Increased anticipatory but decreased consummatory brain responses to food in sisters of anorexia nervosa patients

BackgroundWe have previously shown increased anticipatory and consummatory neural responses to rewarding and aversive food stimuli in women recovered from anorexia nervosa (AN).AimsTo determine whether these differences are trait markers for AN, we examined the neural response in those with a familial history but no personal history of AN.MethodThirty-six volunteers were recruited: 15 who had a sister with anorexia nervosa (family history) and 21 control participants. Using fMRI we examined the neural response during an anticipatory phase (food cues, rewarding and aversive), an effort phase and a consummatory phase (rewarding and aversive tastes).ResultsFamily history (FH) volunteers showed increased activity in the caudate during the anticipation of both reward and aversive food and in the thalamus and amygdala during anticipation of aversive only. FH had decreased activity in the dorsal anterior cingulate cortex, the pallidum and the superior frontal gyrus during taste consumption.ConclusionsIncreased neural anticipatory but decreased consummatory responses to food might be a biomarker for AN. Interventions that could normalise these differences may help to prevent disorder onset.

Download Full-text

Enhanced neural response to anticipation, effort and consummation of reward and aversion during bupropion treatment

Psychological Medicine ◽

10.1017/s003329171600088x ◽

2016 ◽

Vol 46 (11) ◽

pp. 2263-2274 ◽

Cited By ~ 19

Author(s):

Z. Dean ◽

S. Horndasch ◽

P. Giannopoulos ◽

C. McCabe

Keyword(s):

Healthy Volunteers ◽

Reuptake Inhibitor ◽

Primary Motor Cortex ◽

Neural Response ◽

Anterior Cingulate ◽

Therapeutic Effects ◽

Neural Responses ◽

Dorsal Anterior Cingulate Cortex ◽

Ventral Medial Prefrontal Cortex ◽

Increased Activity

BackgroundWe have previously shown that the selective serotonergic reuptake inhibitor, citalopram, reduces the neural response to reward and aversion in healthy volunteers. We suggest that this inhibitory effect might underlie the emotional blunting reported by patients on these medications. Bupropion is a dopaminergic and noradrenergic reuptake inhibitor and has been suggested to have more therapeutic effects on reward-related deficits. However, how bupropion affects the neural responses to reward and aversion is unclear.MethodSeventeen healthy volunteers (9 female, 8 male) received 7 days bupropion (150 mg/day) and 7 days placebo treatment, in a double-blind crossover design. Our functional magnetic resonance imaging task consisted of three phases; an anticipatory phase (pleasant or unpleasant cue), an effort phase (button presses to achieve a pleasant taste or to avoid an unpleasant taste) and a consummatory phase (pleasant or unpleasant tastes). Volunteers also rated wanting, pleasantness and intensity of the tastes.ResultsRelative to placebo, bupropion increased activity during the anticipation phase in the ventral medial prefrontal cortex (vmPFC) and caudate. During the effort phase, bupropion increased activity in the vmPFC, striatum, dorsal anterior cingulate cortex and primary motor cortex. Bupropion also increased medial orbitofrontal cortex, amygdala and ventral striatum activity during the consummatory phase.ConclusionsOur results are the first to show that bupropion can increase neural responses during the anticipation, effort and consummation of rewarding and aversive stimuli. This supports the notion that bupropion might be beneficial for depressed patients with reward-related deficits and blunted affect.

Download Full-text

Mood and neural responses to social rejection do not seem to be altered in resilient adolescents with a history of adversity

Development and Psychopathology ◽

10.1017/s0954579419000178 ◽

2019 ◽

Vol 32 (2) ◽

pp. 411-423

Author(s):

Jessica Fritz ◽

Jason Stretton ◽

Adrian Dahl Askelund ◽

Susanne Schweizer ◽

Nicholas D. Walsh ◽

...

