Stress in our Lives

 by Felix Roth

What is stress? 

 Often, we tend to view stress as an all encompassing idea. We may think that stress is the cause and effect of stressful things. When looking at stress from a medical perspective and the mechanisms at play, it is vital to break down what stress is, why we get stressed and the discrete mechanisms at play. Stress actually refers to stressors, the action or the anticipation of actions that trigger a stress response. A primitive example of this includes seeing a snake, or thinking about seeing a snake in the wild. The stress response refers to the generalised response that occurs as a result of the stressor. 

Hans Seyle was the first to think about how stress can actually make us sick when observing rats. As an undergraduate, he performed numerous studies on rats, naturally as an undergraduate he spent copious amounts of time chasing the rats around and then prodding them with needles. He observed that these rats developed peptic ulcers adrenal gland enlargement and atrophy of immune tissue. In order to explain what was going on, he injected rats with saline solution, noting that they too had peptic ulcers and damage to other tissue. He had just noted the effects of an excessive stress response. 

I use the word excessive as the stress response is actually vital. In vertebrates the stress response has evolved in order to move all energy stores to immediate action in the form of muscular activity as part of the flight of flight mechanism. Examples of this include, increased blood pressure and heart rate, more acute memory recall and improvement of dexterity. As such long term projects such as growth, long term memory and digestion are halted with little to no energy being directed their way. 

Why is stress vital to living and what happens to those who lack proper stress response? 

 As previously mentioned, the basis of the vertebrae stress response is the direction of energy towards muscular action. Developing a stress response allowed those who experienced a risk to make best use of energy stores in their body, energy that they can make up at a later date. The stress response is based around the sympathetic and parasympathetic nervous system. The sympathetic nervous system controls flight, fight, feeding and sexual activity. The parasympathetic nervous does everything else and it important to understand that they inhibit one another. If the heart rate is brought up by the sympathetic nervous system, the parasympathetic nervous system is responsible for bringing it down. 

Firstly when the sympathetic nervous system is activated as part of the stress response, corticotropin releasing hormone (CRH) is released by the hypothalamus. CRH in turn triggers the release of ACTH in the pituitary gland which in turn prompts the adrenal glands to release glucocorticoids. As we will see in a minute, the levels of glucocorticoids can wreak havoc on bodily systems when in excess. This simple mechanism is the generalised stress response, a mechanism that will occur every single time anyone of us is exposed to a stressor. This response is key to life as it not only occurs when one of us sees a snake when walking , but in minute quantities when carrying out every other aspect of our lives. 

Being exposed to excessive stress response can almost certainly cause Ill health however not having a working stress response may prove to be fatal. In Addison’s disease patients are unable to secrete one class of stress hormones. They exhibit perfectly normal characteristics until they experience a major stressor such as car crash, Falling into an addisonian crisis where their blood pressure drops, they are unable to maintain circulation and eventually go into shock. Moreover In Shy-Drager syndrome, secretion of another stress hormone is impaired, patients find it hard to stand up, experience severe drops in blood pressure and rip muscles in pursuit of this simple task. 

Stress and weight gain and loss 

When stressed, some of us may have our appetites interrupted. This is thanks to the chemicals at play in the stress response. When released, CRH not only acts as a chemical that prompts the pituitary gland to release ACTH but actually suppresses appetite. Glucocorticoids, released by the adrenal glands however serve to increase appetite. The differing effects of CRH and glucocorticoids are better understood when observing the time that each spends in the blood stream. CRH may persist for up to 15 minutes in the bloodstream however glucocorticoids can take hours to be banished. As such, glucocorticoids’ appetite increasing powers ensure that an animal that has been in a fight or used energy stores, replenishes them by way of eating. The appetite suppressing powers of CRH ensure that the animal is not craving food in a life or death situation. 

Those more prone to intermittent bouts of stress will be seen to be hyperphagic, meaning they crave food as a result of stress. Those more prone to literal 24/7 stress are determined to be hypophagic as the constant release of CRH suppresses their appetite during the entirety of the stress response. Weight gained as a result of hyperphagia has a propensity to be stored as visceral fat. Therefore, those who are prone to frequent intermittent bouts of stress and therefore hyperphagia, will be gaining visceral fat, fat commonly associated with increased risks of type 2 diabetes and cardiovascular disease. 

Stress and the immune system 

Stress and the immune system have been intensively studies over the last 75 years. The immune system a long term project is not however found to have decreased activity as a result of the stress response. The stress response actually increases the activity of the immune system. More antibodies are sent to sites of infiltration and generic antibodies are released into the saliva in preparation for a potential wound or injury. 

