Tag Archives: stress and obesity

Gaining Weight When Stressed Up

Gaining Weight When Stressed Up — Truth Exposed

Stress

Gaining Weight When Stressed Up. Stress is everywhere around us avoiding stress will go along way in keeping you healthy.

Have you taken a good look at what is happening around you? I mean things that trigger your emotions making you sad or tired in the mind body and spirit? I am referring to things and situations like your job are hanging by a thread probably the board is currently discussing your dismissal, your teenage boy is becoming unruly and he is threatening quitting school for no reason are we together now? These are things that cause us to be very much stressed with life. Irrespective of how you look at it dear reader, stress is actually a way of life in this 21st century. Because of the effects of stress many people are affected in different ways and the effects often go beyond feelings of anxiety and discomfort. For instance have you found yourself eating heavily junk food while trying to beat certain work deadline? Or endlessly stocking and eating cookies in your car while driving and many similar behaviors! Stress is a force which can rearrange your daily programs. It (stress) will increase your appetite causing you to be holding onto fats which interferes with your ability to live a healthy lifestyle. How then does stress leads to weight gain?

Hormones

When your brain senses the presence of any threat whether it is burning fire, irritating employer or an accumulation of debts with no expectation of income to foot the bills, it will triggers the release of adrenaline, CRH (corticotrophin releasing hormone), and cortisol. With the release of these chemicals, your body and brain position themselves to handle the threats by causing you to be more alert and ready to take action and contain any injury which may arise. For a while the adrenaline will help you feel less hungry as your blood flows away from the internal organs and to your large muscles to be ready for fight or flight. However, once the effects of adrenaline wear off, cortisol, known as the stress hormone, stays around and begins signaling the body to replenish your food supply.

Belly Fat

In the days when our ancestors were fighting off tigers and famine, their bodies adapted by learning to store fat supplies for the long haul. The unfortunate result for you and me is that when we are chronically stressed by life crises and work-life demands, we are prone to getting an extra layer of “visceral fat” deep in our bellies. Your belly has an ample supply of blood vessels and cortisol receptors to make the whole process flow more efficiently.

The downside is that excess belly fat is unhealthy and difficult to get rid of. The fat releases chemicals triggering inflammation, which increases the likelihood that we will develop heart disease or diabetes. And it can make it more difficult to fit into those lovely jeans you splurged on, leading to more stress about money wasted! Unfortunately, excess cortisol also slows down your metabolism, because your body wants to maintain an adequate supply of glucose for all that hard mental and physical work dealing with the threat.

Anxiety

When we have a surge of adrenaline as part of our fight/flight response, we get fidgety and activated. Adrenaline is the reason for the “wired up” feeling we get when we’re stressed. While we may burn off some extra calories fidgeting or running around cleaning because we can’t sit still, anxiety can also trigger “emotional eating.” Overeating or eating unhealthy foods in response to stress or as a way to calm down is a very common response. Anxiety can also make you eat more “mindlessly” as you churn around worrying thoughts in your head, not even focusing on the taste of the food, how much you’ve eaten, or when you are feeling full.

Cravings and Fast Food

When we are chronically stressed, we crave for junk foods which tend to be easy to eat, highly processed, and high in fat, sugar, or salt. We crave these foods for both biological and psychological reasons. Stress may mess up our brain’s reward system or cortisol may cause us to crave more fat and sugar. When we are stressed, we also may be more likely to drive through the Fast Food place, rather than taking the time and mental energy to plan and cook a meal.

Less Sleep

Take some time and have adequate sleep. It actually causes you nothing to sleep well yet the benefit is life changing, don’t occupy your mind with the worries of life, they are the reasons why you have insomnia. Even if you’re to sit an exam still read but ensures you have enough sleep because sleep is a powerful factor influencing weight gain or loss. Lack of sleep may disrupt the functioning of ghrelin and leptin—chemicals that control appetite.

Reducing Weight Gain When You’re Stressed

Excessive weight is certainly not good for your health and the best you can do for yourself is to make effort of cutting down on your weight. The following are some of the ways you can use to reduce your weight for a better health ahead of you.

