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Critical Evaluation of of Autism Theories - Term Paper Example

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The author overviews and critically evaluate several theories of autism, each of which highlights different biological mechanisms that are suspected to lead to this developmental disorder. In general, theories of autism emergency can be divided into large categories…
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Critical Evaluation of of Autism Theories
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Introduction Many of us may remember the well-known film “Rain Man”, which depicts a story of a man with autism. For some people, this moving story, along with some other films with similar themes, may serve as the only sources of knowledge about this developmental problem. However, if we take into account available statistics, which convincingly testifies to the surge in the amount of autism cases, as well as of other disorders of childhood and adolescence, during the recent decades (Comer, 2003, ch.17), this situation may not last for long as any one of us is increasingly likely to encounter people affected with autistic disorder. And while in the mentioned films the problem of integration of people with autism in society is considered, modern medical researchers are not less concerned with the problem of uncovering the biological causes of autism. But this task is far from being an easy one, as can be judged from the fact that there are currently several tens of various theories that pretend if not to discover the single cause of autism, but at least to offer clues as to autism`s most fundamental physiological roots (Novartis Foundation, 2003, pp.8-9). In this regard, let us overview and critically evaluate several theories of autism, each of which highlights different biological mechanisms that are suspected to lead to this developmental disorder. In general, theories of autism emergence can be divided into large categories. One group of theories, such as for instance opioid excess theories, views autism as a consequence of certain inborn abnormalities; another group, like for example viral infection theories or the approach that accentuates the increased intestinal permeability, links autism with some acquired abnormalities; and there is a group of theories that aims to investigate the possibility of connection between autism and external factors of influence, such as the effects produced by certain types of vaccines. As can be immediately seen, the range of possible causes of autism is quite diverse. To better asses each type of approaches to autism study, we will overview the mentioned opioid excess theories, the viral infection theory, and the theory of the autism origin due to standard vaccinations of children. Opioids Excess Theories The opioid excess theories of autism emphasise abnormalities in the complex workings and influences of opioids and opioid-like substances in the human organism, and particularly in the brain. Natural opioids produce various effects upon the processes of hormonal regulation, especially if there is an overabundance of them, and in our particular case are thought by some researchers to be responsible for symptoms of autism. Opioids are the agents that bind to specific opioid receptors located mostly in the central nervous system (CNS) and in the gastrointestinal tract. The evidential basis for opioid excess theories of autism is quite circumstantial. For example, endogenous opioid peptides, which are molecules produced in the body that combine two or more amino acids, were identified and isolated by Johnson and Johnson`s physical chemist Dr. Alan Friedman in serum and urine of both normal children and children with symptoms of autism. As the result, it was found that children with autism had around ten times the amount of target opioid peptide particles, such as A-glaidin, germorphin, casomorphine, deltophin II, morphine modulator peptide, and of some other related peptides that interact with neuro-peptides of other types. Besides, dermorphin is present only in children with autistic symptoms, so there are justified reasons to suppose that opioid-like substances may indeed cause autistic manifestations (Novartis Foundation, 2003, pp.115-117). As the mechanism that links excessive opioid peptides with autistic symptoms may serve the so-called gut disorders, and especially what is known as the syndrome of hollow organ dysmotility, when peristalsis, uncoordinated electrical activity in the gut, spasms, and increased gut wall`s muscle tension cause pain. In fact, some disorders of the gastrointestinal nature like the abdominal pain in children with autism may be related to opioids excess as dermorphin and other opioid peptides can interfere with acid output in the stomach, and thus affect digestion (Defelice, 2002, pp.67-81). And while the question of whether those excessive peptides can indeed be fully responsible for many of the aggravated gastrointestinal disorders in autistic children and equally in other people with spastic problems and intestinal motility needs time to be fully answered, what is clear is that the very fact of possible combination of excessive opioid-like substances with the possibility of heightened intestinal permeability may shed