Stress-induced immunosuppression and immune system activation

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

Introduction

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).

Inflammatory

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).

Conclusion

The evolution of stress response was to aid organisms in dealing with fight/flight situations. However, where there is a prolonged activation of the stress response by circumstances and situations that were not in existence in the phases of evolution, there can be pathological results. PTSD pathogenesis is linked to dysfunction of the complement system, including complement classical pathway being in a hyperactive state and the complement terminal pathway being in a hypoactive state as well as the complement terminal pathway being overactivated (Hovhannisyan et al., 2010). Cortisol has vast effects and its effects can be felt in almost the all body and so affect many homeostatic mechanisms. While the effects of cortisol can be registered throughout the body, there are also effects on the transport of ions, immune response and also the memory. The hippocumpus which is the part of the brain where there is processing and storage of memory has several cortisol receptors. While there is no effect on the hippocampus by cortisol levels in the normal range, excess amounts can overwhelm hippocumpus and lead to atrophy (Randal, 2011). PTSD is linked to complement system dysfunction and shows the changed complement system cascade chains.

Module 3 - SLP

Step 1 - which was 'observe and generalize" was made use of in the understanding of immune response and stress. Step 2 was the formulation of a hypothesis and was used in connecting the dots between the influence stress has on the immune response and the possible PTSD effects on inflammatory response, as well as the advancement of depression and various PTSD symptoms.

The hypothesis did not have any information that might be taken as an absolute truth. This is because the connection between the areas is still grey. There is need for more study to help in the understanding of molecular mechanisms that help in PTSD development and to also understand their function in PTSD pathogenesis.

New Technology to Carryout Tests

Brain Imaging

Techniques of brain imaging give researchers and doctors opportunities to view problems as well as activity of the human brain without carrying out invasive neurosurgery. Modern techniques like Magnetic Resonance Imaging (MRI) and PET have become very useful for researchers as they study addiction and the effects of addiction to the brain. Such technologies are allowing researchers to see inside a human brain in the areas reached by drugs and chemicals. Positron Emission Tomography makes use of traces of short-lived radioactive substances and helps in the mapping of the functions of the brain. Positrons are emitted as the materials go through radioactive decay. The detectors pick up these emissions. Areas that show high radioactivity are taken to be the areas with the most brain activity. Functional MRI is another way of measuring the activities of the brain. MRI detects the changes taking place in the flow of blood by the use of radioactive tracers. Blood always flows to the part of the brain with the most activity. The blood supplies oxygen to that part of the brain and so aiding the working cells. The tracking of the changes in blood flow helps in the tracking of brain activity in the course of their happening. MRI machines have giant magnets but have the appearance of PET scanners. Some atoms such as hydrogen which is a water component emit an energy wave when a magnetic field surrounds them. In the MRI machine's magnetic field, hydrogen molecules present in water in blood release energy pulses. The energy amount reflects in the blood flow and so the activity of the brain. This energy is detected by a sensor and it is turned into an image or picture by a computer (Brain Image Technologies, n.d). New technologies like these make up scientific method's phase of "testable prediction."

Carrying out a test

Background: PTSD (Post-traumatic stress disorder has always been linked to lower cortisol levels.

Aims: comparing basal levels of cortisol in adults having PTSD and also in individuals not having any psychiatric disorder.

Method: Systematic meta-analysis and review. SMD - standardized mean differences - in levels of basal cortisol are calculated and there is application of random-effects models through the use of inverse variance weighting.

METHOD

Identification of Studies

There will be identification of relevant studies by searching through Medline, Psychlit, ScienceDirect and EMBASE for articles that were published between the years 1980 and March of 2005. A free-text search is to be performed by the use of terms like cortisol, PTSD or post-traumatic stress disorder or glucocorticoid. The reference list will also be evaluated and checked to find any articles that can be relevant. Researchers will also consider other unpublished works brought to our knowledge or offered by various researchers.

Inclusion Criteria

Inclusion of studies will be done when there is measurement of cortisol in adults (those who are of at least 18 years of age) having PTSD and relatively in control with no prevailing Axis I disorder (according to DSM - III, DSM IV or DSM-III-R; American Psychiatric Association, 1980, 1987, 1994) or PTSD history. The levels of cortisol are to be determined using a typical biological essay. Further, the average levels of cortisol and the S.D. - standard deviations for the two groups shall be presented and described by the authors on request. For the case of multiple papers in one study, just the results of the publication having the most participants will earn inclusion.

