Relationship Between Stress and the Human BodyEssay

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Stress & the Human Body

I caught common cold after a close friend's death that caused psychological stress to me.

You are more prone to sickness when under stress - at least that is how it appears. Research too is showing this to be true. The body's immune system and the stress system are linked and immune system is vastly affected by stress response. The stress response involves activating many neuroendocrine systems plus the hypothalamic-pituitary-gonadal (HPG) axes and HPA as well as the sympathetic nervous system. Discussions on the topic of immune system and the neuroendocrine have found that the two utilize certain similar receptors and ligands to support an inter-system and intra-system communication network. It is understood that the communication happening between the systems is crucial for the maintenance of good health and physiological homeostasis. This communication cycle happening between the immune system and the brain and vice versa allows the immune system-brain crosstalk and for the brain to shut down the system when necessary. Evaluating the cross-talk is like a two-way street, one begins to comprehend the types of illnesses that can be caused in cases of too little or too much communication in any of the two directions (Taub, 2008).

Since one of the ways of dealing with stress is talking about the problems, it might be useful attending a stress management class or group. Some of these might be run community centers or by doctors' surgery centers. The classes aid in the identification of possible causes of the stress and so develop the necessary coping mechanisms. Therefore, stress support is the best option for me. Studies reveal that courses of mindfulness in which participants are instructed on simple meditations for some weeks sequentially helps manage stress and improve the mood of participants (Struggling with stress?, 2014).

Module 3 - CASE


The complement system may be activated by a series of various sequential cascading enzymatic reactions where proteins get sequentially cleaved and activated. The ensuing effector molecules, which are C3a and C5a (also called anaphylatoxins), are highly potent as activation products indicating a wide range of activities on several types of cells from apoptosis to chemo-attraction. The complement system has a crucial place in innate immunity as it helps in the defense against parasitic, viral and bacterial invasion. Complement proteins help in promoting opsonisation and phagocytosis as well as intracellular killing of the pathogens through the use of immune effector cells like neutrophilis and macrophage. Complement proteins, specifically the ones of the classical pathway helps in processing immune complexes as well as the protection against immune complex diseases development (Pundir & Kulka, 2012). Neutrophils are some of the most critical cells in inflammatory response's first stage. They are able to kill since they have molecular weapons known as free radicals that can poison bacteria. The poisons are always hidden in specialized sacks of storage kept separate from tissues of the body. On sensing an injury or infection, a neutrophil undergoes dramatic maneuvers referred to as a respiratory burst. They gulp oxygen to aid in the making of several free radicals like molecule superoxide plus protein-chewing enzymes which rip the walls of the bacterial cells apart. Microorganisms produce exogenous mediators. Endotoxin is very notable and gram-negative bacteria produces it. On getting released in the bloodstream, it ensures the simultaneous activation of all inflammatory mechanisms and so causing a septic shock. Bacteria release exotoxins. In most occasions they are vastly chemotactic, i.e. they attract leukocytes. Inflammatory mediators release leads to localized vasodilation as well as an increase in flow of blood at the injury point. The resultant rise in vascular permeability helps in the promotion of an influx of antibodies, phagocytic cells and antibody to the wounded point (Baranoski & Ayello, 2008). Cytokinine signaling is key in intracellular communication in the body's immune system. It mediates and controls inflammatory and immune processes and coordinates several cells' activities finally leading to adaptive and innate immune responses. Following antigenic stimulation, cytokine level increase mediates several processes like inflammation, T- and B- cell growth as well as differentiation and also activates effector cells. There are complex interactions between inflammation, cytokines as well as the adaptive responses in the maintenance of homeostasis, plus several processes are dependent on activations that are induced by cytokine. Cytokines are protenous and small in size and their production is done by various immune cells (macrophages, natural killer cells and lymphocytes etc.) and are very crucial in cell signaling where the immune system mounts inflammatory responses to cell damage and infection. Production of cortisol is done in the adrenal cortex's zona fasciculate and plays a key part in many physiological systems, even as an anti-inflammatory agent (Baranoski & Ayello, 2008). The weakening effects of cortisol on the response of the immune system have been documented well. T-lymphocytes are a key part of immunity that is cell-meditated. T-cells stage responses to cytokine molecules referred to as interleukins through a signaling pathway. Cortisol ensures the blocking of the proliferation of T-cells through the prevention of interleukin signals from being recognized by some T-cells. It also inhibits inflammation because of the stopping of the secretion of histamine. The ability of cortisol to inhibit immune response promulgation may result in a weakened immunity among people with chronic stress (Randall, 2011),