Seyle was the man to coin the theory that excess stress caused sickness and he was correct. Excessive stress suppresses the formation of new lymphocytes, shortens the time pre existing lymphocytes stay in circulation, inhibits the production of new antibodies, disrupts communication among lymphocytes, inhibits rate immune response and suppresses inflammation. Moreover glucocorticoids, released as a result of the stress response, cause the shrinking of the thymus gland and actually kill lymphocytes. Those with excessive stress are at an increased risk of developing autoimmune diseases, due to an over activation of the immune response as a result of the stress response. 

Glucocorticoids are required to bring the immune function back to normal levels after the increased activity. This can be demonstrated in three ways, 1. Subject low glucocorticoid level rats to stress, immune function increases but never decrease . 2. When removing one adrenal gland from a patient, glucocorticoids levels are halved, during period of decreased glucocorticoid level, patient is much more likely to experience flair up and autoimmune disease. 3. Rats or weird chickens suffering from autoimmune diseases usually have a problem with their glucocorticoid system that has lower levels than normal. 

In summary the stress response actually stimulates the activity of the immune system in preparation for potential injuries however the cause of stress related immune diseases are found in relation to excess glucocorticoid levels. As such the immune function does not return to normal levels but is actually suppressed below normal levels, increasing the risk of ill health through secondary illnesses. 

Stress and sleep 

Sleep consists of two stages, rapid eye movement (REM) and non rapid eye movement sleep (NREM). Whilst in REM sleep, dreaming occurs with the limbic system’s metabolic rate increasing. The limbic system is the part of the brain responsible for controlling emotions. During NREM sleep, energy restoration and memory consolidation occurs. Vitally, the activity of the sympathetic nervous system also decreases during NREM sleep in accordance with glucocorticoid levels. In this way, sleep or sleep deprivation functions as a stressor as glucocorticoid levels never decrease, allowing sex and growth hormones to not be replenished. 

When Kei Cho of Bristol University studied flight attendants from two different airlines who differed in recovery time, it was found that the temporal lobe, where the hippocampus is located, was significantly smaller in the flight attendants who had less recovery time. The stressor of sleep deprivation had manifested into a serious cause for concern. 

Not only can sleep deprivation act as a stressor but stress can cause sleep deprivation. CRH triggers the release of ACTH from the pituitary gland but also acts as a neurotransmitter for fear, anxiety and arousal pathways in the brain, only serving to restrict the quality of one’s sleep. Rats injected with CRH have incredibly difficult times sleeping and studies investigating poor sleepers often found that high levels of glucocorticoids and increased activation of the sympathetic nervous system was common among the sleepers. Lastly, when CRH disrupts sleep, NREM is the stage of sleep found to be affected the most. The stage of sleep is vital to rest and recuperation. 

Stress and pain 

As with appetite, the effects of stress on pain has multiple manifestations. It is first important to understand a simplified version of pain. Pain is modulated by two neurons, X and Y. When a fast fibres is triggered, when you prick your finger on a needle, the nerve impulse is sent along X and then Y, however as soon as Y fires it inhibits the action of X stopping the pain from pressing. Slow fibres that carry throbbing pains inhibit Y allowing X to fire continuously. 

As with a multitude of mechanisms, stress throws all of this out the window and terrorises this system. Analgesia is the lessening of pain perception due to stress and hyperalgesia is the hyperactivity in response to pain. Those with more neurotic personalities are more susceptible to hyperalgesia with hyperalgesia being induced by emotional stressors. Physical stressors however tend to induce analgesia. We see this infamously in war as soldiers suffering from brutal injuries function normally as if the wounds are not present. 

Managing the stress response

The stress response is a generalised response to stressors. In this way, treatment can be generalised as well. 

Whilst there may be many coping and management strategies for stress, I would like to focus on four; 1. Outlets for frustration, 2 . Social networks, 3. Predictability and 4. Control. 

Firstly, the stress response is built around the release of energy. In this way, outlets for frustration allow us to use this energy. Rats who were able to gnaw or bite other rats and run on treadmills had significantly decreased stress responses. In this way, we should use exercise to relieve stress. 

Secondly, social networks are crucial to dealing with stress. Baboons who have a good social network where they play with children and have non sexual grooming bouts had decreased glucocorticoid levels. Moreover, the stress response of public speakers was severely decreased when friends were present. As such we should endeavour to use friends and social networks to manage our stress response. 

When rats were given the luxury of a warning bell before a series of shocks, their incidence of ulcers was significantly less than those who did not receive the warning. Moreover, rats who received a set amount of food at random intervals had a more activated stress response than those who received food at set intervals. Moreover, during the blitz, there was a far higher incidence of ulcers in the suburbs where bombing was sporadic than in London were bombing was routine. Hence, predictability should be emulated when managing our stress response. 

Lastly, control or a perception of control only aids in the management of stress. Rats given a lever to lessen shocks only to have the lever taken away exhibited a massive spike in their stress response. Even when they were given a disconnected lever, the rat’s perceived control lowered their stress response. 

In conclusion, we should endeavour to manage stress through generalised practices, taking advantage of the physiologically mediated nature of the stress response.