Anetylysis Case Study

Generalized Anxiety Disorder (GAD) is one of the most diagnosed mental disorders today, and can often be closely linked to concurrent symptoms or disorders including physiological, behavioral, other anxiety disorders, depression and substance abuse. (Merino, Senra & Ferreiro, 2016) (Cacioppo & Fregberg, 2013, p. 688). GAD most notably produces symptoms of excessive worry and anxiety related to non-specific risks, which often leads to functional decline both socially and professionally (Roberge et al., 2015). GAD reveals instances of links to biological origins such as heredity and biochemistry, as well as, ties to an individual’s cognitive development and socioeconomic environment (Cacioppo & Fregberg, 2013).

This theory creates an issue, as it only looks at nature’s impact as the root cause of phobic disorders and relishes in not accounting for environmental causes, which are posed by nurture. This aspect of nurture which is ignored can be questioned in the twin studies as although Torgersen found that identical twins who share genes are 5x more likely to share an anxiety disorder, it is unclear whether it is the nature of the genetic makeup which causes the disorder, or the nurture of the twins, as they would have both gone through the same things in their environment causing the contamination effect. This is further highlighted through the diathesis stress model formed by Di nardo et al which provides a much more

Despite these concurring viewpoints, there are fundamental differences between these perspectives. The medical/disease perspective focuses on the costs of early stressful experiences, asserting that exposure to early life adversity disrupts normal development, causing dysregulations in biological systems (Ellis & Del Giudice, 2014). As outlined by Del Giudice and Ellis (2016), research from this perspective generally focuses on unfavorable health outcomes associated with early stress exposure, such as reduced performance on intelligence tests and greater prevalence of psychopathology. The evolutionary perspective, in contrast, extends the understanding of epigenetically-based developmental processes by examining the benefits of stress responsivity and its orchestration of adaptive developmental patterns. According to the ACM, organisms have calibrated their systems via environmental cues to adapt physiological and behavioral systems to their current and future environments (Del Giudice & Ellis, 2016). Therefore, despite potential impairments/costs, there should also be adaptations; for example, as discussed by Ellis & Del Giudice (2014), adolescents

In the field of genetics, the study of the effect of various genes is imperative in translation and interpretation. As genetic coding influences phenotypic expression, the analysis of specific genes and any polymorphisms are relevant in a clinical setting. One such example is that of personality traits, which are believed to be influenced by specific neurotransmitters, known as catecholamines. Catecholamines are chemicals released by the adrenal glands in response to stress, and operate dually as hormones and neurotransmitters within the body. Commonly, catecholamines mediate functions within the central nervous system, including those of emotional responses and motor control. Inclusive of dopamine, epinephrine and norepinephrine, the

Oler, et al. (2010) investigates the potential heritability of the anxious temperament (AT) phenotype and its related brain circuity. Perhaps some of the most prevalent mental illnesses are anxiety disorders, where symptoms become noticeable in the prepubescent period. Although many experience feelings of anxiety during adolescence, anxiety disorders are characterized by a continual anxious temperament beginning in youth and extending into adulthood. This anxious temperament is marked by a high degree of both freezing behaviour and a lack of communication in response to strangers or unfamiliar stimuli. Additionally, those with AT will often see an increase in autonomic activity. It is believed that AT has some genetic predisposition. However,

The personality trait anxiousness seems to have a genetic component, because individuals with that have different biological and behavioral variations of the serotonin-transporter-linked-promotor region (5HTTLPR) genotypes indicate that it’s the cause of differential biological stress reactivity. “Susceptibility to stress may have biological roots, especially in the serotonergic system” (Petersen). Different people becoming anxious and reacting to stress differently because of a genotype shows that there’s a strong nature component. One of the parts of the brain that anxiousness can affect is the amygdala, which signals aggression and fear. “Cognitively changing the meaning of emotional stimuli effects evoked responses in the amygdala and other brain areas” (Mocaiber). So trait-anxious individuals sometimes unconsciously change the meaning of a stimulus to an anxious context. Not only are they succeptible to making stimuli a threat, Mocaiber also claims that they can be “abnormally sensitive to threat-related stimuli.” This makes sense that anxious people see more things as threats and can spot an actual threat very easily.

suggested that there is an imbalance of neurotransmitters may be what is contributing to anxiety

The results of the twin study revealed that the DNA segments of the HTR1A gene were identical; neither had the gene missing or inactivated. The data of all the twins’ DNA was tested for differences and the results fit the Hardy-Weinberg equilibrium model, meaning that there were no deviations or major differences in the HTR1A gene between twins. Each twin had identical genes and there was no difference between the twins who had anxiety disorders and depression and those that did not. The data from this study suggests that the HTR1A gene is not the gene, if there is one, that is responsible for anxiety disorders. It is possible that the gene with a combination of other factors, in some people, causes anxiety or depressive behavior. Without knowing a third variable, or perhaps environmental trigger, the HTR1A alone cannot be said to be responsible for anxiety disorders.

