Tag Archives: Stress

Adrenaline, Stress and Obesity-All you need to know

February 10, 2014

Adrenaline, Stress and Obesity-Introduction and background

stress and obesity

The prevalence of obesity has increased dramatically in the last several decades. Obesity, particularly upper body obesity (UBO), is associated with type 2 diabetes (T2DM), dyslipidemia, and hypertension. These associations describe the metabolic syndrome, a clustering of symptoms with insulin resistance as a core cause. Currently, the prevalence of obesity and metabolic syndrome is above average deeming both conditions important public health issues, requiring immediate efforts to understand these diseases and reduce their occurrence.

Stress response:

Role of hypothalamic–pituitary–adrenal axis

Stress is a challenge to the natural homeostasis of an organism. Animals react to stress by producing a physiological stress response to regain equilibrium lost by the stressor. The stress response is characterized by acute behavioral and physical adaptations, including increased cognition, analgesia, gluconeogenesis, lipolysis, and inhibition of reproduction.

There are two major components of the stress response: the autonomic nervous system (ANS), which encompasses the sympathetic and parasympathetic nervous system, and the HPA axis. These systems work centrally and peripherally to produce several responses. The ‘fight or flight response’ is an active reaction to either confront the stressor or escape confrontation.

The ‘defeat response’ is when the individual does not engage in either the fight or flight response and ultimately ‘loses’ the confrontation; this is the primary stress response in modern society and is associated with HPA axis changes. Although the ANS is a key element of the stress response, the purpose of this review is to discuss the role of the HPA axis in obesity and metabolic disease.

Stress can be caused by external stressors such as employment or social strains or by intrinsic stressors such as sleep deprivation. Although an acute short-term stress response is necessary for homeostasis recovery, chronic or prolonged stress responses can be harmful and may cause several disease states. A study on women reported that history of depression was associated with hyperactivity of the HPA axis and decreased bone mineral density. In the past 30 years, numerous studies have shown that obesity and other metabolic risk factors are associated with lower socioeconomic status, job strain, sleep deprivation, and depression

Hypothalamic–Pituitary–Adrenal axis

The HPA axis is one of two major neuroendocrine systems associated with the stress response. Corticotrophin-releasing hormone (CRH), secreted from the Para-ventricular nucleus (PVN) of the hypothalamus, stimulates the synthesis of adrenocorticotropic (ACTH) from the anterior pituitary gland. Other hypothalamic ACTH secretagogues are arginine vasopressin and oxytocin, also produced in the PVN. Physical stressors such as hypoglycemia, hemorrhage, and immune stimuli activate PVN neurons expressing arginine vasopressin and CRH. ACTH stimulates cortisol production from the adrenal cortex.

The first evidence that cortisol levels may be related to obesity and metabolic disease was based on clinical observations of Cushing’s syndrome; the pathological hypercortisolemia in Cushing’s syndrome is associated with UBO, glucose intolerance [impaired glucose tolerance (IGT)], and hypertension. Adrenalectomy in Cushing’s syndrome patients reverses IGT and obesity.Studies in the field of obesity research in the past 10 years have demonstrated that obesity and metabolic syndrome are characterized by chronic inflammation.

Genetic polymorphisms of hypothalamic–pituitary–adrenal axis in obesity

Currently, there are few genetic polymorphisms that present with both functional alterations in the HPA axis and obesity. Several polymorphisms at the level of ACTH synthesis, and in genes associated with glucocorticoid receptor or local cortisol metabolism (11β-HSD1 and 11β-HSD2), which may predict UBO, have been described. The variability in the heritability of obesity makes it difficult to determine the role of these polymorphisms in common obesity.

Fetal programming, stress, and obesity

Stress experienced in early life may also be a risk factor in the development of obesity and metabolic syndrome. A recent study on nonhuman primates reported that juvenile bonnet macaque monkeys exhibit greater weight, BMI, waist circumference, and insulin resistance if their mothers are exposed to food insecurity when the monkeys are young (age 3–5 months).

