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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The multifactorial nature of depression resembles that of other complex disorders such as diabetes mellitus or coronary artery disease. However, while for the latter disorders predisposing and risk factors have been identified, such knowledge is still scarce in depression. In this review we propose to use diabetes mellitus, for which characteristic milestones have been condensed to obesity-hyperinsulinaemia-insulin resistance-diabetes mellitus, as a conceptual analogical model. Based on this model we hypothesize that depression develops according to a similar pattern: prolonged psychological stress-hyperserotonism-serotonin resistance-major depression. We review extensive supporting evidence from human studies and animal models of depression, including stress involvement in the aetiology of depression, evidence for increased synaptic serotonin and decreased 5-HT1A receptor activity. Conceptualizing the pathogenesis of depression as a multi-step process may inspire new concepts, which will eventually lead to delineation of additional preventive and therapeutic interventions similar to those currently practised in diabetes.
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PMID:Major depression as a disorder of serotonin resistance: inference from diabetes mellitus type II. 1725 Jul 76

An increasing number of people report concerns about the amount of stress in their life. At the same time obesity is an escalating health problem worldwide. Evidence is accumulating rapidly that stress related chronic stimulation of the hypothalamic-pituitary-adrenal (HPA) axis and resulting excess glucocorticoid exposure may play a potential role in the development of visceral obesity. Since adequate regulation of energy and food intake under stress is important for survival, it is not surprising that the HPA axis is not only the 'conductor' of an appropriate stress response, but is also tightly intertwined with the endocrine regulation of appetite. Here we attempt to link animal and human literatures to tease apart how different types of psychological stress affect eating. We propose a theoretical model of Reward Based Stress Eating. This model emphasizes the role of cortisol and reward circuitry on motivating calorically dense food intake, and elucidating potential neuroendocrine mediators in the relationship between stress and eating. The addiction literature suggests that the brain reward circuitry may be a key player in stress-induced food intake. Stress as well as palatable food can stimulate endogenous opioid release. In turn, opioid release appears to be part of an organisms' powerful defense mechanism protecting from the detrimental effects of stress by decreasing activity of the HPA axis and thus attenuating the stress response. Repeated stimulation of the reward pathways through either stress induced HPA stimulation, intake of highly palatable food or both, may lead to neurobiological adaptations that promote the compulsive nature of overeating. Cortisol may influence the reward value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (NPY). Whereas glucocorticoids are antagonized by insulin and leptin acutely, under chronic stress, that finely balanced system is dysregulated, possibly contributing to increased food intake and visceral fat accumulation. While these mechanisms are only starting to be elucidated in humans, it appears the obesity epidemic may be exacerbated by the preponderance of chronic stress, unsuccessful attempts at food restriction, and their independent and possibly synergistic effects on increasing the reward value of highly palatable food.
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PMID:Stress, eating and the reward system. 1754 57

Ganglionic long-term potentiation (gLTP) is an activity-dependent sustained increase in the synaptic efficacy of the nicotinic pathway that has been demonstrated in autonomic ganglia. Sustained enhancement in ganglionic transmission as in chronic mental stress may affect the activity of autonomic functions, including blood pressure and heart rate. An increase in sympathetic activity associated with psychosocial stress and stress-prone conditions such as obesity and aging could result in in vivo expression of gLTP leading to hypertension of a neural origin. Recent reports indicated that the prevention of the expression of gLTP in animal models of hypertension prevented or reduced high blood pressure. Although stress-induced hypertension normalizes within a few days of stress relief, prolonged mild-moderate hypertension may contribute to atherosclerotic cardiovascular diseases. The relation between hypertension and enhanced ganglionic transmission as a result of in vivo expression of gLTP is discussed in this review.
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PMID:Role of long-term potentiation of sympathetic ganglia (gLTP) in hypertension. 1765 63

Obesity and type 2 diabetes continue to be major public health burdens with type 2 diabetes rising in epidemic proportions. Since known risk factors do not explain all of the variance in the population, it is important to identify novel risk factors that can lead to development of new preventive measures. Chronic psychological stress and depression are associated with type 2 diabetes but the mechanism remains unclear. Neuroendocrine changes induced by these stressors, specifically activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS), might provide a unifying explanation. The objectives of this review are (1) to summarize the metabolic impact of HPA axis and SNS dysfunction induced by depression and stress, (2) to summarize the relation of neuroendocrine parameters to risk factors for diabetes, (3) to discuss the limitations of assessing neuroendocrine function in population-based and intervention studies, and (4) to summarize the evidence of the impact of stress reduction, by cognitive behavior therapy (CBT), on neuroendocrine factors and on outcomes in diabetes and obesity.
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PMID:A review of the evidence for a neuroendocrine link between stress, depression and diabetes mellitus. 1822 Jun 83