Exclusion Criteria

The seclusion of studies will be when: (a) there is a focus on a condition which is not depression co-morbid with PTSD (like cancer or borderline personality disorder); (b) a lifetime reporting, a twelve-month PTSD diagnosis or partial/sub-threshold PTSD; (c) the level of cortisol was measured in a period of the one month of the trauma; (d) there is pharmacological challenge of the HPA axis (like by dexamethasone) before the cortisol is first measured; (e) there was anticipation of a social stressor on the part of the participants like a combat noise, personalized trauma script or a cognitive stress challenge; (f) the paper reports in a language which is not English. G.V and MM assessed independently every gotten study. Resolutions to the arising diagreements will be found by discussing the problems (Meewisse et al., 2007).

Data Analysis

In each of the identified studies, the researcher calculates the SMD - standardized mean difference in the levels of cortisol between the control groups and associated variances. There will be use of Hedges adjusted g in giving better estimates where the samples used are very small (Rosentall et al., 1994). Random-effects models shall be fitted by the use of inverse variance weighting so as to get SMD poled estimates and the associated 95% CI (Meewise et al., 2007).

In all the analysis, the researcher makes use of the SMD as a measure of outcome to allow pooling in studies that make use of various kinds of measurement (like saliva, plasma, serum or urine) and also as a measure of reducing the measurement problem's impact in relation to the conditions of sampling.

The first analysis of the researcher shall have data drawn from all the studies evaluated and so get the overall pooled estimate and also to do an examination whether or not there exists uniformity of the results reached by the studies. Every study will only be considered once in the overall analysis. If any study gives a report of several times and types of measurements, the hierarchy below shall be used in selecting just one of the measurements. Samples of plasma will be given preference over saliva and saliva over urine. Morning measurement will be preferred to measurements taken in the afternoon or at night/evening. The researcher shall make use of data derived from the earliest sample or at the time of the relation of the measurements to awakening time and the researcher in his selection will choose a sample at 30 minutes following awakening as this is the closest time to when cortisol is highest in the morning. For samples taken in the afternoon, the researcher shall take the latest sample and so compare the circadian curves at nadir of the values of cortisol. There will be a Q test examining if more heterogeneity exists in the results than can be drawn from chance only. This study shall also compute I2 statistic that expresses the total variation percentage which is attributable to heterogeneity instead of chance. Within the set of data, the researcher shall also examine if any systematic differences exist between the various measurement types (Meewise et al., 2007).

The researcher shall carry out many specific analyses at the subgroup level and evaluate if the variances in levels of cortisol between control and PTSD groups is because of other reasons or factors. There will be construction of successive models to help in the examination of if SMD was different significantly in the subgroups that were defined by certain factors. The factors that are to be evaluated are: gender; time of measurement; PTSD group characteristics, including years that have passed since the time of trauma, the kind of trauma and absence or presence of co-morbid depression; whether the group had exposure to trauma or not; as well as the publication year. The results drawn from the analysis of the subgroup are to be presented as average SMD plus 955 CI for every factor level. Further, a test of the different interactions (for instance, if the SMD variances between the factor levels are zero) shall also be carried out so as to avoid the researchers over interpreting the effects existing in the subgroups (Altman & Bland, 2003). P-values that are no more than 0.05 shall be taken to be statistically significant (Meewise et al., 2007).

Module 4 - Background

Discussions

Many things are apparent: (1) gut microbiota are crucial to having good metabolism and the brain functioning optimally, (2) communication pathways of the gut-brain are inclusive of neural connections, (3) gut microbiota are very critical in the initial development stages and can have an influence in the way the stress circuitry is wired in the brain, and (4) 'good bacteria' - probiotics - are shown in science to positively impact mood symptoms in both humans and animals. Commensal bacteria are important in the maintenance of the intestinal tract integrity, and where there is disease or stress, an increased permeability of the intestines contributes to an increase in inflammation. An increase in such permeability is at times called "leaky gut" and can result in the bacteria translocating out of the lumen into the intestinal layer. That is another pathway which pathogenic bacteria and microbiota can use in their communication with the brain through the immune system by activating local neurones in the ENS (enteric nervous system)(Foster & Neufeld, 2013). Stress has been shown to raise intestinal permeability and so give bacteria a chance to translocate and so access ENS neuronal cells and immune cells. This is a possible path where microbiota can have an influence on the ENS through the ENS and the immune system in case of stress. Bidirectional communication between the gut-brain axis components and the gut microbiota do have an influence on homeostasis and can have a hand in disease risk by altering CNS, GI, ANS as well as immune systems. A key question facing neuroscientists is if behavior changes caused by microbiota are due to long-term alterations in the central signaling systems. To date, investigators have given evidence showing that the gut-brain axis has influence on neurotransmitter systems and neuroplasticity-related systems (Foster & Neufeld, 2013).

