Stress – The Effects of Stress on Your Body

Stress is a feeling of emotional or physical tension. It can come from any event or thought that makes you feel frustrated, angry, or nervous. Stress is your body’s reaction to a challenge or demand. In short bursts, stress can be positive, such as when it helps you avoid danger or meet a deadline.

The Stress Response

The body’s stress response is mediated by the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis.

Key Points

A complex interaction of direct influences and indirect feedback mechanisms among the SNS, the hypothalmus, the pituitary gland, and the adrenal glands contributes to the neuroendocrine regulation involved in reactions to stress and other processes.

The SNS is known for its role in mediating the fight-or-flight response. This response is also referred to as the sympatho-adrenal response.

Glucocorticoids of the HPA axis have many important functions, but in excess they may be damaging. Researchers have hypothesized that the hormonal changes brought on by stress may contribute to the neural atrophies seen in many neurodegenerative disease states.

The body’s stress response is mediated by the interplay between the sympathetic nervous system (SNS) and the hypothalmic-pituitary-adrenal (HPA) axis. A complex interaction of direct influences and indirect feedback mechanisms among the SNS, the hypothalmus, the pituitary gland and the adrenal glands contributes to the neuroendocrine regulation involved in reactions to stress.

This is a diagram of the mechanism of stress and stress response in the HPA axis. The hypothalamus secretes corticotropin releasing hormone and the anterior pituitary responds by releasing adrenocortictotropic hormone, that causes the adrenal cortex to activate a physical response.

Mechanism of stress and stress response: The hypothalmic-pituitary-adrenal (HPA) axis is an endocrine cascade that mediates several aspects of physiological stress, including responses to acute stressors (i.e., fight-or-flight response) but it also causes chronic stress.

Sympathetic Component

The SNS plays a key role in mediating the neural response to stress known as the fight-or-flight response. This response is also referred to as the sympatho-adrenal response of the body owing to the fact that the preganglionic sympathetic fibers that end in the adrenal medulla secrete acetylcholine, which activates the release of adrenaline and noradrenaline from the medulla.

This response acts primarily on the cardiovascular system and is mediated directly via impulses transmitted through the sympathetic nervous system and indirectly via catecholamines, such as the adrenaline secreted from the adrenal medulla.

HPA Axis Component

A feedback loop exists among the components of the HPA axis and the SNS. The paraventricular nucleus of the hypothalmus contains neuroendocrine neurons that synthesize and release vasopressin —a hormone that acts in the HPA axis as a vasoconstrictor—and corticotropin releasing hormone (CRH).

These two hormones regulate the anterior lobe of the pituitary gland and stimulate the release of adrenocorticotropic hormone (ACTH), also known as corticotropin. ACTH acts on the adrenal cortices that produce glucocorticoid hormones, like cortisol, which is a stress hormone that exerts many effects throughout the body. In the brain cortisol acts on both mineral corticoid and glucocorticoid receptors that are expressed by many different types of neurons.

CRH and vasopressin are released from nerve terminals. CRH gets transported to the anterior pituitary through the circulatory system and vasopressin is transported by axonal transport to the anterior pituitary. There, CRH and vasopressin act to stimulate the secretion of ACTH from the cells where it is synthesized. ACTH is then transported through the circulatory system to the adrenal cortex where it promotes the biosynthesis of corticosteroids like cortisol and cholesterol.

Glucocorticoids of the HPA axis have many important functions, including the modulation of stress reactions, but in excess they may be damaging. Researchers have hypothesized that the hormonal changes brought on by stress may contribute to the neural atrophies seen in many neurodegenerative disease states.

The Fight-or-Flight Response

The fight-or-flight response is regulated by the release of adrenaline or noradrenaline.

Key Points

The fight-or-flight response refers to the physiological changes made by the body upon sensing a threat.

Major events in the fight-or-flight response include the secretion of cortisol, adrenaline, and noradrenaline from the adrenal gland.

Immediate physiological changes are induced, including acceleration of heart and lung activity, inhibition of digestive activity, shaking, tunnel vision, and loss of hearing.

Physiological changes return to normal following removal of the threat, however some long-term stress illnesses exist where falsely detected threats can induce long-term or repeated fight-or-flight episodes.

Key Terms

noradrenaline: Also known as norepinephrine, it is a key hormone in the fight-or-flight response.

adrenaline: Also known as epinephrine it is a key hormone in the fight-or-flight response.

catecholamine: Any of a class of hormones produced by the adrenal gland.

The fight-or-flight response (also called the acute stress response ) was first described by Walter Bradford Cannon. His theory states that animals react to threats with a general discharge of the sympathetic nervous system, priming the animal for fighting or fleeing. This response was later recognized as the first stage of a general adaptation syndrome that regulates stress responses among vertebrates and other organisms.

