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Childhood obesity is a public health epidemic and is associated with substantial negative physical and psychosocial health consequences. Stress is thought to be one contributor to the development and maintenance of obesity in children and adolescents, yet the linkage between stress and paediatric obesity is a poorly understood phenomenon. This paper furthers the understanding of stress in the context of paediatric obesity by firstly presenting a focused review of what is known about links between chronic and acute stress and paediatric obesity risk and then synthesizing important areas from the literature. These critical areas of focus include the following: (1) physiological stress reactivity; (2) stress-induced eating; (3) stress and physical activity; (4) parent and family influences; and (5) stress in at-risk populations. This review is geared toward facilitating future research on the stress-obesity connection in youth.
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PMID:Stress and paediatric obesity: what we know and where to go. 2381 95

Psychological stress has been proposed as a major contributor to the progression of cardiovascular disease (CVD). Acute mental stress can activate the sympathetic-adrenal-medullary (SAM) axis, eliciting the release of catecholamines (NE and EPI) resulting in the elevation of heart rate (HR) and blood pressure (BP). Combined stress (psychological and physical) can exacerbate these cardiovascular responses, which may partially contribute to the elevated risk of CVD and increased proportionate mortality risks experienced by some occupations (e.g., firefighting and law enforcement). Studies have supported the benefits of physical activity on physiological and psychological health, including the cardiovascular response to acute stress. Aerobically trained individuals exhibit lower sympathetic nervous system (e.g., HR) reactivity and enhanced cardiovascular efficiency (e.g., lower vascular reactivity and decreased recovery time) in response to physical and/or psychological stress. In addition, resistance training has been demonstrated to attenuate cardiovascular responses and improve mental health. This review will examine stress-induced cardiovascular reactivity and plausible explanations for how exercise training and physical fitness (aerobic and resistance exercise) can attenuate cardiovascular responses to stress. This enhanced functionality may facilitate a reduction in the incidence of stroke and myocardial infarction. Finally, this review will also address the interaction of obesity and physical activity on cardiovascular reactivity and CVD.
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PMID:Cardiovascular reactivity, stress, and physical activity. 2422 57

Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body's resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie "palatable" food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.
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PMID:Eating behavior and stress: a pathway to obesity. 2486 May 41

The role that excess adipose tissue plays in chronic inflammation gives rise to its importance as an independent risk factor in cardiovascular dysfunction. Operationalizing chronic stress as obesity, we sought to explore the relationship between obesity, perceived stress and cardiovascular reactivity and recovery from laboratory stressors. Cardiovascular function was assessed using blood pressure and heart rate. Two stress tasks (mental arithmetic and cold pressor) were employed to examine potential differences between type of stress and cardiovascular response. Body mass index (BMI) was able to predict dysfunction in both cardiovascular reactivity and recovery. Participants with a higher BMI exhibited blunted systolic blood pressure and heart rate reactivity to the mental arithmetic task. In contrast, BMI has an incongruent effect on blood pressure reactivity to the cold pressor task that is dependent on the level of perceived stress. This suggests that in some instances the effect of BMI on cardiovascular response to acute stress may be moderated by perceived stress. Further, we found greater adiposity was related to delayed heart rate recovery following both stress tasks.
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PMID:Stress task specific impairments of cardiovascular functioning in obese participants. 2501 62