Module 4 - Case

Tachchardia - a heightened heart rate - is when the heart beats at a rate that is beyond the normal range. Resting heart rate is the rate at which the heart beats when you are sleeping or resting. Several factors may result in a heightened heart rate, although some of the factors can pose more danger. Air temperature, level of activity and stress are some of the factors. In responding to exercise, the heart beats faster. A more physiologically demanding activity causes a higher rate. This is because more blood is needed to be pumped to the muscles to supply nutrients and oxygen and also to take away byproducts from metabolism. An increase in heart rate is common during stress. Stress causes a higher heart rate but prolonged stress can severely affect your health. Some external stresses like humidity, wind, heat, air quality and cold can also heighten the heart rate. Every stress affects the heart differently - the heart rate being one of the responses. Sleep deprivation, rapid blood chemistry changes like sugar levels and reaction to ingested food as well as irritability can affect the heart rate during exercise. Emotions also influence the responses of the heart. Anxiety, fear and anger result in tachycardia while the rate is drastically lower in case of depression. The center for cardiovascular control is at the ventro-lateral medulla. At this place, the rate of the heart reduces on activation by cardiovascular inhibitor center located in the medulla or it is heightened on activation by cardio accelerator. Emotions such as compassion, happiness and compassion lower the rate at which the heart beats.

Studies show that exposure to chronic stress influences blood pressure. Depression has been associated with cardiovascular diseases. The association between heart disease, sudden death and stress has been around for ages. The occurrences of sudden death and heart attack have at times been linked to acute natural disaster stressors like tsunamis and earthquakes as they evoke the response of 'fight or flight.' Coronary heart disease has also been common among people who are under chronic stress and research has been trained at finding a solution for the problem.

Myocardial infraction - a heart attack - is often caused by blood clots which hinders the flow of blood to parts of the muscle of the heart. This is a serious consequence of coronary artery disease. The disease occurs on arteries becoming hardened or narrower because of build-up of plaque cholesterol. More narrowing of the arteries may take place from blood clots (thrombi) that take place on the plaque surfaces. Heart attacks take place on a coronary artery being blocked severely that the flow of blood is braked and so damaging part of the heart muscle - the myocardium. Given the extent of the damage of the heart muscle, the patient might be severely disabled or even succumb to the myocardial infarction. Apart from atherosclerosis, heart attack can also be caused by a temporary spasm or contraction of a coronary artery. On this happening, the artery gets narrowed and the volume of blood flow is reduced significantly or even halted. While the causes of such spasms remain unknown, it can take place in both partly blocked and normal blood vessels. Below are some of the risk factors linked to higher myocardial infarction incidences. Some of them can be controlled (like physical activity and smoking) while others cannot be controlled (like family history or genetics) (Imagins, n.d).

In terms of the risk of myocardial infarction, psychological stress effect was just as significant as the usual factors like obesity, hypertension, smoking and diabetes. Further, a review of twenty-three treatment comparisons drawn from seven-teen random trials that was conducted in those patients having heightened blood pressure, there was a strong effect on reducing blood pressure by transcendental meditations. Gasperin (2009) says that the current meta-analysis had an assessment on the psychological effect of tasks that were stressful on increase in blood pressure among adults that were of between eighteen and sixty-four years of age. People showing tremendous increase in blood pressure in the course of the stressful activity (reactivity) and the people who were recovering from the activities (recovery) showed higher probabilities for the development of increased blood pressure or hypertension. Suggestions have been made that constant increased cardiovascular activity can be a contributor to the development of hypertension by aiding vascular remodeling. Such pathophysiological alterations could then change long-term blood pressure regulation by the kidneys thereby shifting to a higher level the set points of blood pressure. Specifically, an increased cardiovascular activity could be a reflection of enhanced vagal withdrawal at the time of stress or hypersensitivity, while poor cardiovascular recovery can be because of reduced vagal tone, prolonged sympathetic activation or delayed or attenuated vagal rebound after stress termination. Furthermore, many studies have indicated associations between various psychosocial variables and inflammation, an increase in clotting of the blood and vascular function and a reduction in fibrinolysis. A study found out that people going through a stressful activity recovered late from blood pressure, showing that it could be a useful blood pressure increase predictor. Besides, during chronic exposures like stress, people get exposed for a period enough for setting off casual process. Those whose age fall between forty-six and sixty-four are twice as likely to develop increase in blood pressure and hypertension than those who are younger (Gasperin, Netuveli, Dias-da-Costa & Pattusi, 2009).

