The Experts below are selected from a list of 40446 Experts worldwide ranked by ideXlab platform

James M. Swanson - One of the best experts on this subject based on the ideXlab platform.

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-D-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3±3 post 6±3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3±2 post 3±3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r = −0.62, P <0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli was elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction. In addicted individuals exposure to conditioned drug-cues (i.e., places, people and paraphernalia associated with the drug) usually elicits an intense desire for the drug. This subjective experience (described as craving) frequently triggers relapse (O’Brien et al., 1998). Dopamine (DA) is a neurotransmitter involved with reward and with prediction of reward (Wise and Rompre, 1989; Schultz et al., 1997), and DA increases in the nucleus accumbens (NAcc) are associated with the drug-seeking behavior that follows exposure to conditioned-cues (Phillips et al., 2003; Weiss et al., 2000). These DA responses are modulated by glutamatergic projections from the frontal cortex (You et al., 2007; Yun et al., 2004; Taber et al., 1995), including the orbitofrontal cortex (OFC), which signals the motivational value of the conditioned stimuli (Rolls, 1996) and from amygdala and ventral hippocampus (Grace et al., 2007). It has been proposed that disrupted function of frontal regions may contribute to the impaired control over drug taking that characterizes drug addiction (Kalivas, 2004). However, addicted individuals may retain some level of purposeful control over craving, but to our knowledge this has not been specifically evaluated. Here we performed a proof-of-principle study to test the hypothesis that a simple Cognitive control procedure could reduce the subjective report of cue-induced craving in cocaine abusers, and to test the linked hypothesis that this would be associated with objective measures of Inhibition of activity in brain regions (NAcc and OFC) that are implicated in the responses to drug conditioned stimuli. To test these hypotheses we used Positron Emission Tomography (PET) and 2-deoxy-2[18F]fluoro-D-glucose (18FDG) to measure brain glucose metabolism (marker of brain function) ( Sokoloff et al., 1977) in 24 active cocaine abusers. Subjects were tested using a video of cocaine cues that was previously shown to induce the subjective report of craving and to increase objective measures of striatal DA in cocaine abusers (Volkow et al., 2006). The cocaine abusers were scanned during stimulation with the cocaine-cue video twice, both with instruction to try to purposefully inhibit craving (Cognitive Inhibition CI) and without instruction (no-Inhibition NI). A third scan was obtained without the stimulation of drug cues, which was used as a measure of baseline brain metabolic activity. We hypothesized that if Cognitive Inhibition of craving occurred, then it would be accompanied by decreases in metabolic activity in NAcc (in which activity is associated with prediction of reward) and in OFC (in which activity is related to motivational value of conditioned cues). We also assessed if the Inhibition in these brain regions was associated by activation of the right inferior frontal cortex (Brodmann area 44), which is a critical brain region for exerting inhibitory control (Aron et al., 2004).

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.

Nora D. Volkow - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of food craving is a metabolically active process in the brain in obese men
    International Journal of Obesity, 2019
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Joanna S. Fowler, Christopher Wong, Ehsan Shokri Kojori, Kai Yuan, Corinde E Wiers, Peter Manza
    Abstract:

    Obesity is associated with impaired inhibitory control over food intake. We hypothesized that the neural circuitry underlying Inhibition of food craving would be impaired in obesity. Here we assessed whether obese men show altered brain responses during attempted Cognitive Inhibition of craving when exposed to food cues. Sixteen obese men (32 ± 8.7 years old, BMI = 38.6 ± 7.2) were compared with 11 age-matched non-obese men (BMI 24.2 ± 2.5) using PET and FDG. Brain glucose metabolism was evaluated in a food deprived state: no food stimulation, food stimulation with no Inhibition (NI), and food stimulation with attempted Inhibition (AI), each on a separate day. Individualized favorite food items were presented prior to and after FDG injection for 40 min. For AI, participants were asked to attempt to inhibit their desire for the food presented. Self-reports for hunger and food desire were recorded. Food stimulation compared with no stimulation increased glucose metabolism in inferior and superior frontal gyrus, default mode network and cerebellum, in both groups. For both groups, AI compared with NI-suppressed metabolism in right subgenual anterior cingulate, orbitofrontal areas, bilateral insula, and temporal gyri. There was a stimulation-by-group interaction effect in obese (but not in non-obese) men showing increased metabolism in pregenual anterior cingulate cortex (pgACC) and caudate during AI relative to NI. Changes in the food desire from NI to AI correlated negatively with changes in metabolism in pgACC/caudate in obese but not in non-obese men. Obese men showed higher activation in pgACC/caudate, which are regions involved with self-regulation and emotion/reward during AI. Behavioral associations suggest that successful AI is an active process requiring more energy in obese but not in non-obese men. The additional required effort to increase Cognitive control in response to food stimulation in obese compared with non-obese men may contribute to their uncontrolled eating behavior.

