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• W2591166580 abstract "Over the past decades, the number of people with obesity has increased dramatically worldwide. In particular, abdominal obesity is often complicated by metabolic disturbances such as insulin resistance, dyslipidemia, and hypertension, collectively grouped into the term metabolic syndrome (MetS). MetS ultimately leads to cardiovascular disease (CVD), the leading cause of death worldwide (World Health Organization, 2012). An imbalance between energy (food) intake and energy expenditure is currently regarded as the major cause of obesity, with multiple contributing environmental and genetic factors. However, evidence is now mounting that cortisol is a key player in this pandemic. In pathological conditions such as Cushing's disease or use of high doses of exogenous glucocorticoids, increased glucocorticoid exposure can cause all components of MetS and ultimately CVD. It is known that glucocorticoids can (1) increase appetite with a preference for energy-dense food (“comfort food”), (2) cause a redistribution of white adipose tissue to the abdominal region, and (3) suppress the activity of brown adipose tissue, resulting in abdominal obesity and its adverse metabolic sequelae (1). However, evidence for the latter mechanism is mainly derived from in vitro data and animal studies. Interestingly, coinciding with the rise in obesity, MetS, and CVD, the intake of food with a high glycemic index and levels of stress have increased, while the average hours of sleep has decreased. These are all factors known to induce an increase in daily cortisol production. So, from this perspective, it could be hypothesized that a continuous loop may exist between obesity, an unhealthy lifestyle, and increased cortisol, which maintains or worsens obesity and may counteract weight loss (Figure 1). Conceptual model of relationships between and among cortisol, obesity, and an unhealthy lifestyle. The latter comprises high-calorie food (especially with a high glycemic index), alcohol, chronic sleep deprivation, chronic stress, and other biological or environmental factors such as specific medication use, chronic pain, and inflammation. Until now, the majority of studies addressing the relationship between total serum cortisol levels, obesity, and MetS have yielded conflicting data (2). One likely explanation for these conflicting results is that the serum cortisol concentration, which has been used in most studies, is a marker that poorly reflects long-term cortisol exposure and its effects at the cellular level. This is probably due to the circadian rhythm of cortisol, its pulsatile secretion, and daily variation due to changing circumstances like acute stress. Therefore, most matrices used in the past only represent snapshots (serum, saliva) or short-term values (24-hour urine) of cortisol levels instead of chronic cortisol levels in the human body. In the past decade, a novel, noninvasive parameter to measure cortisol using scalp hair has been developed (3), providing the unique opportunity to measure long-term cortisol levels (reflecting mean levels of several months, as hair grows an average of 1 cm per month). In recent years, it has been shown that hair cortisol is an excellent proxy to measure average systemic cortisol levels, thereby overcoming the limitations of measuring highly fluctuating cortisol levels in serum, saliva, or urine (4). These advantages now enable studying cortisol levels over time in large cohorts. Recent case-control studies have shown that, on average, hair cortisol levels are increased in people with obesity compared to normal-weight individuals (5). In this issue of Obesity, Jackson et al. report on a cross-sectional study that showed in a large, population-based sample of 2,527 middle-aged and elderly men and women that hair cortisol levels were positively associated with body weight, body mass index, and waist circumference and were increased in persons with (abdominal) obesity (6). Interestingly, they also showed that long-term cortisol exposure was associated with more persistent obesity over time. This supports the notion that elevated cortisol is a factor in the maintenance of obesity. Another recent study in a large cohort of 3,019 children showed that even at the age of 6 years, the highest hair cortisol concentrations were associated with an almost 10-fold increased risk of obesity (7). Also in this population-based sample, hair cortisol concentrations strongly correlated with abdominal fat mass, one of the typical signs of cortisol excess. An important issue herein is that the causes of the increased chronic cortisol levels in the majority of people with obesity are unclear. In this context, it is of interest that Jackson et al. recently reported that people with obesity who perceived discrimination specifically related to their weight, but not general discrimination, exhibited higher long-term cortisol as measured in hair compared to individuals with obesity who did not perceive unfair treatment because of their weight (8). This indicates that the societal stigma of obesity may contribute to elevated cortisol concentrations and to a vicious circle with obesity. Other factors that are known to stimulate endogenous cortisol production include alcohol intake, chronic stress, sleep deprivation, pain, and inflammation. Also, food intake with a high glycemic index has been shown to elevate cortisol in humans (1), which may be driven by hyperinsulinemia. Hypercortisolism, known to induce insulin resistance, may thus perpetuate a vicious cycle. It has been shown by Ludwig and colleagues that people with obesity with elevated insulin response lost relatively more lean mass and less fat mass during a dietary weight loss intervention than those with low insulin response (9). In addition, they were more prone to weight regain, potentially due to these unfavorable body compositional changes that show remarkable similarities to the adverse body compositional alterations due to hypercortisolism. In addition to increased endogenous production, altered metabolism of cortisol may underlie increased cortisol levels in obesity. This could be due to changes in cortisol metabolizing enzymes (11-β-hydroxysteroid dehydrogenases [11-βHSD], 5α and 5β-reductases, CYP3A4), bile acids, or severe steatosis of the liver as the major site of cortisol clearance (10). Although evidence is rapidly accumulating that, on average, long-term cortisol levels are higher in obesity, it is important to note that not all people with obesity have elevated hair cortisol levels. It is conceivable that we should categorize obesity as ‘'normocortisolistic obesity’’ and ‘'hypercortisolistic obesity.’’ The latter group may be more prone to MetS and CVD and may be a category of patients who could specifically benefit from treatment with cortisol-reducing medications. Medication such as tissue-specific 11-βHSD inhibitors and (selective) glucocorticoid receptor antagonists have been developed in experimental settings (11). Depending on the cause of the hypercortisolism, lifestyle changes (targeting diet, alcohol use, sleep, stress, pain) and psychological and societal interventions to reduce stress and the stigma of obesity may also reduce cardiometabolic consequences in people with hypercortisolistic obesity. Thus, hair cortisol analyses provide a relatively novel way to study the relationships between cortisol and obesity and the cardiometabolic sequelae, now clearly showing that, on average, systemic cortisol levels in people with obesity are elevated. Future studies are needed to further prove that cortisol is an important contributor to obesity, MetS, and CVD in the population. Importantly, insight into the mechanisms underlying increased cortisol exposure in obesity may lead to a more effective implementation of cortisol-lowering therapies and potential new treatment targets." @default.
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• W2591166580 date "2017-02-23" @default.
• W2591166580 modified "2023-10-16" @default.
• W2591166580 title "Obesity and cortisol: New perspectives on an old theme" @default.
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• W2591166580 doi "https://doi.org/10.1002/oby.21774" @default.
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