Why people can and cannot resist food
temptations: the cognitive neuroscience of
self-regulation.
Period: 12-12-2001 until 6-02-2012 ECTS: 10 and Final Date: 21-03-2012
Name: Lizet van Knippenberg, student number 0608866 Supervisor: prof. dr. D.T.D. de Ridder
Co-assessor and UvA Representative: dr. H.A. Slagter
MSc in Brain and Cognitive Sciences, University of Amsterdam: Cognitive science track
Introduction
The ability to control one’s own behaviour is known as self-regulation, which is the process by which people change themselves, including their thoughts, emotions, desires, moods and their impulsive acts in view of their long-term goals (Krendl & Heatherton, 2009). Self-regulation enables us to make plans, selecting between alternatives, control our impulses, inhibit unwanted behaviours or thoughts, and regulate social behaviour. Everyday life is full of temptations that challenge our capacity for self-control and willpower. Although people can delay gratification, control appetite and impulses and obtain long term goals, almost all people show difficulties with self-regulation from time to time. These failures occur in a wide range of contemporary society domains, namely addiction, risky sex, drunk driving, alcohol and drugs abuse, gambling, purchasing, crime, and eating.
Being in a situation in which one needs to make a decision, people can experience two forces that influence them, one tells us to do whatever is reasonable, whereas the other urges us to do what is most pleasurable. For example, when faced with a healthy snack, such as a banana, we know that we should prefer this snack over an unhealthy snack such as a chocolate bar. Yet, we are often tempted to eat the chocolate bar. To be able to choose the healthier, better, more reasonable alternative, we need self-control.
The idea in the current psychological literature is that when in a situation of temptation, there exists a conflict between immediate impulses on one hand and deliberate evaluation of long-term goals, that facilitate self-control on the other (Hofmann, 2009; Baumeister & Heatherton, 1996; Metcalfe & Mischel, 1999). In this dual-system perspective, also known as the ‘hot’/’cool’-system (Metcalfe & Mischel 1999), automatic attitudes are part of an impulsive system and predispose people to approach or avoid a stimulus, or in our case, food. Often impulses are in conflict with deliberate evaluations and long-term goals that reside in the reflective system that may warm against immediate hedonic fulfilment. Human beings have a tremendous capacity to regulate their behaviour and most of the time they are able to successfully control their behaviour and inhibit unwanted responses. Successful self-regulation occurs when the deliberate ‘cool’-system prevails and in that manner aids to withstand the strength of an impulse. Although humans are skilled in regulating themselves, self-regulation failures often occur when people lose control of their behaviour in many circumstances. Self-regulation fails when people are in bad moods, overwhelmed by immediate temptations or impulses and when self-control is impaired. Only in case a person has the motivation to reason in a deliberate way and has enough resources, such as time and cognitive capacity, his or her behaviour will be influenced by controlled and reasoned processes. If either motivation is missing or the opportunities, we act in a more automatic way. In psychological terms, self-regulatory failure occurs when the automatic ‘hot’-system prevails over the ‘cool’-system. The ‘cool’-system is mute when deliberate thinking is overruled by the emotional and rewarding system, for example whenever an impulse is too strong.
Recently, brain imaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) has been used to identify brain regions involved in the exertion of self-regulation. This neuroscientific research has increased our understandings of the neural mechanisms involved in regulation success and self-regulation failure. Right now, it appears that many different brain areas are involved in self-regulation. Psychological dual-system models have received support from neuroimaging research, with substantial evidence of prefrontal-subcortical connectivity and reciprocal activity (Heatherton & Wagner, 2011). However, neuroimaging research on self-regulation and self-regulatory failure is still in its infancy.
Cognitive neuroscience research suggests that successful self-regulation is dependent on top-down control from the prefrontal cortex (PFC) over subcortical regions involved in reward and emotion. Almost all neuroscientific research on decision making and self-regulation has focused mainly on the PFC which is most notable for executive functions which guide a wide range of cognitive processes involved in self-regulation and got its befitting label as ‘chief executive’ of the brain (Curtis & D’Esposito, 2003; Goldberg,
2001). The dorsolateral part of the prefrontal cortex DLPFC is most strongly associated with cold executive function processes such as mechanistic planning, choice, reasoning and problem solving (Grafman & Litvan, 1999) and it is clear that successful self-regulation would not be possible without this brain region. Another brain area implicated in successful self-control includes the anterior cingulate cortex (ACC), which is interconnected with cortical and subcortical brain areas and as such communicates directly with the PFC in monitoring and guiding behaviour and bringing behaviour in line with overarching goals (Gehring & Knight, 2000; Botvinick, Carter, Braver, Barch, Cohen, 2001; Kerns et al, 2004). Apart from correct functioning of different parts of the frontal lobe (PFC, DLPFC, ACC), the hippocampus also contributes to successes in self-control, because of its role in ‘cool’-systems (Metcalfe & Mischel, 1999).
