Mental disorders presently affect a large proportion of world population. The World Health Organization (2012)conducted a status survey, which found that a significant chunk of the world population suffers from various degrees of a wide assemblage of mental disorders. According to the World Health Organization Report (2012), over 350 million people suffer from depression all over the world. In a conflict between, Nature vs. Nurture, scientific community stands divided on the contribution of genetics on Psychiatric disorders and illness. However through this essay, I will put forward arguments based on scientific findings that showcase the contribution of genetics on mental disorders.
Unlike physical disorders, genetic disorders have an early onset age and severely reduces the chances of reproduction in the patient. Based on the selection pressure logic, mental disorders should be naturally selected out of the human population; Uher, (2009) provides interesting insights into the heritability of mental disorders from an evolutionary theory perspective. Gene-environment correlations are also thought to be one of the primary correlates of psychiatric anomalies (Jaffee & Price, 2007). Adolescent depression is a major cause of concern for health agencies, (Silberg, Rutter, Neale, & Eaves, 2001). Owen, Craddock, & Jablensky, (2007) showed how psychosis was closely related to genetic factors and elucidated the underlying mechanisms for psychosis. Schizophrenia, Bipolar Disorder and Autism Spectrum disorder are three most widespread psychotic illness that affects present world population. A paper by Wray, (2013) effectively tried to understand the implications of Single Nucleotide Polymorphisms (SNP) in the development of mental illness. The findings of all these studies and a few more are discussed below.
Heritability of mental disorders
Significant evidence exists that suggest a tangible genetic link between psychotic disorders. Studies on Single Nucleotide Polymorphism by Wray, (2013) effectively showcased that the heritability of mental disorders is often just a few mutations away. Wray (2013) argues that most psychotic disorders are more or less heritable however, the degree of heritability varies widely between different disorders. In the following section, we shall discuss a few scientific papers that effectively proved the role of genetic components as a determinant for some major mental disorders. The biggest achievement of Wray (2013) was that it conclusively showcased that there was tangible genetic link between five different psychological disorders viz., Schizophrenia, Bipolar disorder, Major depressive disorder, autism spectrum disorder, and attention deficit hyperactivity disorder. The shared genetic etiology between these widely varied and highly prevalent diseases indicate that major changes in nosology are required to effectively cure these disorders. Wray (2013) conducted Gene-wide association studies (GWAS) to identify genetic polymorphisms such as Single Nucleotide Polymorphisms (SNPs) at different locations of the genome. Psychiatric ailments need a multi-disciplinary approach so that they may be cured across the wide spectrum of social, behavioral, and psychological contexts in which they occur.
Anxiety in Children
Child anxiety is often considered one of the primary early precursors of mental disorders in children. Anxiety related disorders have an early onset in children however, the reasons behind anxiety in children can vary (Gregory & Eley, 2007). Studies suggest that anxiety disorders in children is often a result of both genetic and environmental factors. Anxiety disorder is characterized by fear, concern or dread and may be related to a specific event or more general (Estes & Skinner, 1941). Most children are likely to show at least some symptoms of anxiety and that can be beneficial but when the fear and anxiety starts interfering with normal development, it might indicate a medical concern. However distinctions need to be made in terms of anxiety as a state and a trait. Every child will show an anxiety state when exposed to a threatening situation, but they will come back to a normalcy soon after the stimulus is removed. On the other hand, children with a disorder display anxiety as a trait and show fear and anxiety as a behavioral response to known and unknown stimuli. Scientists have only recently started examining specific genes that might be involved in the development of anxiety in children. ‘Linkage’ is a family based technique which looks at the presence of specific disorder and traces the origin of that trait alongside a particular section of the genome. This technique is particularly useful while identifying single gene disorders(Huntington’s disease) but fails in case of polygenes(Gregory & Eley, 2007). Anxiety being a fairly complex disease, requires a multi-gene approach, the Quantitative Trait Loci (QTL) technique has been found to be particularly useful in identifying the genes responsible for this disorder(Gregory & Eley, 2007). Serotonin is a chemical that is responsible for emotional states and in case of anxiety related disorder, three other genes which produce dopamine, Catechol-O-Methyltransferase (COMT) and the Corticotrophin releasing hormone (CRH) are also known to play a role in anxiety disorder development in children. While dopamine is associated with the reward pathway, COMT is an enzyme that plays a crucial role in inactivating compounds within both dopamine and serotonin pathways. CRH on the other hand is a part of the Hypothalamic Pituitary Axis (HPA) that is also involved in the fight or flight response and manages stress levels in animals. Therefore, we see that children with anxiety related disorders have skewed reward pathways, may have unpredictable emotional states along with an unregulated stress control mechanism.
