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Eating Behaviours and Food Cravings; Influence of Age, Sex, BMI and FTO Genotype.
Abdella, HM, El Farssi, HO, Broom, DR, Hadden, DA, Dalton, CF
Nutrients. 2019;11(2)
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The development of obesity is influenced by an interaction between genetic, lifestyle, behavioural and psychological factors such as eating behaviours and food cravings. Eating behaviour includes meal size, attitudes to food, meal content and frequency of eating, all of which may have a role in obesity. Food cravings are defined as strong desires to consume specific foods and can be influenced by physical (e.g. appetite) and psychological (e.g. emotions) factors. Recent studies eating behaviours and food cravings have been associated to BMI and obesity. The aim of this study was to investigate the relationship between eating behaviours and food craving, and explore the influence of BMI, gender, age and obesity on these behaviours. The study group consisted of total of 475 participants. The participants completed an 18 question questionnaire so that eating behaviour such as cognitive restraint, uncontrolled eating and emotional eating could be analysed. The study found significant relationships between food cravings and eating behaviours. The authors concluded that gender, genotype and BMI have an influence on eating behaviour and food cravings.
Abstract
Previous studies indicate that eating behaviours and food cravings are associated with increased BMI and obesity. However, the interaction between these behaviours and other variables such as age, sex, BMI and genetics is complex. This study aimed to investigate the relationships between eating behaviours and food cravings, and to examine the influence of age, sex, body mass index (BMI) and fat mass and obesity-associated (FTO) genotype on these relationships. A total of 475 participants (252 female, 223 male, BMI: 25.82 ± 6.14 kg/m², age: 30.65 ± 14.20 years) completed the revised 18-question version of the Three Factor Eating Questionnaire (TFEQ-R18) to assess cognitive restraint, uncontrolled eating and emotional eating, and the Food Cravings Inventory (FCI) to assess cravings for fatty food, sweet food, carbohydrates and fast food. DNA samples were genotyped for the rs9939609 polymorphism in the obesity-linked gene FTO. Questionnaire data was analysed for associations between the TFEQ-R18 and FCI subscales for the whole study group, and the group divided by sex, genotype and age (≤25 years versus >25 years). Finally, mediation analysis was used to explore the relationships between BMI, cognitive restraint and food cravings. FTO AA + AT genotype was associated with increased BMI, but not with differences in eating behavior scores or food craving scores; age was associated with increased BMI and decreases in food craving scores in which this effect was stronger in women compared to men. Increased cognitive restraint was associated with decreased food craving scores in the ≤25 years group. Mediation analysis demonstrated that in this group the association between BMI and reduced food cravings was mediated by cognitive restraint indicating that in this age group individuals use cognitive restraint to control their food cravings. The positive correlation between age and BMI confirms previous results but the findings of this study show that age, sex, FTO genotype and BMI have an influence on the relationships between eating behaviours and food cravings and that these variables interact.
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An acute bout of cycling does not induce compensatory responses in pre-menopausal women not using hormonal contraceptives.
Rocha, J, Paxman, JR, Dalton, CF, Hopkins, M, Broom, DR
Appetite. 2018;:87-94
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Abstract
There is a clear need to improve understanding of the effects of physical activity and exercise on appetite control. Therefore, the acute and short-term effects (three days) of a single bout of cycling on energy intake and energy expenditure were examined in women not using hormonal contraceptives. Sixteen active (n = 8) and inactive (n = 8) healthy pre-menopausal women completed a randomised crossover design study with two conditions (exercise and control). The exercise day involved cycling for 1 h (50% of maximum oxygen uptake) and resting for 2 h, whilst the control day comprised 3 h of rest. On each experimental day participants arrived at the laboratory fasted, consumed a standardised breakfast and an ad libitum pasta lunch. Food diaries and combined heart rate-accelerometer monitors were used to assess free-living food intake and energy expenditure, respectively, over the subsequent three days. There were no main effects or condition (exercise vs control) by group (active vs inactive) interaction for absolute energy intake (P > 0.05) at the ad libitum laboratory lunch meal, but there was a condition effect for relative energy intake (P = 0.004, ηp2 = 0.46) that was lower in the exercise condition (1417 ± 926 kJ vs. 2120 ± 923 kJ). Furthermore, post-breakfast satiety was higher in the active than in the inactive group (P = 0.005, ηp2 = 0.44). There were no main effects or interactions (P > 0.05) for mean daily energy intake, but both active and inactive groups consumed less energy from protein (14 ± 3% vs. 16 ± 4%, P = 0.016, ηp2 = 0.37) and more from carbohydrate (53 ± 5% vs. 49 ± 7%, P = 0.031, ηp2 = 0.31) following the exercise condition. This study suggests that an acute bout of cycling does not induce compensatory responses in active and inactive women not using hormonal contraceptives, while the stronger satiety response to the standardised breakfast meal in active individuals adds to the growing literature that physical activity helps improve the sensitivity of short-term appetite control.
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Pharmacogenomics in psychiatry: the relevance of receptor and transporter polymorphisms.
Reynolds, GP, McGowan, OO, Dalton, CF
British journal of clinical pharmacology. 2014;(4):654-72
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Abstract
The treatment of severe mental illness, and of psychiatric disorders in general, is limited in its efficacy and tolerability. There appear to be substantial interindividual differences in response to psychiatric drug treatments that are generally far greater than the differences between individual drugs; likewise, the occurrence of adverse effects also varies profoundly between individuals. These differences are thought to reflect, at least in part, genetic variability. The action of psychiatric drugs primarily involves effects on synaptic neurotransmission; the genes for neurotransmitter receptors and transporters have provided strong candidates in pharmacogenetic research in psychiatry. This paper reviews some aspects of the pharmacogenetics of neurotransmitter receptors and transporters in the treatment of psychiatric disorders. A focus on serotonin, catecholamines and amino acid transmitter systems reflects the direction of research efforts, while relevant results from some genome-wide association studies are also presented. There are many inconsistencies, particularly between candidate gene and genome-wide association studies. However, some consistency is seen in candidate gene studies supporting established pharmacological mechanisms of antipsychotic and antidepressant response with associations of functional genetic polymorphisms in, respectively, the dopamine D2 receptor and serotonin transporter and receptors. More recently identified effects of genes related to amino acid neurotransmission on the outcome of treatment of schizophrenia, bipolar illness or depression reflect the growing understanding of the roles of glutamate and γ-aminobutyric acid dysfunction in severe mental illness. A complete understanding of psychiatric pharmacogenomics will also need to take into account epigenetic factors, such as DNA methylation, that influence individual responses to drugs.