Possible Connections between Stress, Diabetes, Obesity, Hypertension and Altered Lipoprotein Metabolism that may Result in Atherosclerosis

Abstract

This review has discussed some metabolic and endocrine changes that can be associated with a stress type of metabolism, diabetes, obesity, hypertension, smoking and the consumption of diets rich in fat and refined sugar, or poor in ascorbate. These are some of the risk factors associated with premature atherosclerosis, coronary thrombosis and stroke. It has been proposed that an increased control of metabolism by the 'stress' or counter-regulatory hormones, relative to insulin, is a common feature of these risk factors. Particular emphasis was placed upon the action of the glucocorticoids which can produce insulin insensitivity, leading to hyperglycaemia, hypertriglyceridaemia, hypercholesterolaemia and hyperinsulinaemia. Furthermore, glucocorticoids can decrease energy expenditure and, together with insulin, promote energy deposition. These observations provide a partial explanation for the metabolic changes that can accompany the risk factors and clarify why they interact in promoting atherosclerosis.

Childhood and adult dietary vitamin E intake and cardiovascular risk factors in mid-life in the 1946 British Birth Cohort

“…Other factors that may contribute to this effect, and for which it has not been possible to adjust, include physical and psychosocial stress. Such stresses have been related to elevated cortisol levels that in turn have been associated with central adiposity (Bjorntorp, 2001) and Brindley (Brindley & Rolland, 1989) set out plausible mechanistic pathways. Poorer maternal nutrition in the lower socioeconomic groups might also have compromised foetal nutrition and increased propensity to cardiovascular risk (Barker, 1997).…”

Rorschach Performance Assessment System (R-PAS) and vulnerability to stress: A preliminary study on electrodermal activity during stress

“…Prolonged release of catecholamines, however, may induce serious consequences for both physical and mental health. In fact, high levels of stress hormones increase the risk for phenomena such as hypertension, insulin resistance, hypercholesterolemia, and hyperlipidemia (e.g., Brindley andRolland, 1989, Rosmond et al, 1995), which in turn are primary risk factors for various life-threatening metabolic and cardiovascular conditions. High levels of stress hormones also tend to affect the activity of neurotransmitters important to brain structures such as the amygdala and the hippocampus, increasing the likelihood to develop psychological problems such as anxiety, sleep disorders, or selective cognitive impairments (Arnsten, 1998;Lupien and Meaney 1998;De Kloet et al, 1998;McEwen et al, 1999;Nemeroff, 1996;Rosen and Schulkin, 1998).…”

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

“…For example, the decrease in food intake and body weight gain caused by ADX and loss of CORT may reflect a simultaneous decline in circulating insulin and the loss of its anabolic actions (1 37). Moreover, the increased storage of nutrients and excess body weight gain seen with low-to-moderate levels of circulating CORT replacement may be attributed to the ability of this steroid to induce a counter-regulatory increase in insulin release in ADX animals (17,154,175). With respect to the catabolic effects and weight loss seen at high CORT doses, recent evidence suggests that this may be related to the hyperinsulinemia and an associated state of peripheral insulin resistance (251).…”

“…However, in evaluating the effects on body weight of ADX and hormone replacement at varying doses, it is important to consider all actions of these steroids, including their indirect effects on other endocrine systems. While type 11 receptor activation has anabolic effects geared towards the short-term maintenance of blood glucose and carbohydrate stores, daily carbohydrate intake by itself has little relation to body weight gain (1 11, 114), and chronic type I1 receptor stimulation at high CORT levels has catabolic effects on protein or fat stores (175). The involvement of type I receptors in body weight maintenance is strongly suggested by the potent stimulatory effect of ALDO on fat intake and fat deposition across the feeding cycle (153,159); however, the role of this mineralocorticoid receptor in normal fat oxidation, which is generally associated with high levels of CORT and type I1 receptor activation, remains to be demonstrated (12).…”

“…As described below, this antagonism between CORT and insulin becomes exaggerated when circulating CORT levels are abnormally and chronically high. Under these conditions, such as, in obesity, there occurs a compensatory rise in insulin secretion, and the resulting chronic hyperinsulinemia and hypercortisolemia increase hepatic lipogenesis, while reducing gluconeogenesis, and produce catabolic effects within muscle where CORT's actions outweigh those of insulin (154,174,175).…”