Keyword(s):

Mental Health ◽

Mental Health Problems ◽

Childhood Adversity ◽

Health Problems ◽

Social Rejection ◽

Anterior Cingulate ◽

Neural Responses ◽

Social Feedback ◽

Dorsal Anterior Cingulate Cortex ◽

History Of

AbstractChildhood adversity (CA) increases the risk of subsequent mental health problems. Adolescent social support (from family and/or friends) reduces the risk of mental health problems after CA. However, the mechanisms of this effect remain unclear, and we speculate that they are manifested on neurodevelopmental levels. Therefore, we investigated whether family and/or friendship support at ages 14 and 17 function as intermediate variables for the relationship between CA before age 11 and affective or neural responses to social rejection feedback at age 18. We studied 55 adolescents with normative mental health at age 18 (26 with CA and therefore considered “resilient”), from a longitudinal cohort. Participants underwent a Social Feedback Task in the magnetic resonance imaging scanner. Social rejection feedback activated the dorsal anterior cingulate cortex and the left anterior insula. CA did not predict affective or neural responses to social rejection at age 18. Yet, CA predicted better friendships at age 14 and age 18, when adolescents with and without CA had comparable mood levels. Thus, adolescents with CA and normative mood levels have more adolescent friendship support and seem to have normal mood and neural responses to social rejection.

Download Full-text

Mood and neural responses to social rejection are not altered in resilient adolescents with a history of adversity

10.31219/osf.io/avx6p ◽

2018 ◽

Author(s):

Jessica Fritz ◽

Jason Stretton ◽

Adrian Dahl Askelund ◽

Susanne Schweizer ◽

Nicholas Walsh ◽

...

Keyword(s):

Mental Health ◽

Mental Health Problems ◽

Health Problems ◽

Social Rejection ◽

Anterior Cingulate ◽

Neural Responses ◽

Social Feedback ◽

Dorsal Anterior Cingulate Cortex ◽

History Of ◽

Intermediate Variables

THIS IS A PRE-PRINT OF AN ARTICLE PUBLISHED IN “DEVELOPMENT AND PSYCHOPATHOLOGY (1–13)”. THE FINAL AUTHENTICATED VERSION IS AVAILABLE ONLINE AT: https://doi.org/10.1017/S0954579419000178Childhood adversity (CA) increases the risk of subsequent mental health problems. Adolescent social support (from family and/or friends) reduces the risk of mental health problems after CA. However, the mechanisms of this effect remain unclear and we speculate that they are manifested on neurodevelopmental levels. Therefore, we investigated whether family and/or friendship support at age 14 and 17 function as intermediate variables for the relationship between CA before age 11 and affective or neural responses to social rejection feedback at age 18. We studied 55 adolescents (26 with CA) with normative mental health at age 18 (‘resilient’), from a longitudinal cohort. Participants underwent a Social Feedback Task in the MRI scanner. Social rejection feedback activated the dorsal Anterior Cingulate Cortex (dACC) and the left anterior Insula (AI). CA did not predict affective or neural responses to social rejection at age 18. Yet, CA predicted better friendships at age 14 and age 18, when adolescents with and without CA had comparable mood levels. Thus, adolescents with CA and normative mood levels have more adolescent friendship support and seem to have normal mood and neural responses to social rejection.

Download Full-text

Ketogenic diet reduces alcohol withdrawal symptoms in humans and alcohol intake in rodents

Science Advances ◽

10.1126/sciadv.abf6780 ◽

2021 ◽

Vol 7 (15) ◽

pp. eabf6780

Author(s):

Corinde E. Wiers ◽

Leandro F. Vendruscolo ◽

Jan-Willem van der Veen ◽

Peter Manza ◽

Ehsan Shokri-Kojori ◽

...

Keyword(s):

Ketogenic Diet ◽

Alcohol Withdrawal ◽

Alcohol Use Disorder ◽

Alcohol Intake ◽

Anterior Cingulate ◽

Dorsal Anterior Cingulate Cortex ◽

Beneficial Effects ◽

Alcohol Cues ◽

History Of ◽

To Receive

Individuals with alcohol use disorder (AUD) show elevated brain metabolism of acetate at the expense of glucose. We hypothesized that a shift in energy substrates during withdrawal may contribute to withdrawal severity and neurotoxicity in AUD and that a ketogenic diet (KD) may mitigate these effects. We found that inpatients with AUD randomized to receive KD (n = 19) required fewer benzodiazepines during the first week of detoxification, in comparison to those receiving a standard American (SA) diet (n = 14). Over a 3-week treatment, KD compared to SA showed lower “wanting” and increased dorsal anterior cingulate cortex (dACC) reactivity to alcohol cues and altered dACC bioenergetics (i.e., elevated ketones and glutamate and lower neuroinflammatory markers). In a rat model of alcohol dependence, a history of KD reduced alcohol consumption. We provide clinical and preclinical evidence for beneficial effects of KD on managing alcohol withdrawal and on reducing alcohol drinking.