Sleep deprivation and obesity

stress and obesity

In the past 30 years, the average nightly sleep duration has decreased from 8–9 to 7 h per night. Currently, 30% of all adults in the USA sleep less than 6 h per night. Sleep deprivation has been linked to both increased risk for obesity. Epidemiological studies have reported a negative association between BMI and sleep duration in adults and, children. In laboratory studies, insulin sensitivity was reduced in sleep-restricted individuals.

Sleep deprivation is suggested to be a chronic stressor that may contribute to increased risk for obesity and metabolic diseases, possibly in part through HPA axis dysregulation, although the data are inconsistent. Sleep deprivation resulted in decreased night-time and morning plasma cortisol levels, or increased night-time plasma cortisol levels in other studies. To date, there have been no reported studies on the effect of sleep deprivation on salivary cortisol or UFC.

Conclusion

The present review provides basic support for the relationship between chronic stress, alterations in HPA activity, and obesity. Although animal models provide evidence of the association of stress, HPA axis, and metabolic diseases, human studies have proven to be more challenging, with more understated changes in the HPA axis.

In modern society, where over nutrition, sedentary lifestyle, and sleep deprivation are typical traits, chronic exposure to environmental stress potentially contributes to the development of obesity. This may be at least partially mediated through the HPA axis, although this relationship is complex and many factors, including genetic polymorphisms, tissue-specific cortisol metabolism, chronic inflammation, leptin, ghrelin, and sex hormones, influence the strength of this association. Future studies should address the mechanisms that HPA activity dysregulation contributes to obesity and other metabolic complications. Changes in food intake appear to be a primary target. These actions may be related to effects of leptin and other central signals such as NPY and insulin.

HPA axis dysregulation in obesity is subtle and difficult to assess clinically. Continued research in this field is imperative to define a causal role for chronic stress and obesity, and ultimately develop effective treatment or preventive interventions.

Adrenaline, Stress and Obesity-Introduction and background

 

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Adrenaline, Stress and Obesity-All you need to know

February 10, 2014

Adrenaline, Stress and Obesity-Introduction and background

stress and obesity

Obesity can be avoided by having the right lifestyle!

The prevalence of obesity has increased dramatically in the last several decades. Obesity, particularly upper body obesity (UBO), is associated with type 2 diabetes (T2DM), dyslipidemia, and hypertension. These associations describe the metabolic syndrome, a clustering of symptoms with insulin resistance as a core cause. Currently, the prevalence of obesity and metabolic syndrome is above average deeming both conditions important public health issues, requiring immediate efforts to understand these diseases and reduce their occurrence.

Stress response:

Role of hypothalamic–pituitary–adrenal axis

Stress is a challenge to the natural homeostasis of an organism. Animals react to stress by producing a physiological stress response to regain equilibrium lost by the stressor. The stress response is characterized by acute behavioral and physical adaptations, including increased cognition, analgesia, gluconeogenesis, lipolysis, and inhibition of reproduction.

There are two major components of the stress response: the autonomic nervous system (ANS), which encompasses the sympathetic and parasympathetic nervous system, and the HPA axis. These systems work centrally and peripherally to produce several responses. The ‘fight or flight response’ is an active reaction to either confront the stressor or escape confrontation.

The ‘defeat response’ is when the individual does not engage in either the fight or flight response and ultimately ‘loses’ the confrontation; this is the primary stress response in modern society and is associated with HPA axis changes. Although the ANS is a key element of the stress response, the purpose of this review is to discuss the role of the HPA axis in obesity and metabolic disease.

