- Chronic stress is mainly linked to obesity and visceral fat accumulation and is responsible for the cardiometabolic consequences of obesity, such as type-2 diabetes, hypertension, and cardiovascular disease.
- Α repeated stress response may lead to obesity through different pathways. These pathways implicate (neuro)physiological, behavioral, physiological, metabolic, social, and biochemical adaptations.
- Stress regulation systems develop early in life, and childhood stress exposure likely shapes the risk for later obesity.
The stress response is a biological process that takes place to promote behavioral adaptation under such circumstances. However, when stress exposure becomes prolonged, the stress response becomes maladaptive and can lead to physical and physiological disease. The primary health consequence of stress is depression which nowadays affects over 120 million people worldwide and is projected to be one of the leading causes of death by 2030.
The association between stress and obesity
Stress is a normal biological response that activates under acute threatening conditions (e.g., a barking dog chasing you). Specifically, acute stress mobilizes the body’s energy stores, such as glycogen, so we can respond rapidly and face any threats. Once the threat has passed, the body returns to its baseline state.
However, modern life stressors are not typically physical but psychological, such as financial worries, work problems, health concerns, etc. In this context, the stress response ceases to be beneficial and instead becomes harmful. This type of stress is characterized as chronic stress because the psychological stressor never really passes, and the stress response cannot be regulated adequately. Chronic stress has consistently been linked to obesity in epidemiological studies and meta-analyses. Obesity is a rapidly growing pandemic with significant consequences for public health. It has been directly linked to severe health conditions such as cardiovascular disease, type 2 diabetes, and cancer, among the most common causes of morbidity and mortality worldwide.
As stated in one of our previous Blogspots, obesity is caused by an imbalance between the energy intake of the diet and the body’s voluntary (e.g., physical activity) and/or spontaneous (e.g., resting metabolic rate) energy expenditure.
This imbalance progressively leads to excessive fat accumulation in the body, to an extent where body health is impaired, and health complications like those mentioned above arise.
Multiple pathways are activated during chronic stress, some of which have been recognized as playing a role in the development and maintenance of obesity.
Chronic stress is mainly linked to central obesity and visceral fat accumulation, namely the fat that piles up around organs in the abdominal area and is responsible for the cardiometabolic consequences of obesity, such as type-2 diabetes, hypertension, and cardiovascular disease. From a survival perspective, this is logical since the constant activation of the stress response can be interpreted as living in a continuously unsafe environment, for which it is beneficial to store easy-to-use central fat.
How is a chronically elevated stress response eventually associated with weight gain and obesity?
The chronic stress cascade
Α repeated stress response may lead to obesity through different pathways. These pathways implicate (neuro)physiological, behavioral, physiological, metabolic, and biochemical adaptations.
- Cognition: Chronic stress interferes with the brain areas responsible for self-regulation and can lead to obesity by impeding the cognitive processes required for self-regulation. In other words, chronically stressed individuals are more prone to succumb to dietary misbehaviors in an environment with immense food availability.
- Behavioral: Stress can trigger both orexigenic-like and anorexigenic-like responses, reflecting a variety of factors, such as individual differences, food availability, and/or the type of stress. Typically, chronic stress leads to dietary over-consumption of highly palatable foods, namely foods high in sugar, fat, and calories. This phenomenon implicates the brain’s ‘’reward system’’, where eating palatable foods can relieve stress-related negative emotions. Therefore, when perceived or real chronic stressors are present, eating control may be lost due to the hedonic reward of eating as a counterbalance to the burden of stress. Thus, stress, reward, and highly palatable foods form a positive feedback loop that is very difficult to break free from. It is important to note that although chronic stress can negatively change eating habits in both men and women, not everyone gravitates toward palatable foods and hence gains weight under stress. Stress can also disrupt activity patterns by decreasing physical activity or increasing sedentary behavior. In other words, chronically stressed individuals are more likely to keep away from any form of physical activity and spend more time being sedentary, thus leading to a higher likelihood of obesity. However, some individuals tend to use exercise as a means to cope with stress. Lastly, stress is a known disrupter of sleep. Short sleep duration, in particular, is independently associated with higher body mass index (BMI), higher likelihood of obesity, and other adiposity markers.