Comorbidity studies on 4000 twins aged 4 years was conducted by Gregory & Eley, (2007)to find the genetic and environmental correlates of anxiety related disorders. While shared environmental correlates accounted for 78% of the obsessive compulsive disorder and separation anxiety, general distress showed the largest amount of genetic correlations. This effectively shows that anxiety disorder is caused by both genetic and environmental factors(Gregory & Eley, 2007). Similar comorbidity studies also showed that childhood anxiety was also very closely related to adolescent and adult depression (Silberg et al., 2001). Therefore, until further research proves the existing corpus of information otherwise, we can safely say that anxiety disorders are genetically and environmentally linked.
Autism Spectrum Disorders
First of all Autism is not a single disorder but constitutes an entire spectrum of disorders that constitute many other neurodevelopmental disorders. For many years, autism was considered to have psychogenic etiology. However, based on epilepsy studies and some mental stability analysis the biological origins of the disorder was finally accepted. Autism is one of the prototypical pervasive development disorders that affects 5:10,000 individuals with 75% of the victims being male(Lord & Cook, 2000). Candidate gene studies show that GABA system and serotonergic systems are probable functional candidates for the development of autism spectrum disorders(Turner, Barnby, & Bailey, 2000). Based on the recent findings various preventative measures can be used to reduce the incidences of autism. Genetic counselling, pre-natal and pre-symptomatic counseling can be used to reduce the prevalence of this disorder.
Depression
Depression is considered one of the most prevalent mental disorders presently plaguing human society. The word depression is used to describe two conditions. First, a transient state where individuals go through a phase for a small portion of their lives. Second, a Major Depressive Disorder (MDD) which is a clinical condition with lifelong bio-behavioral ramifications in patients. MDD is a critical and highly prevalent major medical disorder with poorly understood pathophysiology (Fava & Kendler, 2000). Various socio-economic factors have been attributed to the development of depression in adults. However, studies are emerging that showcase that there might be a genetic component to depression, which puts people with immediate family members who suffered from depression in immediate risk of being affected as well. A study by Nestler, Barrot, DiLeone, & Eisch, (2002) suggested that upwards of 20% of present US population suffers from a mild to severe depression. Studies by Nestler and colleagues (2002) and Fava & Kendler, (2000) also clearly linked genetics and depression. According to Fava & Kendler (2000) there is a 40-50% chance that depression can have genetic origins, which is almost the same probability as other diseases like Type II diabetes, asthma etc. However, the genes causing depression are yet to be identified. Levinson, (2006) believes that depression is moderately inheritable and other factors such as childhood and socio-economic factors might determine the occurrence of full-fledged MDD in patients. More studies are required to identify the exact nucleotides and their corresponding chromosomes which when modified can increase chances of MDD occurrence in individuals. Another interesting study by Eaves, Silberg, & Erkanli, (2003) showed that genetic difference ins anxiety can increase chances of depression in adolescents manifold. Eaves and colleagues (2003) also showed that anxiety and life events can have epigenetic effect, which can trigger MDD in adolescents.
