Good Example Of Parental Age And Chromosomal Disorders Essay

Abstract

While women have biological clocks, research studies show that men’s age during the period of conception may also pose risks on the health of the children. In the United Kingdom, average paternal age continues to increase. When a man reaches the age of 41 years and up, the impact of this paternal age is somewhat strong. This paper reviews some articles related to parental age and chromosomal disorders. The primary objective of this paper is to compare and relate the results and claims of the two articles. Arnett (2012) suggests that chromosomal disorders are not likely to be passed on from parent to child. Girirajan (2009) claims the presence of a number various factors related to abnormality in chromosomes. These include advanced maternal age leading to a transformed rate of crossing over between closely connected genes, endocrine imbalances and chromosomal translocations.
Keywords: Parental age, chromosomal disorder, Down syndrome, mitosis, meiosis

Introduction

While women have biological clocks, research studies show that men’s age during the period of conception may also pose risks on the health of the children (Harms, 2012). Studies linked paternal age with autism, miscarriage, schizophrenia, birth defects, and cognitive impairment (Harms, 2012). Researchers contend that increased risk of acquiring health conditions can be associated with age-related genetic mutations. Notwithstanding the increased risks, the overall dangers remain insignificant and less certain compared to those related to advanced maternal age (Harms, 2012).
In the United Kingdom, average paternal age continues to increase (Bray et al., 2006). The implications of this situation to public health remain widely debated and anticipated. Accumulated chromosomal mutations and aberrations happening during the development of male germ cells are held responsible for greater risk of developing certain abnormalities with older fathers (Bray et al., 2006). Increasing evidence demonstrates that the children of old fathers are at greater risk of schizophrenia, birth defects, and some cancers (Bray et al., 2006).
According to Stene et al. (1981), when a man reaches the age of 41 years and up, the impact of this paternal age is somewhat strong. The danger for a fetus to acquire de novo chromosomal aberration increases with advancing age of the father for older mothers compared to that of younger ones (Stene et al., 198). Yang et al. (2006) posits babies who are born to older fathers are observed to have a slightly increased danger of acquiring birth defect. In addition, young paternal age is likewise related to slightly increased danger of a number of selected birth defects in their children (Yang et al., 2006). Nonetheless, provided this weak connection, paternal age seems to perform an insignificant function in the cause of birth defects (Yang et al., 2006).