Functional neuroimaging studies of regulation and its failures suggest that self-regulation involves a balance between brain regions representing reward, salience and emotional value of a stimulus and prefrontal regions associated with self-control (Heatherton & Wagner, 2011). The prefrontal-subcortical balance model suggests that anything that tips the balance in favour of subcortical regions can lead to self-regulatory collapse. These self-regulatory failures are the result of either impairments in top-down prefrontal control of the PFC and overwhelming bottom-up impulses.
The ventromedial part of the PFC (VMPFC) is most strongly associated with ‘hot’ executive function and is strongly implicated in many overt aspects of behavioural self-regulation, in particular emotional processing and expression of inhibition of inappropriate responses. In line with this, the VMPFC is expected to be more active in impulsive behaviour, since it is connected to subcortical limbic areas involved in emotional processing and decision making such as the amygdala (Amaral & price, 1984; Carmichael & Price, 1995). Brown et
al. 2006 suggest that the ability to modulate impulses, experiences and responses is
determined by the functional interplay of corticolymbic arousal and control circuits. Another cortical area, the ventromedial OFC, is particularly implicated in emotional processing, reward and inhibition processes (Elliott, Dolan & Frith, 2000; Rolls, 2000; Volkow & Fowler, 2000).
In case the ‘hot’-system overrules the ‘cool’-system, whenever frontal executive functions are compromised, self-regulation failures occur due to depletion of resources in the brain (local brain glucose store depletion) following alcohol consumption (Crews & Boettiger, 2009), as a results of stress (Sinha, 2005) or drugs use, or as a result of brain damage (Grafman & Goel, 2000).
In this literature thesis we aim to discuss the underlying neurological processes involved in self-regulation and eating behaviour. Specifically, we want to reveal neuroscientific knowledge about the involvement of the psychological dual-system in relation to food consumption behaviour.
Hypothesis
Psychological literature assumes that when being in a ‘hot’-state, deliberate thinking is overruled, which means that in case impulses are too strong, they take over the ‘cool’-system. We will discuss whether neuroscience literature corresponds with this hypothesis based on psychological studies. We also examine whether, whenever we give in to temptation, this is indeed due to overruled prefrontal areas to recruit top-down control by subcortical brain regions.
Based on both the neurological prefrontal-subcortical balance model by Heatherton & Wagner (2011) and the psychological dual-system models and their being in a ‘hot’ or ‘cool’ state by (Metcalfe & Mischel 1999), we assume the strength of the impulse to be finally decisive, when it comes to making decisions about tempting food, regardless of the functioning of the prefrontal cortex.
Operationalization
Based on the afore mentioned hypothesis which states that self-regulation failure in a tempting food environment is primarily caused by the strength of the impulse rather than by functioning of the prefrontal cortex, we formulated the following main question:
Are self-regulation failures in eating behaviour, i.e. giving in to food temptations, caused by top-down control failures as a result of poor PFC functioning, or do they depend on the strength of an impulse?
Sub questions include:
To what extend does giving in to food temptations occur as a result of insufficient top-down controlling, that is to say, poor functioning of among others the PFC?
To what extend are self-regulatory collapses caused by overwhelming bottum-up impulses, when faced with tempting food?
In trying to find an answer to these questions, we searched for relevant literature by making use of Google scholar and the digital library of the University of Amsterdam to find articles concerning self-regulation, impulses, eating, food choices, neuroscience, etc. The following terms were used for searching:
1. Food choice - Food motivation – Food selection - food intake - eating – food stimuli – food craving. AND
2. Neuroscience, neuroimaging, fMRI, neural correlates, neural mechanisms, brain. AND
3. Self-regulation, self-control, self-inhibition, impulsivity and impulse(s), decision making
Soon we found out that a bulk of literature existed which dealt either with food consumption behaviour, self-regulation and its failures and the neuroscience of it. Therefore, we excluded many articles, because we were only interested in neuroimaging studies on self-regulation concerning food choices.