light on the way how these molecules may pass from the gut into the blood and consequently affect people with autism. Among other ways in which opioid-like substances influence the processes of hormonal regulation is the action of dermorphin directed at the increase by means of stimulation of sympathetic nervous system of plasma levels of renin, a hormone that originates in the kidney and elevates blood pressure. Dermorphin also suppresses levels of plasma cortisol, a hormone of steroid type synthesised in frames of the bodily stress response mechanism by the adrenal cortex, and does so by influencing the secretion of the pituitary gland produced hormone termed ACTH. This action of dermorphin might explain the observed alteration in developmentally delayed children of what is called the hypothalamic-pituitary-adrenocortical axis function. Sauvagine is another peptide of opioid type present in high amount in autistic children. Along with dermorphin, this peptide regulates release from pituitary cells of ACTH and of the polypeptide pain-blocking neurotransmitter beta-endorphin, as well as inhibits release of prolactin, another hormone produced by the pituitary gland, which instigates breast development, and the production of milk and of human growth hormone (Tsai, 1999). The opioid excess theories of autism also pay attention to the interrelation between opioids and secretin, the hormone synthesised in the small intestine which regulates the secretion of pancreatic juices. In fact, opioids act to reduce the gastric acid secretion, so, according to one approach to the explanation of the apparent deficiency of secretin witnessed in many patients with autism, the pH in the upper part of duodenum, the first part of the small intestine after the stomach, does not become sufficiently low for secretin to be released by the mucosal cells. Opioids as well work to reduce the amount of hepatic glutathione, a tripeptide antioxidant whose low presence was found in autistic patients. Finally, opioid-like substances due to their action on T-cells may be linked to cases of immunosuppression in many people with autism, as opioids diminish the spread of T-cells through mu-receptors, which are involved into the realisation of rewarding and addictive mechanisms of opioids (Novartis Foundation, 2003, pp.138-142). Viral Infection Theories The viral infection theories of the origin of autism are centred on the processes of immunosuppression, often deemed to occur in the intestinal tract, and on the ability of a viral infection to instigate in the CNS characteristic symptoms of autism. More specifically, secretory immunoglobulin A that protects the intestinal tract from viral infections has been found in deficient amounts in autists. On the other hand, such an infection as viral encephalitis is capable of producing autistic-like symptoms, especially if a person had contracted it at a young age. Among other viruses capable of invading the human gastrointestinal tract is the herpes simplex virus (HSV), which can move intra-neuronally without leading to encephalitis, and thus is capable of travelling from the enteric nervous system into the CNS, the central amygdala, and the temporal lobe and cerebellum (Shaw, 2001, pp.11-24). Being inside the CNS, the HSV virus can sit there for a long time without manifesting itself through detectable markers or other signs, but at the same time can for instance affect person`s language (Novartis Foundation, 2003, pp.225-227). While there are no reasons to suppose that viral infections are the only possible cause of autism, many researchers at least demand the separation of a subgroup of autism-like cases caused by the presence in infants or in children of gastrointestinal pathologies which allow such viruses as HSV to populate their CNS with the consequent emergence of autistic symptoms. Theories of Linkage Between Vaccinations and Autism This group of autism origin theories in essence is similar to those proposing the viral infection as the root cause of this developmental disorder. However, attempts to investigate the possible connection between vaccinations and autism is an extremely important direction of research as it might explain the recent surge of autism cases in countries where, coincidentally, children vaccination programs have been widely implemented. In particular, Dr. Andrew Wakefield theoretised on ground of extensive research that viral infections following the Measles-Mumps-Rubella (MMR), diphtheria-pertussis-tetanus (DPT), and some other vaccinations may be immediately responsible, perhaps as the result of allergic reaction of the human organism to vaccines, for the emergence of autistic symptoms in children with no previous history of developmental disorders (Fitzpatrick, 2003, pp.24-26, 157-176). Interestingly, such an auto-immune response could also affect levels of dipeptydal peptidase, a serine peptidase the deficiency of which, caused either genetically or via the blocking action of dermorphin, is viewed as another possible cause of autism in frames of the opioid theory of autism development (Berney, 2000). The theoretical basis for the claim of connection between autism and vaccination is anchored in the workings of the process of myelination, which is a crucial stage of the development of the human brain. In fact, nerves can