Final paper revision

Development of Autism

Justin Hedberg

Liberty University

Development of Autism

Introduction

Autism ranks among numerous medical conditions that afflict a vast proportion of individuals not only in the United States but also in the rest of the globe. Autism (or autism spectrum disorder) is said to refer to an array of conditions that are typified by difficulties with social capabilities, repetitive conducts, speech and non-verbal communication, in addition to distinctive strong points and differences. Studies conducted over the years have deduced that various types of the condition exist (Mesibov & Shea, 2011 ). Overall, the cause of autism has been ascertained to be diverse combinations of genetic and environmental factors. Further, the most-obvious indications of the condition usually manifest between two and three years of age. However, in a number of instances, a person can be ascertained to be grappling with the condition as early as eighteen months of age.

On a positive note, certain developmental delays that are connected with the condition can be recognized and dealt with even earlier. Due to the gravity of the condition, parents who are concerned with their children are understandably encouraged to seek pursue assessment as early as possible (Mesibov & Shea, 2011). This is owing to the fact that early intervention has the potential to better outcomes for those suffering from autism. In this paper, a great deal of emphasis will be placed on understanding the roots of autism. Certainly, focusing on this aspect of autism can lead to the attainment of an enhanced comprehension of the condition and enable those affected by it to seek the necessary assistance early.

Discussion

Since the discovery of autism a long time ago, there is still a lack of clarity regarding what exactly results in the development of the condition. In a few words, the precise cause of autism remains unknown. Nevertheless, even though the specific cause of the condition is yet to be determined, autism has the potential to crop up due to genetic predisposition, environmental factors, differences in brain biology or because of other factors that are not known. First off, a broad range of studies has determined that autism usually runs in families. Transformations in particular genes have been found to raise the likelihoods of a child ending up developing the condition (Miles, 2011). In case a parent carries 1 or more of these gene transformations, they may end up passing them to their children. The transmission can occur even if the parent themselves do not suffer from the condition. In other instances, these genetic transformations crop up suddenly in an early embryo (De Rubeis et al., 2014 ). Apart from this, the genetic transformations may emerge in the sperm and/or egg, which merge to bring about the embryo. Nevertheless, it is important to point out the greater sum of these gene transformations never result in the development of the condition by themselves. In other words, the changes simply raise the chances of a child developing the disorder.

Further, early studies into the role that genetics may play in the development of autism started with the study of twins, that is, both identical and non-identical ones. Scientists focused their efforts on the study of the concordance of the condition in these sets of twins. The early studies resulted in the finding of a considerably greater concordance in identical twins, who are known to possess mostly indistinguishable DNA. Concisely, the finding suggested that the condition at the center of analysis has a genetic foundation (Mesibov & Shea, 2011). Under present approximations, there is a fifty to eighty percent concordance for identical twins. By comparison, there is an overall 1.5 percent (approximately) likelihood that any 2 individuals will end up having the condition. In situations in which parents have a single child who suffers from the condition, there is a five to twenty percent likelihood that the second child will end up developing the condition.

Currently, scientists have gained knowledge of the fact that as with many other traits (for instance intelligence and height), the condition being evaluated entails several diverse genetic variations that act together. In essence, no single gene has the potential to result in the development of autism. Rather, the more mutations an individual has in certain segments of their DNA, the higher their likelihoods of the diagnosis of the condition (De Rubeis et al., 2014). In a bid to identify the precise parts of DNA that are connected with autism, researchers usually focus their studies on large sums of individuals who are suffering from the condition. This approach is referred to genome-wide association study, and continuing studies are expected to result in the attainment of an even better understanding of the role that genetics play in the development of autism.