Physical Activities

Aerobic exercise has a one-two punch. It can decrease cortisol and trigger release of chemicals that relieve pain and improve mood. It can also help speed your metabolism so you burn off the Learn Mindful Eating

Mindful Eating programs train you in meditation, which helps you cope with stress, and change your consciousness around eating. You learn to slow down and tune in to your sensory experience of the food, including its sight, texture or smell. You also learn to tune into your subjective feelings of hunger or fullness, rather than eating just because it’s a mealtime or because there is food in front of you. A well-designed study of binge-eaters showed that participating in a Mindful Eating program led to fewer binges and reduced depression.

Engage in Rewarding Activities

It is true that food can keep you busy but this would be a very poor option especially when you’re making effort to cutting down on your weight and managing stress. Therefore finding activities like hiking, reading, attending yoga class, getting a massage, patting your dog, or making time for friends and family can help to relieve stress without adding on the pounds.

Although you may feel that you don’t have time for leisure activities with looming deadlines, taking time to relieve stress helps you to feel refreshed, lets you think more clearly, and improves your mood, so you are less likely to overeat.

Finally writing down your healthy eating and exercise goals may make you more conscious of your desire to live a healthier lifestyle and intensify your commitment. Researchers have established that writing expressively or about life goals can improve both mood and health. Finally your good health should be your number one priority. The fact that stress is very common in our day today life is not reason enough to have you get to other life complications relating to weight gain and obesity. It will be necessary that you talk to Dr. Dalal Akoury, Founder of AWAREmed Health and Wellness Resource Center, a professional in her own right and have been of help to many in the same situation. Doctor Akoury has been in practice for the last 20years offering her exclusive NER Recovery Treatment to everyone including other physicians and health care professionals through training, clinical apprenticeships, webinars and seminars. Just like qualified professional are calling her for help in their desire to manage their stress and weight you can also do the same and get your life back on the recovery path for a long and fulfilling life a head of you.

Gaining Weight When Stressed Up — Truth Exposed

 

 

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Relation between Stress and Obesity

Relation between Stress and Obesity – Biochemical changes

Stress

Relation between Stress and Obesity. These are two health conditions that if allowed in ones life then you will be very measurable.

Over the past decades many people have alleged that stress and obesity are linked and now scientific research is bringing forth evidence supporting this connection. Explicit biochemical reactions appear to help explain this link and, the medical professionals understand these reasons better and are in a position to address the prevalence of obesity epidemic facing U.S and the globe in general.

The most disturbing aspect of the link between stress and obesity is that it tends to be self-reinforcing. Very often, when people are stressed they may eat improperly and that may cause them to gain weight which can even cause more stress and therefore ending up causing exactly what you’re trying to fight off.

Relation between Stress and Obesity – The Biological Connection

If you have been keen you must have realized that each time you’re stressed it is always a common practice that you will tend to crave comfort foods which are high in fat or sugar and researchers have established that specific hormones may play a role in this process.

Serotonin – reaching for fattening comfort foods during stressful times may be an attempt to offer self-medication. Consuming carbohydrates raises the body’s serotonin level and serotonin is the body’s feel-good chemical. It makes you feel better. Under normal circumstances people under stress don’t make smart or healthy food choices. Very often their choices of carbohydrates are rich in fat, like muffins, pastries, doughnuts, and cookies which are not necessarily health foods.

Cortisolresearchers have also discovered that chronic stress can cause the body to release excess cortisol, a hormone critical in managing fat storage and energy use in the human body. Cortisol is known to increase appetite and may encourage cravings for sugary or fatty foods.

Neuropeptide Y.recent studies also have established that the human body processes food differently when under stress. One study established that lab mice fed a diet high in fat and sugar added significant amounts of body fat when placed under stressful conditions while those mice fed a normal diet didn’t add as much weight despite stress. This finding has been linked the phenomenon to a molecule called neuropeptide Y which is released from nerve cells during stress and encourages fat accumulation. A diet high in fat and sugar appears to further promote the release of neuropeptide Y.

Relation between Stress and Obesity – Breaking the Cycle

So if we’re wired to seek out unhealthy foods when we are under stress, how do we avoid gaining weight when times get tough?

Don’t allow yourself to become too hungry – When you get irritated on an empty stomach you get a drop in your blood sugar. It’s very hard to think rationally when your blood sugar levels are that low you’ll be motivated to eat anything and to avoid this scenario, be sure you’re not skipping meals.