Upon sensing a threat the brain stimulates the hypothalamus to secrete corticotropin-releasing hormone that induces
adrenocorticotropic hormone from the pituitary to stimulate the release of cortisol from the adrenal cortex to increase blood sugar levels in preparation for fight or flight.

Simultaneously, the adrenal gland also releases catecholamine hormones, such as adrenaline or noradrenaline, into the blood stream. Numerous hormone receptors exist around the body that allow for an immediate, systemic physiological response that can include the following:

  • Acceleration of heart and lung action
  • Paling or flushing, or alternating between both
  • Inhibition of stomach and upper-intestinal action to the point where digestion slows down or stops
  • General effect on the sphincters of the body
  • Constriction of the blood vessels in many parts of the body
  • Liberation of nutrients (particularly fat and glucose) for muscular action
  • Dilation of the blood vessels for muscles
  • Inhibition of the lacrimal gland (responsible for tear production) and salivation
  • Dilation of the pupil (mydriasis)
  • Relaxation of the bladder
  • Inhibition of an erection
  • Auditory exclusion (loss of hearing)
  • Tunnel vision (loss of peripheral vision)
  • Disinhibition of spinal reflexes
  • Shaking

The fight-or-flight response: A diagrammatic representation of the fight-or-flight response.

The stress response halts or slows down various processes, such as sexual responses and digestive systems, to focus on the stressor situation. This typically causes negative effects like constipation, anorexia, erectile dysfunction, difficulty urinating, and difficulty maintaining sexual arousal. These are functions that are controlled by the parasympathetic nervous system and are therefore suppressed by sympathetic arousal.

Prolonged stress responses may result in chronic suppression of the immune system, leaving the body open to infections. However, a short boost to the immune system shortly after the fight-or-flight response is activated has been described. Some think that this may have filled an ancient need to fight the infections in a wound that one may have received during interaction with a predator.

Stress responses are sometimes a result of mental disorders, such as post-traumatic stress disorder (in which the individual shows a stress response when remembering a past trauma) and in panic disorder (in which the stress response is activated by the catastrophic misinterpretations of bodily sensations).

The Resistance Reaction

Resistance is the second stage of the general adaptation syndrome, where the body has an increased capacity to respond to the stressor.

Key Points

Resistance is the second stage of the general adaptation syndrome.

During this stage the body has increased capacity to respond to the stressor.

Due to high energetic costs, the body cannot maintain high levels of resistance to stress forever, and if the stressor persists the body may advance into exhaustion.

This describes how a body reacts to a stressor, real or imagined, in the short term and long term.

Stress typically describes a negative concept that can have an impact on one’s mental and physical well-being, but it is unclear what exactly defines stress and whether or not stress is a cause, an effect, or the process connecting the two. With organisms as complex as humans, stress can take on entirely concrete or abstract meanings with highly subjective qualities, satisfying definitions of both cause and effect in ways that can be both tangible and intangible.

Physiologists define stress as how the body reacts to a stressor (any stimulus that causes stress), real or imagined. Acute stressors affect an organism in the short term; chronic stressors over the long term.

Alarm Stage

Alarm is the first stage, which is divided into two phases: the shock phase and the anti-shock phase.

Shock Phase

During this phase, the body can endure changes such as hypovolemia, hypoosmolarity, hyponatremia, hypochloremia, and hypoglycemia—the stressor effect. The organism’s resistance to the stressor drops temporarily below the normal range and some level of shock (e.g., circulatory shock) may be experienced.

Anti-Shock Phase

When the threat or stressor is identified or realized, the body starts to respond and is in a state of alarm. During this stage, the locus coeruleus/sympathetic nervous system is activated and catecholamines such as adrenaline are produced to create the fight-or-flight response.

The result is: increased muscular tonus, increased blood pressure due to peripheral vasoconstriction and tachycardia, and increased glucose in blood. There is also some activation of the HPA axis, producing glucocorticoids such as cortisol.

Resistance Stage

Resistance is the second stage and the increased secretion of glucocorticoids plays a major role by intensifying the systemic response. This response has lypolytic, catabolic, and antianabolic effects: increased glucose, fat and amino acid/protein concentration in blood.

Moreover, these effects cause lymphocytopenia, eosinopenia, neutrophilia, and polycythemia. In high doses, cortisol begins to act as a mineralocorticoid (aldosteron) and brings the body to a state similar to hyperaldosteronism.

If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.

Exhaustion or Recovery Stage

The third stage is either exhaustion or recovery.