Download Full-text

Acetaminophen Reduces Social Pain

Psychological Science ◽

10.1177/0956797610374741 ◽

2010 ◽

Vol 21 (7) ◽

pp. 931-937 ◽

Cited By ~ 250

Author(s):

C. Nathan DeWall ◽

Geoff MacDonald ◽

Gregory D. Webster ◽

Carrie L. Masten ◽

Roy F. Baumeister ◽

...

Keyword(s):

Brain Activity ◽

Brain Regions ◽

Daily Basis ◽

Social Rejection ◽

Neural Mechanisms ◽

Anterior Cingulate ◽

Neural Responses ◽

Physical Pain ◽

Social Pain ◽

Dorsal Anterior Cingulate Cortex

Pain, whether caused by physical injury or social rejection, is an inevitable part of life. These two types of pain—physical and social—may rely on some of the same behavioral and neural mechanisms that register pain-related affect. To the extent that these pain processes overlap, acetaminophen, a physical pain suppressant that acts through central (rather than peripheral) neural mechanisms, may also reduce behavioral and neural responses to social rejection. In two experiments, participants took acetaminophen or placebo daily for 3 weeks. Doses of acetaminophen reduced reports of social pain on a daily basis (Experiment 1). We used functional magnetic resonance imaging to measure participants’ brain activity (Experiment 2), and found that acetaminophen reduced neural responses to social rejection in brain regions previously associated with distress caused by social pain and the affective component of physical pain (dorsal anterior cingulate cortex, anterior insula). Thus, acetaminophen reduces behavioral and neural responses associated with the pain of social rejection, demonstrating substantial overlap between social and physical pain.

Download Full-text

Postpartum Psychosis

Postpartum Mental Health Disorders: A Casebook ◽

10.1093/med/9780190849955.003.0006 ◽

2020 ◽

pp. 39-50

Author(s):

Nikole Benders-Hadi

Keyword(s):

Bipolar Disorder ◽

Family History ◽

Elevated Risk ◽

Psychotic Symptoms ◽

Postpartum Psychosis ◽

Poor Sleep ◽

Activity Levels ◽

History Of ◽

Infant Hospitalization ◽

Increased Activity

This chapter on postpartum psychosis notes that the risk of postpartum psychosis in the general population is very rare at less than 1%. In a mother with a known history of schizophrenia, this risk increases to 25%. Psychotic symptoms appearing postpartum may also be evidence of a bipolar disorder. The presence of elevated mood, increased activity levels and energy, poor sleep, and a family history of manic episodes all increase the likelihood that a bipolar disorder is present. Women with a personal or family history of a bipolar disorder are at an elevated risk of developing a mania or depression with psychotic symptoms postpartum. Postpartum psychosis due to any cause is a psychiatric emergency and treatment should be initiated early and aggressively to ensure the safety of mother and infant. Hospitalization and/or separation of the baby and mother may be necessary. The use of medication to treat schizophrenia or bipolar disorder during pregnancy may decrease the risk of a postpartum psychosis. With appropriate postpartum medication and support, the majority of women experiencing postpartum psychosis recover well and the risk of recurrent psychotic symptoms can be greatly reduced.

Download Full-text

Intelligence moderates reinforcement learning: a mini-review of the neural evidence

Journal of Neurophysiology ◽

10.1152/jn.00600.2014 ◽

2015 ◽

Vol 113 (10) ◽

pp. 3459-3461 ◽

Cited By ~ 5

Author(s):

Chong Chen

Keyword(s):

Reinforcement Learning ◽

Prediction Error ◽

Dorsolateral Prefrontal Cortex ◽

Anterior Cingulate ◽

Neural Responses ◽

Key Factors ◽

Neural Basis ◽

Dorsal Anterior Cingulate Cortex ◽

Neural Signal ◽

Dorsolateral Prefrontal

Our understanding of the neural basis of reinforcement learning and intelligence, two key factors contributing to human strivings, has progressed significantly recently. However, the overlap of these two lines of research, namely, how intelligence affects neural responses during reinforcement learning, remains uninvestigated. A mini-review of three existing studies suggests that higher IQ (especially fluid IQ) may enhance the neural signal of positive prediction error in dorsolateral prefrontal cortex, dorsal anterior cingulate cortex, and striatum, several brain substrates of reinforcement learning or intelligence.

