Hormones 3: Roles of hormones in stress and growth Flashcards
How and why do different factors influence our response to stress?
How convincing is the evidence that stress affects our physical health?
THINK!
Essay plan:
# * Define stress *
Define stress
A process in which an ‘agent exerts a force on an object’. Stressor: a stimulus that challenges the body’s homeostasis and triggers arousal in humans and animals. Stress responses: Physiological: e.g. increase in heart rate, breathing, decrease in digestive activity, elevated blood pressure, excessive sweating. Behavioural: e.g. social phobia, avoidance, insomnia, obsessive compulsive disorders. Is stress good or bad? –‘Good’ à arousal, e.g. in competitions or if moderate before a performance –Bad if it is strong or constant, in which case it can be debilitating. When does it occur –In presence of a stress-inducing incident or condition (loud noise, traffic, close spaces, social/family demands) –Even in absence of an obvious stressor (thoughts or memory of real stressors). Same physiological response irrespective of the stressor (exciting or frightening). Thanks to the work of our sympathetic nervous system, the “fight or flight” system that takes over when we’re stressed. Behind the wide range of both physical and mental reactions to stress are a number of hormones that are in charge of adding fuel to the fire.
Stress causes a surge of hormones in your body. These stress hormones are released to enable you to deal with pressures or threats – the so-called “fight or flight” response. Once the pressure or threat has passed, your stress hormone levels will usually return to normal. However, if you’re constantly under stress, these hormones will remain in your body, leading to the symptoms of stress.
This essay shall outline models of stress and discuss evidence supporting the facts that stress affects our physical health.
First described stress in the 1950’s: Hans Selye
In the 1950’s, Selye suggested that in the short term, stress helped the animal deal with the environment but long term exposure to stress is maladaptive. He attributed stress to the anterior pituitary-adrenal cortex-system (HPA) which releases glucocorticoids, stress hormones, into the blood stream. This, along with the autonomic nervous system represent the current 2 system view of stress. Both the Hypothalamic–pituitary–adrenal axis (HPA) and autonomic nervous system (ANS) interact to stimulate body organs to prepare the body for the infamous fight or flight response. Selye’s general adaptive syndrome posits we encounter aversive stimuli to which the ANS is activated and glucocorticoids hormones secreted, there then becomes a stage of resistance in which the parasympathetic nervous system returns some functions to normal but the body is still on-alert. If the stressor persists, there becomes a stage of exhaustion in which the individual becomes susceptible to disease. Therefore stress does not automatically lead to dysfunction and illness.
His last inspiration for general adaptation syndrome (GAS, a theory of stress) came from an endocrinological experiment in which he injected mice with extracts of various organs. He at first believed he had discovered a new hormone, but was proved wrong when every irritating substance he injected produced the same symptoms (swelling of the adrenal cortex, atrophy of the thymus, gastric and duodenal ulcers). This, paired with his observation that people with different diseases exhibit similar symptoms, led to his description of the effects of “noxious agents” as he at first called it. He later coined the term “stress”. He empathised stress with a dual nature, in short term it helps respond to a stressor (e.g. mobilisation of energy resources), however, in the long term in produces changes that are maladaptive (e.g. enlarged adrenal glands). The major theory in Selke’s landmark theory is its assertion that both physical and psychological stressors induce the same general stress response.
Ursin et al (1978) studied trainee parachutists jumping on a wire from a 12m tower.
The magnitude of the stress response depends on the stressor and the strategies individuals adopt to cope with the stress. For example, Ursin et al (1978) studied trainee parachutists jumping on a wire from a 12m tower. Various glucocorticoids such as epinephrine and norepinephrine were above normal level on the first day of jumping, but rapidly turned to control levels with each subsequent jump as the trainees were learning to control and predict the situation.If one has no control and predictability over a situation, the high levels of glucocorticoids can have many physical effects on the body, are being Gastric Ulcers. Gastric Ulcers are painful lesions in the stomach and duodenum, which in extreme cases can be life threatening.
Weis (1971) yoked two rats together and delivered electric shocks to both when a signal sounded.
Weis (1971) yoked two rats together and delivered electric shocks to both when a signal sounded. One rat could run in a wheel to avoid the shocks and in doing so also stop the other rat from being shocked. As the wheel running rat was not reliable in running to avoid electric shocks, the other rat had many more gastric lesions. This was due to the fact the rat had no control, but also no predictability of when it would be shocked. Therefore the stress the rat felt had profound ill affects on its physical health. He was found that a bacteria called H. Pylori was a cause of stomach ulcers however although the majority of patients with ulcers have this bacteria, so do 75% of healthy individuals. Therefore other factors relating to the stress outcome must also be influential in affecting our physical health. One factor implicated is cognitive appraisal.
