Despite the plethora of fast food chains, convenience stores, and vending machines providing calorie-dense food in today’s “obesogenic environment,” it is also clear that not everyone is affected by the pandemic.4 The question as to why some people remain lean (the so-called “positive deviants”) while others become large is a complicated combination of genetic, environmental, and psychological factors probably best explained by a biopsychosocial and sociotypic model. The concept of “emotional eating” falls within this model.
From an academic perspective, the origin of this concept comes from Kaplan and Kaplan’s psychosomatic theory of obesity which postulated that due to the anxiety-reducing effects of eating, people learned to eat when anxious, resulting in compulsive eating and obesity.5 Bruch later theorized that obese people had faulty hunger awareness and had incorrectly learnt the signals for hunger, and that they thus felt the same if they were hungry or uncomfortable emotionally, causing them to eat in both situations.6
It has become clear that not all obese or overweight people are emotional eaters, and that not all emotional eaters are overweight; however, the concept remains an important aspect in understanding why some people eat well beyond their caloric needs.7 The Dutch Eating Behavior Scale8 and the Emotional Eating Scale9 have both become useful questionnaires to help tease out “emotional eaters” from “normal” and “restrained” eaters. Those who score as “emotional eaters” consume greater amounts of “palatable” sweet, high-fat foods in response to emotional stress than so-called non-emotional eaters.10 Studies have shown that these self-identified emotional eaters may try to regulate the negative emotions caused by everyday life through eating behavior.11–12 For example, chocolate has been found to lead to an immediate mood increase that is more pronounced among “emotional eaters” than those who score within the normal ranges of these scales.13
Most research in the field of emotional eating has focused on negative emotions, especially stress. However, it is of interest that while emotional arousal may increase food intake, with negative emotions more often leading to “comfort foods,” positive emotions may result in a greater tendency to consume healthier foods.14–16 This area warrants further research. For the purposes of this review we focus on the effects of negative emotions and stress as they relate to obesity.
Emotional Eating and Obesity
Being overweight is neither necessary nor sufficient for classification as an “emotional eater.” As might be expected, however, rates of emotional eating during negative emotional states are reported to be higher among groups of overweight individuals as compared to healthy-weight individuals.17–20
For this reason, much of the research on emotional eating has focused on overweight and obese subjects, including bariatric surgery patients. Among this latter group, emotional eating is a common problem and may affect weight loss outcomes.
In a study of 178 pre-surgical bariatric patients, Walfish21 reported that 40% of patients subjectively felt that there was an emotional cause involved in their weight gain, while around 40% felt that there was not. Amongst the 40% for whom emotions were causal, stress, boredom, and depression were the emotions most strongly implicated. Given the high rates of emotional eating amongst obese bariatric surgery patients, various studies have begun to investigate differential outcomes based on emotional eating status22 as well as pre-surgery coping strategies.23 Results have been inconclusive, partly due to the retrospective nature of the studies combined with the relatively short follow-up times given the characteristic extreme fluctuations in weight post-surgery. A shared conclusion of these studies is the importance of pre-emptively identifying those patients for whom emotional eating was a cause of their obesity, and developing programs to foster healthier coping strategies in order to help prevent relapse a year or two down the road.
In a study of Latino adolescents, Nyugen-Rodriquez and colleagues24 concluded that it is crucial to help vulnerable adolescents develop adaptive coping skills rather than turning to food when faced with stress, to prevent development of poor lifelong eating habits. There is also an ongoing debate as to whether or not obesity is a form of food addiction.25
Mechanism of Emotional Eating
In order to understand the best coping strategies and behavioral modifications to overcome emotional eating, a better appreciation of the phenomenon itself is warranted. There are two hypotheses, both of which may contribute to the ultimate outcome of mood regulation: nutrient-dependent effects and hedonic effects. In the former theory, mood-modulating effects depend on the specific quality of the food and possible biochemical effects that may occur due to these qualities. In the latter theory, mood is regulated due to the pleasure–reward pathway being activated by the brain, which has become conditioned to enjoy palatable foods, often high in sugar and fat.
Nutrient-Dependent Effects. There is much research on the correlation between rates of depression and intake of protein and fatty acid; however, the connection between mood and carbohydrate intake is perhaps most relevant. Experimental diets high in carbohydrates were associated with a better mood than high-protein diets,26 and a carbohydrate-rich drink reduced depression in those with premenstrual syndrome.27 This fits in well with the theory of increased intake of “palatable” food during emotional eating.10
The “Wurtman hypothesis”28 postulated improved mood after carbohydrate consumption due to increased tryptophan crossing the blood–brain barrier, resulting in higher serotonin levels. However, this theory has recently been called into question now that it has been shown that <5% of calories in the meal can be from protein in order for tryptophan to increase significantly. This ratio is not common, even amongst such “high-carbohydrate” foods as chocolate and bread—the protein levels are simply too high.29 Furthermore, the food must be taken in isolation, after all of the previous meal’s protein has left the gut.30 Thus while a soda may indeed affect mood after several hours of fasting via this mechanism, this theory fails to explain emotional eating adequately in general.