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-D-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3±3 post 6±3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3±2 post 3±3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r = −0.62, P <0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli was elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction. In addicted individuals exposure to conditioned drug-cues (i.e., places, people and paraphernalia associated with the drug) usually elicits an intense desire for the drug. This subjective experience (described as craving) frequently triggers relapse (O’Brien et al., 1998). Dopamine (DA) is a neurotransmitter involved with reward and with prediction of reward (Wise and Rompre, 1989; Schultz et al., 1997), and DA increases in the nucleus accumbens (NAcc) are associated with the drug-seeking behavior that follows exposure to conditioned-cues (Phillips et al., 2003; Weiss et al., 2000). These DA responses are modulated by glutamatergic projections from the frontal cortex (You et al., 2007; Yun et al., 2004; Taber et al., 1995), including the orbitofrontal cortex (OFC), which signals the motivational value of the conditioned stimuli (Rolls, 1996) and from amygdala and ventral hippocampus (Grace et al., 2007). It has been proposed that disrupted function of frontal regions may contribute to the impaired control over drug taking that characterizes drug addiction (Kalivas, 2004). However, addicted individuals may retain some level of purposeful control over craving, but to our knowledge this has not been specifically evaluated. Here we performed a proof-of-principle study to test the hypothesis that a simple Cognitive control procedure could reduce the subjective report of cue-induced craving in cocaine abusers, and to test the linked hypothesis that this would be associated with objective measures of Inhibition of activity in brain regions (NAcc and OFC) that are implicated in the responses to drug conditioned stimuli. To test these hypotheses we used Positron Emission Tomography (PET) and 2-deoxy-2[18F]fluoro-D-glucose (18FDG) to measure brain glucose metabolism (marker of brain function) ( Sokoloff et al., 1977) in 24 active cocaine abusers. Subjects were tested using a video of cocaine cues that was previously shown to induce the subjective report of craving and to increase objective measures of striatal DA in cocaine abusers (Volkow et al., 2006). The cocaine abusers were scanned during stimulation with the cocaine-cue video twice, both with instruction to try to purposefully inhibit craving (Cognitive Inhibition CI) and without instruction (no-Inhibition NI). A third scan was obtained without the stimulation of drug cues, which was used as a measure of baseline brain metabolic activity. We hypothesized that if Cognitive Inhibition of craving occurred, then it would be accompanied by decreases in metabolic activity in NAcc (in which activity is associated with prediction of reward) and in OFC (in which activity is related to motivational value of conditioned cues). We also assessed if the Inhibition in these brain regions was associated by activation of the right inferior frontal cortex (Brodmann area 44), which is a critical brain region for exerting inhibitory control (Aron et al., 2004).

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.

  • evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Frank Telang, Millard Jayne, Kith Pradhan, Christopher Wong, Wei Zhu, Panayotis K Thanos, Allan Geliebter, Anat Biegon
    Abstract:

    Although impaired inhibitory control is linked to a broad spectrum of health problems, including obesity, the brain mechanism(s) underlying voluntary control of hunger are not well understood. We assessed the brain circuits involved in voluntary Inhibition of hunger during food stimulation in 23 fasted men and women using PET and 2-deoxy-2[18F]fluoro-D-glucose (18FDG). In men, but not in women, food stimulation with Inhibition significantly decreased activation in amygdala, hippocampus, insula, orbitofrontal cortex, and striatum, which are regions involved in emotional regulation, conditioning, and motivation. The suppressed activation of the orbitofrontal cortex with Inhibition in men was associated with decreases in self-reports of hunger, which corroborates the involvement of this region in processing the conscious awareness of the drive to eat. This finding suggests a mechanism by which Cognitive Inhibition decreases the desire for food and implicates lower ability to suppress hunger in women as a contributing factor to gender differences in obesity.

