Does stress induced cortisol contribute to central obesity - Essay Example

Does stress induced cortisol contribute to central obesity and can diet, exercise and relaxation have a positive effect? Obesity is a multidimensional disease that is increasing in prevalence, especially in the Western countries, including the United States and United Kingdom (Flegal, 2002). Many factors have been observed to be related to its etiopathogenesis. One such factor is stress. Stress is thought to influence human eating behaviour and appears to alter overall food intake in two ways, resulting in under- or overeating, which may be related to the severity of stress. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, basically those that are high in sugar and fat, contributing to the development of obesity (Torres et al, 2007). In clinical practice, obese patients report stress as a primary trigger for binge eating (De Kloeth at al, 1998). Since cortisol is released during stress and can increase hunger and feeding behavior, endogenous cortisol release stimulated by stress may mediate stress-induced eating. The positive association between development of central obesity and increased cortisol levels has been demonstrated by numerous studies (Dimitriou, Maser-Gluth & Remer, 2003; Livingstone et al, 2000; Tiosano et al, 2003). Increased cortisol secretion results in an increased energy intake in both males and females (Epel et al, 2001). The study by Gluck et al (2004) and Gluck (2006) showed that increased cortisol secretion, a major component of the stress response, could play an important role in pathogenesis of binge eating, leading to development of obesity by increasing food intake. Increased basal cortisol levels have also been found in bulimia nervosa contributing to a great amount of hunger and binge eating. An increased cortisol level has been shown to be positively related to central fat distribution in both obese and lean individuals (Bjorntorp, et al, 2000; Douyon et al, 2002). The study by Epel et al (2000) supports the hypothesis that stress-induced cortisol secretion may contribute to central fat and demonstrate a link between psychological stress and risk for disease in women. This relationship holds true in men as well. Besides obesity, increased cortisol levels are also associated with, profound alteration of intermediary metabolism, insulin resistance, changes in lipid metabolism, hypertension and cardiovascular abnormalities (Barker, 1998; De koeth et al, 1998; Girdler et al (1998); Litchfield et al, 1998; Walker et al, 1998; Fraser et al, 1999; Nejtek (2002); Dover et al, 2007; Wei et al, 2007). In these obese subjects, levels of cortisol in plasma, saliva or urine may be significantly higher than those of matched normal subjects (Andrew et al, 1998; Power, Li & Hertzman, 2006). These studies illustrate that increased cortisol levels are associated with an increase incidence of obesity as well as other health related problems in both men and women. Although chronic elevations in cortisol levels can promote insulin resistance and abdominal obesity, the acute elevation of cortisol plays a protective role during stress (Wallerius et al, 2003). However, the biological mechanism underlying this positive relationship between increased cortisol levels and obesity is poorly understood. It has been hypothesized that in patients with bulimia, hypothalamic and pituitary centers controlling adrenal activity have diminished sensitivity to negative feedback inhibition, which may result in excessive cortisol production in these individuals (Plotsky, 1998; Birketvedt et al 1999; Monteleone et al, 1999; Birketvedt et al, 2002). Oral administration of dexamethasone, which mimics cortisol, normally suppresses the morning cortisol rise in normal individuals with intact negative feedback inhibition (Brook, & Nicolas, 2001). Failure to respond to dexamethasone is indicated by morning cortisol >5 µg/dl (Brook, & Nicolas, 2001). However it was observed that in patients with bulimia there is reduced suppression of cortisol after a dexamethasone suppression test (DST) resulting in excessive stimulation of the hypothalamic-pituitary-adrenal (HPA) axis which may produce hypercortisolemia and diminished sensitivity to HPA axis to negative feedback, resulting in development of obesity in long run. (Girdler et al, 1998; Seckl et al, 2004; Tomlinson et al, 2004; Sandeep et al, 2005). Even gloucocorticoids given exogeneously can induce obesity by increasing food intake (koo-Loeb et al, 2000). Numerous studies (Bujalska et al, 1999; Wolf 1999; Bujalska et al, 2002; Bujalska et al, 2006), have defined the permissive role of glucocorticoids in inducing adipocyte differentiation and maturation. In a study by Fraser et al, (1999) it was shown that circulating glucocorticoid levels may be normal or even slightly reduced in obese patients. Thus Fraser et al (1999) proposed that glucocorticoids can be generated within human adipose tissue, specifically in omental depots, at a cellular level. A mechanism involving the increased mRNA expression of the enzyme, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which activates cortisol from cortisone locally within adipose tissue and is essential for the induction of human adipogenesis has been described by Bujalska et al, 2008; Weaver et al, 1998; Wiegand et al, 2007; Buren et al, 2007; Tomlinson et al, 2007; Sandeep et al, 2005; Tomlinson et al, 2004; and Seckl et al, 2004. However, despite of much research in the field, many gaps remain that need to be filled. