Is Autism Environmental or Biological - Essay Example

Running Head: Autism environmental or biological Autism environmental or biological Autism is one of a family of developmental disorders that influences social, communication, and vocational abilities. The aim of this paper is to foster understanding of the causes and course of atypical development of autism that are invariably a result of dynamic interactions between biological, genetic and environmental factors. Though it is also been determined that none of them is proved to be the major cause of Autism. Autism is described clinically as an invasive developmental disorder, with cardinal symptoms of poor social relations, poor communicative capabilities, and a restricted range of interests and activities. It is a distressing childhood neuron-developmental disorder that was first exemplified by Leo Kanner in 1943. Kanner pointed out eleven children with odd and slurred speech, poor human connectedness, and recurring, disturbed behavior. Thus, it would seem appropriate to begin with Leo Kanner's (1943) pioneering paper, in which he descriptively differentiated the syndrome he called early infantile autism from inherent mental defect. Here is his description of Paul, aged five years: There was, on his side, no affective tie to people. He behaved as if people as such did not matter or even exist. It made no difference whether one spoke to him in a friendly or a harsh way. He never looked at people's faces. When he had any dealings with persons at all, he treated them, or rather parts of them, as if they were objects (1943). It is also said that autism comes in families; researchers went on to find out whether this family leaning was due to genetic or to environmental factors. They evaluated the rates of autism in identical and non-identical co twins of twins with autism and found that the identical co twins were much more likely to develop autism than were the non-identical co-twins. As the major difference between identical and non-identical twins lies in their genetic likeness (identical twins are same hereditarily, while non-identical twins simply share about half of their genes), the results of the studies confirmed that genetic factors play a significant role in causing autism. Indeed, the twin concordance rate in identical twin pairs around sixty percent was very much higher than the concordance rate in non-identical twin pairs. The considerable difference in the enormity of the concordance rates, besides other findings, suggests that autism is a composite genetic disorder, possibly requiring the shared action of numerous susceptibility genes (Turner, Barnby and Bailey 2000). The collective impact of environment is an added obscuring factor. Proper studies of identical twins study individuals who have been raised apart, but in autism, it is hard to get sufficient numbers of people who are both identical twins and brought up apart. Though, it is probable that identical twins will have their alleged identities significantly influenced by having a genetically identical other. This might be less significant in studying conditions that do not prove to be correlated to personality; but, with the uncertainty and oblique nature of autism, this will present a more considerable problem. It must also be pointed out that identical twins might in fact have experienced major differences in their environment, starting with their particular positions in the womb. Environmental factors and exposures might interrelate with genetic factors to cause an augmented risk of autism in several families. 1The early maturation of some specialized amygdala-temporal lobe neurons that are selectively responsive to human faces is an exceptionally adaptive development. It supports social expressive face-to-face, vocal relations, and the pattern of emotional affection. Again, conversely, if the infant is brought up in an environment where the mother or caretaker fails to give satisfactorily spurs, these neurons will be unsuccessful to develop usually thus intensely affecting every aspect of social effective behavior. Consider, for instance, several classic signs of autism. The autistic child snubs to make eye-to-eye contact and limbic system aberrations have been linked with deficiency persuaded autistic behavior in primates. This is not to entail that inadequate mothering is the reason of human autism, but rather than inadequate mothering can harm the limbic system and generate autistic behaviors. Diagnostic complexities are usually present, because of the extensive range of severity of the disorder, predominantly in the area of verbal communication. Some autistic individuals are silent, whereas others normally show discreet impairments of language along with language understanding. Obsession with similarity or development of suffering over apparently insignificant changes is a recognized symptom of the disorder. Symptoms are usually noticeable during infancy. The disorder lasts all through life, but its clinical manifestation normally changes, sometimes quite outstandingly, over the years. There is constantly an interruption in language development, but at times there is a prominent development in language in the early school years. Due to the depth of severity of the disorder, it was found to be helpful to distinguish between high and low functioning autism. The normally conventional maximum value is an intelligence test that scores