The Neurological Mechanisms Of Habitual Versus Stress Responding In Eating, Smoking and Online Shopping Behaviours

A working literature review of three topographies (eating, smoking and online shopping) of behaviour, what the evidence suggests, the thoughts it inspires and how this leads to working hypotheses.

The relationship between stress & habitual versus goal directed behaviour

When actions and outcomes are associated, learning is said to be goal-directed (GD). Conversely, the association between a response and its antecedent stimuli is often referred to as Stimulus-Response (or S-R) or habit, which is independent of the outcome. GD responding is dependent on the Pre-frontal Cortex (PFC) which makes sense because goal-directed actions require planning and a flexible learning system. The habitual process uses the dorsal striatum which is inflexible and driven, by past learning outcomes. 

Research focuses on how these two systems are coordinated and one of the factors which determines this is stress. For example, overtraining biases responding towards habit, whereas stress is thought to be the factor for responding being biased towards habit independently of overtraining (Siller-Perez, et al., 2017). This is because stressful events mediate their actions through neurotransmitters, hormones and glucocorticoids, which re-orientate the networks at the expense of executive control processes (Hermans et al., 2011). During stress there is a shift from hippocampal system towards the dorsal striatal system which is implicated in reflexive learning (Schwabe et al., 2007) and is observed after chronic stress. 

Studies of stress have induced modulation of the hippocampal learning system through navigation tasks via outcome devaluation during instrumental learning. It is found that when participants are stressed during learning, they become insensitive to changes in outcome value and this is often interpreted as habitual responding. Stress affects flexible adaptation after the outcome devaluation and is not thought to be down to initial task acquisition. Evidence suggest that there is reduced flexibility because it impairs the goal-directed system. This is particularly true of those with low working memory capacity or chronic stress. 

Stress is found to increase activity in the Amygdala-dorsal striatum and decrease hippocampal connectivity, suggesting the critical role of the amygdala in stress-induced modulation of hippocampal and dorsal striatal learning. This points to the role of noradrenergic (NA) arousal in the amygdala for a stress induced shift towards habit responding. The dorsal lateral striatum is the putamen in humans, injections into this area during a spatial maze task accelerates training towards S-R learning (Vogel et al., 2015). Cross talk between the lateral and medial striatum via the MR in the Amygdala are key for us to understand the mechanisms of stress induced habit learning in navigation and classification tasks. The role of glucocorticoids (GC) and noradrenaline interaction with the amygdala for memory consolidation and retrieval remains has given us mixed data (Roozendaal, McEwan & Chattarji, 2009). On one hand data shows that GC and NA shifts towards habit and in another this was prevented by B-adrenergic antagonists suggesting NA activity is necessary. The combined effect of NA and GC is associated with reduced activity in the Medial Pre-Frontal Cortex (mPFC) and orbitofrontal areas which serve GD action. How these two systems interact to impair GD system and the role of GR in chronic stress is not known. The timescale for stress effects are usually 20-30 minutes and therefore non-genomic. The GC bind to membranes associated with MRs to bring about these effects. The NA and GC activity is synergistic in the amygdala inhibiting cognitive systems and the habit system dominates behaviour. 

Why should we study habit behaviour?

To be able to make a distinction between GD and habit responses is important for many domains, particularly decision making. It is generally considered that there is a mechanism which favours habitual responding over flexibility on tasks which demand higher cognitive resources. It benefits the organism because it allows resources to be conserved, allows quick action and performance under stress. Performance during stress is hindered so this adaptation has benefits and costs. The result in inflexible, rigid behaviour which cannot be generalised to novel situations or link to existing knowledge structures is imperative and the shift between the two is crucial. Not being able to shift between these two mechanisms has implications in mental disorders such as PTSD, addiction, OCD and relapse of disorders which are triggered by stressful events. 


Food consumption, motivation and cue-induced behaviours are deep rooted in our mechanisms for survival and we would not have continued without this drive. The modern era has produced a population which has an unhealthy attitude towards food and is partially responsible for us now being able to categorise people as food addicts. When people eat beyond being full this is a problem and is prevalent in 30% of people who seek weight loss treatment (Smith et al., 1998).