efficiently convey energy only if they have myelin coating, which may be likened to electric wires insulation as the fatty myelin confines pulses in nerves and guards electrical signal integrity in order to maintain a proper signal-to-noise ratio. Of course, if wire`s insulation is damaged or outright absent, electrical current may be impeded and short-circuited (Fitzpatrick, 2003. pp.26-35). Following birth, only the minority of nerve pathways are already insulated by myelin in humans, and the process of myelination is ongoing in the human brain up until twenty years of age or longer. During this period of gradual myelination, before approximately the age of ten large parts of the cortex are yet devoid of myelination, and before the age of twenty vast parts of the frontal lobes are still to be myelinated. In general, myelination starts off in those brain areas that are the oldest developmentally, like for instance the brain stem, and then proceeds to the more recently developed parts of the nervous system, such as the cortex and prefrontal lobe, which are known to greatly influence human behaviour (Deb and Thompson, 1998). In every person the speed of myelination of the nervous system may vary, but for everyone the failure of a proper myelination can impair neural communication, while not always leading to grave damage of the CNS (Davison et al, 2006, p.486). Now, if a person with unfinished myelination is vaccinated by preparations that contain such adjuvants as foreign proteins and biological organisms, aluminium compounds, and mercury, nerves that are yet unprotected may be damaged. Thus, it is this possible biological side effect of vaccines on the nervous system and, correspondingly, on behaviour that forms the backbone of the claims for the linkage between certain types of vaccinations and the emergence of autistic disorders (Fitzpatrick, 2003). The evidence for the destructive action of viruses on both non-myelinated and myelinated parts of the nervous system has been accumulating since early 1920s, when a program of vaccination against smallpox led to the encephalitis outbreak. By the end of 1970s it was already clear that demyelination related disorders, to which autism may be added on solid grounds, were becoming more widespread and serious, and the increased scope of vaccination programs began to be seen as one of the possible causes of that disturbing tendency. However, it is perhaps not surprising that numerous researchers adamantly protect the merits of vaccinations, but nevertheless the facts that the occurrence of autism has greatly increased recently and that there are plausible mechanisms that can facilitate the emergence of this disorder at least in genetically predisposed children demand the further studies. For example, one of the possible directions of such studies may be not the attempt to disqualify the merits of vaccination programs, but rather to assess possible merits of separate administration of various vaccines, which in certain combinations may be more dangerous for children than in isolation (Fitzpatrick, 2003, ch.11). Conclusion All in all, we can see that while different groups of autism origin theories highlight various factors that may actually trigger the onset of its symptoms, many of them are interlinked in one way or another. For one, auto-immune responses instigated by viral infections may interfere with the activity of opioid-like substances investigated by opioid excess group of theories, and theories about the role of vaccination in the growth of the number of autism cases actually build on the mechanisms offered by the viral infection theories. What can be added, though, is that none of the theories we have outlined is seemingly capable of providing a single conclusive account for such a complex phenomenon as autism (Prior, 1987, pp.15-16). Moreover, there are other theoretical approaches to this developmental disorder that highlight yet another biological mechanisms of influence. In this situation, it seems warranted to suppose that in the end it may turn out that autism may have different underlying mechanisms of its development, and that it may be necessary to perceive its real-life manifestations in frames of the existence of the whole spectrum of autism-like disorders. Sources Berney, T., P. (2000). “Autism — an evolving concept”, The British Journal of Psychiatry ,vol.176, viewed 16 November, 2006, Comer, R., J. (2003). Abnormal Psychology, 5th ed. Worth Publishers Davison, G., C., and Neale, J., M., Kring, A., M., and Johnson, S., L. (2006). Abnormal psychology. John Wiley & Sons Deb, S., and Thompson, B. (1998). “Neuroimaging in autism”, The British Journal of Psychiatry, vol. 173: 299-302 Defelice, K., L. (2002). Enzymes for Autism and other Neurological Conditions. Thundersnow Interactive Fitzpatrick, M. (2003). MMR and Autism. Routledge Novartis Foundation. (2003). Autism: Neural Basis and Treatment Possibilities. John Wiley & Sons Prior, M., R. (1987). “Biological and neuropsychological approaches to childhood autism”, The British Journal of Psychiatry ,vol. 150: 8-17 Shaw, W. (2001). Biological Treatments for Autism and PDD. Sunflower Pub Tsai, L., Y. (1999). “Psychopharmacology in Autism”, Journal of Psychosomatic Medicine, vol. 61:651-665 Read More
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