Failures of self-regulation are common, leading to many of the most vexing problems facing contemporary society, from overeating and obesity to impulsive sexual behavior and STDs. One reason that people may be prone to engaging in unwanted behaviors is heightened sensitivity to cues related to those behaviors; people may overeat because of hyperresponsiveness to food cues, addicts may relapse following exposure to their drug of choice, and some people might engage in impulsive sexual activity because they are easily aroused by erotic stimuli. An open question is the extent to which individual differences in neural cue reactivity relate to actual behavioral outcomes. Here we show that individual differences in human reward-related brain activity in the nucleus accumbens to food and sexual images predict subsequent weight gain and sexual activity 6 months later. These findings suggest that heightened reward responsivity in the brain to food and sexual cues is associated with indulgence in overeating and sexual activity, respectively, and provide evidence for a common neural mechanism associated with appetitive behaviors.
Brain Scan Predicts Weight Gain And Sexual Activity
Neural and physiological reactivity to drug cues predicts important behavioral outcomes, such as smoking cessation (Janes et al., 2010) and cocaine relapse (Back et al., 2010). Does such reactivity predict long-term outcomes for non-drug behaviors? An open question is whether individual differences in brain activity, specifically in regions associated with reward motivation, are associated with an increased proclivity for indulgence and thereby predict future weight gain and/or sexual promiscuity. We hypothesized that individual differences in NAcc activity in response to viewing food items and sexual scenes would predict future weight gain and sexual behavior.
It seems likely that the stress associated with the first year of college may be a contributing factor to changes in behavior. Research in nonhuman animals indicates that stress weakens prefrontal control over behavior (Arnsten, 2009) while also sensitizing reward systems to biologically salient stimuli (Piazza and Le Moal, 1998). Thus, stress may disrupt self-regulatory efforts because it is associated with reduced top-down control from prefrontal cortex in conjunction with heightened hedonic responses to appetitive stimuli (Heatherton and Wagner, 2011). For instance, a considerable amount of research demonstrates that stress and other types of negative affect produce increases in eating, particularly for those trying to control their weight (Heatherton and Baumeister, 1991). Other factors, such as less frequent exercise, living away from parental influence, and changes in daily routines and sleep and their hormonal consequences may all be contributing factors to weight gain and changes in sexual behavior observed among college students. Future research is needed to disentangle these putative mechanisms.
As noted, cue exposure increases activity in brain reward regions, but it also produces spontaneous activity in the action observation network, such as when smokers spontaneously engage action representation brain areas when viewing others smoking (Wagner et al., 2011). According to contemporary research in social cognition, exposure to appetitive cues primes behavior outside of people's intentions or awareness (Bargh and Morsella, 2008). The putative mechanism for behavioral priming is that cue exposure activates mental representations that lead to unconscious goal pursuit, which ultimately produces the same outcomes that consciously pursuing goals does (Dijksterhuis et al., 2007). Indeed, even if people are aware of being exposed to appetitive cues, they may be unaware of the effect such cues have on their behavior (Stacy and Wiers, 2010). From this perspective, exposure to food or sexual images activates mental representations of their attendant behaviors and activates unconscious goals to engage in those behaviors.
Certain health conditions, including bulimia and obesity, have already been linked to high nucleus accumbens activity in response to food-related cues. Kelley and his colleagues wanted to find out if there was any predictive power to such linkages. So the researchers recruited 58 female college freshmen for a study in which they weighed the women and calculated their body mass index, or BMI (a measure of fatness). College freshmen were chosen because of the dreaded "Freshmen 15" weight gain, Kelley said. The researchers wanted a group of volunteers who might be at risk for putting on pounds. [8 Reasons Our Waistlines are Expanding]
The women whose nucleus accumbens responded more strongly to pictures of food were the ones most likely to gain weight over the next six months, the researchers report Wednesday (April 18) in The Journal of Neuroscience. About half of the women were sexually active, so researchers checked on sexual behavior, too. It turned out that women with a stronger nucleus accumbens reaction to erotic images were more likely to report at least one sexual partner during the six months following the brain scans. A strong nucleus accumbens reaction was also linked with more sexual desire, as reported on questionnaires.
Importantly, these reactions were behavior-specific. Weight gain was linked only with a nucleus accumbens response to food pictures, not to sexy images or neutral environmental scenes. And sexual desire and activity were linked only to the response to sexy pictures. That means specific temptations, not just an overactive nucleus accumbens, trigger these behaviors, Kelley said.
Epidemiological evidence supports a link between sleep loss and obesity. However, the detrimental impact of sleep deprivation on central brain mechanisms governing appetitive food desire remains unknown. Here we report that sleep deprivation significantly decreases activity in appetitive evaluation regions within the human frontal cortex and insular cortex during food desirability choices, combined with a converse amplification of activity within the amygdala. Moreover, this bi-directional change in the profile of brain activity is further associated with a significant increase in the desire for weight-gain promoting high-calorie foods following sleep deprivation, the extent of which is predicted by the subjective severity of sleep loss across participants. These findings provide an explanatory brain mechanism by which insufficient sleep may lead to the development/maintenance of obesity through diminished activity in higher-order cortical evaluation regions, combined with excess subcortical limbic responsivity, resulting in the selection of foods most capable of triggering weight-gain.
