20 January 2012,
 5

Does Dieting Change the Brain?

 

Gaining an understanding of what underlies the impulsive urge to overeat has been the focus of significant contemporary research. If dieting was as ‘easy’ as substituting carrots for chocolate, we wouldn’t have an obesity crisis. The pleasure part of the equation is fundamental to understanding why and how we are motivated beyond our energy requirements. The neural pathways and functions that primarily reside in the cortico limbic structures of the brain are responsible for what scientists call ‘hedonically motivated feeding,’ which is the type of eating that is governed by cognitive and emotional choices, as opposed to the physical necessity for energy (i.e. calories).

 

Before we start, I should mention: The decision to eat is astoundingly complex, reliant upon not only psychological factors, but rather metabolic, endocrine and genetic factors (Lowe & Butryn, 2007). Significant progress has been made to understand the metabolic feedback signals and neural systems, most of which are located in the hypothalamus. The hypothalamus has thus been proposed to be the ‘homeostatic regulator’ in the body (Berthoud, 2011). The decision to eat for pleasure- as opposed to physiological need- can be traced to networks that run between both frontal and subcortical areas in the brain, including the orbitofrontal cortex, ventral medial, amygdala and mid brain regions (Beaver et al., 2006; K. Berridge, 1996; K. C. Berridge & Robinson, 1998, 2003; Davis et al., 2007; Kelley et al., 2002; Lowe, van Steenburgh, Ochner, & Coletta, 2009).

 

…Understanding how the two systems interact, i.e. one that governs physiological need and the other by emotional desire, starts to disentangle why we are so compelled to reach for another cookie.

 

In terms of mechanisms in the brain, both addiction and obesity are characterized by altered activity in the mid brain dopamine system. Scientists are beginning to tease apart the relationship between the sensation of pleasure in the brain, and its neural underpinnings, and it seems that both obese individuals, and those vulnerable to the rewarding effects of drugs, have a condition that manifests itself in the tendency for natural rewards to lose their value more rapidly.

 

Individuals with substance dependence and obese individuals are known to have decreased dopamine receptors (DA D2) availability in the striatum, which possibly indicates lower dopaminergic activity. In order to correct for this imbalance, one could externally ingest those things that provoke dopamine, like highly palatable foods (or drugs), thus correcting for this imbalance. Or, this imbalance might make a person ultra sensitive to the rewarding effects of food or drugs, thus making the act of seeking out rewarding substances, such as food or drugs all the more compelling. So, maybe biology in a way is destiny: the lack of tonic dopamine could explain why one person needs to eat an entire box of smarties, as opposed to the lucky dopamine-rich individual who is able to stop with one or two candies.

 

Psychologists talk about Bottom Up or Top Down processing. The ‘Top’ part of the equation refers to the ‘frontal’ regions of the brain like the cortex, whereas the ‘Bottom’ refers to the midbrain and brain stem (the limbic and cortico limbic areas). When a decision is based on Top Down processing, it means that it is future oriented, and contingency based. This kind of future oriented thinking is responsible for careful planning and goal setting. Bottom Up processing refers to the kinds of impulsive choices we make, because they feel great at the time. Research is beginning to uncover the fact that through multiple exposures to rewarding substance, changes in the brain happen so that the ‘Bottom Up’ processing occurs before the Top Down.

 

Neurobioligical data predicts a down regulation of dopamine receptors would hypothetically produce a faulty reinforcement system (Volkow, Fowler, & Wang, 2004; Volkow, Wang, & Baler, 2011), yielding a tendency for generalized impulsive responding (Dalley, Everitt, & Robbins, 2011), or greater ‘Bottom Up’ processing. Experimental psychology verifies this hypothesis; the impairments suggested here can be detected in deficits of impulse control on tasks that psychologists use called Delayed Discounting Tasks, where the preference for immediate small rewards hold greater value than larger future gains (Dawe & Loxton, 2004; Nederkoorn, Jansen, Mulkens, & Jansen, 2006). Both overweight, obese, and drug addicted individuals show highly significant impulsive responding on DDT tasks in contrast with healthy controls.

 

Spookily enough, it may also be the case that through multiple exposures to a highly rewarding substance (food or drugs), may evoke this ‘pruning’ effect. This is to say, we don’t know if someone who suffers addiction has a genetic predisposition or if the exposure to the rewarding substance leads to the down regulation of dopamine receptors. By flooding the brain with dopamine, and then restricting access, the brain must overcompensate twice to correct for a new influx of euphoria inducing hormones. Over time, this kind of cycle exhausts the receptors, pruning what is available in the cortico limbic areas of the brain (likely the striatum) leading to permanent neuroadaptations. These permanent neuroadaptations prime the individual for even more sensitivity to the euphoric effects of the rewarding substance, and making it harder and harder to resist.

 

How does this relate to dieting?

 

Let’s take someone who has become accustomed to a diet rich in sweet, pleasant tasting foods. When this person restricts access to this kind of food (in order to lose weight), it registers as a general dip in pleasure in the brain. Lest we forget that our bodies have not changed all that much within the last few thousands of years, where as our food environment has changed radically within the last thirty.  The pictures and paraphernalia that represent food speak directly to the midbrain/ limbic system: as soon as we see them, we can’t help but continue to think about them. Those pictures speak directly to our midbrain, the cortico limbic, ‘Bottom’ part of the Top Down processing.

