Stress and Emotional Eating
Are you an emotional eater? Then this scientific article is for you!
For years, I would have no appetite in the but found my cravings were highest at night. I always wondering how my response to stress and lack of sleep may have played in my dysfunctional appetite regulation. In fact, I do recall when I had major dysfunctional sleep patterns, my cravings for hyperpalatable foods were the highest. And I also had bouts of compulsive overeating which I called “emotional eating”. I now realize that this association by be mediated by alterations in the HPA axis, glucose metabolism, insulin sensitivity and other appetite related hormones and hypothalamic neuropeptides (Yau & Potenza, 2013). And much of this may have beee lifestyle related, not getting the proper amount of sleep, staying up too late and not taking charge of my stress levels.
Interestingly, chronic stress can affect parts of the brain involved in stress/motivation such as the mesolimbic dopaminergic system, which can together affect a person’s food preference and seeking out hyperpalatable foods, in a similar way as additive drugs potentiate. The problem is, the metabolic changes that results in these patterns can result in weight gain, and obviously is an unhealthy pattern. Acute bouts of stress or periods of good stress called “eustress” may increase motivation and goal directed outcomes, but chronic stress can dysregulate homeostatic responses. The response varies within different personality traits, emotional states and individual physiological responses that contribute to the experience of “distress”. “Stress is a challenge to the natural homeostasis of an organism; in turn, the organism may react to stress by producing a physiological response to “regain equilibrium lost by the impact of the stressor”. One such homeostasis that is disrupted is that of feeding behavior” (Yau & Potenza, 2013). Below are some key points I took on stress as it relates to feeding behavior. It helps expand the understanding on how sleep can contribute to changes in feeding behavior.
- Acute stress and HPA axis- The hypothalamus is a critical region in the stress-response circuit as well as in the regulation of feeding and energy balance. There is a release of catecholamines (adrenaline and noradrenaline) during periods of acute stress, due to activation of the adrenal medullary system. Secondly, stress stimulates corticotropin-releasing factor (CRF) from the paraventricular nucleus (PVN) of the hypothalamus which stimulates adrenocorticotropic hormone (ACTH), that ultimately triggers glucocorticoids (GC) from the adrenal cortex. Cytokines can also stimulate the HPA axis at the levels of the hypothalamus, anterior pituitary gland, and the adrenal cortex. Acute stress and GC release can promote energy mobilization, including heightened cardiac output, blood pressure, gluconeogenesis, triglyceride levels, and redirection of blood flow to fuel various parts of the body such as the heart, brain and muscles. These types of responses are evolutionarily adaptive and serve to promote an immediate fight-or-flight reaction (Yau & Potenza, 2013). This can impair appetite (reduce), as well as digestion. This is why we often lose our appetite during short term periods of high stress. It should be pointed out that the hypothalamus is also responsive to insulin concentrations, which is an integral partner in glucose metabolism and other hormones such as leptin and ghrelin.
- Chronic stress and HPA axis-Chronic stress can disrupt the HPA axis, which can alter glucose metabolism, promote insulin resistance, and influence multiple appetite related hormones and hypothalamic neuropeptides. Prolonged stress induced GC secretion can promote abdominal fat deposition, together with insulin, which can decrease HPA axis activity. As a result, those who have chronic stress will actually eat more when they have additional acute stress, and will show a heightened preference for hyperpalatable, energy dense foods high in sugar and fat (processed foods).
Activation of the HPA is linked to activation of the mesolimbic dopaminergic system, a network strongly related to reward. As a result, it is thought that food and drug abuse may exploit similar pathways in the brain including dopaminergic and opioidergic systems (Yau & Potenza, 2013). Several studies have examined the consumption of high-fat, high-sugar diets and activity of the HPA axis. Dopamine has been associated with reward sensitivity, conditioning and control with respect to both food and drugs of abuse, and increased dopamine has been associated with reward sensitivity, conditioning and control (Yau & Potenza, 2013). Even more interesting, repeated stimulation of the dopaminergic reward pathways may trigger neurological adaptation that can promote progressively worse compulsive behavior. Essentially what that means is, regular consumption of these “comfort foods” may lead to changes in neuronal networks, disrupting carbohydrate and fat metabolism, insulin sensitivity and appetite hormones. These changes can modify food choice and selection, cravings for certain foods and motivation to eat specific foods. “Given the rewarding properties of food, it is hypothesized that hyperpalatable foods may serve as “comfort food” that acts as a form of self-medication to dispel unwanted distress” (Yau & Potenza, 2013). In addition, palatable non-nutritious foods (processed foods) can dampen HPA access responses, which is why it often can temporarily relieve stress, which is why they are often called comfort foods.
Where does sleep come into play? Sleep deprivation is a common stressor that may contribute to the risk of metabolic changes discussed above during stress. It is estimated that roughly 30% of all adults in the United States sleep less than 6 hours per night, where the optimal recommendation seems to be around 7.5 hours (Noseworthy, n.d.). “Cross-sectional analyses have found a significant association between short sleep duration and increased prevalence of obesity or higher BMI in both adult and child sample” (Yau & Potenza, 2013) Sleep deprivation can dysregulate HPA axis, decrease insulin sensitivity, and change plasma cortisol levels. As a result, which I have experienced myself, sleep deprivation can increase cravings for comfort, hyperpalatable foods, and increase the risk for compulsive eating. Long term this can increase the risk for obesity and other metabolic diseases such as abdominal obesity, insulin resistance, HTN, atherosclerosis, and can predispose individuals to develop CV disease and T2D.
Noseworthy, S (n.d.) Module 10 : Motor Systems Role in Health and Wellness Part 5: Sleep. [presentation] Retrieved http://coursecontent.muih.edu/NUTR834/NUTR%20834%20Module%202%20Week%2010%20Motor%20System%20in%20Health%20and%20Wellness%20Part%204%20Sleep/
Yau, Y. H., & Potenza, M. N. (2013). Stress and eating behaviors. Minerva Endocrinol, 38(3), 255-267