Human Traits - Heredity and Environment - Essay Example

 Human Traits - Heredity and Environment Introduction: The nature-nurture debate seeks to explain individual phenotypes on the basis of the influence of one or the other aspect. The debate rages ever fierce, as some individuals attribute causal factors for behavioral disorders as originating naturally at birth vis a vis others who contend that such disorders are triggers by environmental factors. However, in specific reference to homosexuality and schizophrenia, it is demonstrated below that heredity and the environment cannot be separated as distinct and separate entities, rather the appropriate conclusion that must be drawn is that both heredity and the environment may play a role in the determination of individual phenotypes. Homosexuality: Freud characterized homosexuality as “inversion” - that all humans are born bisexual but unresolved oedipal conflicts and a failure to break the maternal bond in early years develops into adult homosexuality. (Freud 1975: 5). According to Gagnon, sexuality is learnt on the basis of script templates conditioned by the norms of social behavior and individual interpretation. (Gagnon 1990:6). Bozett and Sussman (1989) offer insight on several studies indicating the negative feedback that homosexuals receive from society and their own families, arising from religious notions that it is an aberrant and evil condition. These studies appear to support the learned model of sexual behavior. Studies have shown that differences in brain structure between homosexual and heterosexual men. LeVay(1991) found neuroanatomic differences between homosexual and heterosexual males. The interstitial nucleus of the anterior hypothalamus – the INAH3 – was similar to women in homosexual men – three times larger than heterosexual men. Swaab et al (1995) found that the suprachiasmatic nuclear area of the homosexual hypothalamus contained double the number of cells, thereby corroborating the possible influence of brain structure on homosexuality. Honekopp et al (2007) have recently corroborated earlier studies on prenatal angrogenization of human behavior, as reflected in the relative length of the index finger to the ring finger. Hall and Kimura (1994) examined the relationship between dermatoglyphic asymmetry or fingerprint markers and sexual orientation. They found that only homosexual men demonstrated a tendency towards leftward asymmetry. Similarly, Allen and Gorski (1992) found that the anterior commisure in the brain is typically larger in homosexual men, just as in the case of women. The functional implications of the last two studies are not clear, however differences in brain plasticity may play a role in sexual orientation. Interestingly enough, Swaab et al (1995) found that young adult men generally had twice as many cells in the pre-optic area of the hypothalamus – the Sexually Dimorphic Nucleus, but no deviations occurred between homosexual and heterosexual men. Therefore, there appears to be some correlation between brain structure and homosexual orientation. Hormonal factors may play a role in gender differentiation; a study by McFadden (2002) found masculinization effects in the auditory systems of homosexual and bisexual female and opposite sex twins. He suggests that this may have been caused by reception of higher androgen levels during prenatal development. However, another study conducted by Banks and Gatrell (1997) questions the theory that angrozenization leads to sexual dimorphic behavior. These authors found no causal link between natal hormonal levels and sexual orientation, hence no definitive conclusions can be reached. There is also increasing support for the hypothesis that the neurological framework of adult sexual orientation may be determined within the mother’s womb itself.(Rahman, 2005). For example, the fraternal birth order effect seems to play a significant role in determining sexual orientation and has been a consistent finding in several studies (Blanchard, 2001; Blanchard et al, 1998; Bogaert 2005). For every additional older brother there is a 33% higher chance of a male being homosexual. The reasons for this phenomenon may lie in the immune system of the mother. Each male fetus is associated with the production of histocompatibility H-Y antigens that are Y-linked, however with each male fetus, an increasing level of immunization takes place in the mother’s womb. As a result, anti H-Y antibodies are produced in the mother’s body, which impact upon the component of the fetal brain that is associated with sexual differentiation (Blanchard, 2001). A study on twins by Hamer et al (1993) showed that the incidence of homosexuality was higher among brothers, which suggests that heredity may play a role in sexual orientation, since brothers share the same mother’s womb. Moreover, while Blanchard’s study (1998) demonstrated the auto immune effect in the mother’s body with successive male fetuses, this was not the case with successive female fetuses, where no impact was demonstrated as far as sexual differentiation