We thus excluded neuroscientific literature on eating, which mainly deals with the effects of macronutrient composition or food intake on brain processes. Food intake, food selection and food choice is determined by sensory properties of food like texture, taste, smell and sight. These food-specific properties induce preabsorptive physiological responses, which are collectively referred to as cephalic phase responses (Smeets et al., 2010). Neuroimaging studies on sensory signals, i.e. neuroscience of eating, mainly focus on the effect of being satiated (pre compared to post ingestion) on taste responses with
positron emission tomography (PET) or by measuring blood-oxygen-level-dependent (BOLD) responses. Research on studying the process of satiation is still in its infancy (Spetter et al, 2012). In these neuroimaging studies on satiation, often hormones and other substances like leptin, ghrelin, PYY, CCK, BDNF, glucose, insulin and amylin important in the regulation in food intake and choice are taken into account.
We also excluded a body of research on self-control of food consumption highlighting the role of motivation for food as addressed in studies on wanting and liking (Berridge, 2009). Third, we excluded *animal studies, *studies about individual differences in food regulation and food consumption behavior and *studies about food craving and neuroimaging of craving (has more to do with addiction and drugs), as well as *studies about food choices and purchasing.
When combining all our searching terms with all possible combinations, we found out that neuroscience about the self and self-regulation, deals with this topic only and does not tell us anything about food consumption. On the other hand, neuroimaging studies on eating, food consumption, food choices etc. focusses on the effect of looking at food stimuli, searched with fMRI or PET, and does not tell us anything about self-regulation. Understanding the neurobiology of food choices and behaviour with a link to self-control thus appeared to be quite hard. Besides, we mainly tried to find neuroimaging articles about these subjects in normal healthy subjects. Soon we concluded that we needed to include a wider range of studies to answer our questions. First, normal healthy people show normal self-regulation, but can also show an abnormal pattern of self-regulation after the use of alcohol, drugs or being influences by stress. Secondly, it appeared that, research on controlling eating and the brain was often studied in studies with obese, restrained eaters or subjects suffering from anorexia or bulimia nervosa. So, we included studies who used abnormal people as their subjects of interest. Next to that, to emphasize the role of some particular brain areas involved in self-regulation and neuroscience, we included leasioned subjects. By this, one could see how self-regulation is impaired as a results of a lesion in a particular area. This resulted in a set of recent studies (2003 – 2012) on self-regulation in tempting food choice occasions and food motivation on a neuronal level.
Finally, my goal in this thesis is to combine neuroscientific findings from the literature on self-regulation (research on addictions, obesity, impulsivity and lesion studies) on one hand, and existing data from neuroimaging studies on food consumption and choices on the other hand. This article has attempted to frame the existing literature in such terms to answer the main question about whether or not resisting food temptations. At first, I’ll give an overview of brain areas which are known to be implicated in self-regulation (success or failure) concerning food consumption. Second, I’ll describe brain areas involved in making food choices, (looking at food pictures, while being scanned with mainly an MRI scanner) and food motivation.
Results
After filtering out all neuroscientific researches on eating according to our exclusion criteria described afore, 15 studies were left over. All these studies are neuroimaging studies concerning eating and food choices. That means that in all articles pictures of food and sometimes non-food, where shown to participants, who were either healthy normal weight subjects or restrained eaters or obese. An overview of the articles and a short description, is known in table 1.
Table 1.: Included neuroimaging studies concerning eating behaviour.
Wang et al, 2004 PET/ FDG Whole brain Questionnaires about favorite foods and interest N = 12 7 female, 5 male Mean age 28. Food deprived Food exposure: view, taste, smell it. OFC important for desire for food. Holsen et al, 2005 fMRI N = 9 5 female, 4 male Mean age 13 Normal weight/ healthy BMI 4h fasting before scanned. Pre en post scan. Pictures were Food, Animals Blurred & Control Increased activation to food images in the amygdala, medial frontal/ OFC and insula in the pre-meal condition Killgore et al, 2003 fMRI N = 13 13 female Age between 21-28 BMI 22 90 min before food deprived. 500 kcal intake 6h before Pictures of food High calorie Low calorie dining related utensils. Amygdala activated by food, VMPFC for reward value of food.