Changes in food composition and availability have contributed to the dramatic increase in obesity over the past 30-40 years in developed and, increasingly, in developing countries. The brain plays a critical role in regulating energy balance. Some human studies have demonstrated increased preference for high fat and high sugar foods in people reporting greater stress exposure. We have examined neurochemical changes in the brain in rodent models during the development of obesity, including the impact of obesity on cognition, reward neurocircuitry and stress responsiveness. Using supermarket foods high in fat and sugar, we showed that such a diet leads to changes in neurotransmitters involved in the hedonic appraisal of foods, indicative of an addiction-like capacity of foods high in fat and/or sugar. Importantly, withdrawal of the palatable diet led to a stress-like response. Furthermore, access to this palatable diet attenuated the physiological effects of acute stress (restraint), indicating that it could act as a comfort food. In more chronic studies, the diet also attenuated anxiety-like behavior in rats exposed to stress (maternal separation) early in life, but these rats may suffer greater metabolic harm than rats exposed to the early life stressor but not provided with the palatable diet. Impairments in cognitive function have been associated with obesity in both people and rodents. However, as little as 1 week of exposure to a high fat, high sugar diet selectively impaired place but not object recognition memory in the rat. Excess sugar alone had similar effects, and both diets were linked to increased inflammatory markers in the hippocampus, a critical region involved in memory. Obesity-related inflammatory changes have been found in the human brain. Ongoing work examines interventions to prevent or reverse diet-induced cognitive impairments. These data have implications for minimizing harm caused by unhealthy eating.
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PMID:Why is obesity such a problem in the 21st century? The intersection of palatable food, cues and reward pathways, stress, and cognition. 2549 5

Cortisol measurements in blood, saliva and urine are frequently used to examine the hypothalamus-pituitary-adrenal (HPA) axis in clinical practice and in research. However, cortisol levels are subject to variations due to acute stress, the diurnal rhythm and pulsatile secretion. Cortisol measurements in body fluids are not always a reflection of long-term cortisol exposure. The analysis of cortisol in scalp hair is a relatively novel method to measure cumulative cortisol exposure over months up to years. Over the past years, hair cortisol concentrations (HCC) have been examined in association with a large number of somatic and mental health conditions. HCC can be used to evaluate disturbances of the HPA axis, including Cushing's syndrome, and to evaluate hydrocortisone treatment. Using HCC, retrospective timelines of cortisol exposure can be created which can be of value in diagnosing cyclic hypercortisolism. HCC have also been shown to increase with psychological stressors, including major life events, as well as physical stressors, such as endurance exercise and shift work. Initial studies show that HCC may be increased in depression, but decreased in general anxiety disorder. In posttraumatic stress disorder, changes in HCC seem to be dependent on the type of traumatic experience and the time since traumatization. Increased hair cortisol is consistently linked to obesity, metabolic syndrome and cardiovascular disease. Potentially, HCC could form a future marker for cardiovascular risk stratification, as well as serve as a treatment target.
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PMID:Clinical applications of cortisol measurements in hair. 2592 11

In utero, hypoxia is a significant yet common stress that perturbs homeostasis and can occur due to preeclampsia, preterm labor, maternal smoking, heart or lung disease, obesity, and high altitude. The fetus has the extraordinary capacity to respond to stress during development. This is mediated in part by the hypothalamic-pituitary-adrenal (HPA) axis and more recently explored changes in perirenal adipose tissue (PAT) in response to hypoxia. Obvious ethical considerations limit studies of the human fetus, and fetal studies in the rodent model are limited due to size considerations and major differences in developmental landmarks. The sheep is a common model that has been used extensively to study the effects of both acute and chronic hypoxia on fetal development. In response to high-altitude-induced, moderate long-term hypoxia (LTH), both the HPA axis and PAT adapt to preserve normal fetal growth and development while allowing for responses to acute stress. Although these adaptations appear beneficial during fetal development, they may become deleterious postnatally and into adulthood. The goal of this review is to examine the role of the HPA axis in the convergence of endocrine and metabolic adaptive responses to hypoxia in the fetus.
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PMID:Fetal endocrine and metabolic adaptations to hypoxia: the role of the hypothalamic-pituitary-adrenal axis. 2617 60