Stress can be caused by external stressors such as employment or social strains or by intrinsic stressors such as sleep deprivation. Although an acute short-term stress response is necessary for homeostasis recovery, chronic or prolonged stress responses can be harmful and may cause several disease states. A study on women reported that history of depression was associated with hyperactivity of the HPA axis and decreased bone mineral density. In the past 30 years, numerous studies have shown that obesity and other metabolic risk factors are associated with lower socioeconomic status, job strain, sleep deprivation, and depression

Hypothalamic–pituitary–adrenal axis

The HPA axis is one of two major neuroendocrine systems associated with the stress response. Corticotrophin-releasing hormone (CRH), secreted from the Para-ventricular nucleus (PVN) of the hypothalamus, stimulates the synthesis of adrenocorticotropic (ACTH) from the anterior pituitary gland. Other hypothalamic ACTH secretagogues are arginine vasopressin and oxytocin, also produced in the PVN. Physical stressors such as hypoglycemia, hemorrhage, and immune stimuli activate PVN neurons expressing arginine vasopressin and CRH. ACTH stimulates cortisol production from the adrenal cortex.

The first evidence that cortisol levels may be related to obesity and metabolic disease was based on clinical observations of Cushing’s syndrome; the pathological hypercortisolemia in Cushing’s syndrome is associated with UBO, glucose intolerance [impaired glucose tolerance (IGT)], and hypertension. Adrenalectomy in Cushing’s syndrome patients reverses IGT and obesity.Studies in the field of obesity research in the past 10 years have demonstrated that obesity and metabolic syndrome are characterized by chronic inflammation.

Genetic polymorphisms of hypothalamic–pituitary–adrenal axis in obesity

Currently, there are few genetic polymorphisms that present with both functional alterations in the HPA axis and obesity. Several polymorphisms at the level of ACTH synthesis, and in genes associated with glucocorticoid receptor or local cortisol metabolism (11β-HSD1 and 11β-HSD2), which may predict UBO, have been described. The variability in the heritability of obesity makes it difficult to determine the role of these polymorphisms in common obesity.

Fetal programming, stress, and obesity

Stress experienced in early life may also be a risk factor in the development of obesity and metabolic syndrome. A recent study on nonhuman primates reported that juvenile bonnet macaque monkeys exhibit greater weight, BMI, waist circumference, and insulin resistance if their mothers are exposed to food insecurity when the monkeys are young (age 3–5 months).

Sleep deprivation and obesity
stress and obesity

Obesity Effects

In the past 30 years, the average nightly sleep duration has decreased from 8–9 to 7 h per night. Currently, 30% of all adults in the USA sleep less than 6 h per night. Sleep deprivation has been linked to both increased risk for obesity. Epidemiological studies have reported a negative association between BMI and sleep duration in adults and, children. In laboratory studies, insulin sensitivity was reduced in sleep-restricted individuals.

Sleep deprivation is suggested to be a chronic stressor that may contribute to increased risk for obesity and metabolic diseases, possibly in part through HPA axis dysregulation, although the data are inconsistent. Sleep deprivation resulted in decreased night-time and morning plasma cortisol levels, or increased night-time plasma cortisol levels in other studies. To date, there have been no reported studies on the effect of sleep deprivation on salivary cortisol or UFC.

Conclusion

The present review provides basic support for the relationship between chronic stress, alterations in HPA activity, and obesity. Although animal models provide evidence of the association of stress, HPA axis, and metabolic diseases, human studies have proven to be more challenging, with more understated changes in the HPA axis.

In modern society, where over nutrition, sedentary lifestyle, and sleep deprivation are typical traits, chronic exposure to environmental stress potentially contributes to the development of obesity. This may be at least partially mediated through the HPA axis, although this relationship is complex and many factors, including genetic polymorphisms, tissue-specific cortisol metabolism, chronic inflammation, leptin, ghrelin, and sex hormones, influence the strength of this association. Future studies should address the mechanisms that HPA activity dysregulation contributes to obesity and other metabolic complications. Changes in food intake appear to be a primary target. These actions may be related to effects of leptin and other central signals such as NPY and insulin.

