Stress and the Metabolic Syndrome

Hjemdahl, Paul

doi:10.1161/01.cir.0000041502.43564.79

Cited by 87 publications

(20 citation statements)

References 19 publications

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“…These integrated actions are clearly evolutionarily highly appropriate for organisms that may be confronted by drought and famine, and must have both the motivation, memory and energy stores to enable movement to a less hostile environment if they are to sustain life. However, with the rapid pace of many societies that are progressing toward, or have arrived at the nearly instant availability of hedonically rewarding, highly palatable highfat and sugar-laden foods with the expenditure of little to no effort, as well as with the perceived increase in social stressors in modern times, the tonic effects of elevated glucocorticoids may contribute to the current epidemic of obesity [57][58][59][60][61][62]. This, together with ageing, and the sleepdeprivation that occurs in individuals with Alzheimer's Disease, may serve to worsen this catastrophic disease.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids, the Etiology of Obesity and the Metabolic Syndrome

Dallman¹,

Akana²,

Pecoraro³

et al. 2007

CAR

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In mammals, glucocorticoid actions appear to have evolved to maintain and enhance energy stores to be used for life-saving gluconeogenesis. They act on the brain to stimulate search behaviors, palatable feeding and emotionally relevant memories, and they act on the body to mobilize stored peripheral energy and direct it to central depots that serve the substrate needs of the liver. Our work in rats shows that searching and intake of palatable foods (sucrose, saccharin and lard) are stimulated by corticosterone in a dose-related fashion. Adrenalectomized rats gain weight poorly, have low fat content, increased sympathetic neural and hypothalamo-pituitary-adrenal outflow, and altered behaviors. Replacement with corticosterone reverses these effects. Surprisingly, when such rats are provided with 30% sucrose to drink, in addition to saline, all of the usual effects of adrenalectomy are corrected without corticosterone. We hypothesize that there is a metabolic feedback system that decreases stress-responsiveness. Although we have not yet identified the signal associated with sucrose drinking, the weight of mesenteric fat correlates inversely with hypothalamic corticotropin-releasing factor (CRF). When rats eat lard and sucrose ad libitum, fat stores increase and CRF, ACTH and corticosterone responses are reduced. During stress, chow intake decreases but intake of lard and sucrose does not. Our current working model suggests that palatability signals and neural signals from fat stores act on brain to reduce activity in the central stress response system. Correlative results from a clinical study support the powerful role of small changes in glucocorticoids in type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

Glucocorticoids, the Etiology of Obesity and the Metabolic Syndrome

Dallman¹,

Akana²,

Pecoraro³

et al. 2007

CAR

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“…t has often been hypothesized that stress leads to the metabolic syndrome (1)(2)(3). Dysregulation of one of the main stress systems-the autonomic nervous systemcould lead to insulin resistance, altered lipid metabolism, and increased blood pressure (BP) (4 -8).…”

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confidence: 99%

Dysregulation of the Autonomic Nervous System Predicts the Development of the Metabolic Syndrome

Licht

Geus

Penninx

2013

The Journal of Clinical Endocrinology &Amp; Metabolism

120

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Context:Stress is suggested to lead to metabolic dysregulations as clustered in the metabolic syndrome. Although dysregulation of the autonomic nervous system is found to associate with the metabolic syndrome and its dysregulations, no longitudinal study has been performed to date to examine the predictive value of this stress system in the development of the metabolic syndrome.Objective: We examined whether autonomic nervous system functioning predicts 2-year development of metabolic abnormalities that constitute the metabolic syndrome.Design: Data of the baseline and 2-year follow-up assessment of a prospective cohort: the Netherlands Study of Depression and Anxiety was used.Setting: Participants were recruited in the general community, primary care, and specialized mental health care organizations.Participants: A group of 1933 participants aged 18 -65 years. Main outcome measures:The autonomic nervous system measures included heart rate (HR), respiratory sinus arrhythmia (RSA; high RSA reflecting high parasympathetic activity), pre-ejection period (PEP; high PEP reflecting low sympathetic activity), cardiac autonomic balance (CAB), and cardiac autonomic regulation (CAR). Metabolic syndrome was based on the updated Adult Treatment Panel III criteria and included high waist circumference, serum triglycerides, blood pressure, serum glucose, and low high-density lipoprotein (HDL) cholesterol.Results: Baseline short PEP, low CAB, high HR, and CAR were predictors of an increase in the number of components of the metabolic syndrome during follow-up. High HR and low CAB were predictors of a 2-year decrease in HDL cholesterol, and 2-year increase in diastolic and systolic blood pressure. Short PEP and high CAR also predicted a 2-year increase in systolic blood pressure, and short PEP additionally predicted 2-year increase in diastolic blood pressure. Finally, a low baseline RSA was predictive for subsequent decreases in HDL cholesterol. Conclusion:Increased sympathetic activity predicts an increase in metabolic abnormalities over time. These findings suggest that a dysregulation of the autonomic nervous system is an important predictor of cardiovascular diseases and diabetes through dysregulating lipid metabolism and blood pressure over time.

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“…Encouraged by the development of molecular biology, by sophisticated modern biotechnologies and, in general, by modern neuroscience, we have in the last few years started the still diffi cult task of understanding the biological correlates of psychological functions [1] . This fascinating adventure is only at the beginning, but we are getting a deeper knowledge of psychobiological correlates [2][3][4] , impact of social life style, individual perception of adverse effects, and major chronic debilitating diseases, such as obesity, type 2 diabetes mellitus and cardiovascular diseases [5] . The article by Ryff et al [6] published in this issue focuses on an interesting question in psychology: 'Is well-being merely the fl ip-side of studying psychological maladjustment' to adverse internal or external factors, 'or do well-being and ill-being constitute separate, independent dimensions of mental functioning?'…”

mentioning

confidence: 99%

The Biological Balance between Psychological Well-Being and Distress: A Clinician’s Point of View

Pasquali¹

2006

Psychother Psychosom

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Stress and the Metabolic Syndrome

Cited by 87 publications

References 19 publications

Glucocorticoids, the Etiology of Obesity and the Metabolic Syndrome

Glucocorticoids, the Etiology of Obesity and the Metabolic Syndrome

Dysregulation of the Autonomic Nervous System Predicts the Development of the Metabolic Syndrome

The Biological Balance between Psychological Well-Being and Distress: A Clinician’s Point of View

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