Discussion Question On Stress: Is There Significant Evidence

Discussion Question Onestressthere Is Significant Evidence That Stres

Discussion question one: Stress There is significant evidence that stress causes a number of changes in the brain and body. The changes are significantly different between acute and chronic stress. Discuss the difference between acute and chronic stress, and discuss whether or not either of these conditions are beneficial in humans. Respond to at least two of your classmates’ posts no later than Monday discussion question two: Schizophrenia Discuss the dopamine theory of schizophrenia. What are its implications regarding treatment? (For example, does the dopamine hypothesis of schizophrenia suggest that the only successful treatment for this disorder is a pharmacological approach?) Identify at least two research studies to support the position you take on this. Respond to at least two of your classmates’ posts no later than Monday, Day 7.

Paper For Above instruction

Stress is an intrinsic part of human life, triggering a complex array of physiological and psychological changes within the body and brain. The distinctions between acute and chronic stress are fundamental to understanding their respective impacts and potential benefits or detriments to health. Acute stress, characterized by a sudden and temporary response to a perceived threat, can be beneficial in certain contexts by enhancing alertness, focus, and physical performance. This 'fight-or-flight' response is evolutionarily advantageous, preparing individuals to confront or escape danger. For example, acute stress can improve reaction times and decision-making in emergency situations, potentially saving lives (McEwen & Stellar, 1993). Additionally, brief episodes of stress have been associated with increased resilience and improved coping skills over time (Seery et al., 2010). Conversely, chronic stress, which persists over an extended period, can have deleterious effects on health. It leads to sustained activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in elevated cortisol levels and sustained physiological arousal (Lupien et al., 2009). Chronic stress has been linked to numerous adverse outcomes, including cardiovascular disease, immune suppression, depression, and cognitive impairment (McEwen, 2006). The maladaptive effects of prolonged stress underscore its potential harm rather than benefit. While acute stress may sometimes foster adaptive responses and resilience, chronic stress tends to be detrimental, impairing bodily systems and contributing to disease (Lupien et al., 2009). Therefore, the beneficial or harmful nature of stress depends heavily on its duration and context, with acute stress serving potentially positive functions and chronic stress predominantly posing health risks.

Schizophrenia and the Dopamine Theory

The dopamine hypothesis of schizophrenia posits that dysregulated dopamine activity in the brain, particularly hyperactivity in mesolimbic pathways, underpins the positive symptoms of the disorder such as hallucinations and delusions (Howes & Kapur, 2009). This theory has significant implications for treatment, primarily endorsing the use of dopamine antagonists or antipsychotic medications to mitigate symptoms. The role of dopamine in schizophrenia was initially supported by the observation that drugs increasing dopaminergic activity, such as amphetamines, can induce psychosis-like symptoms in healthy individuals (Laruelle & Abi-Dargham, 1999). Conversely, antipsychotics that block dopamine receptors effectively reduce positive symptoms, further reinforcing this connection (Kapur & Remington, 2001). However, the dopamine hypothesis does not entirely explain all aspects of schizophrenia, particularly negative symptoms and cognitive deficits. Research evidence supporting the dopamine hypothesis includes PET studies demonstrating increased dopamine synthesis and release in patients with schizophrenia (Howes et al., 2012) and clinical trials where dopamine antagonists effectively alleviate positive symptoms (Kapur et al., 2000). Nonetheless, the reliance solely on dopamine-blocking medications has limitations, as they often produce significant side effects and do not address negative or cognitive symptoms comprehensively. Emerging models now consider other neurotransmitter systems, such as glutamate and serotonin, in the pathophysiology of schizophrenia (Moghaddam & Javitt, 2012). Therefore, while dopamine antagonists are vital in managing positive symptoms, a more integrated treatment approach that incorporates pharmacological and psychosocial therapies is increasingly advocated.

References

• Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—the final common pathway. Schizophrenia Bulletin, 35(3), 549–562.
• Howes, O. D., et al. (2012). Dopamine synthesis capacity prior to the onset of psychosis: a prospective PET imaging study. The American Journal of Psychiatry, 169(12), 1314-1321.
• Kapur, S., & Remington, G. (2001). Serotonin-dopamine interaction in schizophrenia: developments in pharmacology. Trends in Pharmacological Sciences, 22(9), 438–444.
• Kapur, S., et al. (2000). The dopamine hypothesis of schizophrenia: clinical and preclinical evidence. Journal of Psychiatry & Neuroscience, 25(4), 342–350.
• Laruelle, M., & Abi-Dargham, A. (1999). Dopamine as the wind of the psychotic fire: New evidence from brain imaging studies. Journal of Psychiatry & Neuroscience, 24(4), 341–352.
• Lupien, S. J., et al. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434–445.
• McEwen, B. S., & Stellar, E. (1993). Stress and brain plasticity: consequences for behavior. Neuroscience & Biobehavioral Reviews, 17(1), 27–34.
• McEwen, B. S. (2006). Protective and damaging effects of stress mediators: central role of the brain. Dialogues in Clinical Neuroscience, 8(4), 367–381.
• Moghaddam, B., & Javitt, D. (2012). From revolution to evolution: The glutamate hypothesis of schizophrenia and its implication for treatment. Neuropsychopharmacology, 37(1), 4–15.
• Seery, M. D., et al. (2010). Cardiovascular stress reactivity and resilience: Foundations for future research. Frontiers in Behavioral Neuroscience, 4, 59.