Previous studies have reported that psychological stress is associated with greater food consumption, particularly consumption of high fat foods. We are unaware of any studies that have examined stress-induced eating among African Americans (AAs). The goals of the current study were to examine the relationship between perceived stress and high fat eating behaviors in a sample of AAs, to examine whether this relationship is stronger among overweight and obese participants, and to examine whether haphazard meal planning mediates the relationship between perceived stress and high fat eating behaviors. One hundred fifty-nine adults from a metropolitan area completed the Perceived Stress Scale (PSS-10), the Eating Behaviors Pattern Questionnaire (EBPQ), a demographic questionnaire, and body mass was assessed with BMI. Perceived stress was associated with haphazard planning and emotional eating, but not related to other high fat eating domains in the overall sample. These findings held for overweight and obese participants with the addition of snacking on sweets. High fat eating behaviors were not mediated by haphazard meal planning. These findings are consistent with other studies which demonstrate a link between stress and eating. Long-term interventions for high fat consumption and obesity should include an examination of perceived stress among AAs.
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PMID:Perceived stress and eating behaviors in a community-based sample of African Americans. 1832 91

Obesity, lipid disorders, type 2 diabetes, high blood pressure and coronary heart disease are frequently encountered in wealthy populations. All these disorders frequently occur as clusters, constituting the metabolic syndrome. It is currently admitted that insulin resistance plays a central role in the pathogenesis of this syndrome. Stress responses include activation of the sympathetic nervous system and stimulation of epinephrine and cortisol release. These hormones may over the long term reduce insulin sensitivity. Cortisol may also favour the development of central obesity. In healthy individuals, mental stress increases heart rate, but simultaneously decreases vascular resistance in skeletal muscle. This results in a moderate increase in blood pressure, and an acute increase in insulin-mediated glucose disposal. In obese patients, mental stress elicits responses which differ widely from those of healthy individuals. While mental stress enhances catecholamine-mediated energy expenditure in obese patients to the same extent as in lean subjects, it fails to decrease systemic vascular resistance due to endothelial dysfunction. This leads to enhanced blood pressure responses and the absence of stimulation of glucose disposal in obese subjects during mental stress. It can be hypothesized that repeated professional or social stress may activate the sympathoadrenal system, resulting in high cortisol levels, stimulation of the sympathetic nervous system, and epinephrine secretion. All these factors may eventually lead to the development of central obesity and insulin resistance. Furthermore, the blood pressure responses to mental stress may be enhanced in insulin-resistant individuals, favouring the development of vascular complications.
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PMID:Stress and metabolism. 1837 Jul 4

Obesity results from a number of factors including socio-environmental influences and rodent models show that several different stressors increase the preference for calorically dense foods leading to an obese phenotype. We present here a non-human primate model using socially housed adult female macaques living in long-term stable groups given access to diets of different caloric density. Consumption of a low fat (LFD; 15% of calories from fat) and a high fat diet (HFD; 45% of calories from fat) was quantified by means of a custom-built, automated feeder that dispensed a pellet of food when activated by a radiofrequency chip implanted subcutaneously in the animal's wrist. Socially subordinate females showed indices of chronic psychological stress having reduced glucocorticoid negative feedback and higher frequencies of anxiety-like behavior. Twenty-four hour intakes of both the LFD and HFD were significantly greater in subordinates than dominates, an effect that persisted whether standard monkey chow (13% of calories from fat) was present or absent. Furthermore, although dominants restricted their food intake to daylight, subordinates continued to feed at night. Total caloric intake was significantly correlated with body weight change. Collectively, these results show that food intake can be reliably quantified in non-human primates living in complex social environments and suggest that socially subordinate females consume more calories, suggesting this ethologically relevant model may help understand how psychosocial stress changes food preferences and consumption leading to obesity.
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PMID:Quantifying food intake in socially housed monkeys: social status effects on caloric consumption. 1848 58