was concerned. The possible explanation for this lies in the fact that the mother’s body is also female, thus the fetus is not seen to be alien, like the male fetus. The studies above appear to suggest that homosexuality is linked to nurture. However, there may also be a genetic predisposition to homosexuality. Studies using DNA linkage analysis were conducted by Hamer et al (1993) on homosexual twins and their families, which indicated that a specific gene may be involved in determining homosexual orientation. This study found that polymorphic markers were present on the Xq28 chromosome, which is located in the subtelomeric region of the longer arm of the chromosome pair, where increased sharing of alleles took place. Statistical correlation between the presence of the marker and homosexual orientation was very high. This study seems to implicate a possible genetic causal root of homosexuality. However, the results of this study have been contradicted in another study conducted by Rice et al (1999). In examining the purported genetic link in homosexuality, they conducted studies on twin homosexual sibling pairs. The focus of their study was the Xq28 chromosome at four different markers – DXS 1113, Factor 8, BGN and DXS 1108. But they did not find any evidence to support increased sharing of alleles at any of these marker locations, therefore this does not support the X-chromosome linked genetic theory of homosexuality and no consensus exists on this theory. Twins offer the best means to examine the relative contribution of genetics and environment to an individual’s phenotype. Whitman et al (1993) included several monozygotic and dizygotic twins in his participant samples. The results of his study showed that almost 1/3 of the fraternal twins had homosexual co twins, however among the monozygotic twins, two thirds of the participant sample had a homosexual co-twin. This provides additional support for the hypothesis that genetics may also play a role in homosexuality. The results obtained in the study by Whitman et al (1993) were also corroborated in the study conducted by Bailey and Pillard (1993) who used a much larger sample of fraternal and monozygotic twins. Their study found a 22% correlation among 56 pairs of male fraternal twins and a correlation of 52 % among 56 identical twins. Bailey et al (1993) also conducted a similar study with female co-twins and demonstrated similar results – about half the sample of monozygotic twins also had a homosexual co-twin, while 16% of the fraternal reported the existence of a homosexual co-twin. Therefore, the genetic predisposition to homosexuality seems to be implicated in these studies and it must be concluded that both hereditary and genetic factors appears to play a role in determining the individual phenotype. Schizophrenia: Existing research on mental disorders is based on the polygenic theory, wherein certain factors in the environment, such as drug dependency or stress for example, may result in the development of schizophrenia in a person with an already existing genetic predisposition to the disease. Schosser and Aschauer (2004) identify a region on Chromosome 22q11 which when deleted in microlevels, is associated with velo-cardio-facial-syndrome and a high incidence of schizophrenia, although further research is necessary in this area (Zinkstok et al, n.d). Such deletion in chromosome is also associated with the gene coding for proline dehydrogenase and Catechol-O-methyltransferase (COMT), both of which are believed to modulate the glutamatergic activity in the brain, with the enzyme COMT also regulating dopamine levels. According to Diaz et al (2006), COMT causes the degradation of dopamine, which results in interfere with memory functions. Gene variants of COMT have been implicated in memory deterioration and impairment of cognitive function. COMT may also impair the functioning of the glutamatergic system, which is believed to be linked to schizophrenia, since a reduced level of glutamate functioning in the brain is one of the characteristic features of schizophrenia. Schosser and Aschauer (2004) have suggested that genes that cause hypofunctioning in this system are Neuregulinl,(NGRI) Dysbindin D-amino-acid-oxidase (DAAO) and G72. NGRI is also implicated in another recent study as a gene that may contribute to the risk of developing schizophrenia. (Bjarnadottir et al, 2007). NGRI signaling results in the activation of certain kinases. These kinases cause a short term alternation in the plasticity of nerve synapses through the dys-functioning of the NDMA receptor, which also regulates glutamate activity and may thus be a factor in abnormal behavior. Similarly, Corfas et al (2005) also identify the gene NGRI as a potential susceptibility gene for the development of schizophrenia. DAAO and G72 were the subject of the study by Boks et al (2007). They have suggested that the G72 gene activates DAAO, which in turn regulates the oxidation of D-serine. D-serine is associated with the functioning of the NDMA receptor, therefore any reductions in D-serine production levels produce concomitant reduction in activity levels of the NDMA receptor and may trigger schizophrenia. In addition, the locus of schizophrenia has been specifically pinpointed on chromosome no: 5q31-35, where it may affect the activity of the GABA system. Disinhibition of GABA is believed to lead to increased dopamine levels which is linked to the development of the schizophrenic condition.