With respect to environmental causes of autism, recognition has grown in the recent past that certain facets of the environment may also play a role in the development of the condition. However, in spite of significant research, not a single environmental factor has been ascertained to be a definite cause of the condition being evaluated. Further, the most broadly employed research approach to examining environmental risk factors for the condition relates to epidemiology (Landrigan, 2010). Succinctly, epidemiology entails the examination of how often, as well as why, medical conditions crop up in diverse clusters of individuals. To start with, many environmental factors in the course of prenatal life have been ascertained to some extent raise the likelihood of an offspring developing the condition. This could be as a result of dangerous infectious organisms being passed on from the mother to the fetus via the placenta. Apart from this, the mother’s immune response may be harmful to the fetus’ developing brain, hence increasing its chances of developing autism.

Other factors in the mother that are suspected to have the potential to increase the chances of an offspring developing autism comprise the existence of gestational diabetes, shortage of folic acid during conception, as well as the use of particular antidepressants in the course of pregnancy. Nevertheless, it is critical to note that there is no conclusive proof for any of the environmental links discussed. Moreover, being an older parent (in particular, an older father) continues to be suspected to raise the chances of having a child who grapples with the condition. As male people become older, the sum of sperm that carry de novo genetic mutations rises (Krumm et al., 2014). Even though a number of the de novo genetic mutations usually have negligible or no impact on the resultant baby, certain mutations have the potential to result in the brain of the baby developing differently. In addition, a vast body of research has determined that fathers aged more than fifty years at the time of conception tend to have an enhanced likelihood of transmitting de novo mutations, as well as an increased chance of having a child who grapples with autism.

A clear, yet highly critical, observation relates to the fact that not each and every individual who is exposed to these environmental factors ends up having a positive diagnosis of autism. A possible explanation for this relates to a phenomenon referred to as gene-environment interaction (Landrigan, 2010). Concisely, the phenomenon refers to the situation in which the genetic composition of 2 different individuals pushes them to react in a different way to an environmental factor.

Moreover, for a considerable period of time, researchers have been looking for a conspicuous brain difference that may result in an individual demonstrating autistic conducts. However, researchers are yet attain concrete results in this regard, with only a handful of studies identifying brain features that are shared by diverse people found to be suffering from the condition. Such findings may represent a further indication of the fact that the condition has several dissimilar causes (Courchesne, Campbell, & Solso, 2011). Apart from this, the findings may also be a reflection of the challenges that researchers continue to confront in their bid to attain a clearer understanding of the brain. At the moment, researchers employ an array of ingenious approaches with a view to understanding the brain’s function and structure, for instance, X-rays, magnetic fields, as well as radioactive chemicals. Despite the amazing capabilities of these approaches, they are still unable to offer a complete measure of the remarkable complexity of the manner in which the brain functions.

Furthermore, it is also improbable that the condition under focus affects just a single region of the brain alone. Succinctly, the complex conducts of people grappling with autism (these comprise language, cognitive, as well as sensory problems) make it challenging to point out just a single region of the brain that may be affected. Nonetheless, a number of encouraging hints have demonstrated the manner in which diverse brain pathways may result in autistic conducts. In particular, there is growing proof that dissimilarities in brain development may commence prenatally in a number of people with the condition. Numerous studies revolving around prenatal ultrasound measurements have managed to unearth proof for dissimilarities in the growth patterns of the brain when it comes to fetuses that went on to be diagnosed with the condition (Courchesne, Campbell, & Solso, 2011 ). On top of this, newborns who go on to be diagnosed with the disorder are more often than not said to have large heads at the time of birth, a condition referred to as macrocephaly.

Far from the differences in brain biology, there are other biological factors that may contribute to the development of autism in an individual. First off, there exists preliminary proof that a number of (but not all) people grappling with the disorder are exposed to elevated degrees of testosterone in the womb. Concisely, extremely elevated concentrations of testosterone in the bloodstream may end becoming detrimental and bring about the death of cells, in particular, within the brain (Kapp et al., 2013). This is quite worrying owing to the fact that the brain tends to be extremely sensitive to transformations in the levels of hormone. Some researchers have posited that the pattern of cell death brought about by elevated levels of testosterone may end up altering the development of the brain in a manner that results in autistic conducts in childhood. However, this postulation has not been verified. Moreover, it is definite that not every individual suffering from the disorder is exposed to extreme degrees of testosterone in the womb (Kapp et al., 2013).