Keep portion size in mind – when people are stressed out they are likely to careless about what they are feeding on and to what quantity. It is important to note that smaller portions can help keep your total calorie intake under control.

Eat healthy snacks – it is advisable to take those snacks combine with protein and carbohydrates because the body digests them more slowly allowing you to feel for longer duration for example you may want to feed on almond butter and whole-grain crackers, or cheese and a piece of whole-grain bread but by all means void snacks high in fat and sugar.

Think about what you’re eating – often when people are really stressed, they tend to think that paying attention to their diet will cause more stress. Actually it’s just the opposite. Don’t forget that food is fuel for your body and your brain and when you eat properly well you’re just fueling your body to fight stress.”

Deal with your stress – this may not be easy as it may look but all the same you must find better ways of manage your stress because this is very essential to your overall health you may choose trying yoga, tai chi, or meditation and in all these ensure regular exercise and avoid isolation desire spending time with friends, seek counseling and reduce the number of stressors in your life.

If you find yourself reaching for high-fat, sugary snacks when you’re feeling stressed, know that you’re not alone. Fortunately though, you can break this cycle. Find ways to minimize stress in your life and focus on making better food choices. Stress may be a part of life, but it doesn’t have to lead to weight gain.

Finally take not of what I have just said and I repeat “Stress may be a part of life, but it doesn’t have to lead to weight gain” The phenomenon of obesity being among chronic diseases makes Dr. Akoury of AWAREmed Health and Wellness Resource Center very resourceful for you. She will help you achieve optimal weight loss in the most natural way possible. She is a medical professional with over two decades of practicing experience and together with her team of experts doctor Akoury will focus on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE. I assure you that with the help of Dr. Akoury your problem is sorted out for good.

Relation between Stress and Obesity – Biochemical changes

 

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Stress and Obesity the Missing Link!!!

Stress and Obesity-Not a Union

Stress

Research has found that stress leads to specific reactions in the body that cause induced cravings and lead to obesity

Obesity is a burgeoning problem in the developed world, and certain behaviors, such as increased portion sizes and reduced physical activity, can help explain why the obesity epidemic is spreading. Job strain might also contribute to the prevalence of obesity, and the current study addresses this issue in a cohort of civil servants followed over time. Obesity continues to be one of the largest public health concerns of the developed world. Analysis of data from the 2001-2002 National Health and Nutrition Examination Survey (NHANES) found that the prevalence rates of overweight and obesity among US adults were 31.5% and 30.5%, respectively. The prevalence of overweight in children was 16.5%. Compared to the previous NHANES survey (1988-1994), the body mass index (BMI) greater than 30 among adults had doubled. (Of note, the prevalence of overweight and obesity were fairly stable between the 1999-2000 and 2001-2002 examination periods.)

Stress and Obesity-Understanding obesity

While the problem of obesity has been well publicized, clinicians should also understand that societal factors play a prominent role in obesity. In research sponsored by the World Health Organization involving 26 different populations worldwide, surveys of over 30,000 subjects found an inverse trend between BMI and highest educational level attained. Women with lower educational attainment were significantly more likely to be obese compared with men with similar educational backgrounds, although lower educational levels in both sexes were associated with higher obesity. Moreover, the negative association between educational attainment and obesity increased over the 10-year study period, indicating that the obesity gap between well-educated and poorly educated individuals was increasing. To reinforce these data, another study limited to developed countries found that increased income disparity was associated with not only higher rates of obesity, but also diabetes mortality as well among subjects at the lower end of the income scale. Other societal trends can affect obesity as well. In the United States, more individuals are choosing to eat at restaurants than at home, and the easiest and least expensive option in dining is often preferred. Such choices can increase the risk of developing obesity. Ecological research from 21 developed countries found that girls who ate fast food at least twice a week were more likely to become obese compared with those who ate fast food less frequently. Unfortunately, the assimilation of other cultures into American society may not help improve the obesity problem. In one study, while regularly eating at fast food restaurants increased the risk of overweight in adults and children in Mexican-American families by a factor of 2.2, the risk of overweight associated with eating at buffet-style restaurants was slightly worse (odds ratio = 2.8). Families who ate food at Mexican restaurants, however, were less likely to be overweight.

