not lose sight of the fact that statistical evidence is often no more than circumstantial. Circumstantial evidence must always be interpreted. Unfortunately, it can so easily be misinterpreted.
The role of the environment
It may be useful to present an example of how unwise it can be to base conclusions on statistics only. Until recently, the inhabitants of a town not too far from my hometown were allowed to use well-water for domestic purposes. The water, when used as drinking water, caused a discoloring of the front teeth. Except in the case of a person with dentures, all the members of the family — father, mother, and children — would then have discolored front teeth. The concordance must have been 100%. As already indicated, however, the discoloring of the teeth was not caused by genetics, but by the circumstances and conditions that the family members shared: they all drank the same water.
One of the main objections to studies on genetics and dyslexia is that the statistics may be misinterpreted (Bishop, 2015). The fact that dyslexia “runs in families” cannot necessarily be attributed to genetics, but may be caused by the fact that the family members share the same unique environment.
I do not deny that genes may play a role in human capabilities and talents. However, determining the relative importance of the role of genes and the environment will forever be impossible. Take Mozart as an example. He was one of the most brilliant musicians of all time. All his family members were musicians, and from birth, he was continually exposed to music. Suppose he had been adopted immediately after birth by other parents who played no music. Would we then have known about Mozart? It is possible but highly unlikely.
The brilliant work done by the late Shinichi Suzuki of Japan also shows how musical talent may be developed by exposure. Suzuki trained thousands of violinists, who from a very young age took part in concerts lasting more than two hours, playing works by Mozart, Beethoven, and Liszt. He started stimulating these future violinists from before birth. Based on his research, Suzuki concluded that what a child becomes is dependent on education. “Talent is not an accident of birth,” he said.
The Glenwood State School
Research on the role of the environment in children’s intellectual development has shown that a stimulating environment can dramatically increase IQ, whereas a deprived environment can lead to a decrease in IQ. A particularly interesting project on early intellectual stimulation involved 25 children in an orphanage. These children were seriously environmentally deprived because the orphanage was crowded and understaffed. Thirteen babies of the average age of 19 months were transferred to the Glenwood State School for retarded adult women, and each baby was placed in the personal care of a woman. Skeels, who conducted the experiment, deliberately chose the most deficient of the orphans to be placed in the Glenwood School. Their average IQ was 64, while the average IQ of the 12 who stayed behind in the orphanage was 87.
In the Glenwood State School, the children were placed in open, active wards with the older and relatively brighter women. Their substitute mothers overwhelmed them with love and cuddling. Toys were available, they were taken on outings, and they were talked to a lot. The women were taught how to stimulate the babies intellectually and how to elicit language from them.
After 18 months, the dramatic findings were that the children who had been placed with substitute mothers, and had therefore received additional stimulation, on average showed an increase of 29 IQ points! A follow-up study was conducted two and a half years later. Eleven of the 13 children originally transferred to the Glenwood home had been adopted and their average IQ was now 101. The two children who had not been adopted were reinstitutionalized and lost their initial gain. The control group, the 12 children who had not been transferred to Glenwood, had remained in institution wards and now had an average IQ of 66 (an average decrease of 21 points).
More telling than the increase or decrease in IQ, however, is the difference in the quality of life these two groups enjoyed. When these children reached young adulthood, another follow-up study brought the following to light: “The experimental group had become productive, functioning adults, while the control group, for the most part, had been institutionalized as mentally retarded.”
High heritability does not imply immutability
From the example above and many other cases in the literature, I contend that, even if it were possible to inherit a learning disability, a human being is not merely a slave to his genes but can learn to overcome his problems. All too often it is assumed that if genetic effects are found, the child will be untreatable. Yet, high heritability does not imply immutability. 
Genetic research does not lead us to write off children who are poor readers, but rather to recognize that they may need more individualized instruction tailored to their specific needs (Bishop, 2015).
Human life can be compared to a game of cards. At birth, every person is dealt a hand of cards — his genetic make-up. Some receive a good hand; others a less good one. Success in any game, however, is almost always a matter of erudition. It is undeniably so that there are often certain innate qualities that will give one person an advantage over another in a specific game. However, without having learned the game and without regular and rigorous practice, nobody will ever become a champion at any game.
In the same way, the outcome of the game of life is not solely determined by the quality of a person’s initial hand of cards, but also by how he takes part in the game of life. His ability to take part in the game of life satisfactorily, perhaps even successfully, will be determined to a very large extent by the quality and quantity of education that he enjoyed.
In his book The Idea of Man Matson already stated in 1976, “Man has been shown to hold the power, not only to act upon his heredity — not only to change his world, but to change his own being.” Perhaps it is high time that we take note of this possibility.
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References:
Bishop, D. V. M. (2015). The interface between genetics and psychology: Lessons from developmental dyslexia. Proceedings of the Royal Society B, 282.
DeFries, J. C., & Alarcón, M. (1996). Genetics of specific reading disability. Mental Retardation and Developmental Disabilities Research Reviews, 2, 39–47.
DeFries, J. C., Singer, S. M., Foch, T. T., & Lewitter, F. I. (1978). Familial nature of reading disability. The British Journal of Psychiatry, 132(4), 361–367.