Interestingly, calorie dense foods are found to increase the neuropeptides associated with pleasure (Kelley et al., 2005) regulation, increase dopamine circuits, the striatal extracellular system, metabolism in the executive functioning region (orbitofrontal cortex) and the motivation and decision making areas of the brain (Wang, Volkow & Thanos, 2009). This pattern is similarly observed in drugs of abuse such as cocaine, alcohol and methamphetamines, therefore, they share a pathway. Serotonin serves to provide a stop eating signal and agonists are often used to decrease the frequency of this behaviour (Appolinario & McElroy, 2004). similarly when dopamine (D2) receptor activity reduces, this decreases the metabolism in the PFC (prefrontal cortex) which modulates appetitive behaviours (Blundell, 1984). Given these findings it suggests that binge eating does fit into the framework of addictive disorders but they have had limited success using Selective Serotonin Re-uptake Inhibitors (SSRI’s) for treatment.

Thought 1: the use of pharmacological intervention without a constructive behaviour plan is only part of the story here and without proper understanding of the context or the complexities of the S-R and R-O relations and its role in addictive behaviour, we are not going to be able to successfully treat people with these addictions. It is likely that findings from research should inform policy on advertising and educating the next generation before these behaviours have a chance to develop in the first place. It is a much better investment of our time to prevent rather than treat. There could even be legal implications for the way companies market and target people to sell their product.

Stress & eating

Food that is palatable stimulates endogenous opioid release. This protects against the effects of stress by decreasing the activity of the Hypothalamic Pituitary Axis (HPA) attenuation of the stress response, by elucidating endocrine mediators in the relationship between stress and eating. These neurobiological adaptations through HPA stimulation and high calorie foods promote the behaviour of overeating. In addition, cortisol influences the value of food through neuropeptides such as leptin, insulin & Neuropeptide-Y (NPY) and the glucocorticoids are antagonised by insulin and leptin.

When there is chronic stress, the system becomes dysregulated, leading to increased food intake and visceral fat accumulating. This is exacerbated by chronic stress, unsuccessful food restriction and other synergistic effects on increasing the reward value of highly palatable food. Emotional eating scores show that emotional eaters eat the same or more during an emotional response which is not in line with how the system is activated for the fight and flight response because there is decreased gastric motility, release of sugar in the blood stream and hunger is suppressed (Gold & Chrousos, 2002). It is found that those that eat through emotional agitation are often found to be adolescents with inadequate parenting, genetic vulnerability, poor coping skills, poor interoceptive awareness and high alexithymia (Larsen, Van Strien, Eisenga, & Egnels, 2006). However, the results of the Emotional Eating Subscale are mixed and it could be due to misclassification of the scale as it is shown that stressed emotional eaters eat more sweet, high-fat foods when there has been an ego-threat compared to a control task (Evers, de Ridder, & Adriaanse, 2009).  

Studies showing high scores on the Trier Social Stress Test (TSST; Birkett, 2011) and low on the Dutch Eating Behaviour Questionnaire (Van Strien et al., 1986) along with measures of hunger and affect were correlated with higher food intake in emotional eaters, particularly when there is a sad movie or stress. Hunger after stress is not typical of the HPA response due to hypo activation. The increased food intake is not in parallel with post stress hunger, implying emotional agitation and the lack of responding to internal hunger cues supports poor interoceptive awareness.

Thought 2: Are we more likely to engage in S-R responding with stress if we have a propensity towards this behaviour anyway? Scores on these questionnaires can be correlated with those in study 2 which can look at the effect of outcome devaluation in trained and non trained tasks to see how stress manifests on behaviour. It is expected that overtraining will be insensitive to devaluation when there is stress. In addition, is it actually poor interoceptive awareness of cue-related cues which are independent of the outcome which drive the stress related response to eating?

  • Is food more reinforcing when there is negative mood?
  • Is there a heightened sensitivity to reward (Bohon et al., 2009) 
  • Does hypo-dopaminergic functioning underlie the development of emotional eating and explain why food is used to self-medicate blunt negative emotions?- possible neuroimaging application
  • Is down regulation of dopamine neuroadaptation, overstimulation using food and heightened sensitivity to reward? (inferred)
  • Does the moderator effect for emotional eating extreme scores reveal categorical rather than continuous analysis of this variable if the questionnaire correlates with the experiment then there is concordance between these two measures.
  • The validity of the emotional eating scale is not independent of cues to which is it related to emotionally
  • Given the comorbidity and lack of DSM processes identified, it would be worth investigating whether or not the lawfulness of behaviour is playing a part here in terms of Arbitrary Applicable Relational Responding (AARR) and working out the Pavlovian/Operant mechanisms responsible (might be a potential study 4/5 with brain imaging)

It is found that fear does not increase eating of obese or dieting individuals or reduce it in non-dieters (Herman & Polivy, 1975). If there is uncertainty (aka people not able to label their source of emotional arousal) obese people eat more when distressed rather than calm, this result is also found in public speaking tasks (Oliver et al., 2000; Wallis and Hetherington, 2004). Emotional eating effects on food intake were only borderline but higher eaters do so in response to ego threat by TSST and in response to a sad movie. Distress induced food intake was predicted here but it is unlikely that people will overeat in a laboratory setting Krantz (1978). The assessment of palatability ratings was a limitation. 