Download Full-text

Lithium in a Case of Severe Anorexia Nervosa

The British Journal of Psychiatry ◽

10.1192/bjp.140.5.526 ◽

1982 ◽

Vol 140 (5) ◽

pp. 526-528 ◽

Cited By ~ 21

Author(s):

G. S. Stein ◽

S. Hartshorn ◽

J. Jones ◽

D. Steinberg

Keyword(s):

Anorexia Nervosa ◽

Depressive Symptoms ◽

Family History ◽

Affective Disorder ◽

Complex Relationship ◽

Psychological Treatments ◽

Treatment Of Depression ◽

History Of

Anorexia nervosa may sometimes be resistant to all forms of therapy, with cases running through a gamut of somatic and psychological treatments. One possible explanation for this may be that the illness is of heterogeneous aetiology (Kay and Leigh, 1938; King, 1963; Feighner et al, 1972), although others regard anorexia as a single condition that tends to breed true though having protean manifestations (Russell, 1970; Crisp et al, 1980). In most of the larger series of cases, a proportion have depressive symptoms both during the illness (Dally, 1969; Theander, 1970; Crisp et al, 1980) and some years later (Morgan and Russell, 1975; Hsu et al, 1979), and a family history of affective disorder is also commonly reported (Dally, 1969; Theander, 1970; Morgan and Russell, 1975). Cantwell et al (1977) have reviewed the complex relationship between depression and anorexia nervosa and have suggested that some of the remedies used in the treatment of depression merit further exploration in the management of anorexia nervosa. We report here a patient who was in hospital for over four years and in whose eventual improvement lithium may have played an important role.

Download Full-text

Insulin sensitivity affects corticolimbic brain responses to visual food cues in polycystic ovary syndrome patients

Hormone Molecular Biology and Clinical Investigation ◽

10.1515/hmbci-2015-0048 ◽

2015 ◽

Vol 24 (2) ◽

Cited By ~ 2

Author(s):

Hanin M. Alsaadi ◽

Dean A. Van Vugt

Keyword(s):

Polycystic Ovary ◽

Brain Regions ◽

Anterior Cingulate ◽

Food Cues ◽

Ovary Syndrome ◽

Insulin Resistant ◽

Brain Responses ◽

Glucose Challenge ◽

Visual Food Cues ◽

Food Pictures

AbstractThis study examined the effect of insulin sensitivity on the responsiveness of appetite regulatory brain regions to visual food cues.Nineteen participants diagnosed with polycystic ovary syndrome (PCOS) were divided into insulin-sensitive (n=8) and insulin-resistant (n=11) groups based on the homeostatic model assessment of insulin resistance (HOMA2-IR). Subjects underwent functional magnetic resonance imaging (fMRI) while viewing food pictures following water or dextrose consumption. The corticolimbic blood oxygen level dependent (BOLD) responses to high-calorie (HC) or low-calorie (LC) food pictures were compared within and between groups.BOLD responses to food pictures were reduced during a glucose challenge in numerous corticolimbic brain regions in insulin-sensitive but not insulin-resistant subjects. Furthermore, the degree of insulin resistance positively correlated with the corticolimbic BOLD response in the medial prefrontal cortex (mPFC), orbitofrontal cortex (OFC), anterior cingulate and ventral tegmental area (VTA) in response to HC pictures, and in the dorsolateral prefrontal cortex (DLPFC), mPFC, anterior cingulate, and insula in response to LC pictures following a glucose challenge. BOLD signal in the OFC, midbrain, hippocampus, and amygdala following a glucose challenge correlated with HOMA2-IR in response to HC-LC pictures.We conclude that the normal inhibition of corticolimbic brain responses to food pictures during a glucose challenge is compromised in insulin-resistant subjects. The increase in brain responsiveness to food pictures during postprandial hyperinsulinemia may lead to greater non-homeostatic eating and perpetuate obesity in insulin-resistant subjects.

Download Full-text