How Parental Age Impacts Chromosomal Disorders

In an article by Dolan (2005) titled Impact of Parental Age on the Occurrence of Chromosomal Abnormalities, it was stated that maternal age has been long acknowledged as the main risk element for nondisjunction particularly during meiosis. This leads to the development of trisomy 21 or Down syndrome. According to Dolan (2005), Down syndrome happens to about 1 in 800 births. A 20-year trend study demonstrates consistently snowballing rates of live birth to women age 30 and up. This trend may posit an increase in the percentages of births impacted with Down syndrome. Nevertheless, increased accessibility to screening as well as diagnostic methods for the prenatal uncovering of trisomy 21, such as options for first-trimester risk evaluation, has transformed the epidemiology of birth with Down syndrome.
Arnett (2012) claims that chromosomal disorders are not likely to be passed on from parent to child. In addition, a stronger link is found between chromosomal disorders and maternal age (Arnett, 2012). There may be a relationship between chromosomal disorders and paternal age; however, it is not as clear as it is among mothers’ age (Arnett, 2012). In addition, exposure of mothers to various teratogens increases the risk of developing abnormalities to the unborn child. Some of the major teratogens present in both progressive and emerging nations include infectious disease, malnutrition, tobacco, and alcohol (Arnett, 2012).
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Source: Human Development: A Cultural Approach by Jeffrey Jensen Arnett (2012)
One of the chromosomal disorders often encountered in some children is Down syndrome. The primary cause of Down syndrome is a gene-dosage imbalance that results from chromosome-21 trisomy (Girirajan, 2009). Down syndrome is also the typically the most diagnosed congenital malformation syndrome and mental retardation condition. A pioneer study about Down syndrome was conducted by John Langdon Down in 1866 (Girirajan, 2009). The study emphasized the distinct clinical characteristics of cases from diverse ethnic backgrounds. In a 1994 report by Penrose, it was indicated that a number of credible etiological elements are attributed to Down syndrome. These include advanced maternal age leading to a transformed rate of crossing over between closely connected genes, endocrine imbalances and chromosomal translocations, a robust hereditary element in familial cases with decreased mean maternal age, as well as maternal-fetal genotype-specific vulnerability (Girirajan, 2009). Penrose also postulated that the cases of Down syndrome affected by maternal age could be brought about by chromosomal non-disjunction, the inability of chromosomes to detach properly during the meiosis stage (Girirajan, 2009). According to Girirajan (2009), the paternal versus maternal basis for errors in meiosis are demonstrated by their physiological timeline.
Source: Girirajan, S. (2009). Parental-age effects in Down syndrome
In a research conducted by Terry Hassold and Stephanie Sherman, the origin of aneuploidy in humans, including trisomy 21, was found. Maternal nondisjunction consist >90% of trisomy 21 cases while only 5%–10% were caused by paternal nondisjunction, and the remaining <5% were brought about by mitotic errors (Girirajan, 2009). The male and female sex cells have diverse timelines for meiotic and mitotic events in the evolving ovary and testis. In the men’s fetal testis, following the first mitotic arrest, there transpires a prolonged mitotic proliferation until the beginning of puberty when certain meiotic events are started and completed. Production of sperm goes on all through the timeline. On the other hand, in the women’s ovary, following a smaller event of mitotic proliferation, the sex cells go into protracted first and second meiosis periods (Girirajan, 2009). Following the homologous recombination, meiosis I is arrested during the prophase stage and is completely following the ovulation, at the beginning of puberty. The second meiosis is then started simply to be arrested again in the second metaphase. Second meiosis reaches its completion following fertilization (Girirajan, 2009).
Girirajan (2009) posited that increased biological ageing of the women’s ovaries is the leading component for aneuploidy or a condition in women termed as “limited oocytes pool.” This hypothesis suggests that ovarian ageing is linked to accessibility of restricted and less ideal oocytes for fertilization. While a number of associations with ovarian biological ageing, such as cigarette smoking, history of ovariectomy, as well as hormonal levels still under assessment, the median age for menopausal was mostly perceived to be 0.9–1 year earlier in women having trisomic pregnancies (Girirajan, 2009).

Conclusion

Parental age has significant effects to the development of chromosomal disorders. Nevertheless, there is a greater risk of chromosomal disorder occurrence among women aged 35 and up compared to men. The findings of chromosomal disorder links to paternal age are insignificant. Studies associated paternal age with miscarriage, autism, schizophrenia, birth defects, as well as cognitive impairment. Greater risk of acquiring health conditions can be related to genetic mutations in connection to age. Notwithstanding the increased risks, the dangers of age continue to be insignificant and less certain compared to those related to advanced maternal age.

References

Arnett, J. (2012). Human development. Upper Saddle River, N.J.: Pearson.
Bray, I., Gunnell, D., & Smith, G. (2006). Advanced paternal age: How old is too old?. Journal Of Epidemiology & Community Health, 60(10), 851-853. doi:10.1136/jech.2005.045179
Dolan, S. (2005). Impact of Parental Age on Chromosomal Abnormalities. Medscape.com. Retrieved 21 March 2015, from http://www.medscape.com/viewarticle/496962
Girirajan, S. (2009). Parental-age effects in Down syndrome. J Genet, 88(1), 1-7. doi:10.1007/s12041-009-0001-6
Harms, R. (2012). Paternal age: How does it affect a baby?. Mayoclinic.org. Retrieved 21 March 2015, from http://www.mayoclinic.org/healthy-living/getting-pregnant/expert-answers/paternal-age/faq-20057873
Stene, J., Stene, E., Stengel-Rutkowski, S., & Murken, J. (1981). Paternal age and Down's syndrome data from prenatal diagnoses (DFG). Human Genetics, 59(2), 119-124. doi:10.1007/bf00293059
Yang, Q., Wen, S., Leader, A., Chen, X., Lipson, J., & Walker, M. (2006). Paternal age and birth defects: how strong is the association?. Human Reproduction, 22(3), 696-701. doi:10.1093/humrep/del453