Thought 3: Conduct full preference assessments for reinforcers using (DeLeon & Iwata, 1996). Correlate this with scores on the SRBAI or SRHI (Gardner & Lally, 2011) and the ratio of reinforcement in the natural setting compared with the study 2 setting. It is expected that the way that habit preferences contact their reinforcers are more similar to a variable interval rather than a fixed ratio. It will be expected that reinforcers that are not on a VI will remain goal directed and not habitual. This could be a confound for study 1-study 2 comparing a more naturalistic approach (qualitative data and questionnaire data gathering) with the experimental manipulations in study 2.

Online shopping

There are two types of shopping addiction, utilitarian and hedonistic with the latter carrying more risk (Gunuc & Keskin, 2016). If people are not able to control these impulses then it can develop into an addiction as a way of seeking excitement and enjoyment (Gunuc, 2013). Factors which lay the ground work for a shopping addiction are enjoyment, happiness, relaxation and entertainment and this works together with indirect factors such as stress, depression, boredom and loneliness. If people spend money to alleviate worries and stress, then it can turn into a buying addiction (Johnson & Attmann, 2009).  Uncontrolled buying can lead people to excessive internet use and harm to well-being due to online shopping being so popular (Panwar & Chahal, 2013.)

Thought 4: To understand the symptoms, causes and effects of online shopping and how this relates to performance on behaviour automaticity measures and performance on outcome devaluation tests using food items. Is there a relationship between online shopping and performance on habit questionnaires and tests? 

  • comparison of scores on the hedonic scale for those responses relating to shopping, smoking and drinking alcohol should reveal no significant difference between experimental manipulation using outcome devaluation compared to each other. If the mechanisms are the same then there should be no differences between subjects because the mechanism is the same.

It was found that shopping scores when compared with variables such as experiencing problems with one’s environment and lying, the hedonic scores increased. Participants who reported to feel relaxed and happy after were higher than those reporting no change compared with no change in emotions. Feelings of excitement, happiness, relaxation, and pleasure may also be considered related to the concept of hedonism and indicate addiction or be addictive themselves. In addition, lying and problems with the environment are factors which relate to hedonic impulses, including the existence of cheap products, psychological factors (such as boredom and stress). Online shopping has no external inhibitors and the individual can focus more on the hedonistic factors (pleasure).

Thought 5: Are the responses on the hedonic scale standardised across all three addiction areas?

Stress buying

Shopping is often used as a coping behaviour when people are going through stress (Zheng et al., 2020). Personality traits, values, goals, self-concepts and psychological distress (stress, depression and anxiety) play a role for compulsive buying (Darrat, Darrat, & Amyx, 2016). In addition, low mood and other negative moods are also risk factors along with perceived stress are the most commonly studied. Perceived stress is when there is reflection of the global evaluation of the personal and environmental challenges and how difficult they are to deal with (Cohen, Kamarck & Mermelstein, 1983). Compulsive buying or ‘retail therapy’ is a common approach used by women to regulate negative emotions or find positive experiences which alleviate negative ones (Otero-Lopez & Villardefrancos, 2014).

Negative coping is a risk factor for addictive behaviours. Online shopping is a form of escape and is particularly risky because it is available 24/7 (Otero-Lopez & Villardefrancos, 2014).  Teasing out the mechanisms in which perceived stress is associated with online compulsive buying is important so that interventions can be developed. The escape (relief) from negative emotions is combined with the positive emotions with little resource consumption (Dittma et al., 2007; He et al., 2018) which is also linked to the perceived stress and compulsive behaviour associated with compulsion (Dreier, Wolfling, Duven, Giralt, Beutel, & Muller, 2017).

Is self-esteem, conservation of resources (Hobfoll, 1989) or perceived stress a risk factor for negative coping which leads to compulsive buying?