HPA axis dysregulation in obesity is subtle and difficult to assess clinically. Continued research in this field is imperative to define a causal role for chronic stress and obesity, and ultimately develop effective treatment or preventive interventions.

Adrenaline, Stress and Obesity-Introduction and background

 

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Stress Slow Killer is Serious Business

December 4, 2013

Stress Slow Killer

Dr. Dalal Akoury

 

Stress Slow Killer is Serious Business

Stress Slow Killer affects us physically and emotionally. The stress response is mediated through HPA axis and activation of the autonomic nervous system. The aim is to mobilize energy for the “fight or flight” response. This brings about changes in almost all organs and tissues as a whole. In an acute event, after the stressor disappears, the homeostasis or internal equilibrium is regained. In case where the stress continues it leads to chronic disorders involving many organs and this also depends on the nature of stress.

The effects of Stress Slow Killer on each organ

Stress Slow Killer and the Nervous System:

Stress leads to activation of HPA axis once the hypothalamus receives signals from cerebral cortex which are perceived as stress. Then hypothalamus releases corticotropin releasing hormone which stimulates the anterior pituitary to produce adrenocorticotropic hormone (ACTH). ACTH is secreted into the systemic circulation and stimulates the adrenal glands to produce stress hormone called cortisol.

There is stimulation of autonomic nervous system which is caused by direct stimulation of both sympathetic and parasympathetic systems. This is done by hypothalamus. The sympathetic activation leads to release of adrenaline and noradrenaline by the adrenal medulla. These hormones increase the heart rate, raise blood pressure, increase glucose levels in the blood and suppress digestive and reproductive functions. This stimulation is more obvious when the stressor is strong like acute pain. In people with chronic pain, this effect is weak and not clinically obvious unless there is aggravation of symptoms. After the stressor disappears, the parasympathetic nervous system helps in reverting back to normal and regain of internal equilibrium. The autonomic nervous system also interacts with the enteric nervous system and has anti-inflammatory properties.

Stress Slow Killer and the Musculoskeletal system

Due to the effect of stress, the muscle tone increases as the body is prepared for the “fight or flight” response. It results in tension headache and back pain.

 Stress Slow KillerStress Slow Killer and the Respiratory system

Stress increases respiratory rate to increase the availability of oxygen to all organs and muscles so as to prepare for the stress response. This occurs due to direct stimulation of the respiratory center. An excessive stimulation may bring panic attack in some individuals.

Stress Slow Killer and the Cardiovascular system

Acute stress causes activation of the cardiovascular system. This occurs mainly due to release of noradrenaline and adrenaline from the adrenal medulla. These hormones act on the heart to produce the effects which include rapid heart rate, stronger contractions of heart and palpitations. The blood flow to the skeletal muscles and heart increases due to dilatation of blood vessels. These changes occur with acute stress.

Chronic stress is associated with inflammation of arteries of heart (coronary arteries) and may lead to heart attack. There is also higher incidence of hypertension, stroke and atherosclerosis.

Stress Slow Killer and the Endocrine system

Stress related ACTH stimulation results in enlargement of adrenal glands which are required to produce increased amounts of stress hormones. The adrenal cortex produces cortisol and adrenal medulla secretes noradrenaline and adrenaline. These three adrenal hormones play a crucial role in the stress response.

Stress Slow Killer and the Gastrointestinal system

Stress promotes increased consumption of palatable food. Severe stress is associated with nausea and vomiting. It may result in reflux esophagitis. Under the effects of cortisol and adrenaline, liver produces more glucose which is used for energy production by various organs and skeletal muscles. Stress affects digestion adversely and may modulate gut motility to produce diarrhea or constipation.

 

Stress Slow KillerStress Slow Killer and the Reproductive system

The stress response leads to suppression of reproductive function. Chronic stress impairs testosterone secretion in the testes. The sperm production is reduced and infertility may occur. In women, the menstrual cycles become irregular and painful or may develop complete amenorrhea. The sexual desire is reduced significantly.