Lazarus & Folkman (1984) suggest 2 stages of cognitive appraisal in regards to stress.
Lazarus & Folkman (1984) suggest 2 stages of cognitive appraisal in regards to stress. The first is to evaluate the threat and the 2nd is to assess whether one has the resources to cope (overcome or prevent harm). Kasaba (1979) studied business executives and the effects of long term stress. Results showed those individuals that appraised stressors as challenges coped with stress better and did not suffer from ill health as a result. Therefore, there is evidence that stress and poor cognitive appraisal can increase susceptibility to disease and this is studied in psychoneuroimmunology.
Psychoneuroimmunology
Psychoneuroimmunology is the study of interactions among psychological factors such as those outlined above, the nervous system and the immune system. In the immune system, adrenal steroids suppress swellings of injuries in order for the animal to remain mobile during threat. Only once it is safe does healing begin. However, if one remains stressed, healing can be compromised.
This was shown in a study by Marucha et al (1998).
This was shown in a study by Marucha et al (1998). A small wound was placed on a hard palate of 11 dental students during the summer holidays and healing was monitored. A second wound was placed on the opposite side 3 days before an exam. Healing took 40%longer 3 days before an exam in response to the stress participants were encountering. Similarly stress is correlated to ill physical health even for colds. Cohen (1998) exposed individuals to 1 of 2 cold viruses and found although 84% became infected, only 40% developed a cold. Those who did had an average endured more chronic stressors for at least a month compared to those who did not. Even though other factors such as smoking and poor sleep contributed to the chances of developing cold, this study shows strong support for the fact stress affects our physical health.
Psychoneuroimmunology: Then and Now: Fleshner and Laudenslager, 2004
It was found that brief stressors produce physiological reactions that participate in the body’s inflammatory responses. Most notably, brief stressors produce increase in blood levels of cytokines, a group of peptide hormones that are released to many cells and participate in a variety of physiological and immunological responses, causing inflammatory and fever. The cytokines are now classified with the adrenal hormones as major stress hormones. Abstract: Today, we recognize that the highly complex immune system interacts with an equally complex nervous system in a bidirectional manner. Evolutionarily old signals continue to play a role in these communications, as do mechanisms for protection of the host. The disparity between physical and psychological stressors is only an illusion. Host defense mechanisms respond in adaptive and meaningful ways to both. The present review will describe a new way of thinking about evolutionarily old molecules, heat shock proteins, adding to a body of evidence suggesting that activation of the acute stress response is a double-edged sword that can both benefit and derail optimal immunity.
Organizational vs activating effects:
Organizational effects: Semi- or permanent changes in the structure of part of the nervous system. When? During ‘’sensitive periods’’ in early development. How? Steroids hormones cross cell membrane and act on cell’s DNA to influence the production of proteins. Activating effect: A transient change in the properties of cells. When? Any time a hormone occupies a cell’s receptor. How long? For as long as a hormone is present at a cell or a short time after its removal. The structure of the hormone is unchanged.
Adrenaline:
What It Is: Commonly known as the fight or flight hormone, it is produced by the adrenal glands after receiving a message from the brain that a stressful situation has presented itself. What It Does: Adrenaline, along with norepinephrine (more on that below), is largely responsible for the immediate reactions we feel when stressed. Along with the increase in heart rate, adrenaline also gives you a surge of energy – which you might need to run away from a dangerous situation – and also focuses your attention.
Norepinephrine:
What It Is: A hormone similar to adrenaline, released from the adrenal glands and also from the brain. What It Does: The primary role of norepinephrine, like adrenaline, is arousal. “When you are stressed, you become more aware, awake, focused,” he says. “You are just generally more responsive.” It also helps to shift blood flow away from areas where it might not be so crucial, like the skin, and toward more essential areas at the time, like the muscles, so you can flee the stressful scene. Although norepinephrine might seem redundant given adrenaline (which is also sometimes called epinephrine), a type of backup system.