seventy. There tends to be a prevalent recognition by researchers that an intelligence test is the best key to understanding the severity of autistic disorder. Though the issue remains fairly contentious, there is some agreement that individuals with elevated functioning or with low functioning autism suffer from the same disorder, and that their disorders are not expected to have contradictory etiologies. The mental retardation often linked with autism is considered to be a part of the disorder, not a separate illness. While the genetic mechanisms accountable for behavioural disorders are studied, techniques have been formulated that allow for the consistent diagnosis of autism, when estimates are carried out by highly- trained personnel and for quantitative appraisal of the severity of different aspects of the disorder (Cohen, Schmidt-Lackner, Romanczyk, & Sudhalter, 2003). However, autism might only be one division of a broader phenotype of behavioural dysfunction that is innate in families. This broader phenotype is distinguished by peculiarities in language and/or social skills, with or devoid of the presence of recurring or ritualistic behaviors; and there is proof that such a broader phenotype is present in several first degree and comprehensive relatives of affected children. Whether it is better to centre on well-defined cases or to include this broader phenotype in studies of genes that might cause autism is not clear. Thus, in recent years, further environmental factors have been implied as the cause in the development of autism. Interactions between genetic vulnerability and toxic exposures that might prompt those genetic factors are the matter of substantial research into the causes of autism. Every theory and the proof that supports it has attracted staunch, forthright advocates, several of whom have organized networks and organizations devoted to additional research, services for affected individuals, and treatment. There are substantial distinctions among individuals in the degree to which autistic symptoms are present. Though many do fit the typical pattern of extreme social withdrawal, stereotypes such as rocking, hand waving, lack of language and gesticulation, and severe cognitive impairment, others are drastically less impaired, though they still appear somewhere along the autistic continuum of disability. It is also important to know that, like other individuals, children with autism do develop. Thus, although the pathway of their development is certainly very diverse from that of other children, they will act in a different way at different points in their development (Cohen, Paul, & Volkmar, 1987). The majority of investigators, distinguish that language, cognition, and social behaviour are thoroughly interrelated in development (Fein, Pennington, Markowitz, Braverman, & Waterhouse, 1986) now tend to agree that the social inconsistency of autism is most fundamental to the disorder, and that this inconsistency pervasively affects development in all other areas, leading to the distinctive syndrome of autism (Mundy & Sigman, 1989a). A current focus of discrepancy concerns the explicit nature of the social shortfall. There are currently numerous competing theories that stress the failure of autistic children to know other people's ways of thinking and feeling. Several investigators have construed this problem in terms of an impaired development of the theory of mind (Baron-Cohen, 1988; Baron-Cohen, Leslie, & Frith, 1985; Leslie, 1987), such that the autistic person has little awareness of what other people discern. Another view is that autistic persons are fundamentally deficient in interpersonal responsiveness, comprising understanding of other people's thoughts and sentiments, and that this insufficiency begins very early in development (Hobson, 1989a). 1The basis of behavior might be a composite blend of genetic and environmental influences that is, a combination of nature and nurture: Children who take more than two copies of a transmuted form of a single gene on chromosome twelve will be incapable to fail the amino acid phenylalanine that is a general constituent of food proteins. If this insufficiency, called phenylketonuria (PKU), goes concealed, the child will develop mental retardation, a state with observable behavioral consequences. Thus, a single gene can have intense effects on behavior, here by disturbing normal behavior. Unfortunately, a usual test conducted on each newborn in the United States can distinguish PKU soon after birth, and a special diet that reduces phenylalanine can avert retardation. In PKU, geneticists have dogged that retardation is suitable to genetics that is a mutated phenylalanine hydroxylase gene and the environment that are a phenylalanine-containing diet. Thus, Due to genetic or environmental causes, nonconforming patterns of development and certain considerable losses occur regarding these mental capabilities are why we see the aspects of Autism seem to appear throughout early childhood. Studying individuals who expand in different ways achieves approaching into typical development. Baron-Cohen and Staunton (1994, p. 241) studied the inflections of children and young adults with autism. These were the progeny of immigrants; their mothers spoke English with a foreign inflection. The non-autistic siblings of these children spoke English without a foreign pronunciation, but more than eighty percent of