Everyone with any mental health disorder always wonders if linkage of genetics is part of the disorder they have. People have said that risk of genetics being a factor in anxiety disorders is less likely to be a switch more than a problematic mix of genetics that can put a person at risk. Researchers have said that anxiety disorders can be due to hostile childhood experiences. Efforts to identify the specific DNA mutations to the heritability of anxiety disorders establish any independent, suspicious loci, but any genetic study for anxiety faces some obstacles also. The fine line between healthy and pathological anxiety is unclear, and the phenotypic and genetic barriers between scientific anxiety disorders

Investigations clearly show that both nature and nurture play significant roles in the origin of psychopathology. Many studies based on adoption, twins and family have confidently recognized the roles of both genes and environment in mental disorders. Having a close relative with a mental health disorder is typically the most predictable risk factor for increasing that disorder to you, but the relationship is not inevitable. Even identical twins with identical genes sometimes do not develop the same psychiatric disorder. It remains difficult, to determine if genes for disorder are characterize by certain ecological conditions or psychopathology. The reason for this difficulty lies in the complex nature of mental disorders. Many disorders such

Mitra, Adamex & Sapolsky (2009) investigated the individual differences that appear in managing stress and anxiety. Despite many people undergoing traumatic events within their lifetime, most do not develop an anxiety disorder as a consequence. Why is this the case? Correlational studies have proposed that individual characteristics, as well as our genes and personal experiences, contribute to the development of PTSD. One factor thought to be critical in this process is a change in the functioning of the seratonin transporter (5-HTLPR); the basolateral amygdala (BLA) is important for fear responses, and the degree of its reactivity is regulated by the 5-HTLPR. Through a technique called predator stress exposure, anxiety-like characteristics can be displayed in rodents and manifested in the brain as an increase in signal communication between the amygdala and other structures. This increase in communication increases the sensitivity of the BLA. An important mechanism in this increased excitation in the BLA is thought to be the structure of it’s dendrites: different dendrite structures could affect the reaction a rodent has to a predator stressor. In cases of anxiety or stress, larger dendrites in BLA are present. Similarly, if the length of dendrites is decreased, the anxiety characteristics decrease as well.

The true cause of anxiety has yet to be discovered and it is necessary to know what causes people to have this disorder. This article describes what occurs genetically when a child is being conceived. It expresses how “genes make the right proteins at the right time” (What causes anxiety? 4). This means that when a child is being created, each parent’s genes are being combined. “But if the genes get it wrong, they can alter your biology in a way that results in your mood becoming unstable. This biological tendency toward anxiety man be latent for years until an exceptionally stressful event triggers its expression” (What causes anxiety? 4). Anxiety is already a very depressing and life altering condition and some individuals have to cope with

Personality is an amalgamation of characteristics and traits that an individual develops as they grow; this can affect the way they think, feel and behave. However, in some cases certain fragments of an individual’s personality can progress in a way which makes it difficult for the person to live their life. This can affect an individual negatively in their daily lives as well as the people around them; this is known as a personality disorder (Stoddart, n.d.). Personality disorders are long-term behaviours and are usually exhibited in late childhood or adolescence and can continue into adulthood; it can cause a great amount of distress and impairment to an individual (Rubin, 2011). Genetics is the study of inherited characteristics and variations in genes amongst individuals (Genetics, n.d.). It is believed to play a large role in determining and underpinning many personality disorders. This essay will be critically discussing the genetic components of various personality disorders such as Borderline personality disorder (BPD), Anti-social personality disorder (ASPD), Avoidant personality disorder (AVPD) and Obsessive-compulsive personality disorder (OCPD) and lastly Dependent personality disorder (DEPD), with the use of relevant theories and research.

The scale measures the fear and avoidance in social and performance situations. They then gathered DNA from the volunteers from leukocytes. The results from these methods of research showed that lower expressing serotonin polymorphism genotypes were associated with decreased reappraisal and increase social anxiety. But, not only did they state this information, they gave a possible solution for increasing or bettering reappraisal. Through cognitive-behavioral psychotherapy low-expressing genotypes can improve.

Around 10-17% of the general population will develop an anxiety disorder at some point in their lives (Kessler et al., 2007), and affected individuals are typically severely impaired in their social and occupational function. In order to improve current treatment options, a detailed understanding of the neural circuits that underlie fear behavior, and their dysregulation in patients with anxiety disorder, is critical. Neuronal circuits encoding fear include the amygdala, PAG, and dMT, among several other regions. The amygdala integrates fear-related sensory input and initiates fear responses through CeM output projections targeting brainstem or hypothalamic nuclei. Generally, input signals to the amygdala are relayed from LA to CeM via the