Cortisol:
What It Is: A steroid hormone, commonly known as the stress hormone, produced by the adrenal glands. What It Does: It takes a little more time – minutes, rather than seconds – for you to feel the effects of cortisol in the face of stress. because the release of this hormone takes a multi-step process involving two additional minor hormones. First, the part of the brain called the amygdala has to recognize a threat. It then sends a message to the part of the brain called the hypothalamus, which releases corticotropin-releasing hormone (CRH). CRH then tells the pituitary gland to release adrenocorticotropic hormone (ACTH), which tells the adrenal glands to produce cortisol. Whew! In survival mode, the optimal amounts of cortisol can be life saving. It helps to maintain fluid balance and blood pressure, while regulating some body functions that aren’t crucial in the moment, like reproductive drive, immunity, digestion and growth. But when you stew on a problem, the body continuously releases cortisol, and chronic elevated levels can lead to serious issues. Too much cortisol can suppress the immune system, increase blood pressure and sugar, decrease libido, produce acne, contribute to obesity and more. Of course, estrogen and testosterone are also hormones that affect how we react to stress, as are the neurotransmitters dopamine and serotonin. But the classic fight-or-flight reaction is mostly due to the three major players mentioned above.
Sex Differences in Endocrine and Psychological Responses to Psychosocial Stress in Healthy Elderly Subjects and the Impact of a 2-Week Dehydroepiandrosterone Treatment; Kudielka, et al 1998
Abstract: Evidence from animal as well as human studies has suggested that significant sex differences exist in hypothalamus-pituitary-adrenal axis (HPA) activity. As gonadal steroids could be important modulators of HPA sex differences, stress responses were investigated in subjects of advanced age after dehydroepiandrosterone (DHEA) or placebo treatment. After a 2-week treatment with 50 mg DHEA daily or placebo, 75 men and women (mean age, 67.6 yr) were exposed to the Trier Social Stress Test (TSST). The TSST is a brief psychosocial stress that consists of a free speech and mental arithmetic task in front of an audience. The results show that the TSST induced significant increases in ACTH, salivary free cortisol, total plasma cortisol, norepinephrine, and heart rates (all P < 0.0001) as well as decreased positive affect in the elderly (P = 0.0009). Men showed larger stress responses in ACTH (P = 0.004), salivary free cortisol (P = 0.044), and plasma total cortisol (P = 0.076) compared to women. No sex differences were observed in norepinephrine, epinephrine, or heart rate responses. In contrast to ACTH and cortisol response differences, women reported that they were significantly more stressed by the TSST than men (P = 0.0051). Women treated with DHEA showed ACTH stress responses similar to those of men, but significantly enhanced compared to those of women taking placebos (P < 0.009). No other stress response differences emerged between DHEA and placebo groups. Finally, DHEA treatment did not result in an improvement of subjective well-being. We conclude that elderly men show larger HPA responses than women to psychosocial stress, as studied in the TSST. Estrogen effects on hypothalamic CRF-producing neurons might be responsible for these sex differences.
Fast and slow acting stress responses
Activating a stress response: 1.Body mobilizes its resources 2.Deals with the challenge psychologically and behaviourally 3.Then it shuts down the stress response. Fast acting: (A) Nervous system response: sympathetic pathway (autonomic nervous system) (B) Hormonal response: adrenaline and noradrenaline (from adrenal medulla). Actions: (fight or flight) Cell metabolism stimulated so body cells are ready for action (Liver released glucose for energy). Increase in heart rate •Increase in breathing •Decrease in digestive activity (don’t feel hungry) •Immune system is excited to protect in case of injury or infection during fight. Slow acting: (A)Hormonal response: HPA axis (from adrenal cortex). Slow-acting Fast-acting Adrenal medulla: •Is part of the autonomic nervous system (where activities are generally performed without conscious control) •It secretes the hormone adrenaline among others, which activates ‘sympathetic’ responses (for instance when occupy receptors on the cardiac muscle, the frequency of the heartbeat increases). Activating a slow-acting stress response: Hormonal response: HPA axis (from hypothalamus pituitary gland adrenal cortex producing among others gluco-corticoids hormones, e.g. cortisol). Actions: Glucose released from fats and proteins by the liver (gluconeogenesis), fatty acids released from adipose tissue. •Other effects: –All the bodily systems not required to deal with stressor are turned off, e.g. •Reproductive functions off, no growth hormone •Activity of the immune system inhibited or down-regulated.
Hippocampus and stress response:
Contains high density of cortisol receptors (in red) •Has axons projecting into the hypothalamus •Hence it can easily detect cortisol in the blood and it can instruct the hypothalamus to reduce blood-cortisol levels. Too much cortisol •If a stress-inducing situation continues •Constant high level of cortisol damage the hippocampus •The damaged hippocampus cannot do its work of reducing the level of cortisol in the blood. A vicious circle: •High cortisol àcell death in the hippocampus à less negative feedback à higher cortisol •The hippocampus undergoes progressive degeneration and cortisol levels are not controlled. A fine balance: – Brief cortisol exposure increases activity in the hippocampus and helps one remember an acute stressor. – Lengthy high levels increase cell death and decrease the formation of new neurons.