(Petryshen et al, 2005). The dopamine receptor (D4) gene is believed to cause impairment in memory and abnormal behavior through the polymorphism of the C allele with the T allele, which reduces the efficiency of transcription by 40% as compared to the C allele. C allele frequencies that were significantly higher than normal were found in 252 Japanese schizophrenics.(Okuyama et al, 1999). Another gene that has been implicated in schizophrenia due to its elevation of dopamine levels is the RGS9-2 gene. A study conducted by Seeman et al compared the levels of the gene in animals with schizophrenia and tissue from a dead schizophrenic’s brain and found similar reduced levels of the RSG9-2 gene. All the above studies indicate that there may be significant genetic components that may play a role in the development of schizophrenia. Disorders in behavior, and the behaviors that serve as symptoms for mental illnesses may be the result of disorders in the function of the mind, however, the subject’s environment could also influence the development the disorder (Mohr, 2003). A combination of genetic susceptibility and the neuroplasticity that comes with life experiences is often required for certain mental disorders to appear (Mohr, 2003) Krabbendum and Os (2005) did a review of several studies that have been conducted on the disease. Their findings are that more than 10 studies have shown consistently that the occurrence of schizophrenia depends upon certain triggering factors in the environment, which affect children and adolescents, such that they later begin to develop symptoms of the disease with progressive mental and cognitive deterioration. This study specifically examined the differences between a rural and urban environment and has concluded that urbanicity is a factor since high risk individuals often move into urban areas, which may generate high levels of stress. Wicks et al (no date) examined the risk for the development of schizophrenia in the case of individuals subjected to adversity and poverty in childhood. Their findings suggest that poor socio-economic conditions and adversity in childhood are clearly associated with the risk of schizophrenia. Another theory is based on the belief that a virus may cause schizophrenia, since there is a higher incidence of schizophrenia with physical birth abnormalities or during winter months, which is a time when utero-viral infections most commonly occur.( Kaplan and sadoc, 1991:320-342). Complications during labor were also found to affect brain sizes in monozygotic twins and prolonged labor or trauma during birth are believed to be associated with the brain abnormalities of schizophrenia.(McNeil et al, 2000). One way that biologists have studied the interaction of nature and nurture in the transmission of mental disorders is to study monozygotic twins. Research about the rates of concordance of schizophrenia in monozygotic twins, for example, has shown the existence of a factor called a “second hit.” This sort of factor became an object of interest after the concordance of schizophrenia for monozygotic twins was only 40% to 50%, and 10% to 15% in dizygotic twins (Torgerson, Onstad, and Skre, 1993), thus indicating an environmental impact in the progression of the disorder. All of these studies suggest that environmental factors may play an equally important role in schizophrenia as genetic factors. Conclusion: The evidence presented above appears to suggest that genetic loci may exist for both homosexuality and schizophrenia. In the case of homosexuality, studies on the role of the Xq28 chromosome are still at a preliminary stage, however several genes have been implicated in schizophrenia, with the influence of genes on dopamine and glutamate activity in schizophrenia being reiterated in several studies. Viewed in the context of the nature-nurture debate, this could boost the arguments of those ascribing nature as the primary determinant of individual phenotypes. However, nurture has also been shown to play a significant role, since to a large extent, individual characteristics may be the result of prenatal influences or brain plasticity. Therefore, in the light of the evidence, it cannot be definitively concluded that nature or nuture alone determine individual phenotypes. Rather, the correct conclusion would be that both heredity and the environment play a role. References: * Allen LS, Gorski RA, 1992: Sexual orientation and the size of the anterior commissure in the human brain. Proc Natl Acad Sci USA 89:7199­7202. * Bailey, J. M., and Pillard, R. C, 1991. “A genetic study of male sexual orientation”. 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