Hare et al, 2011 fMRI
food choice task N = 33 23 female, 10 male Mean age 25 Stop eating 3 hours before scanning Pictures of food items, junk food, and healthy snacks. Attention focus on health, taste or control condition.
Health cues let people make healthier choices. Neural mechanisms of successful self-control activated by exogenous health cues. Hare et al, 2009 fMRI
food choice task by self-reported dieters N = 37 Self-controllers: 19 Non self-controllers 18 Status: unknown Rated 50 different food items VMPFC involved in incorporating both taste and health aspects of food pictures in
self-ROI: VMPFC and DLPFC Health vs. taste of food pictures controllers, NOT in non-self-controllers. Demos, Kelley & Heatherton, 2011 fMRI whole brain, but with ROIs.
N = 100 Dieters: 50 Non dieters: 50 Either consumed water or a milkshake Pictures of animal, environment, people, appetizing food NAcc & Amygdala Dieters showed greatest activity after food pictures in NAcc, after milkshake.
Lowe & Coletta,
2008. fMRI N = 19 Normal weight REs: 9 UREs: 10 Participant studies in fasted and fed status Pictures looking of highly and moderately palatable food. Fed status in REs increased reward value of palatable food. Coletta et al, 2009 fMRI N= 19 Normal weight REs: 9 UREs: 10
Fasted and fed status Pictures of High & moderate palatable food and neutral objects When fed, RE s activity in reward and desire areas. So RE find food more appealing then UREs when fed. Bruce et al, 2010 fMRI N = 20 Obese: 10, age between 11-16 Non-obese/HW: 10, age between 10-17 Pre (fasting 4h) and post meal Food pictures Nonfood: animals Blurred pictures Greater activation in response to food pic in PFC and OFC in obese group. Obese children thus hyper responsive to food stimuli compared to HW children. Martin et al, 2009 fMRI N = 20 Obese adults: 10, (BMI 34) HW adults: 10, (BMI 22) Pre-meal (fasting 4h) and post-meal status (direct after eating 500 kcal). Pictures of Food and Non-food Higher activation in ACC and VMPFC in obese adults during pre-meal condition. Davids et al,
Obese: 22 HW: 22 Mean age 13
and neutral. obese children. HW higher activity in hippocampus & caudate to food pictures. Obese have increased inhibitory control?! Batterink, 2010 fMRI self-report of impulsivity behavioral data: go no-go task N = 39 girls Mean age 16 Stop eating 4-6hours before scanning Go/no-go task: Pictures of Food vegetables deserts Higher BMI: worse response inhibition and reduced activation in prefrontal inhibitory areas + show greater activity in food reward areas, and thus may use more neural resources for processing appetitive characteristics of stimuli. Page et al, 2011 fMRI behavioral measurement of interest in food hyperinsulinemi c euglycemic-hypoglycemic clamp N = 21 9 female, 12 male Mean age 31 N=14 5 female, 9 male Obese: 5 (BMI, 30.9) Non obese: 9 (BMI 22,8) Received a standardized lunch 2h before session pictures: High or Low calorie food & Non-food Higher circulating glucose in prefrontal areas less interest in food stimuli. This was absent in obese people. Glucose influences inhibitory control over food motivation. Woolley et al, 2007 VBM N = 50 18 Healthy people 32 subjects with neurodegenerati ve disease. Stayed intern for 5 days Binge eating in subjects with atrophy in OFC, insula, striatum. Born et al, 2010 fMRI N = 9 female Fasted subjects
Pictures of food Under stress, reward signalling lower, thus increased energy intake. Reduced activity in
amygdala, hippocampus, ACC.
Functional neuroimaging studies on eating behavior point to the pivotal role of the PFC in the control of eating behavior. While the hypothalamus is most studied in relating to eating, prefrontal subcortical networks regulate eating, via connections with the hypothalamus, as representations of hunger and satiety are found in prefrontal-subcortical systems (Spinella & Lyke, 2004). Neuroimaging studies indicate that the PFC and particularly the OFC, play a role in reinforcing value of food by assessing reward values of taste (Rolls, 2004).