Additionally, the connection between gastrointestinal issues and autism relates to another scientific realm that has and continues to receive an immense measure of attention. Currently, researchers have attained an enhanced comprehension of this link, with studies indicating that between thirty and fifty percent of people suffering from the condition tend to grapple with noteworthy gastrointestinal issues, for instance, constipation, diarrhea, as well as an irritable bowel. For a long time, this phenomenon was mysterious (Kapp et al., 2013). However, very encouraging proof exists to aid in the explanation of this occurrence these days. In a few words, the multifaceted community of microbes in the gut has been ascertained to play a critical role in the development of human beings and is vital for not healthy endocrine and immune systems but also for the brain.

A number of researchers are of the belief that a disturbance in the natural balance of these important bacteria may result in the development of autism. Just to cite an instance, antibiotics are often employed with babies in Western societies. On a worrying note, these medications have been ascertained to destroy not only the “bad bacteria” but also the “good bacteria” that they were prescribed for in an individual . An alteration in the community of microbes (on which human beings have evolved to rely upon immensely) may end up disrupting the development of the brain and result in the development of the disorder (Kapp et al., 2013). Currently, the proof for this likely origin of the condition is not that sturdy. Nevertheless, continued research into this sphere is expected to be undertaken in the future so that a greater understanding of the connection can be gained.

Conclusion

The research picture with respect to the causes of autism remains complicated to date. Concisely, the condition does not have a single cause. However, there exists an extremely sturdy genetic component to the origin of the disorder. In a number of instances, there exist discernible genetic defects that result in the development of the condition. In other instances, the genetic dissimilarities tend to be extremely complicated and have not been discovered. Further, even though no evidence presently exist for any given potential environmental cause of autism, it is likely that subtle environmental influences may end up affecting people in a different manner contingent on their genetic composition.

Concisely, it is highly possible that the most appropriate response to what brings about the disorder will not only rest in genetics or in environmental factors. Rather, a combination of these potential causes is highly likely to result in an individual developing the condition. Irrespective of the factors that end up going into the mix, it is safe to surmise that they typically have their impact in the course of fetal life owing to the fact that an individual with the condition tends to be born with it. Moreover, even though receiving the news that one’s child is suffering from autism is certainly bound to be distressing, seeking the necessary care for them as early as possible has the potential to result in the betterment of their condition.

References

De Rubeis, S., He, X., Goldberg, A. P., Poultney, C. S., Samocha, K., Cicek, A. E., ... & Singh, T. (2014). Synaptic, transcriptional and chromatin genes disrupted in autism. Nature, 515(7526), 209-216 .

Mesibov, G. B., & Shea, V. (2011). Evidence-based practices and autism. Autism, 15(1), 114-133.

Lloyd, M., MacDonald, M., & Lord, C. (2013). Motor skills of toddlers with autism spectrum disorders. Autism, 17(2), 133-146.

Miles, J. H. (2011). Autism spectrum disorders—a genetics review. Genetics in Medicine, 13(4), 278-285.

Krumm, N., O’Roak, B. J., Shendure, J., & Eichler, E. E. (2014). A de novo convergence of autism genetics and molecular neuroscience. Trends in neurosciences, 37(2), 95-105.

Landrigan, P. J. (2010). What causes autism? Exploring the environmental contribution. Current opinion in pediatrics, 22(2), 219-225.

Courchesne, E., Campbell, K., & Solso, S. (2011). Brain growth across the life span in autism: age-specific changes in anatomical pathology. Brain research, 1380, 138-145.

Kapp, S. K., Gillespie-Lynch, K., Sherman, L. E., & Hutman, T. (2013). Deficit, difference, or both? Autism and neurodiversity. Developmental psychology, 49(1), 59-65 .

�Dear Justin,

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�Numbers less than 10 should be spelled out (APA 4.31). For example, use “two” instead of “2.”

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