There is increased prevalence of abdominal pain and diarrhea and decreased gastric sensation with increased body mass index (BMI). Our hypothesis is that increased BMI is associated with increased colonic motility and sensation. The study aim was to assess effect of BMI on colonic sensory and motor functions and transit. We used a database of colonic tone, compliance, and perception of distensions measured by intracolonic, barostat-controlled balloon, and gastrointestinal transit was measured by validated scintigraphy in healthy obese and nonobese subjects. Regression analysis was applied to assess the association of BMI with colonic sensory and motor functions. We included adjustments for sex differences, age, height, balloon volumes during distension, and psychological stress. Among 165 participants (87 women, 78 men), increased BMI was associated with decreased colonic compliance (P < 0.006, adjusted), decreased pain rating during distensions (P = 0.02, adjusted), and a higher threshold for pain (P = 0.042, adjusted). Sensation for gas, colonic tone, and contraction after meal ingestion were not significantly associated with BMI. Transit was assessed in 72 participants (41 women, 31 men); colonic transit was faster with BMI >30 kg/m(2) (P = 0.003 unadjusted, P = 0.08 adjusted for gender). In conclusion, BMI >25 kg/m(2) is associated with decreased colonic compliance and pain sensation; colonic transit is accelerated particularly with BMI >30 kg/m(2) in women. These data suggest that colonic dysfunction may contribute to diarrhea, but the cause of increased abdominal pain in obesity is not explained by the studies of colonic sensation and requires further study of afferent, spinal, and central mechanisms.
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PMID:High body mass alters colonic sensory-motor function and transit in humans. 1861 55

White blood cell (WBC) count is well known to be an independent risk marker for cardiovascular disease. The aim of this study is to examine the relationships of WBC counts to seven health practices including obesity, eating habits, smoking, alcohol intake, sleeping, physical activity, and perceived mental stress, and then clustering the relevant healthy practices. The subjects were 1,492 male and 316 female Japanese workers aged 40 yr and over in 2002. Each of seven health practices from a self-administered questionnaire was categorized as a 'healthy' or 'unhealthy' practice, and WBC counts from fasting blood samples were determined by automated particle counters. The means of age and WBC counts were 49.5 yr and 5,375 cells/microl in men, and 48.6 yr and 4,890 cells/microl in women, respectively. After multivariate adjustments for all health practices and age, the estimated WBC counts were significantly lower in normal weight subjects and never or former smokers (p<0.01). Age-adjusted WBC counts decreased significantly by 204.9+/-23.7 cells/microl (means+/-SE) and 117.6+/-53.2 cells/microl for each increase in one healthy practice (p<0.05), respectively, suggesting that cultivating healthier practices would lead to lower WBC counts. This study recommends modifying unhealthy practice one by one and maintaining healthy practices as an effective strategy for the prevention of atherosclerotic diseases, in addition, to quit smoking or abstain from heavy smoking especially in men is important to prevent the low-grade inflammation.
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PMID:Having more healthy practice was associated with low white blood cell counts in middle-aged Japanese male and female workers. 1871 82

Obesity is associated with an elevated risk of hypertension and cardiovascular disease. The adipocyte hormone leptin, which stimulates energy expenditure in animals by activating the sympathetic nervous system (SNS), is believed to play a role in this association. However, evidence in humans remains sparse. We investigated the relationship between circulating leptin and cardiovascular and inflammatory responses to acute psychological stress in humans. Participants were 32 men and 62 women aged 18-25 years. Cardiovascular activity was assessed using impedance cardiography at baseline, during acute laboratory stress, and during a 45-min recovery period. Plasma cytokines were measured in blood drawn at baseline and 45-min poststress. In women only, baseline plasma leptin was significantly associated with stress-induced changes in heart rate (beta = 0.53, P = 0.006), heart rate variability (HRV) (beta = -0.44, P = 0.015), and cardiac preejection period (PEP) (beta = -0.51, P = 0.004), independent of age, adiposity, and smoking. Women's plasma leptin levels also correlated with stress-induced elevations in the proinflammatory cytokine interleukin-6 (IL-6) (beta = 0.35, P = 0.042). Circulating leptin is an independent predictor of sympathetic cardiovascular activity, parasympathetic withdrawal, and inflammatory responses to stress in women. Because cardiovascular and inflammatory stress responses are predictive of future cardiovascular disease, leptin may be a mechanism mediating the adverse effects of stress and obesity on women's cardiovascular health.
Obesity (Silver Spring) 2008 Dec
PMID:Circulating leptin and stress-induced cardiovascular activity in humans. 1882 Jun 49


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