Taste and olfactory processing occur in the OFC, because the OFC receives input about foods from multiple sensory modalities, including gestation, olfaction, vision and somatosensation. The OFC also has a great impact on food choice and selection (Zald, 2009). The OFC is important for food selection and decision making by coding rewards and satiety and also negative valuations that influences food choices, such as costs, health consequences. Furthermore, it has been suggested that the OFC may be the strongest candidate for linking food to hedonic experiences and hedonic drives for food (Kringelbach, 2004) and thus may underlie motivation to consume food (Wang et al, 2004). The ACC, striatum and insula may also be candidates for representing subjective pleasantness in foods and play a part in hedonic networks in the human brain (Kringelbach, 2004).
The first 4 studies include studies with healthy normal weight adults or children as subjects (Wang et al., 2004; Holsen et al., 2005; Killgore et al., 2003 &
Hare, 2011;). Our first study done on healthy adults points to the role of the OFC in food desire (Wang et al., 2004). Food deprived normal weight subjects were exposed with food stimuli and showed increased activity in the OFC and insula as measured with PET and FDG. They suggest that the OFC is important for drive, en thus may underlie motivation to consume food. Heightened sensitivity to food pictures may ultimately contribute to obesity (Wang et al, 2004).
Holsen et al. (2005) also revealed specific neural patterns of activity during hunger, including increased activity to presentation of food pictures in the OFC, amygdala, MFC, insula, parahippocampal gyrus, cingulate gyrus, and fusiform gyrus. Habituation to presentation of food stimuli was found explicitly in the amygdala. This study on children thus revealed activation to food stimuli in limbic and paralimbic brain regions during fMRI scans while food deprived for 4 hours.
Killgore et al., (2003) applied functional magnetic resonance imaging (fMRI) to study the cerebral responses of 13 healthy normal-weight adult women as they viewed colour photographs of food. The motivational salience of the stimuli was manipulated by presenting images from three categories: high-calorie foods, low-calorie foods, and nonedible dining-related utensils. Both food categories were associated with bilateral activation of the amygdala and ventromedial prefrontal cortex VMPFC. High-calorie foods yielded significant activation within the medial and dorsolateral prefrontal cortex, thalamus, hypothalamus, corpus callosum, and cerebellum. Low-calorie foods yielded smaller regions of focal activation within medial orbitofrontal cortex; primary gustatory/somatosensory cortex; and superior, middle, and medial temporal regions. Findings suggest that the amygdala may be responsive to a general category of biologically relevant stimuli such as food, whereas separate ventromedial prefrontal systems may be activated depending on the perceived reward value or motivational salience of food stimuli.
All studies thus underscore the role of the OFC and the amygdala in food motivation (Ongur et al, 2003; Rolls, 2004) seeing their direct connections with the VMPFC. The VMPFC on its turn, is connected to the DLPFC, which influences decision making and goal directed behavior by modulating the value signal encoded in the VMPFC, which was
found by Hare et al. (2009). This study focussed on external exogenous attention ‘health’ cues influencing neural mechanisms of successful self-control concerning eating. It appeared that external health cues influence specific parts of the brain important for self-control of food intake. The VMPFC responded more to pictures of food when in presence of health cues, and the DLPFC seemed to modulate this effect.
Studies on dieters or restrained eaters (Demos et al., 201; Lowe & Coletta., 2008; Coletta et al., 2009) also emphasize the important role of the PFC for successful regulating food intake. In all studies participants where scanned in a fasted and fed status, i.e. receiving a preload or not. In Demos et al., 2011 this was tested by examining the effect of breaking a diet on neural cue-reactivity to appetizing foods in dieters. Compared to non-dieters, those who had their diet broken by the intake of a milkshake, showed increased cue-reactivity to appetizing food pictures in the Nucleus Accumbens (NAcc) and amygdala. Initial intake of food thus serves as a hedonic prime and thereby brain regions involved in reward and are freed from the regulatory influence of the PFC. Again, a fed status in restrained eaters (REs) increased the reward value of palatable food (Lowe & Coletta, 2008). This has been further emphasized by a study by Coletta., (2009), which revealed that REs who received a pre-meal, showed increased brain activity in reward and desire areas. Apparently, REs find food more appealing then unrestrained eaters (UREs) when being fed. These studies underline the overruling role of reward areas such as the Nacc and the amygdala in restrained eaters or dieters, and the mute role of the PFC. Again, control over prefrontal regions appeared to be important for succeeding in inhibiting food cravings.