Gene-jack Wang - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of food craving is a metabolically active process in the brain in obese men
    International Journal of Obesity, 2019
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Joanna S. Fowler, Christopher Wong, Ehsan Shokri Kojori, Kai Yuan, Corinde E Wiers, Peter Manza
    Abstract:

    Obesity is associated with impaired inhibitory control over food intake. We hypothesized that the neural circuitry underlying Inhibition of food craving would be impaired in obesity. Here we assessed whether obese men show altered brain responses during attempted Cognitive Inhibition of craving when exposed to food cues. Sixteen obese men (32 ± 8.7 years old, BMI = 38.6 ± 7.2) were compared with 11 age-matched non-obese men (BMI 24.2 ± 2.5) using PET and FDG. Brain glucose metabolism was evaluated in a food deprived state: no food stimulation, food stimulation with no Inhibition (NI), and food stimulation with attempted Inhibition (AI), each on a separate day. Individualized favorite food items were presented prior to and after FDG injection for 40 min. For AI, participants were asked to attempt to inhibit their desire for the food presented. Self-reports for hunger and food desire were recorded. Food stimulation compared with no stimulation increased glucose metabolism in inferior and superior frontal gyrus, default mode network and cerebellum, in both groups. For both groups, AI compared with NI-suppressed metabolism in right subgenual anterior cingulate, orbitofrontal areas, bilateral insula, and temporal gyri. There was a stimulation-by-group interaction effect in obese (but not in non-obese) men showing increased metabolism in pregenual anterior cingulate cortex (pgACC) and caudate during AI relative to NI. Changes in the food desire from NI to AI correlated negatively with changes in metabolism in pgACC/caudate in obese but not in non-obese men. Obese men showed higher activation in pgACC/caudate, which are regions involved with self-regulation and emotion/reward during AI. Behavioral associations suggest that successful AI is an active process requiring more energy in obese but not in non-obese men. The additional required effort to increase Cognitive control in response to food stimulation in obese compared with non-obese men may contribute to their uncontrolled eating behavior.

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-D-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3±3 post 6±3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3±2 post 3±3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r = −0.62, P <0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli was elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction. In addicted individuals exposure to conditioned drug-cues (i.e., places, people and paraphernalia associated with the drug) usually elicits an intense desire for the drug. This subjective experience (described as craving) frequently triggers relapse (O’Brien et al., 1998). Dopamine (DA) is a neurotransmitter involved with reward and with prediction of reward (Wise and Rompre, 1989; Schultz et al., 1997), and DA increases in the nucleus accumbens (NAcc) are associated with the drug-seeking behavior that follows exposure to conditioned-cues (Phillips et al., 2003; Weiss et al., 2000). These DA responses are modulated by glutamatergic projections from the frontal cortex (You et al., 2007; Yun et al., 2004; Taber et al., 1995), including the orbitofrontal cortex (OFC), which signals the motivational value of the conditioned stimuli (Rolls, 1996) and from amygdala and ventral hippocampus (Grace et al., 2007). It has been proposed that disrupted function of frontal regions may contribute to the impaired control over drug taking that characterizes drug addiction (Kalivas, 2004). However, addicted individuals may retain some level of purposeful control over craving, but to our knowledge this has not been specifically evaluated. Here we performed a proof-of-principle study to test the hypothesis that a simple Cognitive control procedure could reduce the subjective report of cue-induced craving in cocaine abusers, and to test the linked hypothesis that this would be associated with objective measures of Inhibition of activity in brain regions (NAcc and OFC) that are implicated in the responses to drug conditioned stimuli. To test these hypotheses we used Positron Emission Tomography (PET) and 2-deoxy-2[18F]fluoro-D-glucose (18FDG) to measure brain glucose metabolism (marker of brain function) ( Sokoloff et al., 1977) in 24 active cocaine abusers. Subjects were tested using a video of cocaine cues that was previously shown to induce the subjective report of craving and to increase objective measures of striatal DA in cocaine abusers (Volkow et al., 2006). The cocaine abusers were scanned during stimulation with the cocaine-cue video twice, both with instruction to try to purposefully inhibit craving (Cognitive Inhibition CI) and without instruction (no-Inhibition NI). A third scan was obtained without the stimulation of drug cues, which was used as a measure of baseline brain metabolic activity. We hypothesized that if Cognitive Inhibition of craving occurred, then it would be accompanied by decreases in metabolic activity in NAcc (in which activity is associated with prediction of reward) and in OFC (in which activity is related to motivational value of conditioned cues). We also assessed if the Inhibition in these brain regions was associated by activation of the right inferior frontal cortex (Brodmann area 44), which is a critical brain region for exerting inhibitory control (Aron et al., 2004).