Recent research shows that blunted cardiovascular and cortisol reactions to acute psychological stress are associated with adverse behavioural and health outcomes: depression, obesity, bulimia, and addictions. These outcomes may reflect suboptimal functioning of the brain's fronto-limbic systems that are needed to regulate motivated behaviour in the face of challenge. In support of this, brain imaging data demonstrate fronto-limbic hypoactivation during acute stress exposure. Those demonstrating blunted reactions also show impairments of motivation, including lower cognitive ability, more rapid cognitive decline, and poorer performance on motivation-dependent tests of lung function. Persons exhibiting blunted stress reactivity display well established temperament characteristics, including neuroticism and impulsivity, characteristic of various behavioural disorders. Notably, the outcomes related to blunted stress reactivity are similar to those that define Reward Deficiency Syndrome. Accordingly, some individuals may be characterised by a broad failure in cardiovascular and cortisol responding to both stress and reward, reflecting fronto-limbic dysregulation. Finally, we proffer a model of blunted stress reactivity, its antecedents and sequelae, and identify future research priorities.
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PMID:The behavioural, cognitive, and neural corollaries of blunted cardiovascular and cortisol reactions to acute psychological stress. 2825 28

The relationship between testosterone deficiency (TD) syndrome and surgical resilience has a great impact in the modern approach to male elderly patients. There is good evidence that low levels of T are a strong marker for cardiovascular risk; also, TD is frequently associated with increased cardiovascular and all-cause mortality especially in cardiac older frail men. Screening for low T should be mandatory in high risk groups candidate to surgery including those with diabetes, metabolic syndrome and obesity, even though benefits from T-treatment on survival rates are unclear. The low-T3 syndrome, named non-thyroidal illness (NTI) that occurs during critical illness refers to a syndrome with different faces in both sexes. The acute stress or critical illness-induced alterations within the thyroid axis occur in the first days of critical illness i.e. post-surgery and are brought about at least in part by the concomitant macronutrient deficit. The NTI that occurs in prolonged critically ill patients or in post-surgical resilience patients who continue to be dependent on intensive medical care for weeks or months, may have an impact on surgical outcomes because of frequent occurrence of cardiac arrhythmias. Future directions should better routinely investigate circulating thyroid hormones in population at risk before surgery after excluding iatrogenic drug interferences, and investigate the effect of possible treatments on survival rates after surgery.
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PMID:Testicular and thyroid function as survival predictors in the elderly patient candidate to surgery. 2896 25

The dynorphin/kappa opioid receptor (KOR) system is implicated in the "dark side" of addiction, in which stress exacerbates maladaptive responses to drug and alcohol exposure. For example, acute stress and acute ethanol exposure result in an elevation in dynorphin, the KOR endogenous ligand. Activation of KORs results in modulation of several neurotransmitters; however, this chapter will focus on its regulatory effects on dopamine in mesolimbic areas. Specifically, KOR activation has an inhibitory effect on dopamine release, thereby influencing reward processing. Repeated stimulation of KORs, for example, via chronic drug and/or stress exposure, results in increased function of the dynorphin/KOR system. This augmentation in KOR function shifts the homeostatic balance in favor of an overall reduction in dopamine signaling via either by reducing dopamine release or by increasing dopamine transporter function. This chapter examines the effects of chronic ethanol exposure on KOR function and the downstream effects on dopamine transmission. Additionally, the impact of chronic cocaine exposure and its effects on KOR function will be explored. Further, KORs may also be involved in driving excessive consumption of food, contributing to the risk of developing obesity. While some studies have shown that KOR agonists reduce drug intake, other studies have shown that antagonists reduce addiction-like behaviors, demonstrating therapeutic potential. For example, KOR inhibition reduces ethanol intake in dependent animals, motivation to self-administer cocaine in chronic stress-exposed animals, and food consumption in obese animals. This chapter will delve into the mechanisms by which modulation of the dynorphin/KOR system may be therapeutic.
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PMID:Dynorphin/Kappa Opioid Receptor Signaling in Preclinical Models of Alcohol, Drug, and Food Addiction. 2905 56


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