Articles on obese children or adults include Bruce et al, 2010; Martin et al, 2009;
Davids, et al, 2010; Batterink, 2010 & Page et al., 2011. A review by Carnell et al., 2011 showed us that obesity is associated with heightened and abnormal responses in visual food cues in brain regions involved in reward and motivation (striatum, OFC), emotion and memory (amygdala, hippocampus) and cognitive control (PFC and ACC).
Martin et al. (2009) used fMRI to examine changes in the hemodynamic response in obese and healthy weight (HW) adults while they viewed food and nonfood images in pre-meal and post-pre-meal states. During the pre-pre-meal and post-pre-meal condition, obese participants showed increased activation, compared to HW participants, in the anterior cingulate cortex (ACC) and medial prefrontal cortex (MPFC) – regions implicated in motivational processing. This study thus revealed increased activation in prefrontal and limbic brain regions in obese adults and these findings are in line with previous fMRI studies in obese compared to HW individuals when viewing food pictures. It indicates that obese and HW adults differ in their brain function associated with food motivation. Bruce et al. (2010) shows us a similar pattern of abnormalities in neural networks involved in food motivation in obese children. HW and obese children were shown food pictures in a hungry and satiated status. Both groups of children showed increased brain activation to food images in the limbic and paralimbic regions (PFC/OFC). However, obese children were hyper-responsive to food stimuli as compared with HW children. In addition, unlike HW children, brain activations in response to food stimuli in obese children failed to diminish significantly after eating. Obese children thus show hyper activation to food pictures in brain networks linked to motivation, reward and cognitive control. Another study by Davids et al. (2010) also provides evidence that obesity, even among children, is associated with abnormalities in neural networks involved in food motivation. Obese and HW children were shown pictures of food during functional magnetic resonance imaging. Obese children showed higher activation in the dorsolateral prefrontal cortex (DLPFC) in response to food pictures. This increased prefrontal activation in reaction to food stimuli might be, as they suggest, associated with increased inhibitory control. Because of their strong inhibitory control, obese children cannot be affected easily by external cues and reconcile them with internal body needs with leads to disorders of food intake regulation, eating behavior and ultimately obesity.
This finding is in contrast with Carnell et al. (2011) and Batterink & Stice (2010), which suggest that obese people are lacking inhibitory control in the PFC instead of having a strong inhibitory control according to Davids et al., 2010. In Batterink & Stice (2010), it
was shown again that people at risk for overeating or elevated weight may show hypo functioning of inhibitory control regions (OFC, VMPFC, PFC) and increased responses in food reward regions of the brain such as the insula Activation in food reward areas (insula & temporal operculum) after looking at food images correlated with higher scores on BMI. Overeating could thus be either a result of sluggish homeostatic responses to satiety and reduced inhibitory response in the DLPFC, or increased inhibitory control but wrongly reconciling external cues with body needs and in that way becoming obese.
Important for all these brain areas at work when making decisions about food, is enough glucose supply to brain areas important for self-control, such as the PFC and reward areas. Acts at self-regulation can also affect depletion of brain glucose levels which influences decision making in food. Circulating glucose in the brain plays a role in modulation of inhibitory control over food motivation (Page et al , 2011). Obese and non-obese adults were shown pictures of high and low calorie food pictures and non-food pictures while being scanned by and fMRI scanner and simultaneously blood samples were drawn. Higher circulating glucose in prefrontal areas was associated with reduced interest in food stimuli. This pattern was absent in obese people. Glucose levels thus influences inhibitory control over food motivation. This study suggest that indeed glucose does buffer against the effects of self-regulatory depletion.
That stress could also have an impact on food control appears from a study by Born et al 2010. This study suggested that stress significantly decreases the rewarding value of food, leading to non-homeostatic eating in the absence of hunger with food choices that result in higher energy intakes. Reward signaling and reward sensitivity were significantly lower under stress, coinciding with increased energy intake from food choice for more crispiness and fullness of taste. Reduced activity was found in reward areas such as the amygdala, hippocampus, ACC and putamen. The changes in putamen activation may reflect specifically decreased reward prediction sensitivity.
Damage to the VMPFC (Woolley et al, 2007) leads to breakdowns in self-control and
restraint, but also results in failures to regulate primary physiological drives. Participants with a lesion in the VMPFC may show excessive overeating which points to difficulties in inhibiting appetitive behaviours.