Stress Slow Killer and the Immune system

Stress leads to suppression of immunity so as to conserve energy. In case of chronic stress, this increases the risk of infections due to poor immunity.

Stress Slow Killer and the Cellular and molecular effects of stress

Stress increases intracellular calcium. This effect is seen in association with message induced stress which stimulates the mast cells to release histamine which causes local vasodilatation and improves perfusion.

On exposure to stress, the cells generate heat shock proteins which promote cell survival. Exposure of cells to temperature of 3 to 5 °C above normal, reactive oxygen species causes induction of heat shock proteins 27 and 70. These proteins inhibit apoptosis and promote survival.

Apoptosis or programmed cell death occurs if a cell is partially damages due to stress or fails to sustain stress. During this process, special enzymes called caspases are activated which bring about protein changes resulting in cell death.

Autophagy is characterised by self-destruction of cell organelles like mitochondria and cytoplasmic proteins. Autophagy is observed in cells exposed to stressors like starvation, ischemia reperfusion injury, increased intracellular calcium and endoplasmic reticulum stress.

So Stress Slow Killer affects each system in the body, each organ and each cell.

Stress Slow Killer is Serious Business

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Weight Loss and Stress the Missing Link

October 23, 2013

Understanding Weight Loss and Stress

Weight loss and Stress are linked, it is hard to lose weight when– Stress…Is Everywhere! says Dr. Dalal Akoury

Weight Loss and Stress

Understanding Weight Loss and Stress

Lets face it people, stress will always be in our lives… to a certain degree anyways.  It is almost a way of life in the 21st century.  Stress can be a major prohibiting factor to weight loss and can even contribute to weight gain.  Chronic stress can be tied to an increase in appetite and ultimately stress-induced weight gain.  It all starts in our neuroendocrine system.  This system activates a hormones in response to stress or life threatening situations.  The hormones released during this response is adrenaline, corticotrophin releasing hormone (CRH), and cortisol.  Elevated levels of adrenaline and CRH cause a decreased appetite.  This result is usually temporary.  Cortisol on the other hand is there to support and replenish our body after the stressors have gone.  This elevated level of cortisol remains for a long period of time and tends to increase appetite.  For most people, increased appetite means increase in weight gain!

 Weight Loss – Stress A Tyrannosaurs Rex  or a Late Electric Bill?

This response from the neuroendocrine system is doing what it is supposed to do but it was not designed for the 21st century stressors.  The increase in hormones was intended for life threatening situations such as, a tyrannosaurs rex trying to eat your entire family as it was in the time of cavemen.  The calories or stored food in the body we would have used to fight off the tyrannosaurs rex in the beginning of time is not being expended in modern day.  Now “we” mope around and fuss and dwell on our stressors and anger.  Eating has become our stress reliever.  At this point or neuroendocrine system is confused and has not received the necessary signals to know if we fought off that tyrannosaurs rex or not.  This causes us to feel hungry because the hormones are still being released to restore calories lost and our depleted food stores.

AWAREmed Health and Wellness Resource Center team and Dr. Dalal Akoury reminds us that – Weight Loss  a ndStress – Cortisol and the Adrenals – are all connected

Cortisol is actually made in the Adrenal Cortex.  It controls the strength of our immune system, normalizes blood sugar, and regulates blood pressure.  This production is due to adrenal cortical stimulating hormone (ACTH) produced in the pituitary gland.  If the adrenals are producing to much of the cortisol, the motions for increased susceptibility to infections and cancer will occur, along with weight gain around the belly area and your immune system can be compromised.  Opposite of that, if too little cortisol is produced chronic fatigue can occur and so can exhaustion.  An overactive immune system could develop as could autoimmune disease.

Dr. Dalal Akoury founder of AWAREmed Health and Wellness Resource Center describes the Weight and  Stress connection – Let’s Correct That Cortisol Level!!