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the relationship between stress and obesity how the etiopathology of stress related obesity might be linked to hormones (typically cortisol) that control appetite. Role of diet, exercise and relaxation Obesity adversely affects cardiac function, and increases the risk factors for numerous health related problems including atherosclerosis, stroke, coronary heart disease, type II diabetes, insulin resistance etc (Despres et al, 2000; Folsom et al, 2000; Couillard et al, 2002; Janssen et al, 2002; Lemieux et al, 2000; Miyazaki et al, 2002; Nguyen-Duy et al, 2003; Nieves et al, 2003; Caterson et al, 2004). Current therapies available for weight management primarily include lifestyle modifications mainly in form of dietary intervention, increased physical activity, mental relaxation, pharmacotherapy, and surgery (European Task Force members, 2007; O’Neil and Nicklas, 2007; Praet & Van Loon, 2007; Meka et al, 2008; Metsios et al, 2008; Janiszewski et al, 2008; Ungvari et al, 2008). Behaviour modification to enhance dietary and exercise habits forms an important component of all of these treatments. The statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism (2004), after reviewing the relationship between obesity and the cardiovascular system, evaluated the effect of weight loss on the risk of coronary heart disease. The study demonstrated that weight loss and physical activity can prevent and treat obesity-related coronary heart disease and should be considered a primary therapy for obese patients with cardiovascular disease. Modest weight loss can reduce the person’s risk for coronary heart disease by improving diastolic function. In STRRIDE: a randomized, controlled study analyzing the effect of exercise intensity and amount on weight gain (Slentz et al, 2005), one hundred and seventy-five sedentary, obese men and women with mild to moderate dyslipidemia were randomly assigned to either participate for 6 months in a control group or for 8 months in one of three exercise groups: first group in which low amount, moderate intensity exercise, equivalent to walking 12 miles/wk (19.2 km), with 40–55% of peak oxygen consumption was prescribed. In the second group, low amount, vigorous intensity exercise, equivalent to jogging 12 miles/wk at 65–80% of peak oxygen consumption was prescribed. While in the third group, high amount, vigorous intensity, equivalent to jogging 20 miles/wk (32.0 km) was prescribed. Abdominal fat was analyzed using computed tomography scan. The results of the study showed that Exercises, equivalent of 11 miles of exercise per week, at either intensity, prevented significant accumulation of visceral fat, where as the controls showed a significant gain in amount of visceral fat (8.6 ± 17.2%; P = 0.001). Besides causing a reduction in fat accumulation, exercises also help in improving metabolic abnormalities, underlying the metabolic syndrome of obesity. Abnormalities in free fatty acid (FFA) metabolism are evident in the metabolic syndrome (Arner, 2002), especially reduced lipid oxidation (Turpeinen et al, 1999; Blaak et al, 2000) and increased abdominal fat distribution (Miyazaki et al, 2002; Nguyen-Duy et al, 2003; Pietilainen et al, 2005). Impaired lipid oxidation leads to a higher concentration of circulating FFAs in the blood, resulting in increased tissue FFA uptake, especially by the skeletal muscle and liver. Exercises help in decreasing hepatic FFA (free fatty acid) uptake, but have no effects on skeletal muscle or myocardial FFA uptake (Slentz et al, 2005). Effect of diet Current guidelines from the National Cholesterol Education Program (NCEP, 2001) and the American Heart Association (AHA, 2000) to reduce risk for coronary heart disease in obese individuals by normalizing plasma lipids include weight reduction, increased physical activity, and decreasing consumption of total fat, saturated fat and cholesterol in the diet. Marked changes in dietary fat intake, particularly reduction in levels of saturated fat have been associated with improvements in the lipid profile (Howell et al, 1997; Nieman et al, 2002; Mullis et al, 2004). A 10% to 15% decrease in weight, especially that associated with decreased intake of energy, primarily, along with reduced intake of saturated fats and increased uptake of omega-3 fatty acids may be sufficient to show favourable changes in the lipid profile by causing increase in HDL and significant reduction in the quantity of LDL, VLDL and triglycerides, body mass, body mass index, percent body fat, and total serum cholesterol levels (Redman et al, 2007; Boucher et al, 2007). There is an ongoing debate regarding the individual and combined effects of dieting and increased physical activity on improving metabolic risk factors (body mass Index and fat distribution). Redman et al (CALERIE team, 2007) carried out a randomized, controlled trial (CALERIE) to test the effect of a 25% energy deficit by diet alone or diet plus exercise for 6 months on body composition and fat distribution. The results of the study showed that exercise plays an equivalent role to calorie restriction in terms of improving body mass Index and fat distribution balance. However, exercise has an added benefit of improving aerobic fitness, which has other important cardiovascular and metabolic implications. Physical activity is known to prevent and enhance impaired FFA metabolism (Goodpaster et al, 2001; De Glisezinski et al, 2003) resulting in increased uptake of FFAs by the cells and enhanced use of intramyocellular lipid storage. There have also been questions regarding the optimal amount of weight to be lost. The recommendation by National Heart, Lung, and Blood Institute (2000) is to lose 5–10% of body weight for health benefits. There still are questions whether low fat diet is more beneficial than low energy diet. A meta-analysis of the randomized controlled trials by Nordman et al (2006) showed that after 6 months, those individuals who followed a low-carbohydrate ( Read More