Exhaustion

Exhaustion is the depletion and inability to maintain normal function and often results in physical illness.

Key Points

During the exhaustion phase the body’s resources are completely depleted and the body is unable to maintain normal function.

Initial autonomic nervous system symptoms may reappear.

If the exhaustion stage is extended, long-term damage may result.

Key Terms

  • decompensation: The inability of a diseased or weakened organic system or organ to compensate for its deficiency, which then results in functional deterioration.

Physiologists define stress as how the body reacts to a stressor (a stimulus that causes stress), real or imagined. Acute stressors affect an organism in the short term; chronic stressors over the long term.

Alarm

,

The alarm is the first stage. When the threat or stressor is identified or realized, the body’s stress response is in a state of alarm. During this stage, adrenaline will be produced in order to bring about the fight-or-flight response. The organism’s resistance to the stressor drops temporarily below the normal range and some level of shock may be experienced.

Resistance

Resistance is the second stage. If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.

Exhaustion

Exhaustion is the third and final stage in the general adaptation syndrome model. At this point, all of the body’s resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.).

If stage three is extended, long-term damage may result, as the body’s immune system becomes exhausted, and bodily functions become impaired and result in decompensation. The result can manifest itself in obvious illnesses such as ulcers, depression, diabetes, trouble with the digestive system, or even cardiovascular problems, along with other mental illnesses.

Stress and Disease

Over-activation of the stress response can result in pathology and disease.

Key Points

Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after exposure to psychological trauma.

While cortisol release typically facilitates increased memory, chronic exposure leads to hippocampal damage that can lead to memory loss.

Clinical depression is characterized by an increased HPA- axis function, primarily through a decrease in the normal negative feedback of the system.

Additionally, clinical depression is associated with lower serotonin and noradrenaline levels.

Excessive production of cortisol has been correlated with an increased risk of heart disease.

Key Terms

  • post-traumatic stress disorder: A serious condition that develops following an intensely stressful situation or event.

Exhaustion is the third and final stage in the general adaptation syndrome model. At this point, all of the body’s resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.).

If stage three is extended, long-term damage may result, as the body’s immune system becomes exhausted, and bodily functions become impaired and result in de-compensation. The result can manifest itself in obvious illnesses such as ulcers, depression, diabetes, trouble with the digestive system, or even cardiovascular problems, along with other mental illnesses.

Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. Diagnostic symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased arousals, such as difficulty falling or staying asleep, anger, and hypervigilance.

This is an illustration of the brain with its regions in associated with stress and PTSD highlighted. The regions are the prefontal cortex, the medial prefrontal cortex, the ventromedial prefrontal cortex, and the amygdala.

Regions of the brain associated with stress and PTSD: Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after exposure to psychological trauma.

Sensory input, memory formation, and stress response mechanisms are affected in patients with post-traumatic stress disorder. The regions of the brain involved in memory processing that are implicated in PTSD include the hippocampus, amygdala, and frontal cortex, while the heightened stress response is likely to involve the thalamus, hypothalamus, and locus coeruleus.

There is consistent evidence from MRI volumetric studies that hippocampal volume is reduced in post-traumatic stress disorder. This atrophy of the hippocampus is thought to represent decreased neuronal density.

However, other studies suggest that hippocampal changes are explained by whole-brain atrophy, and generalized white matter atrophy is exhibited by people with PTSD.

Memory

Cortisol works with epinephrine (adrenaline) to create memories of short-term emotional events; this is the proposed mechanism for the storage of flashbulb memories and may originate as a means to remember what to avoid in the future.

However, long-term exposure to cortisol damages cells in the hippocampus, which results in impaired learning. Furthermore, it has been shown that cortisol inhibits memory retrieval for already stored information.

Depression

Many areas of the brain appear to be involved in depression, including the frontal and temporal lobes and parts of the limbic system, including the cingulate gyrus. However, it is not clear if the changes in these areas cause depression or if the disturbance occurs as a result of the etiology of psychiatric disorders.

The Hypothalamic-Pituitary-Adrenal Axis in Depression

In depression, the hypothalamic-pituitary-adrenal (HPA) axis is up-regulated by a down-regulation of its negative feedback controls. The corticotropin-releasing factor is over-secreted from the hypothalamus and induces the release of adrenocorticotropin hormone (ACTH) from the pituitary.

ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands. Adrenal hypertrophy can also occur due to this repeated stimulation. The release of cortisol into the circulatory system has a number of effects, including the elevation of blood glucose.

The negative feedback of cortisol to the hypothalamus, pituitary and immune systems is impaired. This leads to continual activation of the HPA axis and excess cortisol release. The cortisol receptors then become desensitized, which causes an increase in the activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.