 Weight Loss and Stress the Missing Link

Stress reduction is an essential part of all efforts to normalize cortisol. Stress is the stimuli that caused the cortisol levels to get out of hand to begin with. Each individual should explore and find the stress reduction techniques that work best for themselves. Meditation, physical activities, attitude changes, just to name a few are good paths to explore. Without stress reduction, therapeutic and support measures will ultimately fail.

Get plenty of rest.  Rest must be handled as a scheduled and straight forward strategy, choice, and course of action. That may sound obvious but how well do you really schedule your rest?  Otherwise it gets lost and forgotten in the high strung pace of life.

A low glycemic diet is also important. Sugar handling stress increases cortisol levels. Elevated cortisol, then disturbs the sugar handling situation, contributing towards the development of high insulin levels and possibly diabetes. Diet alone without stress reduction will not help you lose weight because weight loss and stress are connected.

Weight Loss and Stress

Understanding Weight Loss and Stress

Nutritional supplementation is highly recommended in restoring normal cortisol levels. We suggest a Integrative Therapeutic Cortisol Manager.  Our product will support a healthy sleeping habit without using habit forming ingredients.  Due to the more normal sleeping pattern, the stressors associated with the unhealthy sleeping pattern will disappear.  Phosphatidylserine is the main active ingredient in our Integrative Therapeutic Cortisol Manager and is believed to facilitate the repair of the cortisol receptors in the hypothalamus. It is believed that the cortisol receptors get damaged by high cortisol levels reducing the ability of the hypothalamus to sense and correct high cortisone levels. Because Phosphatidylserine helps repair the feedback control apparatus, it is useful in correcting both high and low cortisol levels.

Another nutritional supplement that is necessary are adaptogen herbs.  Adaptogens are an entire category of herbs that assist the body in coping with stress by restoring hypothalamic cortisol receptor sensitivity.  A combination of these adaptogens are all researched for their effects on increasing stamina, mental alertness and work performance.

The AWAREmed Health and Wellness Resource Center team and it’s founder Dr. Dalal Akoury  describe that Weight gain is caused by  Stress and Having Healthy SEX will help weight loss

The adrenals are a big deal in many people’s sex lives. People usually feel sexier on vacation when the stress level is down. They can relax and also make up their sleep deficit. Many couples complain that they are just too tired to be interested in sex. A great rule for rebuilding the adrenals is “rest is best.” I can guarantee that if one spouse is feeling fearful and anxious, he or she is definitely not feeling very sexy. Remember Weight loss and stress are closely linked.

All of the adrenal hormones, and all the sex hormones for that matter, are steroids. Steroids are made from cholesterol. You need good sources of cholesterol. Forget the margarine and only eat butter. Keep up a good protein intake, which will also provide good sources of cholesterol.  Remember, healthy sex equals healthy adrenals!

 

Understanding Weight Loss and Stress!

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Do You Really KNOW Stress Management!?

September 13, 2012
Stress Management

Dr. Dalal Akoury

Do You Really KNOW Stress Management!?

Your body is hard-wired to react to stress in ways meant to protect you against threats from predators and other aggressors. Such threats are rare today, but that doesn’t mean that life is free of stress.

Stress Management

Stress Management

On the contrary, you undoubtedly face multiple demands each day, such as shouldering a huge workload, making ends meet, taking care of your family, or just making it through the morning rush hour. Your body treats these so-called minor hassles as threats. As a result you may feel as if you’re constantly under assault. But you can fight back. You don’t have to let stress control your life.

Stress Management: Fight or Flight

If your mind and body are constantly on edge because of excessive stress in your life, you may face serious health problems. That’s because your body’s “fight-or-flight reaction” — its natural alarm system — is constantly on.