Discussion & Conclusion
Concluding from both studies on healthy subjects, dieters & restrained eaters and obese people, we can underline the role of the PFC and DLPFC on one hand, while on the other hand reward areas in the brain are important for successful and unsuccessful regulating eating behaviour. From neuroimaging studies on healthy normal weight subjects, it appeared that the DLPFC is important for making food choices and inhibiting unwanted food choices. Also the role of the OFC is underscored again, seeing it’s previously found role in food selection and decision making. Findings suggest that the amygdala may be responsive to a general category of biologically relevant stimuli such as food, whereas separate VMPF systems may be activated depending on the perceived reward value or motivational salience of food stimuli.
Research on restrained eater and dieters also point to the role of the PFC. The PFC seems to be mute and overruled by increased activation in reward areas. When being satiated, REs find food more appealing then unrestrained eaters (UREs). It seems like food is still appealing to them, even when hunger is absent. However, these REs do have a normal weight. Even their rewarding system may be different from UREs i.e. normal people, they do not show an increased weight. This finding of increased activity in rewarding systems in a satiated status is in contrast with findings from studies on stress. These studies indicated that reward sensitivity was lower under stress, decreasing the rewarding value of food and therefore leading to food choices resulting in higher energy intake. So on one hand, stress decreased the rewarding value of food and let people eat more, while on the other hand increased activity in reward areas in restrained eaters or dieters also leads to food intake ultimately.
From our data it seemed that obesity is associated with heightened and abnormal responses in visual food cues in brain regions involved in reward and motivation (striatum & amygdala, VMPFC, OFC & ACC) and cognitive control (PFC and DLPFC). Hypo activity in top-down control areas as the PFC, combined with increased activity in reward areas correlated with higher BMI scores (Batterink & Stice, 2010). In addition, obese seemed to be hyper sensitive to food stimuli (Bruce et al., 2010), which could indicate that their rewarding system may overrule their PFC recruiting. Oddly enough, Davids et al. (2010) showed that increased activity in the DLPFC might be associated with increased inhibitory control.
Overeating could thus be either a result of sluggish homeostatic responses to satiety, reduced inhibitory response in the PFC/DLPFC in combination with increased activity reward areas, or increased inhibitory control but wrongly reconciling external cues with body needs and in that way becoming obese, according to Davids et al, (2010).
Based on our included articles we cannot give an answer to the ‘to what extend’ part of our two main questions; ‘To what extend does giving in to food temptations occur as a result of insufficient top-down controlling, that is to say, poor functioning of among others the PFC?’ and ‘To what extend are self-regulatory collapses caused by overwhelming bottum-up impulses, when faced with tempting food?’
Apparently, it is the combination of insufficient top-down control and overwhelming bottum-up impulses when it comes to decision making about food. Active or inactive prefrontal control areas in combination with increased activity in reward and desire areas in a tempting food environment determine whether one can successfully inhibit unwanted behavior. To what extend either systems play a role, cannot be answered on the selected articles in this thesis but also in general, literature is lacking concerning this topic. Apparently, neuroimaging research on self-regulation success and failure concerning food choices is in its infancy.
Important to mention is the diversity in the design of the studies. Some use pictures of only food, different kind of food, differing in palatability and energy content. Others also use neutral pictures, pleasant/unpleasant pictures, or non-food pictures, which could differ a lot. Number of participants varies from 9 until 100, also the gender differs. Some studies look at the whole brain, others other at specific regions of interest ROIs. Time until the last eating occasion varies also between studies, that means some participants were allowed to eat up till 4 hours before being scanned, while other only 2. Sometimes subjects were given a preload by the researchers, while other studies did not. Apparently, neuroimaging studies with a similar design are lacking. Future research should further elucidate separate effects of methodological and physiological factors on between-study variations.
Therefore in the field of neuroscience and eating, clearly research is needed which is comparable in their research design and method and deal with self-regulation and control in food selection tasks. Besides, research could be of interest in which participants need to choose between healthy and unhealthy foods on different parts of the day when in a normal status and when depleted of cognitive top-down resources. We also need to discover in which specific circumstances bottom-up impulses are overwhelming and overrule the top-down system. Does they take over in all situations, only when being in a fasted and hungry status, or do they overrule the cool-system when the stimulus itself is that attracting and appealing and forces us to consume it.
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