It is thought that perceived self-esteem mediates the relationship between perceived stress and internal (sadness, anxiety) and external (alcohol, tobacco) negative behaviours (Carter, 2018; Jiang, Liang, Yang, & Ke, 2015). In Conservation Of Resources (COR) theory, Kim, Hogge, and Salvisberg, (2014) suggest that self-esteem is a protective factor and women with lower self-esteem and the more stress they are under, the more likely they are to maintain bulimic symptoms over time (Vohs, Bardone, Joiner Jr, & Abramson, 1999). Perceived stress is a predictor of online compulsive buying, higher perceived stress is a factor which is partially mediated by negative coping and there is a weaker effect in women with high self-esteem. Negative coping occurs in women with low self-esteem along with the experience of high perceived stress (also known as the stress buffering hypothesis; Carver & Vargas, 2011) which supports the stress coping theory and use of avoidance behaviour (Carver & Vargas, 2011; Lazarus & Folkman, 1984). These behaviour patterns are maladjustments that women with low self esteem adopt when they perceive stress and buying possibly serves to improve their self-evaluation through the value of goods which is in line with the social comparison theory (Festinger, 1954). Conversely, women who have higher self esteem are less likely to suffer from this lack of self control around resources (Grodzinsky et al., 2015. 

Thought 6: Interventions which build self-esteem e.g. group interventions, loving those around you and compassionate action could allow people to have more resources to deal with the challenges of life stress and the direct effects of perceived stress (such as Acceptance and Commitment Therapy; ACT)

  • Future research may use experimental research to confirm the causal relationships in the theoretical model. The self-report method has been used widely. Data from multi-method and multi-informant methods looking at other coping such as emotion focused, problem focused and avoidance coping could be looked at for mediating roles (Nicholls & Polman, 2007). 
  • Examination of people who score low on self-esteem tasks, high on perceived stress and high on negative coping could be experimentally examined in the laboratory to understand how these factors will related to a basic habit-forming test using outcome devaluation.
  • People who score low on self esteem and negative coping will be far more likely to continue responding in study 2, despite outcome devaluation. AKA they are more likely to show habitual responding, despite the scores on topographies of behaviour
  • Higher scores in SRBAI and SRHI will reflect stronger habits are formed in those with low negative coping and low self-esteem.

What is compulsive buying disorder?

There is a diagnostic criterion for this (McElroy et al., 1995) and a scale (Claes et al., 2011; Black et al., 2001) and it carries comorbidities such as mood disorders (21-100%), eating disorders (8-85%), substance abuse disorders (24-46%) and 60% meet criteria for at least one personality disorder (Black, 2007). Serotonergic and dopaminergic systems play a role, SSRIs have mixed effects and L-DOPA precursor increases compulsive shopping and other addictions, increases risk taking and reward learning (Pessiglione et al., 2006) suggesting its role.  The behavioural features associated with this disorder are escalation, tolerance and more spending to receive fulfilment from spending money. 

A compulsion is a series of repetitive actions which are not stoppable. They function to escape by relief from anxiety and they reinforce by doing this too. They also increase euphoric feelings which defines an addiction which includes experience or substance. They are defined by impulsivity and hedonic qualities which give a rush or high (Grant, Brewer, Potenza, 2006). 

Thought 7: Do these symptoms originate from the primary disorder, or are they secondary manifestations of an underlying psychiatric illnesses such as; mood disorder, anxiety disorders, ADHD or personality? Is the function of this repetitive behaviour simply an adaptation to avoid discomfort? It is found that when influenced by comorbidities or environmental stimuli addiction and related disorders appear to work on a spectrum. 

Despite the link between substance and non-substance addictions there is limited research which evaluates the shared neurobiology. There is a need for uniform diagnostics, valid screening and definitions of the biological system driving these disorders. The study of non-drug behaviours is a way we can gain a better understanding of behavioural addictions and a stronger understanding of the mechanisms comprising our perception of addiction. 

Stress & smoking

Smoking is a serious health issue and responsible for 5.4 million deaths per year according to WHO (2010). Smoking contains nicotine and is a chronic relapse condition along with other substance use disorders. It is reported that 70% of people want to quit but few do (CDC and preventions, 2002). Stress is a primary mechanism for maintaining and relapse. It converges with negative affect, craving and full-blown relapse (Shiffman et al., 1996). It is found that stress decreases the ability to resist smoking, potentiates intensity and reward (McKee, Sinha, Weinberger, Sofuoglu, Harrison, Lavery & Wanzer, 2010). Factors found to contribute to smoking and relapse when examining HPA axis reactivity (Childs & de Wit, 2009) is tobacco craving (Buchman et al., 2010) mood reactivity (Back et al., 2008; Childs & de Wit, 2009) mechanisms associated with stress-precipitated smoking lapse behaviour. 