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.

  • evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Frank Telang, Millard Jayne, Kith Pradhan, Christopher Wong, Wei Zhu, Panayotis K Thanos, Allan Geliebter, Anat Biegon
    Abstract:

    Although impaired inhibitory control is linked to a broad spectrum of health problems, including obesity, the brain mechanism(s) underlying voluntary control of hunger are not well understood. We assessed the brain circuits involved in voluntary Inhibition of hunger during food stimulation in 23 fasted men and women using PET and 2-deoxy-2[18F]fluoro-D-glucose (18FDG). In men, but not in women, food stimulation with Inhibition significantly decreased activation in amygdala, hippocampus, insula, orbitofrontal cortex, and striatum, which are regions involved in emotional regulation, conditioning, and motivation. The suppressed activation of the orbitofrontal cortex with Inhibition in men was associated with decreases in self-reports of hunger, which corroborates the involvement of this region in processing the conscious awareness of the drive to eat. This finding suggests a mechanism by which Cognitive Inhibition decreases the desire for food and implicates lower ability to suppress hunger in women as a contributing factor to gender differences in obesity.

Christopher Wong - One of the best experts on this subject based on the ideXlab platform.

  • Inhibition of food craving is a metabolically active process in the brain in obese men
    International Journal of Obesity, 2019
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Joanna S. Fowler, Christopher Wong, Ehsan Shokri Kojori, Kai Yuan, Corinde E Wiers, Peter Manza
    Abstract:

    Obesity is associated with impaired inhibitory control over food intake. We hypothesized that the neural circuitry underlying Inhibition of food craving would be impaired in obesity. Here we assessed whether obese men show altered brain responses during attempted Cognitive Inhibition of craving when exposed to food cues. Sixteen obese men (32 ± 8.7 years old, BMI = 38.6 ± 7.2) were compared with 11 age-matched non-obese men (BMI 24.2 ± 2.5) using PET and FDG. Brain glucose metabolism was evaluated in a food deprived state: no food stimulation, food stimulation with no Inhibition (NI), and food stimulation with attempted Inhibition (AI), each on a separate day. Individualized favorite food items were presented prior to and after FDG injection for 40 min. For AI, participants were asked to attempt to inhibit their desire for the food presented. Self-reports for hunger and food desire were recorded. Food stimulation compared with no stimulation increased glucose metabolism in inferior and superior frontal gyrus, default mode network and cerebellum, in both groups. For both groups, AI compared with NI-suppressed metabolism in right subgenual anterior cingulate, orbitofrontal areas, bilateral insula, and temporal gyri. There was a stimulation-by-group interaction effect in obese (but not in non-obese) men showing increased metabolism in pregenual anterior cingulate cortex (pgACC) and caudate during AI relative to NI. Changes in the food desire from NI to AI correlated negatively with changes in metabolism in pgACC/caudate in obese but not in non-obese men. Obese men showed higher activation in pgACC/caudate, which are regions involved with self-regulation and emotion/reward during AI. Behavioral associations suggest that successful AI is an active process requiring more energy in obese but not in non-obese men. The additional required effort to increase Cognitive control in response to food stimulation in obese compared with non-obese men may contribute to their uncontrolled eating behavior.