- Physiological-Metabolic: Stress causes the activation of multiple physiological systems pertinent to obesity, with hypothalamic-pituitary-adrenal (HPA) axis activation being the most important one. The HPA axis is a major neuroendocrine system that controls reactions to stress and regulates many body processes. When an individual perceives stress, a physiological cascade occurs in the HPA axis. The result of this hyperactivity is the increased production of the glucocorticoid hormone (any steroid hormone produced by the adrenal gland) cortisol. In cases of chronic stress, the HPA axis activity is constantly elevated; hence, cortisol levels invariably increase. Cortisol has a complex role in energy balance and metabolic control. Specifically, chronically elevated cortisol levels promote visceral fat accumulation and loss of muscle mass and bone mass. High cortisol levels can also increase appetite with a preference for palatable foods by reducing the brain’s sensitivity to leptin, regulating neuropeptide Y (NPY) stimulation, and potentiating the brain’s reward pathways. Subsequently, cortisol also causes the excess adipose tissue created due to the caloric surplus to redistribute to the abdominal region. The subsequent visceral obesity increases the risk of metabolic syndrome since abdominal obesity is one of its core symptoms, along with hypertension and metabolic alterations, such as insulin resistance and dyslipidemia. Therefore, a vicious cycle where stress, increased cortisol action, and abdominal obesity interact and amplify each other, ultimately leading to poor metabolic and cardiovascular health. However, not all individuals respond to stress similarly (interindividual variation in the biological response to stress). Moreover, biological factors that disrupt cortisol’s daily levels (cortisol is normally high on waking, surge in the 30-40 minutes after waking, and then drops rapidly, reaching rock-bottom around bedtime), such as decreased sleep and/or shift work can potentially lead to higher cortisol levels and thus make certain people more prone to weight gain, obesity, and subsequent health complications. The same holds for other environmental and behavioral factors, such as food intake with a high glycemic index, excessive alcohol use, and chronic pain, possibly leading to increased cortisol levels and higher body weight. The harmful effects of cortisol relative to obesity are readily evident in Cushing’s syndrome, in which individuals have congenitally high cortisol levels (endogenous hypercortisolism). People suffering from Cushing syndrome have increased abdominal body fat, high blood pressure, and insulin resistance, an identical metabolic profile to chronically stressed individuals.
- Biochemistry: In addition to activating physiological systems, chronic stress can also directly modulate levels of hormones that are relevant to weight and obesity. Leptin, ghrelin, and NPY may respond to chronic stress such that the interaction of these hormones stimulates lipogenesis in terms of both the number and the size of adipocytes in the fat tissue. In particular, NPY’s release, which potently increases food intake through its effects on the brain, is reinforced under stress. Similarly, ghrelin, an orexigenic hormone acting through the brain’s ‘’reward system’’ is also increased under chronic stress. On the other hand, chronically stressed individuals are more likely to be leptin-resistant and hence more likely to gain weight, given that leptin is a hormone that suppresses appetite. Chronic stress also leads to a chronic inflammatory state, with high concentrations of inflammatory cytokines (small proteins that regulate the immune system and mediate inflammatory responses). When abdominal obesity coexists, which can very well be an outcome of chronic stress too, visceral fat also secretes cytokines, exacerbating the inflammatory state. Since the cardiometabolic complications of chronic stress are pathologies where inflammation plays a significant role in their development and progression, this is another pathway in chronic stress, obesity, and disease are interrelated.
Weight stigma as a component of the chronic stress vicious cycle
One common but often overlooked aspect of obesity is that obesity is a stressful state in itself. In other words, obesity per se can lead to increased chronic stress to varying degrees, depending on the individual’s personality. It has been found that people experiencing weight stigma are at risk of experiencing chronic stress and its resulting cascade of negative consequences.
Some studies link weight stigma to exercise avoidance or decreased physical activity. The evidence also shows that weight stigma predicts future weight gain and a greater likelihood of obesity. Consequently, the vicious cycle of chronic stress is fueled by so many factors that are also interrelated and all favor an obesogenic state.
Are some people steered to be eternally knocked by stress?
Early life stress exposure likely shapes the risk for later obesity and/or unhealthy fat deposition patterns (visceral fat) through biological pathways deep in our gastrointestinal tract. Gut microbiota or gut microbiome, i.e., the genetic makeup of the community of microbes that inhabit the human body, differs between children with obesity or overweight and children with average weight. Also, specific characteristics of infant gut microbiota predict early weight gain.
Moreover, different gut microbiota compositions can affect how prone and responsive to stress an organism is and affect the levels of the orexigenic (appetite-stimulating) hormones ghrelin and NPY.
These data are pretty novel and, at the moment, can just manifest how complicated and inextricable the relationship between chronic stress and obesity is.
Stress is a normal biological process that protects us from physical and psychological threats. However, it can become detrimental when its effectors are constant, and the stress regulation systems cannot turn it down anymore.
The relationship between chronic stress and obesity is rather complex and is fueled by different pathways, which all end up in a toxic fat deposition pattern in the abdominal area. Therefore, chronic stress creates a metabolically unfavorable body fat accumulation, which harms cardiovascular health.
However, healthy dietary behavior and regular physical activity can help someone escape the vicious cycle of chronic stress and its consequences.
Remember, the energy balance is a somewhat workable equilibrium, and it’s never late for someone to try and tip it over.
If you would like to speak to our health and wellness coach regarding metabolic testing, please call us at 865-218-9000 or book a free consult at medispa-choto.com.
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