High blood pressure or hypertension is a condition where the arteries have heightened blood pressure consistently. Every instance the heart beats, blood is pumped to the entire body. Blood pressure refers to the force by which the blood is pushed up against the walls of the blood vessels. When the blood pressure is higher, the heart is forced to pump harder. This can lead to organs being damaged or the development of illnesses like stroke, heart failure or heart attack. Suggestions have been put forth that consistent psychological stress can lead to high blood pressure and so lead to the development of hypertension. A study involving more than 3000 young adults indicated that impatience/urgency behavior as well as hostility as assessed in young adulthood was linked strongly to a much higher risk of hypertension fifteen years later. Some other exposures like anxiety and depression were reported as well. Chronic stress caused by financial problems is reported as a prediction of blood pressure 3 years following the follow up. Despite the results not being significant, other methods for fighting stress like biofeedback, stress management training and relaxation has been shown to register positive results. Such therapies can be helpful in reducing blood pressure among patients.

Someone may experience excess demand and pressure outside of the work environment just as they do in at work. I found out that the way someone handles stress away from work like at home is very important in deciding the development of hypertension or undergoing a heart attack. Stress often compiles over a long period because of a host of factors which might not be related in any way to work. Conflicting household and work demands might lead to someone being extremely stressed out. Heightened cortisol levels and cortisol are linked to inflammation, cardiovascular disease and blood pressure, etc.

Module 4 -SLP

Part I: Stress and Weight Gain

On detecting a threat, several chemicals are released by the brain including CRH, cortisol and adrenaline. Adrenaline is crucial in helping an individual not feel hungry since the blood is driven into the large muscles from the internal organs as a preparation for fight/flight. Nonetheless, when the effects go away, the 'stress hormone' - cortisol remains and the body receives a signal to have the food supply replenished. Anxiety can cause this. An increase in adrenaline in a fight/flight situation, we become fidgety. While just a little calorie is burnt because of moving around simply because of restlessness, "emotional eating" is triggered. Consuming unhealthy food or overindulgence as a means of calming down is quite common. People who are stressed chronically crave "comfort foods" like ice cream or potato chips. Such foods are not hard to eat but are high in salt, sugar and fat. The cravings are both psychological and biological. Sleep can also influence weight loss or gain. Inadequate sleep can disrupt leptin or ghrelin functioning -the chemicals that aid in controlling appetite. This means that chronic stress may lead to one getting "visceral fat" in the belly. The belly possesses several cortisol receptors and blood vessels to aid and so ensure the process is smooth. The problem comes because of the unhealthiness of the belly fat and the difficulty of getting rid of it. Stress for a sustained period of time is bad for your weight (Greenberg, 2013).

Part II: Blood Sugar Regulation

Randall (2011) states that cortisol counters insulin through promoting higher levels of blood sugar and also stimulating gluconeogenesis which is the metabolic pathway which synthesizes glucose. Cortisol presence triggers the release of enzymes to useful in gluconeogenesis and so facilitating the rise is production of glucose. Conversely, there is also stimulation of synthesis of glycogen in the liver that lowers net blood sugar levels (11). In such ways, the level of glucose is carefully regulated. Cortisol is beneficial to metabolism: at the time one is fasting - when there is depletion of levels of glucose in the blood, it makes sure the blood is steadily supplied with glucose through gluconeogenesis (Randall, 2011). As per Len Kravitz and Schneider (n.d) besides hypertension and hyperlipidemia, hyperglycemia has been associated with high levels of cortisol. Under conditions of stress, cortisol is capable of giving protein to the body for the production of energy through the process of gluconeogenesis. Amino acids are converted to glucose in this process in the liver (Len Kravitz & Schneider, n.d). Greenberg (2013) states that in case of a threat, a series of chemicals are released. The chemicals include cortisol, CRH and adrenaline. In the short-term adrenaline aids in having the person not to feel as hungry since the blood is flowing away to the large muscles from the internal organs in readiness for fight or flight. A person at this day and age who lounges on the couch worrying about paying the bill or working at his/her desk trying to beat a deadline, doesn't use much of the energy as they deal with the stressor. The body, unfortunately, still undergoes this loop and so the brain will still give instructions that you need the cookie anyway. Stress results in a drop in blood sugar which causes fatigue (Greenberg, 2013).