Stress and Obesity-The Environment

The work environment can contribute to obesity as well. In a study of 208 male workers in Japan, obesity was associated with psychological tension and anxiety, much of which was derived from high demands and poor decision latitude at work. The authors also found that higher degrees of stress negatively affected subjects’ diets, which contributed to higher rates of obesity. The current study examined the 10,308 civil servants from the Whitehall II study, all of whom were between the ages of 35 and 55. Work stress was assessed by the Job Strain Questionnaire and defined by poor work social support, high job demands, and low job control. Overall, work strain was associated with increased risk of BMI obesity by a maximum odds ratio of 1.73, and of waist obesity by a maximum odds ratio of 1.61. There was a dose-response relationship between the number of reports of stress and obesity. There were some interesting nuances related to the study’s main finding. Men were more likely than women to suffer the negative effects of job strain in terms of obesity, to the point that women did not experience a significant increase in waist obesity with stress. Overall, poor social support at work was the most important singular factor of job strain in increasing the risk of obesity in this study. The study was strengthened by analyzing individuals prospectively over time and employing repeated measures of job stress as participants advanced through their careers. However, the study was limited by examining a very specific group of employees — civil servants — in a first-world country.

Stress and Obesity-Health Risk

Obesity may just be a part of the overall increased health risk associated with work stress, with the sum of these risks being an increased prevalence of cardiovascular disease. In a study of nearly 7000 individuals, the prevalence of smoking was elevated among subjects with greater job strain, while men with low degrees of decision latitude were also more likely to be sedentary. However, no job environment factor in this study was independently related to increase BMI. A case-control analysis of 609 workers in France found that job strain increased the risk of developing hypertension. The odds ratios for hypertension associated with job strain were 3.20 in women and 2.60 in men. Low social support at work was not related to hypertension, and, moreover, higher levels of social support did not mitigate the effects of job strain on hypertension. Another study of female nurses and male factory workers generally corroborated these results. Researchers found that increased duration of shifts during work was associated with increased systolic blood pressure among men over age 30. Both BMI and waist-to-hip ratio increased with increasing shift duration among nurses. The study of nurses and factory workers failed to find an association between blood glucose levels and the duration of shift work. In another analysis of the Nurses’ Health Study II cohort, working overtime was associated with an increased risk of developing type 2 diabetes, while women who worked less than 20 hours per week had a lower risk of diabetes. There is also evidence that serum markers associated with an increased risk of cardiovascular disease may increase with job stress. A study of adults in Sweden found that men reporting high effort and low reward at work had increased levels of total cholesterol and the total cholesterol/high-density lipoprotein cholesterol ratio after adjustment for possible confounders. Women whose jobs required more effort had higher levels of low-density lipoprotein cholesterol. The association between stress at work and cardiovascular risk factors such as BMI, hypertension, and lipid levels points to a possible larger relationship between work stress and cardiovascular disease. The researchers of the Whitehall study have previously examined this issue in their study cohort. They demonstrated that the hazard ratio for coronary heart disease was increased with low decision latitude among men (adjusted hazard ratio 1.43), but low decision latitude did not significantly increase the risk of coronary heart disease among women. However, both men and women experienced increased risks of coronary heart disease with higher demands at work. This increased risk of coronary heart disease was increased with job stress at all employment grades in the organization. This research echoed previous studies in that greater social support at work failed to improve cardiovascular outcomes associated with significant job stress.

Stress and Obesity-Effects
Stress

The harmful health effects of stress-induced obesity.

The effects of stress at work constitute a major public health issue. As clinicians, the best we can do is counsel patients about the potential cardiovascular and metabolic events associated with high levels of stress and encourage healthy life choices for patients at risk. While it may be unrealistic to ask employers to reduce job stress at all levels in our competitive economy, these same employers should understand that their employees’ health is critical to their success. There is a dearth of data regarding stress reduction programs at work and cardiovascular outcomes, and future researchers should address this issue. The phenomenon of obesity being among chronic diseases makes Dr. Akoury of AWAREmed Health and Wellness Resource Center very resourceful for you. She will help you achieve optimal weight loss, the Dr. Focus on Neuroendocrine Restoration (NER) to reinstate normality through realization of the oneness of Spirit, Mind, and Body, Unifying the threesome into ONE. With the help of Dr. Akoury your problem is sorted out for good.

Stress and Obesity-Not a Union

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Adrenaline, Stress and Obesity-All you need to know

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

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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