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Biomedical subjects

Iain C Campbell

Publications and source records attributed to Iain C Campbell.

15 recordsLinked to original sources
PubMed2006

Differential motivational responses to food and pleasurable cues in anorexia and bulimia nervosa: a startle reflex paradigm.

BACKGROUND: Abnormal perceptions of food and shape underpin the cognitive behavioural model of eating disorders (EDs). The aim of this study was to investigate motivational processing of disorder-specific and standard emotional cues in anorexia (AN) and bulimia nervosa (BN) using startle eyeblink modulation (SEM). SEM was used because it is sensitive to motivational states of approach (appetitive response) and withdrawal (aversive response), which are independent of conscious intentional control. METHOD: Acoustically elicited SEM and subjective anxiety ratings were measured in 30 female patients with an ED (n=15 AN, n=15 BN) and 30 female control subjects while they viewed ED-relevant stimuli (food, female bodies) and standardized emotional pictures. RESULTS: BN subjects showed an appetitive response (startle inhibition) to food relative to neutral cues that differed significantly from AN subjects. By contrast, self-reports indicated significantly increased anxiety related to food cues across both ED groups. To female body picture (relative to neutral) cues, no significant between-group differences were found for SEM. ED subjects unexpectedly showed an aversive response (startle potentiation) to positive cues, in contrast to controls, who showed the established startle attenuation. CONCLUSIONS: These preliminary results suggest that BN patients demonstrated an exaggerated appetitive response to food but not to standardized positive cues, whereas SEM in AN patients points to a generalized failure to activate the appetitive motivational system. Differences in motivational salience to food cues are in line with distinctions between AN and BN in eating behaviour and food consumption and support differential treatment requirements.

Adult↗
PubMed2006

Difference in susceptibility to activity-based anorexia in two inbred strains of mice.

Food restricted rodents develop activity-based anorexia in the presence of a running wheel, characterised by increased physical activity, weight loss and decreased leptin levels. Here, we determined trait differences in the development of activity-based anorexia between C57BL/6J and DBA/2J inbred mouse lines previously reported as having low and high anxiety, respectively. C57BL/6J mice housed with running wheels and exposed to scheduled feeding reduced their wheel activity, in contrast to DBA/2J mice which exhibited increased behavioural activity under these conditions. Food restriction induced hypoleptinemia in both strains, but the decline in plasma leptin was stronger in DBA/2J mice and correlated with increased activity only in that strain. These data suggest that plasma leptin level dynamics rather than hypoleptinemia alone influences the development of activity-based anorexia and that recombinant inbred panels based on these progenitor lines offer opportunities for the identification of molecular determinants for anorexia nervosa related behavioural traits.

Animals↗
PubMed2006

Behavioral, physiological, and molecular differences in response to dietary restriction in three inbred mouse strains.

Food restriction paradigms are widely used in animal studies to investigate systems involved in energy regulation. We have observed behavioral, physiological, and molecular differences in response to food restriction in three inbred mouse strains, C57BL/6J, A/J, and DBA/2J. These are the progenitors of chromosome substitution and recombinant inbred mouse strains used for mapping complex traits. DBA/2J and A/J mice increased their locomotor activity during food restriction, and both displayed a decrease in body temperature, but the decrease was significantly larger in DBA/2J compared with A/J mice. C57BL/6J mice did not increase their locomotor activity and displayed a large decrease in their body temperature. The large decline in body temperature during food restriction in DBA/2J and C57BL/6J strains was associated with a robust reduction in plasma leptin levels. DBA/2J mice showed a marked decrease in white and brown adipose tissue masses and an upregulation of the antithermogenic hypothalamic neuropeptide Y Y(1) receptor. In contrast, A/J mice showed a reduction in body temperature to a lesser extent that may be explained by downregulation of the thermogenic melanocortin 3 receptor and by behavioral thermoregulation as a consequence of their increased locomotor activity. These data indicate that genetic background is an important parameter in controlling an animal's adaptation strategy in response to food restriction. Therefore, mouse genetic mapping populations based on these progenitor lines are highly valuable for investigating mechanisms underlying strain-dependent differences in behavioral physiology that are seen during reduced food availability.

Adipose Tissue↗
PubMed2006

Hippocampal volume and cognitive function in anorexia nervosa.