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-D-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3±3 post 6±3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3±2 post 3±3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r = −0.62, P <0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli was elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction. In addicted individuals exposure to conditioned drug-cues (i.e., places, people and paraphernalia associated with the drug) usually elicits an intense desire for the drug. This subjective experience (described as craving) frequently triggers relapse (O’Brien et al., 1998). Dopamine (DA) is a neurotransmitter involved with reward and with prediction of reward (Wise and Rompre, 1989; Schultz et al., 1997), and DA increases in the nucleus accumbens (NAcc) are associated with the drug-seeking behavior that follows exposure to conditioned-cues (Phillips et al., 2003; Weiss et al., 2000). These DA responses are modulated by glutamatergic projections from the frontal cortex (You et al., 2007; Yun et al., 2004; Taber et al., 1995), including the orbitofrontal cortex (OFC), which signals the motivational value of the conditioned stimuli (Rolls, 1996) and from amygdala and ventral hippocampus (Grace et al., 2007). It has been proposed that disrupted function of frontal regions may contribute to the impaired control over drug taking that characterizes drug addiction (Kalivas, 2004). However, addicted individuals may retain some level of purposeful control over craving, but to our knowledge this has not been specifically evaluated. Here we performed a proof-of-principle study to test the hypothesis that a simple Cognitive control procedure could reduce the subjective report of cue-induced craving in cocaine abusers, and to test the linked hypothesis that this would be associated with objective measures of Inhibition of activity in brain regions (NAcc and OFC) that are implicated in the responses to drug conditioned stimuli. To test these hypotheses we used Positron Emission Tomography (PET) and 2-deoxy-2[18F]fluoro-D-glucose (18FDG) to measure brain glucose metabolism (marker of brain function) ( Sokoloff et al., 1977) in 24 active cocaine abusers. Subjects were tested using a video of cocaine cues that was previously shown to induce the subjective report of craving and to increase objective measures of striatal DA in cocaine abusers (Volkow et al., 2006). The cocaine abusers were scanned during stimulation with the cocaine-cue video twice, both with instruction to try to purposefully inhibit craving (Cognitive Inhibition CI) and without instruction (no-Inhibition NI). A third scan was obtained without the stimulation of drug cues, which was used as a measure of baseline brain metabolic activity. We hypothesized that if Cognitive Inhibition of craving occurred, then it would be accompanied by decreases in metabolic activity in NAcc (in which activity is associated with prediction of reward) and in OFC (in which activity is related to motivational value of conditioned cues). We also assessed if the Inhibition in these brain regions was associated by activation of the right inferior frontal cortex (Brodmann area 44), which is a critical brain region for exerting inhibitory control (Aron et al., 2004).

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.

  • evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Frank Telang, Millard Jayne, Kith Pradhan, Christopher Wong, Wei Zhu, Panayotis K Thanos, Allan Geliebter, Anat Biegon
    Abstract:

    Although impaired inhibitory control is linked to a broad spectrum of health problems, including obesity, the brain mechanism(s) underlying voluntary control of hunger are not well understood. We assessed the brain circuits involved in voluntary Inhibition of hunger during food stimulation in 23 fasted men and women using PET and 2-deoxy-2[18F]fluoro-D-glucose (18FDG). In men, but not in women, food stimulation with Inhibition significantly decreased activation in amygdala, hippocampus, insula, orbitofrontal cortex, and striatum, which are regions involved in emotional regulation, conditioning, and motivation. The suppressed activation of the orbitofrontal cortex with Inhibition in men was associated with decreases in self-reports of hunger, which corroborates the involvement of this region in processing the conscious awareness of the drive to eat. This finding suggests a mechanism by which Cognitive Inhibition decreases the desire for food and implicates lower ability to suppress hunger in women as a contributing factor to gender differences in obesity.

Kith Pradhan - One of the best experts on this subject based on the ideXlab platform.