the children and young adults with autism had maintained the foreign accent of their mothers. Baron-Cohen and Staunton accredited this outcome to a lack of the usual drive to recognize with peers. Several other theories of mind behaviors rely more seriously on explicit (verbal) ways of thinking, as in recursive problems where actual conditions are not observed but rather talked about. In such cases awareness of the human environment for self and other is still essential, but other skills linking symbol use are also significant. Further compatible with an environmental approach is the theory of Hobson (1989a, 1989b), who argues that a discrepancy in personal relatedness is vital to autism. In Hobson's view, the normally developing infant is biologically ready to be accustomed to emotional expressions from other people and to be properly receptive to these expressions. This early form of inter-subjectivity then forms the foundation for the development of more refined interpersonal actions including communication. Therefore, Hobson's (1989b) description of the relations among human affective expressions and environmental events lends itself readily to interpretation in terms of affordances: . . . Biologically based signals of emotion, and biologically based responsiveness (including emotional responsiveness) to those signals, constitute an important device for promoting interpersonal coordination. The effectiveness of this device depends upon a sufficiently regular association with the different expressions of particular emotions, and upon the consistency in the ways these expressions relate to environmental events and to the individuals' propensity to particular forms of action. If it were frequently the case that children smiled broadly and then ran away, we should question the sense in which children's smiles were "smiles." (p. 24) Affordances specify and inform relationships between individuals and the 'environment.' (http://www.trincoll.edu/depts/ecopsyc/UK95abs.html) Conclusion Autism prevalence is normally thought to be rising, though altering diagnostic criteria and increased reporting are probable to be contributing to some extent to that increase. Genetic and biological factors are imperative in the causation of autism but are not fully explanatory. Different environmental factors, are known, suspected, or speculated to play a role, also. Thus, it is a multifaceted disorder of unidentified etiology in the majority cases. Although environmental factors are expected to play a role in the illness, it is also clear that certain individuals inherit a genetically determined vulnerability to developing autism. Over the past ten years, medical science has made extraordinary strides in discovering out the specific genetic defects that cause several human diseases. The majority of these diseases are rather unlike autism, being caused by a defect in a single gene, frequently with no or restricted contribution from biological or environmental factors. Current approximations suggest that changes in as many as ten or twenty different genes may be implicated in the inherited component of autism. References: Gardner Murphy; Personality: A Biosocial Approach to Origins and Structure Harper & Brothers, 1947 Cohen, D. J., Paul, R., & Volkmar, F. R. (1987). Issues in the classification of Pervasive Developmental Disorders and associated conditions. In D. J. Cohen & A. M. Donellen (Eds.), Handbook of autism and pervasive developmental disorders (pp. 20-40). New York: Wiley. Fein, D., Pennington, B., Markowitz, P., Braverman, M., & Waterhouse, L. (1986). "Toward a neuropsychological model of infantile autism: Are the social deficits primary" Journal of the American Academy of Child Psychiatry, 25, 198-212. Mundy, P., & Sigman, M. (1989a). Specifying the nature of the social impairment in autism. In G. Dawson (Ed.), Autism: Nature, diagnosis, and treatment (pp. 3-21). New York: Guilford. Baron-Cohen, S. (1988). "Social and pragmatic deficits in autism: Cognitive or affective" Journal of Autism and Developmental Disorders, 18, 379-402. Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the autistic child have a "theory of mind" Cognition, 21, 37-46. Leslie, A. M. (1987). Pretence and representation: The origins of "theory of mind. Psychological Review, 94, 412-426. Loveland, K. (1990, May). Autism, affordances and the self. Paper presented at the Conference on the Interpersonal Self, Atlanta, GA. Zaff, B. (1989, July). Super-vision: Perceiving affordances for other people. Paper presented at the Fifth International Conference on Event Perception and Action, Miami, OH. Kanner, L. (1943). "Autistic disturbances of affective contact". Nervous Child, 2, 217-250. Hobson, R. P. (1989a). Beyond cognition: A theory of autism. In G. Dawson (Ed.), Autism: Nature, diagnosis, and treatment (pp. 22-48). New York: Guilford. Hobson, R. P. (1989b). "On sharing experiences". Development and Psychopathology, 1, 197-203. Lovaas, 0.1. (1977). The autistic child. New York: Irvington. Turner, M., Barnby, G. and Bailey, A. (2000)Genetic clues to the biological basis of autism. Molecular Medicine Today, 6, pp. 238-244. Cohen, I. L., Schmidt-Lackner, S., Romanczyk, R., & Sudhalter, V. (2003). The PDD Behavior Inventory: A rating scale for assessing response to intervention in children with PDD. Journal of Autism and Abnormal Development, 33 http://www.trincoll.edu/depts/ecopsyc/UK95abs.html Read More