Part III: Conclusions

Indeed, chronic and acute stress can have severe effects on human health. High stress levels, even in a short period and in varying contexts, cause the same results. Long-term exposure to cortisol because of chronic stress leads to other symptoms like a decrease in thyroid function, impaired cognition as well as accumulation of belly fat, which can also affect the heart. It is apparent that both acute stress episodes and prolonged stressful situations worsens health and they should be both minimized. In extreme cases, Cushing's syndrome which involves alarmingly high levels of cortisol can also result. Individuals suffering from Cushing syndrome gain weight rapidly, and experience hypercalcemia and hyperhidrosis plus other endocrine and psychological problems. Suggestions have been made that chronic psychological stress exposure can result in an increase in blood pressure and so lead to the development of hypertension. Over the short-term, adrenaline is useful in ensuring that a person feels less hungry as he/she prepares for "fight or flight." Nonetheless, on the adrenaline effects wearing off, the stress hormone cortisol hangs around and begins giving signals to the body to replenish supply of food. Prolonged periods of stress when a person has poor coping mechanisms and habits can cause chemical, hormonal and physical imbalances and so resulting in disease or even death if not managed. High levels of cortisol cause storage of fat and relocation of excess circulating fat to the abdomen which can cause obesity.

Reflective Essay

The class assisted me in knowing more of the brain's role in stress response as it determines stress response and also the behavioral and physiological responses that can be either damaging or adaptive. Stress is about communication of the brain with immune, cardiovascular as well as other systems through endocrine and neural mechanisms. This communication is two-way. Besides the response of "fight or flight" to acute stress, there are other responses to stress that take place in everyday life and over time wear the body. But stress hormones give protection to the body in the short-term and promote its adaptation. Brains are stress targets, and the first region of the brain to be recognized as a glucocorticoids target apart from the hypothalamus was the hippocumpus. Stress hormones and stress have both maladaptive and adaptive effects on the hippocampus throughout life. Events occurring early in life influence the entire life of a person. The prefrontal cortex, amygdala and the hippocumpus alters physical and behavioral responses. Stress is a word denoting experiences that are physiologically and emotionally challenging.

The course has allowed me to appreciate the place of stress in activating autonomic nervous system as well as the HPA axis and also the "fight or flight" response in various stressful circumstances. Surviving such circumstances requires stress hormone response. Humans undergo sustained periods of heightened activities and such systems ensure our survival. Such long periods could be caused by anxiety, exposure to unfriendly environment, lifestyle, etc. The course has made me appreciate the significance of these responses as a protective response as well as the possible harm that might result if not properly managed. I now understand how the brain evaluates threats and tailors specific responses to them to protect the body. Also, I have looked into the brain parts which are key in helping in making decisions, and also those responsible for anxiety and memory.

I now understand the effects of stress on human reproductive systems as well as in excretion. Learners are better off when they actively engage with the content instead of just passively absorbing information. Giving learners a chance to experiment and play games reinforces learning. Quizzes and assessments have also helped me absorb the material better. Ultimately, any course is evaluated by the nature of the content. Many times, supplemental content was added unnecessarily and so resulting in bloated course content. A relevancy review should be done and any content that is not specifically relevant ought to be eliminated. Also, more visuals should be used and they should be constructive and help the learners form good attitudes and impressions of the course material. They should be attractive visually and be up date. Visually unattractive material makes the material untrustworthy and harms the learners' experience. There should also be active learning to reinforce the content learned in the course. Active learning involves talking, processing and thinking about the course material (Active Learning, n.d).

The method of measuring progress of the course in future is being aware of the truth that stress profoundly affects my health and so I should try minimizing or avoiding stress to the best of my ability. I will have the ability to identify what is happening in other people's lives when they exhibit responses similar to the ones I have learned. Informing them of what is actually happening and my ability to express that in a way that is easy to understand is a good way of measuring my progress in the course. I have the belief that I have gotten the desired course outcomes even though some of the tasks have been a bit challenging.