Serotonin Pathways in Depression

Serotonin transmission from both the caudal raphe nuclei and rostral raphe nuclei is reduced in patients with depression compared with non-depressed controls. Increasing the levels of serotonin in these pathways by reducing serotonin re-uptake, hence increasing serotonin function, is one of the therapeutic approaches to treating depression.

The Noradrenaline Pathways in Depression

In depression, the transmission of noradrenaline is reduced from both of the principal noradrenergic centers. An increase in noradrenaline in the frontal/prefrontal cortex modulates the action of selective noradrenaline re-uptake inhibition and improves mood. Increasing noradrenaline transmission to other areas of the frontal cortex modulates attention.

Heart Disease

Excessive cortisol release also has a negative impact on heart health. High levels of cortisol correlate with an increased risk of heart disease. This is due to the increases in blood sugar and blood pressure levels that cortisol imparts along with it’s pro-inflammatory effects.

Ways to manage stress

If you take practical steps to manage your stress, you may reduce the risk of negative health effects. Here are some tips that may help you to cope with stress:

  • Be observant. Recognize the signs of your body’s response to stress, such as difficulty sleeping, increased alcohol and other substance use, being easily angered, feeling depressed, and having low energy.
  • Talk to your health care provider or a health professional. Don’t wait for your health care provider to ask about your stress. Start the conversation and get proper health care for existing or new health problems. Effective treatments can help if your stress is affecting your relationships or ability to work.
  • Get regular exercise. Just 30 minutes per day of walking can help boost your mood and improve your health.
  • Try a relaxing activity. Explore relaxation or wellness programs, which may incorporate meditation, muscle relaxation, or breathing exercises. Schedule regular times for these and other healthy and relaxing activities.
  • Set goals and priorities. Decide what must get done now and what can wait. Learn to say “no” to new tasks if you start to feel like you’re taking on too much. Try to be mindful of what you have accomplished at the end of the day, not what you have been unable to do.
  • Stay connected. You are not alone. Keep in touch with people who can provide emotional support and practical help. To reduce stress, ask for help from friends, family, and community or religious organizations.
  • Consider a clinical trial. Researchers at the National Institute of Mental Health (NIMH) and other research facilities across the country are studying the causes and effects of psychological stress as well as stress management techniques. You can learn more about studies that are recruiting by visiting Join a Study or ClinicalTrials.gov (keyword: stress).

How can you help yourself?

  • Recognize when stress is a problem – It’s important to connect the physical and emotional signs you’re experiencing to the pressures you are faced with. Don’t ignore physical warning signs such as tense muscles, tiredness, headaches, or migraines. Think about what’s causing your stress. Sort them into issues with a practical solution, things that will get better with time, and things you can’t do anything about. Take control by taking small steps towards the things you can improve. Make a plan to address the things that you can. This might involve setting yourself realistic expectations and prioritizing essential commitments. If you feel overwhelmed, ask for help and say no to things you can’t take on.
  • Review your lifestyle – Are you taking on too much? Could you hand over some things to someone else? Can you do things in a more leisurely way? You may need to prioritize things and reorganize your life so you’re not trying to do everything at once.
  • Build supportive relationships – Find close friends or family who can offer help and practical advice that can support you in managing stress. Joining a club or a course can help to expand your social network and encourage you to do something different. Activities like volunteering can change your perspective and have a beneficial impact on your mood.
  • Eat healthily – A healthy diet can improve your mood. Getting enough nutrients (including essential vitamins and minerals) and water can help your mental wellbeing.
  • Be aware of your smoking and drinking – Cut down or cut out smoking and drinking if you can. They may seem to reduce tension but actually make problems worse. Alcohol and caffeine can increase feelings of anxiety.
  • Exercise – Physical exercise can help manage the effects of stress by producing endorphins that boost your mood. Even a little bit of physical activity can make a difference, such as walking for 15-20 minutes three times a week.
  • Take time out – Take time to relax and practice self-care, where you do positive things for yourself. Striking a balance between responsibility to others and responsibility to yourself is vital in reducing stress levels.
  • Be mindful – Mindfulness meditation can be practiced anywhere at any time. Research has suggested it can be helpful for managing and reducing the effect of stress and anxiety.
  •  Get some restful sleep – If you’re having difficulty sleeping, you can try to reduce the amount of caffeine you consume and avoid too much screen time before bed. Write down a to-do list for the next day to help you prioritize, but make sure you put it aside before bed.
  • Don’t be too hard on yourself – Try to keep things in perspective and don’t be too hard on yourself. Look for things in your life that are positive and write down things that make you feel grateful.

References

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