Despite the frequent use of the term ‘stress’ both in scientific and everyday speech, a standard definition of the condition is absent, and the term has been defined and redefined over decades [7,8,9,10]. A commonly used definition by Torres and Nowson defines stress as ‘the generalised, non-specific response of the body to any factor that overwhelms, or threatens to overwhelm, the body’s compensatory abilities to maintain homeostasis’ [7]. To further understand the development of the scientific notion of stress, the term can be divided into the three sub-terms: ‘stressor’, ’stress response’, and ‘allostasis’.

A ‘stressor’ can be any kind of stimuli which is perceived as stressful by the individual. Thus, it can be anything from a specific working task to a traumatic life event, such as death in the near family. This also implies that all major life events can be deemed as stressful, even the positive events of getting married, having children, and going on vacations. Therefore, many different attempts have been made at defining the stressful events of life for the purpose of being able to measure the magnitude of stress and the adaption needed [3,11,12]. Nevertheless, there is still little agreement as to what defines a stressful event [12].

The ‘stress response’ is a term in stress research which finds it origin in the work of Lazarus and Folkman [1,3,12], who focused on the appraisal of threats posed during life, and the ability to effectively ‘cope’ with these threats. From this perspective, stress occurs when an individual perceives an event as threatening or harmful, and simultaneously experiences having inadequate coping resources available [3,10,11]. If coping with the stressors is successful, the imbalance between the demands of the stressful situation and the resources needed is levelled out, and possible discontent and discomfort are reduced. Oppositely, if coping is not successful, the imbalance and discontentment will proceed and perhaps worsen, and can lead to both physiological and mental symptoms of stress, e.g., headaches, exhaustion, memory loss, or anxiety [10].

A central concept in relation to the stress response is that of ‘allostasis’, first introduced by Bruce McEwen [3,13]. Allostasis is the physiological process, by which the body responds to a stressor, adapts to that specific stressor, and thus, reaches homeostasis again. Thereby, allostasis is also the physiological and behavioral mechanisms that allow people to cope with challenges, stressors, or high demands, and once the challenge is over, shuts off and allows the body to return to a normal relaxed state. Furthermore, McEwen defines the term ‘allostatic load’ as ‘the wear and tear that results from chronic overactivity or underactivity of allostatic systems’ [13], which can have pathophysiologic consequences. Allostatic load can be relieved in many ways. Most often, people will turn to behavioral changes, such as the consumption of alcohol and tobacco, increased sleep, less physical activity, and perhaps, an unhealthy diet too [1,9,12,13].

In biological stress research, the focus is often on the sympathetic–adrenal–medullary system (SAM) and the hypothalamic–pituitary–adrenal axis (HPA), as well as the cardiovascular, metabolic, and immune systems as allostatic systems, all of which protect the body from stressors [9,11]. In addition, it is important to understand and discriminate between chronic and acute stress, as the implications of allostasis are quite diverse for the two states of stress. In the event of acute stress, allostasis systems will activate as an appropriate and beneficial reaction, allowing the body to perform fast on a high level. This primarily happens through the SAM system, by the release of stress hormones, which will increase blood pressure and heart rate, expand the heart and muscular blood vessels, as well as accelerate the metabolism of macronutrients for the release of energy [3,9,11,14]. In the case of chronic stress, a completely different effect of allostatic systems is seen. A prolonged exposure to stress has proven to cause a long and varied list of clinically defined diseases. These health effects are caused by activation of the HPA axis and alterations of health behavior and affective regulation, which can potentially result in diseases such as depression, cardiovascular diseases, diabetes, and infectious and neurodegenerative diseases [9,13,14,15].

The complex relationship between stress and eating behavior has long been acknowledged. Stress can cause irregular eating patterns, altered food behaviors and preferences, and is believed to cause alterations in the perception of pleasure from food [9,16,17]. Research has shown that being stressed can cause non-homeostatic hunger, as food consumption has proved to have calming capacities on the physiological and behavioral stress responses [9,16,17,18]. Oppositely, other studies report a reduced intake due to activation of the SAM system [8,19,20,21]. Thus, approximately 40–70% of people suffering from stress report an increase in food intake, whereas 30–60% report a reduction under stress [8,22]. Yet, the underlying psychobiological mechanisms that shape the direction of change are largely unidentified [21,23]. In the case of chronic stress, it is largely believed that the stress response is governed by an activation of the HPA axis, with a consequent rise in the secretion of glucocorticoids. Glucocorticoids directly and indirectly stimulate food intake, especially highly palatable foods, by activating secretion of the appetite hormones, insulin, leptin, and NPY [8,16]. At the same time, food intake can dampen the physiological stress response by deactivating the HPA axis [16,24]. This deactivation is very often credited to the hedonic effects of the food, as eating will activate neural substrates, such as dopamine, in a similar manner to drug abuse [16,25,26]. Dopamine functions in multiple ways; however, in the context of eating, it is first and foremost a neurotransmitter, which codes for pleasure and enhances the desire for food. Furthermore, dopamine supports the deactivation of the HPA axis [16,26]. Experienced pleasure from food may, therefore, be the main explanation for this comforting effect of food under stressful conditions. In this manner, food intake as a reaction to the physiological and behavioral stress response will concurrently stimulate the reward pathways, and thus, possibly lead to neurobiological adaptations which will promote stress-induced eating in the future too [27,28,29]. Thus, if eating is learned to be an effective coping strategy, then it is likely that highly palatable foods could become addictive, in the same manner as other highly hedonic substances (e.g., alcohol, drugs, or tobacco) [26,30,31].

Hedonia, or, in larger degree, its contradistinction, anhedonia, have been studied primarily as symptoms of mental illnesses such as depression, anxiety, and schizophrenia [26,32,33]. Anhedonia is defined as the lack of ability to perceive pleasure, and thus, the term anhedonic traits is frequently used to describe how anhedonia is expressed in the individual. Prior human studies commonly assume that relatively mild acute stressors, as well as chronic stressors, can lead to impairments in reward function, and thus, result in anhedonic symptoms [34,35]. In fact, animal studies have found that exposure to stressors induce anhedonic and depression-like behavior, as well as dysfunctions in the dopaminergic reward pathways [26,35]. In addition, it is believed that anhedonia is heterogeneous across different mental disorders, depending on which part of the reward pathway is involved [32]. For instance, in depression, anhedonia can be regarded as a transient state, whereas in schizophrenic patients, anhedonia reflects a trait-like characteristic [32]. Many different self-report scales have been constructed for measuring anhedonia, primarily in patients of mental diseases. Examples which have been widely used include the Chapman Physical and Social Anhedonia Scale, the Fawcett–Clark Pleasure Scale, and the Snaith–Hamilton Pleasure Scales [36,37,38]. Though these scales differ, what is common for all these scales is the focus on pleasure from the perspective of anhedonia, thereby only giving attention to the dysfunctional reward systems. Moreover, these scales address anhedonia from a general perspective with respect to food, which means that specific pleasure from food and food experiences is either addressed by a single question or not at all [32,39,40]. Recently, Andersen et al. (2021), at the Department of Food Science, Aarhus University and Department of Psychology, University of Chinese Academy of Sciences, developed a scale for solely evaluating pleasure from food-related experiences [40]. Thereby, it has become possible to investigate the specific relationship between pleasure perception and eating behavior in various consumer groups. Furthermore, this scale lays the foundation for a deeper understanding of why some consumers experience having issues in terms of keeping a healthy diet or making more sustainable food choices, in addition to aiding the development of strategies for alleviating these issues.

3. The Effect of Chronic Stress on Appetite, Meal Patterns, and Food Preferences