 

So, it has been suggested that weight-loss dieting in an environment of supranormal rewarding foods and food cues can be stressful. By the way, anything deep fried fits the definition of ‘supranormal’. The stress leads to episodes of loss of control, and we regain control by focusing on one thing: how great that doughnut tastes. So, pairing the deluge of food advertisements and cues with an articificially imposed rule to simply ‘eat less’, or ‘stop eating chocolate’ only makes that food more attractive. Under periods of hunger, the rewarding properties of the food are ever the more enhanced. Thus, the loss-of-control episodes associated with dieting may be hazardous since they may induce neuroplastic changes to dopamine receptors, ingraining corresponding behaviour and ultimately contributing to binge pathology.

 

We should consider the robust and reliable finding that food deprivation not only increases the reinforcing value of food but also drugs. Which is to say, when you are hungry food not only tastes better, but drugs also feel better. This is a homely example of how similar regions in the brain are implicated in the sense of natural and external rewards. A recent study of fasting, hungry healthy human contrasted high-calorie versus low-calorie foods. Interestingly,  the high-calorie foods selectively increased neural activity in reward related areas in the brain: the Pictures of chocolates and cookies elicited activity in the orbitofrontal cortex, ventral striatum, amygdala, and anterior insula; this wasn’t the case with less pleasant tasting food, such as carrot sticks. The neurobiological data matches the participants psychological response, unsurprisingly, the participants also rated the pleasant tasting food more positively. These findings suggest that some fasting-related signal, a signal conveying ‘caloric need’, modulates the hedonic value assigned to specific familiar foods triggered by looking at pictures, and that these foods will be preferred if available for eating, and especially if one is hungry.

 

So, by placing an arbitrary rule to ‘simply’ eat less, you may inadvertently increase the hedonic and emotional attraction of said forbidden food.

 

Impulsive eating can be explained by the over activation of reward system components, those areas in the brain that are related to the sensation of pleasure. For this reason, there is significant support for the idea that overeating may be a form of addictive behaviour. Critically, by eating less, you also induce the sensitivity to the rewarding effects of pleasant tasting food.

 

It seems that the system governed by psychological/ emotional desire is most likely to be exploited, particularly in our current food environment, rife with food that is highly caloric despite not having many nutrients. In other words, we have created a system that caters to our emotional desires for sweet and pleasant tasting food. Controlling our desire for these types of foods, if current obesity statistics are to be believed, is an incredibly challenging undertaking for the  majority of people in developed, and developing, countries.

 

 

Beaver, J. D., Lawrence, A. D., van Ditzhuijzen, J., Davis, M. H., Woods, A., & Calder, A. J. (2006). Individual differences in reward drive predict neural responses to images of food. J Neurosci, 26(19), 5160-5166.

Berridge, K. (1996). Food reward: Brain substrates of wanting and liking. Neurosci Behav Rev, 20, 1-25.

Berridge, K. C., & Robinson, T. E. (1998). What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Brain Res Rev, 28(3), 309-369.

Berridge, K. C., & Robinson, T. E. (2003). Parsing reward. Trends Neurosci, 26(9), 507-513.

Berthoud, H. R. (2011). Metabolic and hedonic drives in the neural control of appetite: who is the boss? Curr Opin Neurobiol, 21(6), 888-896.

Dalley, J. W., Everitt, B. J., & Robbins, T. W. (2011). Impulsivity, compulsivity, and top-down cognitive control. Neuron, 69(4), 680-694.

Davis, C., Patte, K., Levitan, R., Reid, C., Tweed, S., & Curtis, C. (2007). From motivation to behaviour: a model of reward sensitivity, overeating, and food preferences in the risk profile for obesity. Appetite, 48(1), 12-19.

Dawe, S., & Loxton, N. J. (2004). The role of impulsivity in the development of substance use and eating disorders. Neurosci Biobehav Rev, 28(3), 343-351.

Kelley, A. E., Bakshi, V. P., Haber, S. N., Steininger, T. L., Will, M. J., & Zhang, M. (2002). Opioid modulation of taste hedonics within the ventral striatum. Physiol Behav, 76(3), 365-377.

Lowe, M. R., & Butryn, M. L. (2007). Hedonic hunger: A new dimension of appetite? Physiol Behav.

Lowe, M. R., van Steenburgh, J., Ochner, C., & Coletta, M. (2009). Neural correlates of individual differences related to appetite. Physiol Behav.

Nederkoorn, C., Jansen, E., Mulkens, S., & Jansen, A. (2006). Impulsivity predicts treatment outcome in obese children. Behav Res Ther.

Volkow, N. D., Fowler, J. S., & Wang, G. J. (2004). The addicted human brain viewed in the light of imaging studies: brain circuits and treatment strategies. Neuropharmacology, 47 Suppl 1, 3-13.

Volkow, N. D., Wang, G. J., & Baler, R. D. (2011). Reward, dopamine and the control of food intake: implications for obesity. Trends Cogn Sci, 15(1), 37-46.

 

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