Thought 8: Are HPA, craving, mood and physiological reactivity factors associated with the decision to start smoking following stress and the reward value of smoking?

Payne et al., (1992) Used imagery of smoking and looked at measures of sensitisation, increased rate, volume, duration, pleasure and arousal (Zinser et al., 1992; Koob & Le Moal, 1997 & Sinha, 2001). They found that imagery undermines the ability to resist smoking when deprived. Also stress and negative affect are known to decrease self-control, executive function and the inability to delay gratification for rewarding substances (Arnsten, 1998).  It is also found that stress increases craving along with self-control for addicted individuals (Sinha, 2001). After a stressful trigger subjects smoke more intensely with more puffs and greater inhalation and less time between puffs. The higher Carbon Monoxide (CO) readings suggest deeper inhale (Payne et al., 1992). Also the rating of reinforcing properties of smoking is higher following stress which correlates with the inability to resist. When people start to smoke the HPA axis and ACTH activity increases, with a more gradual increase in cortisol with nicotine exposure (Mello, 2010). Nicotine associated HPA activation is potentiated in the context of stress. Higher cortisol and ACTH are associated with reduced ability to resist smoking after stress. In addition, CRF and HPA plays a role in nicotine reinforcement (Goeders, 2002; Koob et al., 2004), increased craving (Buchmann et al., 2010) and plays a role in restoring homeostasis in the HPA system following stress (McEwen, 2000). Evidence suggests that negative emotion increases during stress but once the decision is made to smoke this decreases (Baker et al., 2004). Therefore, smoking alleviates negative emotion, craving and withdrawal following negative mood induction. The sensory aspects of smoking are more important than nicotine suggesting more S-R mechanism cues are enough to maintain smoking. Theories suggest that the reinforcing properties are disconnected from the affective outcomes (Belin et al., 2009)

Thought 9: Does stress and negative affect increase motivation to smoke but not affect the reinforcement?

Others have found that smoking when there is negative affect rate cigarettes less satisfying (Kirchner 2009). It is unlikely that negative affect relief plays a central role in smoking behaviour. But the current study shows that stress decreases the latency of smoking, increased the intensity or self-administration and its reinforcement. The post stress craving and HPA axis levels were associated with cigarette reward. It is possible that stress only influences craving and latency to smoke and it effects smoking intensity and reward as a function of differences in craving and latency to smoke, the results support theories which posit that stress and negative affect play a central role in drug use (Baker et al., 2004).  Stress coactivates the brain stress circuits (CRF, ACTH & Cortisol) and the mesocorticolimbic dopaminergic system (reward circuitry) simultaneously and provides a neural substrate which enhances the drug taking experience following acute withdrawal stress can sensitize or enhance the behavioural or neurochemical response to drugs and this study shows that overnight deprivation and exposure to stress enhances sensitivity to the rewarding value of cigarettes. 

Thought 10: Are the stress effects specific to smoking or attributable to non-specific increases in behavioural responses? No control for non-specific responses.  If this is the case there would be less stress effects on smoking reward and biological stress effects on smoking behaviour AND are these effects unique to the habit in question?


Do these symptoms originate from the primary disorder or are they secondary manifestations of an underlying psychiatric illnesses such as; mood disorder, anxiety disorders, ADHD or personality? Is the function of this repetitive behaviour simply an adaptation to avoid discomfort? If so, is the function of a habit always about escape? What about addictions which happen to the exclusion of all other consequences? are they maintained by multiple functions? It is found that when influenced by comorbidities or environmental stimuli, addiction and related disorders appear to work on a spectrum. However, taking a behavioural stance on this make much more sense because it helps us to draw out the relationship between the neurological underpinnings and the lawfulness of behaviour. Understanding the use of behavioural interventions such as ACT will make much more sense to implement if we can identify these mechanisms. The tools of diagnosis such as the DSM are probably a guide but not the rule book especially if we can prove a propensity towards this type of responding in a laboratory setting. What we are really trying to understand here, is whether or not the topography is unimportant and the function the same for all addictions. 

Despite the link between substance and non-substance addictions there is limited research which evaluates the shared neurobiology. There is a need for uniform diagnostics, valid screening and definitions of the biological system driving these disorders. The study of non-drug behaviours is a way we can gain a better understanding of behavioural addictions and a stronger understanding of the mechanisms comprising our perception of addiction.

The foregoing are the conclusions of the author of this paper. Comments and feedback are invited to:

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