Taking an opposite approach, there have been suggestions that carbohydrates may improve mood through reduction of hypoglycemia. Research among starvation victims also showed large increases in irritability, anxiety, and mood swings,31 and in the laboratory setting insulin clamp-induced hypoglycemia may result in a tense tiredness state in non-diabetic subjects, perhaps due to hypoglycemic activation of the autonomic nervous system in an attempt to return to euglycemia.32 A thorough review of this field of research by Bolton33 has shown higher rates of aggressiveness in studies of Quolla Indians, violent offenders, and college students for those individuals who more readily entered a hypoglycemic state during a glucose tolerance test, or who had generally poor glucose control.33–36 Taken collectively, these studies suggest that hypoglycemia may indeed affect mood, and glucose intake would most quickly return blood glucose to normal, thereby elevating mood. While it has been noted that true reactive hypoglycemia is quite rare as the body controls blood glucose levels very carefully,37 Donahoe and Benton have shown that very low blood glucose levels are not necessarily associated with greater aggressiveness.38 Perhaps most promising are studies among children39 and adolescents,40 which have shown decreased irritability and frustration when playing an impossible computer game if given a glucose drink; these changes were observed rapidly. Without more evidence it is difficult to reach any conclusions except that the relationship between insulin release and the propensity for emotional eating should be studied further.
Hedonic Effects. Theories of obesity often revolve around the disruption of control of a “set point” which may be located in the hypothalamus,41 but may perhaps have evolved only to deal with the more common historic problem of undersupply rather than surplus.42–45 In recent years several gut hormones have been discovered and shown to control a significant amount of hunger and satiety signaling.46 Disruptions in leptin signaling, for example, may lead to obesity, but a genetic defect in this pathway is rare.47 Recent studies have combined various study designs with neuroimaging in attempts to elucidate pathways further and understand patterns of eating behavior. More complex systems postulate the regulation to be beyond the hypothalamus, including the pleasure–reward system.48 Activation of the mesolimbic dopamine system49,50 and increases in dopamine in the nucleus acccumbens (the brain’s reward center), upon consumption of palatable food,51–53 certainly support this theory. Carnell et al.54 recently reviewed this literature, including emotional eating. Emotional eating was shown to represent a different neural process than restrained eating and is hypothesized to occur via a dopaminergic response seen on neuroimaging studies to gustatory and olfactory cues.55 Additionally, Bohon et al.56 used fMRI to examine a group of girls, divided into “emotional eaters” and non-emotional eaters, for responses to the idea of drinking a milkshake while in a negative or neutral mood. The emotional eaters showed greater activation in the parahippocampal and anterior cingulate in anticipation of the milkshake, and greater activation of the left caudate nucleus and left pallidum on actual receipt of it, versus a control tasteless solution. By contrast, non-emotional eaters showed decreased reward region activation during a negative mood. These results indicate a general activation of the reward center, indicating perhaps that emotional eaters have a greater sensitivity in their reward centers during negative emotional states. However, the lack of activation of emotional areas may indicate that while increased reward may promote a tendency to binge, food does not necessarily decrease the negative affect.
In addition, these effects are frequently related to palatability and so-called “comfort foods” which are often high in sugar and fat. Chocolate is well known as a food that people crave. Macht and Mueller showed that there is an immediate response in mood when subjects were given a palatable chocolate (of their choosing). This dependency of the response on palatability and immediacy suggests that the dependency is not due to specific components of the chocolate, but rather a conditioned response. Furthermore, these results were correlated with emotional eating: respondents with higher emotional eating scores showed greater mood change effects.13
These changes are hypothesized to occur via endorphin release, since spontaneous eating increases the release of beta-endorphins in rats,57 and beta-endorphins are known to inhibit GABA and thus cause an increased release of dopamine. This theory is also supported by the observation that opioid antagonists decrease feeding behavior in rats57 as well as thinking about food, feelings of hunger, and preference for sucrose in humans.58 Thus overall, while the exact mechanism remains to be elucidated, there is a large body of evidence that supports the theory that eating involves the pleasure–reward system of the brain, and that this may pathologically become dysregulated in “emotional eaters.” The role of the endocannabinoid system is also relevant both in maternal bonding and later food preferences.59
Emotional Eating and Stress
As previously noted, stress has been well documented as a key negative emotion involved in emotional eating.21
Oliver et al.10
recorded an increase in consumption of high-sweet/fat foods pre-public speaking, widely considered to be a stressful event. Stress caused by an ego-threatening Stroop color-naming task, in which participants determine the color of “ego-threatening” words on a computer screen (e.g. worthless) versus neutral words, has been shown to enhance intake of chocolate among females.60
Ego-threatening stressors are also generally associated with the intake of highly palatable, often high-calorie, foods.61–64
Dallman and colleagues65 theorized that comfort food intake may reduce stress by acting on the hypothalamic–pituitary–adrenal (HPA) axis. In rats, higher cortisol levels were found to increase comfort food intake, while chronically high glucocorticoids increased the salience of pleasurable activities. They hypothesized that this mechanism was related to depression in humans: “atypical” depressives gain weight, but maintain normal levels of cerebrospinal fluid (CSF) cortisol, while “melancholic” depressives have increased cortisol. Atypical depressives may experience hyperphagia in order to reduce the activity of their stress network. Thus, the hedonic effects of comfort food may be augmented by subsequent endocrine effects, especially in persons experiencing high levels of stress. On the contrary, Wallis and Hetherington66 suggest that stress-related eating is not an effective coping mechanism. Studies have shown that eating does not serve to reduce distress during, or after, eating.64,67 Furthermore, consumption of “forbidden” highly palatable food may also cause post-consumption guilt resulting in negative affects and undoing any positive changes that may have occurred, especially among women.68,69
Whether or not eating represents an effective coping mechanism for stress in terms of elevating affect, two facts remain clear: one is that emotional eating is a real phenomenon and is present in a large portion of the overweight population; second, this coping mechanism is not a healthy one for most of those who use it. Emotional eaters who struggle to remain at a healthy weight need help to modify their behavior into healthier patterns.
Large, naked, raw carrots are acceptable as food only to those who live in hutches eagerly awaiting Easter.
(Fran Lebowitz (1946–): Metropolitan Life; 1978)