PTSD and the Complement System-brain

As per the results gotten, the average values of serum C4H50, C2H50 and Chapter 50 in patients with PTSD were 1.6, 1.2 and 2.1 times significantly higher than was the case in healthy subjects. Contrarily, the average values of serum fDH50, fBH50, AH50 and C3H50 in PTSD patients were 2.3, 1.6, 1.7 and 1.5 times relatively significantly lower than the healthy subjects. The changes detected were positive and also significantly correlated (p < 0.05) having total (intensity and frequency) cluster PTSD symptom of avoidance, hyper-arousal and re-experiencing. Correlation analysis demonstrates that in subjects affected by PTSD, there is a strong correlation between C4H50 and C2H50 (r=0.72; p=0.002; r=0.5; p=0.05 respectively) and there is a significant correlation between AH50 and C3H50 (r= 0.57; p =0.027). Nonetheless, there was no observation of any significant correlations in the cases of measured PTSD parameters. There was no significant correlation among the healthy subjects in the parameters mentioned (Hovhannisyan et al. 2010). The study's focus was on the main inflammation's mediators' functional state. The obtained results indicate that complement system dysfunction can be linked to PTSD. They give evidence in inflammator component involvement in PTSD pathogenesis as demonstrated in various studies. The researchers here make the hypothesis that neuroendocrine mechanisms associated with PTSD that modulate immunity might put up a fight against the first stages of the inflammatory cascade and so influence changes in the major mediator's functioning (Hovhannisyan et al., 2010).


In the past the peripheral immune system and the CNS were imagined to be operating independently. Nonetheless, fresh evidence has pioneered significant advances in the understanding of the way peripheral events related to immunity influences the CNS processes and so changing mood, behavior and cognition. The advances suggest that inflammation might pose implications to the brain that are long-term. The cytokines participating in the production of inflammatory response are responsible for the initiation of CNS communication process. There is a surge in the brain and so reach the brain, where, while they are made of large proteins and so can't cross into the brain, the chemical signals they carry are carried into the brain through active transport (Maier & Watkins, 2012).

Inflammation is a swelling or redness and heat and is a component of the first response of the immune system to various infections. The defense isn't limited to the infection site. Following the infection, there is development of a pattern which includes what is known as 'acute phase response (APR)' as well as 'sickness behavior.' Sickness behavior can be recognized by someone who has had flu. They are reductions in food intake, activity, sexual behavior and social interaction as well as mood sags. It isn't easy forming fresh memories, there are changes in sleep and pain sensitivity increases. In most circumstances, mechanisms that evolved to help in handling emergencies result in outcomes not intended by nature if they remain active for long. In the course of an infection, neuroinflammation and the resultant adaptive sickness behaviors go on for a number of days. Nevertheless, if the responses are prolonged or exaggerated, the outcomes can be established thereby causing cognitive impairment instead of just a brief disruption of memory, there is depression in place of a reduction in mood, or fatigue in place of inactivity as well as chronic pain where there would be acute pain. Repeated or prolonged peripheral inflammatory issues lead to the production of continuous immune-to-CNS signaling. An example is as in the classic cases - cancer chemotherapy, surgery, peripheral nerve damage as well as myocardial infarction. Such conditions do produce prolonged and large peripheral inflammation (Maier & Watkins, 2012).


The evolution of stress response was to aid organisms in dealing with fight/flight situations. However,… [END OF PREVIEW]

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