Schizophrenia and Bipolar Disorder
Schizophrenia and Bipolar Disorder are two dissimilar mental diseases that have been found to possess a similar genetic basis. Previously, Autism Spectrum Disorders were considered a form of childhood schizophrenia because of small similarity in symptoms. However, recently scientific articles have started focusing on the genetic correlation between Adult Schizophrenia and Bipolar Disorder has been drawn due to the sharing of a polygenic component that contributes to both diseases (Purcell et al., 2009). Purcell and colleagues (2009) genotyped a large sample of individuals for up to 1 million Single Nucleotide Polymorphisms and found that there was a strong polygenic component to both disorders, at the first intron of Myosin on Chromosome 22 and more than 450 SNPs on chromosome 6p that spanned the Major Histocompatibility Complex. This study not only proved the genetic components that may lead to schizophrenia and Bipolar disorder but also connected the two disorders through a polygene component and the most likely cause was Single Nucleotide Polymorphisms. Polimeni & Reiss, (2003) tried to understand the basis of schizophrenia from the evolutionary theory perspective. The authors present some interesting reasoning behind the persistence of schizophrenia in the human population. Some of the various advantages of schizophrenia include increased survival in children(Avila, Thaker, & Adami, 2001), increased immune-response in surviving family members of schizophrenics. Scientists exploring the evolutionary basis of schizophrenia believe that this disorder must be genetically transmitted because apart from having certain negative connotations to it, it might provide a certain service to the maintenance of human societal structure.
The Paradox
The paradox of confirming genetic variation as a causative agent for mental illness lies in the fact that mental illness is often associated with reproductive disadvantage in adults(Uher, 2009). If most mental disorders were genetically inherited, then it is quite probable that most of them would be under high selection pressure and thus would be naturally purged out from the population. If that is the case, why is the prevalence of mental disorders increasing worldwide? The second problem lies in the fact that it is becoming increasingly difficult to pinpoint the exact portions of human genome responsible for certain diseases (like in MDD). A previously prevalent hypothesis called the Common Disease/Common Variant (CD-CV) advocated that small changes in genome is not expressed readily in individuals and passes through generations and the additive effect of such variations result in mental illness. Upon evaluating the CD-CV hypothesis under the light evolution theory and epidemiological theories Uher (2009) explained that this theory needs to be integrated with a Genome Wide Association Studies (GWAS) to comprehensively understand the role of genes in mental illness. Uher explains that the heritability of mental illnesses can be explained through two plausible mechanisms. First, the gene-environment interaction and second, the accumulation of small changes over the course of time that manifests into mental disorders. However, Uher (2009) argues that only these two factors cannot account for the wide variety of mental disorders known to modern medicine. Probably different mental disorders occur from varied contributions of the two factors i.e. gene-environment interaction and pleiotropic events (Uher, 2009). So more research is required to understand the evolutionary mechanisms that regulate mental disorders in human populations.
Discussion
Based on the evidences presented from scientific research conducted within the last few decades, we can safely conclude that mental disorders are a result of genetic and environmental factors. There are various competing theories that try to validate the existence of mental disorders in human population based on the evolutionary perspective. Some research has also been conducted on the selective advantages imparted to patients with mental disorders that might lead to the transference of such genes into the next generation. From the literature, it can be safely deduced that although some mental disorders have single gene origins, others may have a polygene origin. For diseases that have a polygene inheritance and are also dependent on environmental factors, etiological studies run into roadblocks. However, through familial studies based on QTL it has become easier to identify the exact constellation of genes responsible for certain disorders. One of the most important studies was that conducted by Wray (2013) where it was conclusively shown that five psychiatric disorders might share certain molecular risk factors. The study did not provide any clear idea about the nature or degree of the relationships but based on Gene Wide Association Studies (GWAS) it showed that Single Nucleotide Polymorphisms or SNPs were shared between five different psychological disorders. This study and the others provided in the above literature review effectively showcase the molecular basis of psychiatric disorders. Further research is required to understand the moral, social and evolutionary implications of the psychiatric ailments in order to better understand the origins of such diseases and thereby treat them more effectively. Further studies should focus on a range of disorders with similar symptoms in order to identify all parts of the genome that might play a role in creating such ailments. Therefore I support the idea that mental disorders do have a certain degree of genetic basis.
References
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