We hypothesised that hippocampal volume would be reduced in underweight anorexia nervosa (AN) and associated with impaired hippocampus-dependent cognitive function. Hippocampal and whole brain volumes were measured in 16 women with AN and 16 matched healthy women using magnetic resonance imaging (MRI) and a manual tracing method. Participants also completed the Doors and People Test of hippocampus-dependent memory and an IQ test. After adjustment for total cerebral volume, there was significant bilateral reduction in hippocampal volume in the AN group (8.2% right; 7.5% left). There was no evidence of impaired hippocampus-dependent cognitive function and no evidence of a relationship between hippocampal volume and clinical features of AN. The reduced hippocampal volume in anorexia nervosa is not associated with changes in cognitive function. To understand the cause and consequence of hippocampal size and function, it will be important to integrate endocrine, neuropsychological and neuroimaging studies.

Adolescent↗
PubMed2006

An investigation of hypothalamic-pituitary-adrenal axis hyperactivity in anorexia nervosa: the role of CRH and AVP.

We hypothesised that hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in anorexia nervosa (AN) is associated with (a) elevated arginine vasopressin (AVP) activity and (b) enhanced pituitary sensitivity to AVP, as it is in depressive illness. 16 Healthy women and 18 women with active AN participated in a combined dexamethasone (DXM)/corticotrophin releasing hormone (CRH) challenge test and an AVP challenge test. This combination of tests is designed to assess the functional contribution of AVP to HPA axis activity. 10 of the active AN group repeated participation after weight gain. The cortisol response to AVP was reduced by 138% in the active AN group, suggesting an impairment of pituitary sensitivity to AVP, which began to normalise with weight gain. The cortisol and adreno-corticotrophin (ACTH) responses to the DXM/CRH test were not significantly enhanced in the active AN group, suggesting that there was no elevated endogenous AVP activity augmenting the response to CRH in AN. Weight gain was associated with blunting of the endocrine response to the DXM/CRH test, which may have been related to rising oestrogen levels. Thus, contrary to the hypotheses, we did not find (a) evidence of upregulated AVP activity or (b) enhanced pituitary sensitivity to AVP in AN. These findings suggest that the mechanism of HPA axis hyperactivity differs in depression and AN, with greater involvement of AVP in depressive disorder and perhaps more reliance on CRH to drive the axis in AN. The powerful anorexigenic effect of CRH could contribute to the severity of weight loss associated with AN.

Adolescent↗
PubMed2006

Cerebral processing of food-related stimuli: effects of fasting and gender.

To maintain nutritional homeostasis, external food-related stimuli have to be evaluated in relation to the internal states of hunger or satiety. To examine the neural circuitry responsible for integration of internal and external determinants of human eating behaviour, brain responses to visual and complex gustatory food-related stimuli were measured using functional magnetic resonance imaging in 18 healthy non-smokers (10 women, 8 men). Each individual was studied on two occasions, the order of which was counterbalanced; after eating as usual and after 24 h fasting. Raised plasma free fatty acids and lower insulin and leptin concentrations confirmed that participants fasted as requested. When fasted, participants reported more hunger, nervousness and worse mood and rated the visual (but not gustatory) food-related stimuli as more pleasant. The effect of fasting on hunger was stronger in women than in men. No circuitry was identified as differentially responsive in fasting compared to satiety to both visual and gustatory food-related stimuli. The left insula response to the gustatory stimuli was stronger during fasting. The inferior occipito-temporal response to visual food-related stimuli also tended to be stronger during fasting. The responses in the occipito-temporal cortex to visual and in the insula to gustatory stimuli were stronger in women than in men. There was no interaction between gender and fasting. In conclusion, food reactivity in modality-specific sensory cortical areas is modulated by internal motivational states. The stronger reactivity to external food-related stimuli in women may be explored as a marker of gender-related susceptibility to eating disorders.

Adult↗
PubMed2005

Effect of left prefrontal repetitive transcranial magnetic stimulation on food craving.

BACKGROUND: Dysfunction of the prefrontal cortex is implicated in craving for drugs and food. This study explores the effect of prefrontal cortex stimulation on food craving. METHODS: In a randomized double-blind parallel group study, 28 women, who reported frequent cravings for food were exposed to foods that typically elicit strong cravings before and after a single session of real or sham 10-Hz repetitive transcranial magnetic stimulation to the left dorsolateral prefrontal cortex at an intensity of 110% individual motor threshold. RESULTS: Self-reported food craving during exposure to the experimental foods remained stable before and after real stimulation compared with sham stimulation in which cravings increased over the experimental session. Consumption of snack foods within a 5-min period after stimulation did not differ between groups. CONCLUSIONS: Prefrontal stimulation inhibits the development of craving. A longer period of observation is necessary to establish whether there is an effect on food consumption.