When you encounter perceived threats — a large dog barks at you during your morning walk, for instance — your hypothalamus, a tiny region at the base of your brain, sets off an alarm system in your body. Through a combination of nerve and hormonal signals, this system prompts your adrenal glands, located atop your kidneys, to release a surge of hormones, including adrenaline and cortisol.

Adrenaline increases your heart rate, elevates your blood pressure and boosts energy supplies. Cortisol, the primary stress hormone, increases sugars (glucose) in the bloodstream, enhances your brain’s use of glucose and increases the availability of substances that repair tissues.

Cortisol also curbs functions that would be nonessential or detrimental in a fight-or-flight situation. It alters immune system responses and suppresses the digestive system, the reproductive system and growth processes. This complex natural alarm system also communicates with regions of your brain that control mood, motivation and fear.

Stress Management means Take Control

The body’s stress-response system is usually self-regulating. It decreases hormone levels and enables your body to return to normal once a perceived threat has passed. As adrenaline and cortisol levels drop, your heart rate and blood pressure return to baseline levels, and other systems resume their regular activities.

But when the stressors of your life are always present, leaving you constantly feeling stressed, tense, and nervous or on edge, that fight-or-flight reaction stays turned on. The less control you have over potentially stress-inducing events and the more uncertainty they create, the more likely you are to feel stressed. Even the typical day-to-day demands of living can contribute to your body’s stress response.

The long-term activation of the stress-response system — and the subsequent overexposure to cortisol and other stress hormones — can disrupt almost all your body’s processes. This puts you at increased risk of numerous health problems, including:

  •                Heart disease
  •                Sleep problems
  •                Digestive problems
  •                Depression
  •                Obesity
  •                Memory impairment
  •                Worsening of skin conditions, such as eczema

That’s why it’s so important to learn healthy ways to cope with the stressors in your life.

Stress Management means identify your Unique Stressors

Your reaction to a potentially stressful event is different from anyone else’s. How you react to stressors in your life includes such factors as:

  •                Genetics. The genes that control the stress response keep most people on a fairly even keel, only occasionally priming the body for fight or flight. Overactive or underactive stress responses may stem from slight differences in these genes.
  •                Life experiences. Strong stress reactions sometimes can be traced to early environmental factors. People who were exposed to extremely stressful events as children, such as neglect or abuse, tend to be particularly vulnerable to stress as adults.

You may have some friends who seem laid-back about almost everything and others who react strongly at the slightest stress. Most reactions to life stressors fall somewhere between those extremes.

Stress Management teach how to React to Life Stressors 

Stressful events are a fact of life. And you may not be able to change your current situation. But you can take steps to manage the impact these events have on you. You can learn to identify what stresses you out, how to take control of some stress-inducing circumstances, and how to take care of yourself physically and emotionally in the face of stressful situations.

Stress Management: Means Move that Body and Exercise!

Stress Management

Stress Management

Any activity that raises your heart rate and makes you sweat will greatly lighten your mood, increase energy, sharpen focus, and relax both the mind and body. For maximum stress relief, try to get at least 30 minutes of activity on most days.

Eat right

Low blood sugar can make you feel anxious and irritable, while eating too much can make you lethargic. Eat small, but frequent meals throughout the day to maintain an even level of blood sugar and avoid these swings in mood.

Get enough sleep

Not only can stress and worry cause insomnia, but also a lack of sleep can leave you vulnerable to even more stress. When you’re well rested, it’s much easier to keep your emotional balance.

When job and workplace stress threatens to overwhelm you, there are simple steps you can take to regain control over yourself and the situation. Your coworkers will love your self-control and may try to adopt your habits, too.

 

 

Stress management strategies include:

  •                Eating a healthy diet and getting regular exercise and plenty of sleep
  •                Practicing relaxation techniques
  •                Fostering healthy friendships
  •                Having a sense of humor
  •                Seeking professional counseling when needed

The payoff of managing stress is peace of mind and — perhaps — a longer, healthier life.

 

AWAREmed: Do You Really KNOW Stress!?

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