Despite such population-level as well as peripheral body evidence, the central brain mechanisms explaining the impact of sleep deprivation on appetitive food desire that can lead to weight-gain remain unknown. Discovering such neural dysfunction may represent a critical component to understanding the link between sleep loss and obesity2. It would further contribute to a central nervous system explanation for the failure to appropriately regulate dietary intake and thus develop or maintain obesity under conditions of insufficient sleep. Using a food-desire task in combination with human functional MRI (fMRI), here we sought to characterize the impact of sleep loss on the brain mechanisms governing appetitive food desire.
The study focused a priori on a discreet set of well-characterized cortical and subcortical regions of interest (ROIs) known to be instrumental in appetitive desire and food stimulus evaluation4. At the cortical level, the anterior insular cortex, lateral orbital frontal cortex and anterior cingulate cortex, all have well established roles in signalling stimulus value across contexts, including appetitive choices, and in integrating food features that govern preferences (for example, the odour and flavour of food)5,6. Moreover, disrupted functional activity within frontal cortex, including these anterior cortical regions, is widely considered to be one hallmark of sleep loss7. At the subcortical level, both the amygdala and the ventral striatum have been strongly implicated in governing the motivation to eat4. The amygdala has consistently demonstrated responsivity to food stimuli, especially when the salience of food stimuli is high8. Activity in the ventral striatum in response to foods accurately predicts immediate food intake9, binge eating10 as well as real-world weight gain11. Moreover, previous work has demonstrated that activity in the amygdala and striatum in other (non-appetitive) affective tasks is elevated following sleep loss12,13.
Building on this established literature, the current study sought to test two non-mutually exclusive hypotheses regarding the central brain mechanisms that may lead to weight-promoting food choices following sleep loss. One hypothesis is that failure to recruit cortical regions necessary for optimal evaluation of food stimuli (the anterior cingulate, the lateral orbitofrontal cortex and the anterior insula) leads to improper food choice selection (that is, choosing items with greater weight-gain potential). A second hypothesis is that excessive reactivity in two subcortical regions known to signal food salience and promote eating behaviour (the amygdala and the ventral striatum) may exaggerate food salience and motivated consumption for appetitive food stimuli, also leading to weight-gain potential. The findings reported here demonstrate not only reduced recruitment of all three key cortical regions necessary for food stimulus evaluation but also amplified subcortical amygdala (yet not ventral striatal) reactivity under sleep deprivation. Such changes offer a novel explanatory brain mechanism by which insufficient sleep may lead to altered food choices and thus the development or maintenance of obesity.
Third, and congruent with these predictions, these changes in neural reactivity to food desirability under sleep deprivation were additionally accompanied by a significant shift in preferences for food items carrying the highest caloric content. While a shift in food desire ratings was observed following sleep deprivation, the controlled eating schedule of the study precluded the ability to measure actual changes in caloric intake under ad libitum (rather than controlled) food availability. Interestingly, this alteration in food desire, coinciding with changes in brain activity, is consistent with previous behavioural findings describing increases in actual caloric intake following sleep loss when ad libitum food conditions are presented3,22 and increased cravings for higher caloric food categories (for example, sweet, salty and starchy foods)23. Given the established increase in energy needs induced by sleep deprivation22,24,25, the shift towards increased caloric intake and high-calorie choice preferences identified in the current experiment, supports an adaptive homoeostatic function to recover such energy expended. However, a recent study that assessed ad libitum caloric intake as well as energy expenditure in sleep-restricted humans reported increased calorie consumption beyond that which could be explained by expended energy or altered metabolic rate22. Moreover, this increase in calorie intake resulted in significant gains in weight. This finding leads to the hypothesis that changes in central nervous system disruption due to sleep loss, such as the alterations in appetitive brain signaling discovered in the current study, may trigger decisions that lead to increased calorie consumption in excess of energy expenditure changes, one consequence of which is weight gain. Consistent with this proposal, we additionally demonstrated that the magnitude of change (increase) in desire for high-calorie foods was positively correlated with the perceived subjective severity of sleep deprivation across participants (indexed in the measure of sleepiness). These neural and behavioral data provide indirect support linking the state of sleep deprivation, and the subjective severity of this state, to altered internal homoeostasis following extended time awake, consistent with already established alterations in other primal homeostatic functions such as metabolic balance and temperature regulation following sleep loss26,27. This may reflect a progressive deterioration in the brain and body systems that regulate and maintain optimal energy balance, one expression of which is select cortical and subcortical dysfunction leading to increases in energy consumption through heightened desire for high-calorie foods. 2ff7e9595c
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