Adolescent↗
PubMed2005

Functional neuroanatomy of body shape perception in healthy and eating-disordered women.

BACKGROUND: Abnormalities in perception and evaluation of body shape are a hallmark of eating disorders. METHODS: Brain responses to line drawings of underweight, normal weight, and overweight female bodies were measured with functional magnetic resonance imaging in 9 women with bulimia nervosa, 13 with anorexia nervosa, and 18 healthy women. Participants rated the stimuli for fear and disgust. RESULTS: In the three groups, the lateral fusiform gyrus, inferior parietal cortex, and lateral prefrontal cortex were activated in response to body shapes compared with the control condition (drawings of houses). The responses in the lateral fusiform gyrus and in the parietal cortex were less strong in patients with eating disorders compared with healthy control subjects. Patients with eating disorders rated the body shapes in all weight categories as more aversive than did healthy women. In the group with eating disorders, the aversion ratings correlated positively with activity in the right medial apical prefrontal cortex. CONCLUSIONS: Processing of female body shapes engages a distributed neural network, parts of which are underactive in women with eating disorders. The considerable variability in subjective emotional reaction to body shapes in patients with eating disorders is associated with differential activity in the prefrontal cortex.

Adult↗
PubMed2005

Neuropsychological studies in anorexia nervosa.

Neuropsychological findings in eating disorders are somewhat inconsistent. This may be because individual studies have used a broad range of tests on relatively small, heterogeneous clinical groups, thus limiting the detection of subtle neuropsychological differences in these patients. Therefore, rather than using broad assessments of a variety of neuropsychological functions, adoption of a more focused, hypothesis-driven approach based on clinical practice is proposed. This will allow more in-depth investigations of targeted functions and will improve the chances of detecting a problem, of exploring its ecologic validity, and of tailoring a treatment. We have demonstrated this approach using our neuropsychological studies of cognitive flexibility in anorexia nervosa (AN).

Anorexia Nervosa↗
PubMed2004

Medial prefrontal cortex activity associated with symptom provocation in eating disorders.

OBJECTIVE: The authors sought to identify neural correlates of eating disorders in order to contribute to the debate on the genesis and classification of eating disorders and provide endophenotypes for genetic research. METHOD: Twenty-six female patients with eating disorders (10 with bulimia nervosa, 16 with anorexia nervosa) and 19 healthy female comparison subjects matched for age and education were presented with food and aversive emotional images while brain activity was recorded with functional magnetic resonance imaging. RESULTS: Women with eating disorders identified the food stimuli as threatening and disgusting. In response to these stimuli, the women with eating disorders had greater activation in the left medial orbitofrontal and anterior cingulate cortices and less activation in the lateral prefrontal cortex, inferior parietal lobule, and cerebellum, relative to the comparison group. In addition, women with bulimia nervosa had less activation in the lateral and apical prefrontal cortex, relative to the comparison group. Between-group differences in response to nonspecific emotional stimuli were found in the occipital cortex, parietal cortex, and cerebellum. CONCLUSIONS: A medial prefrontal response to symptom-provoking stimuli was identified as a common feature of anorexia and bulimia nervosa. This finding supports a conceptualization of eating disorders as being transdiagnostic at the neural level. The abnormal prefrontal reaction is associated with symptom-related material, whereas the occipital and cerebellar differences are nonspecific. An abnormal propensity to activate medial prefrontal circuits in response to inappropriate stimuli is common to eating, obsessive-compulsive, and addictive disorders and may account for the compulsive features of behavior in these conditions.

Adult↗
PubMed2003

Recovery and chronicity in anorexia nervosa: brain activity associated with differential outcomes.

BACKGROUND: The course of anorexia nervosa varies from rapid recovery to a chronic debilitating illness. This study aimed to identify functional neural correlates associated with differential outcomes. METHODS: Brain reactions to food and emotional visual stimuli were measured with functional magnetic resonance imaging in nine women who had long-term recovery from restricting anorexia nervosa. These were compared with age- and education-matched groups of eight women chronically ill with restricting anorexia nervosa and nine healthy control women. RESULTS: In response to food stimuli, increased medial prefrontal and anterior cingulate activation, as well as a lack of activity in the inferior parietal lobule, differentiated the recovered group from the healthy control subjects. Increased activation of the right lateral prefrontal, apical prefrontal, and dorsal anterior cingulate cortices differentiated these recovered subjects from chronically ill patients. Group differences were specific to food stimuli, whereas processing of emotional stimuli did not differ between groups. CONCLUSIONS: Separate neural correlates underlie trait and state characteristics of anorexia nervosa. The medial prefrontal response to disease-specific stimuli may be related to trait vulnerability. Lateral and apical prefrontal involvement is associated with a good outcome.