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-D-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3±3 post 6±3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3±2 post 3±3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r = −0.62, P <0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli was elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction. In addicted individuals exposure to conditioned drug-cues (i.e., places, people and paraphernalia associated with the drug) usually elicits an intense desire for the drug. This subjective experience (described as craving) frequently triggers relapse (O’Brien et al., 1998). Dopamine (DA) is a neurotransmitter involved with reward and with prediction of reward (Wise and Rompre, 1989; Schultz et al., 1997), and DA increases in the nucleus accumbens (NAcc) are associated with the drug-seeking behavior that follows exposure to conditioned-cues (Phillips et al., 2003; Weiss et al., 2000). These DA responses are modulated by glutamatergic projections from the frontal cortex (You et al., 2007; Yun et al., 2004; Taber et al., 1995), including the orbitofrontal cortex (OFC), which signals the motivational value of the conditioned stimuli (Rolls, 1996) and from amygdala and ventral hippocampus (Grace et al., 2007). It has been proposed that disrupted function of frontal regions may contribute to the impaired control over drug taking that characterizes drug addiction (Kalivas, 2004). However, addicted individuals may retain some level of purposeful control over craving, but to our knowledge this has not been specifically evaluated. Here we performed a proof-of-principle study to test the hypothesis that a simple Cognitive control procedure could reduce the subjective report of cue-induced craving in cocaine abusers, and to test the linked hypothesis that this would be associated with objective measures of Inhibition of activity in brain regions (NAcc and OFC) that are implicated in the responses to drug conditioned stimuli. To test these hypotheses we used Positron Emission Tomography (PET) and 2-deoxy-2[18F]fluoro-D-glucose (18FDG) to measure brain glucose metabolism (marker of brain function) ( Sokoloff et al., 1977) in 24 active cocaine abusers. Subjects were tested using a video of cocaine cues that was previously shown to induce the subjective report of craving and to increase objective measures of striatal DA in cocaine abusers (Volkow et al., 2006). The cocaine abusers were scanned during stimulation with the cocaine-cue video twice, both with instruction to try to purposefully inhibit craving (Cognitive Inhibition CI) and without instruction (no-Inhibition NI). A third scan was obtained without the stimulation of drug cues, which was used as a measure of baseline brain metabolic activity. We hypothesized that if Cognitive Inhibition of craving occurred, then it would be accompanied by decreases in metabolic activity in NAcc (in which activity is associated with prediction of reward) and in OFC (in which activity is related to motivational value of conditioned cues). We also assessed if the Inhibition in these brain regions was associated by activation of the right inferior frontal cortex (Brodmann area 44), which is a critical brain region for exerting inhibitory control (Aron et al., 2004).

  • Cognitive control of drug craving inhibits brain reward regions in cocaine abusers
    NeuroImage, 2010
    Co-Authors: Nora D. Volkow, Joanna S. Fowler, Gene-jack Wang, Frank Telang, Jean Logan, Millard Jayne, Kith Pradhan, Christopher Wong, James M. Swanson
    Abstract:

    Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to Cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-Inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic Inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with Cognitive Inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.

  • evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation
    Proceedings of the National Academy of Sciences of the United States of America, 2009
    Co-Authors: Gene-jack Wang, Nora D. Volkow, Frank Telang, Millard Jayne, Kith Pradhan, Christopher Wong, Wei Zhu, Panayotis K Thanos, Allan Geliebter, Anat Biegon
    Abstract:

    Although impaired inhibitory control is linked to a broad spectrum of health problems, including obesity, the brain mechanism(s) underlying voluntary control of hunger are not well understood. We assessed the brain circuits involved in voluntary Inhibition of hunger during food stimulation in 23 fasted men and women using PET and 2-deoxy-2[18F]fluoro-D-glucose (18FDG). In men, but not in women, food stimulation with Inhibition significantly decreased activation in amygdala, hippocampus, insula, orbitofrontal cortex, and striatum, which are regions involved in emotional regulation, conditioning, and motivation. The suppressed activation of the orbitofrontal cortex with Inhibition in men was associated with decreases in self-reports of hunger, which corroborates the involvement of this region in processing the conscious awareness of the drive to eat. This finding suggests a mechanism by which Cognitive Inhibition decreases the desire for food and implicates lower ability to suppress hunger in women as a contributing factor to gender differences in obesity.