Adult↗
PubMed2003

A neurodevelopmental model for anorexia nervosa.

This paper integrates genetic and biological data on aetiological risk for anorexia nervosa (AN) with cognitive and psychosocial explanatory models. We have reviewed clinical and basic science data from each of these domains and then used a developmental perspective to formulate a multifactorial threshold model. By positioning interpersonal stress as a central component of this model, psychological, social and biological conceptualisations of AN can be used to generate a data driven, neurodevelopmental hypothesis for the aetiology of this complex disorder.

Adaptation, Psychological↗
PubMed2003

Evidence for metabolic and endocrine abnormalities in subjects recovered from anorexia nervosa.

Subjects with anorexia nervosa (AN) at low weight display metabolic, endocrine, and behavioral abnormalities. Whether these various differences are a consequence of the condition and persist after recovery is unclear. We tested the hypothesis that abnormalities in the insulin and leptin axes and in the desire to eat persisted in subjects who had recovered from AN in terms of body mass index (BMI) and menstrual function. Endocrine, metabolic, and psychological parameters were assessed by sampling under fasting conditions and serially in response to a standard meal. Subjects included 18 females recovered from AN and 18 female controls and measures included plasma insulin, leptin, glucose and beta-hydroxybutyrate (beta-HBA) concentrations together with desire to eat. Fasting glucose concentrations were normal in both groups, but fasting insulin concentrations were significantly lower and the fasting glucose/insulin ratio significantly higher in the recovered subjects. The glucose concentration was significantly higher at the end of the meal period in the recovered group. The peak increase of insulin during the meal was significantly less in the recovered group and in response to the meal, glucose/insulin ratios were significantly higher for the first 45 minutes indicating a delayed insulin response. Fasting beta-HBA concentrations were not significantly different between groups, but postmeal decreases were significant and larger in the recovered AN group. Fasting and meal-related leptin concentrations were not significantly different between the groups and in both groups were correlated with BMI. In controls, but not in recovered subjects, the reported desire to eat was correlated with plasma glucose and leptin concentrations. The insulin, glucose and beta-HBA data indicated the presence of insulin hypersensitivity in the recovered subjects. As the insulin response to the meal was blunted and apparently delayed, there may be a persistent alteration in pancreatic function as a long-term pathological consequence of the anorexia. Alternatively, these data indicate a possible trait marker for AN.

3-Hydroxybutyric Acid↗
PubMed2003

Estrogen administration does not reduce the rate of recurrence of affective psychosis after childbirth.

BACKGROUND: High rates of postpartum relapse occur in women with histories of bipolar or schizoaffective disorder. These relapses may be triggered by the postdelivery fall in circulating estrogen through alteration of central neurotransmitter (especially dopaminergic) systems. This study tested the hypothesis that estrogen administration after childbirth would prevent postpartum relapse and would alter dopamine receptor sensitivity. METHOD: Twenty-nine pregnant women with a Research Diagnostic Criteria diagnosis of hypomania (bipolar II), mania (bipolar I), or schizoaffective disorder participated in an open clinical trial. Three transdermal dose regimens of estrogen (17beta-estradiol) were tested. Starting doses were 200 (N = 13), 400 (N = 3), and 800 (N = 13) micro g/day, beginning within 48 hours after delivery and reduced by one half every 4 days for a total of 12 days. On the fourth day after starting estradiol therapy (before relapse occurred), subjects participated in a neuroendocrine challenge test that measured the sensitivity of the central nervous system (tubero-infundibular) dopaminergic system (plasma prolactin and growth hormone responses to apomorphine). RESULTS: Estradiol at all dose regimens did not reduce the rate of relapse. However, of the 12 women who relapsed, those who had taken the highest dose of estradiol (800 micro g/day) needed less subsequent psychotropic medication (fewer chlorpromazine equivalents) and were discharged sooner than those who had taken either of the 2 lower doses. No differences in neuroendocrine responses to apomorphine were detected between women receiving the high-dose and the lower-dose regimens. CONCLUSION: The results do not support the hypothesis that a fall in circulating concentrations of estrogens precipitates relapse in subjects at risk of postpartum affective psychosis. The use of prophylactic estrogen in such circumstances is therefore highly questionable.

Administration, Cutaneous↗