635 resultados para Appetite.


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Berridge's model (e.g. [Berridge KC. Food reward: Brain substrates of wanting and liking. Neurosci Biobehav Rev 1996;20:1–25.; Berridge KC, Robinson T E. Parsing reward. Trends Neurosci 2003;26:507–513.; Berridge KC. Motivation concepts in behavioral neuroscience. Physiol Behav 2004;81:179–209]) outlines the brain substrates thought to mediate food reward with distinct ‘liking’ (hedonic/affective) and ‘wanting’ (incentive salience/motivation) components. Understanding the dual aspects of food reward could throw light on food choice, appetite control and overconsumption. The present study reports the development of a procedure to measure these processes in humans. A computer-based paradigm was used to assess ‘liking’ (through pleasantness ratings) and ‘wanting’ (through forced-choice photographic procedure) for foods that varied in fat (high or low) and taste (savoury or sweet). 60 participants completed the program when hungry and after an ad libitum meal. Findings indicate a state (hungry–satiated)-dependent, partial dissociation between ‘liking’ and ‘wanting’ for generic food categories. In the hungry state, participants ‘wanted’ high-fat savoury > low-fat savoury with no corresponding difference in ‘liking’, and ‘liked’ high-fat sweet > low-fat sweet but did not differ in ‘wanting’ for these foods. In the satiated state, participants ‘liked’, but did not ‘want’, high-fat savoury > low-fat savoury, and ‘wanted’ but did not ‘like’ low-fat sweet > high-fat sweet. More differences in ‘liking’ and ‘wanting’ were observed when hungry than when satiated. This procedure provides the first step in proof of concept that ‘liking’ and ‘wanting’ can be dissociated in humans and can be further developed for foods varying along different dimensions. Other experimental procedures may also be devised to separate ‘liking’ and ‘wanting’.

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Background We have used serial visual analogue scores to demonstrate disturbances of the appetite profile in dialysis patients. This is potentially important as dialysis patients are prone to malnutrition yet have a lower nutrient intake than controls. Appetite disturbance may be influenced by accumulation of appetite inhibitors such as leptin and cholecystokinin (CCK) in dialysis patients. Methods Fasting blood samples were drawn from 43 controls, 50 haemodialysis (HD) and 39 peritoneal dialysis (PD) patients to measure leptin and CCK. Hunger and fullness scores were derived from profiles compiled using hourly visual analogue scores. Nutrient intake was derived from 3 day dietary records. Results Fasting CCK was elevated for PD (6.73 ± 4.42 ng/l vs control 4.99 ± 2.23 ng/l, P < 0.05; vs HD 4.43 ± 2.15 ng/l, P < 0.01). Fasting CCK correlated with the variability of the hunger (r = 0.426, P = 0.01) and fullness (r = 0.52, P = 0.002) scores for PD. There was a notable relationship with the increase in fullness after lunch for PD (r = 0.455, P = 0.006). When well nourished PD patients were compared with their malnourished counterparts, CCK was higher in the malnourished group (P = 0.004). Leptin levels were higher for the dialysis patients than controls (HD and PD, P < 0.001) with pronounced hyperleptinaemia evident in some PD patients. Control leptin levels demonstrated correlation with fullness scores (e.g. peak fullness, r = 0.45, P = 0.007) but the dialysis patients did not. PD nutrient intake (energy and protein intake, r = -0.56, P < 0.0001) demonstrated significant negative correlation with leptin. Conclusion Increased CCK levels appear to influence fullness and hunger perception in PD patients and thus may contribute to malnutrition. Leptin does not appear to affect perceived appetite in dialysis patients but it may influence nutrient intake in PD patients via central feeding centres.

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Objective: To assess the effect of graded increases in exercised-induced energy expenditure (EE) on appetite, energy intake (EI), total daily EE and body weight in men living in their normal environment and consuming their usual diets. Design: Within-subject, repeated measures design. Six men (mean (s.d.) age 31.0 (5.0) y; weight 75.1 (15.96) kg; height 1.79 (0.10) m; body mass index (BMI) 23.3(2.4) kg/m2), were each studied three times during a 9 day protocol, corresponding to prescriptions of no exercise, (control) (Nex; 0 MJ/day), medium exercise level (Mex; ~1.6 MJ/day) and high exercise level (Hex; ~3.2 MJ/day). On days 1-2 subjects were given a medium fat (MF) maintenance diet (1.6 ´ resting metabolic rate (RMR)). Measurements: On days 3-9 subjects self-recorded dietary intake using a food diary and self-weighed intake. EE was assessed by continual heart rate monitoring, using the modified FLEX method. Subjects' HR (heart rate) was individually calibrated against submaximal VO2 during incremental exercise tests at the beginning and end of each 9 day study period. Respiratory exchange was measured by indirect calorimetry. Subjects completed hourly hunger ratings during waking hours to record subjective sensations of hunger and appetite. Body weight was measured daily. Results: EE amounted to 11.7, 12.9 and 16.8 MJ/day (F(2,10)=48.26; P<0.001 (s.e.d=0.55)) on the Nex, Mex and Hex treatments, respectively. The corresponding values for EI were 11.6, 11.8 and 11.8 MJ/day (F(2,10)=0.10; P=0.910 (s.e.d.=0.10)), respectively. There were no treatment effects on hunger, appetite or body weight, but there was evidence of weight loss on the Hex treatment. Conclusion: Increasing EE did not lead to compensation of EI over 7 days. However, total daily EE tended to decrease over time on the two exercise treatments. Lean men appear able to tolerate a considerable negative energy balance, induced by exercise, over 7 days without invoking compensatory increases in EI.

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The objective of this investigation was to compare the acute effects of exercise and diet manipulations on energy intake, between dietary restrained and unrestrained females. Comparisons of two studies using an identical 2 x 2 repeated-measures design (level of activity (rest or exercise) and lunch type (high-fat or low-fat)) including thirteen dietary unrestrained and twelve restrained females were performed. Energy expenditure during the rest session was estimated and the energy cost of exercise was measured by indirect calorimetry. Relative energy intake was calculated by subtracting the energy expenditure of the exercise session from the energy intake of the test meal. Post-meal hedonic ratings were completed after lunch. Energy intake and relative energy intake increased during high-fat conditions compared with the low-fat, independently of exercise (P < 0.001). There was a positive relationship between dietary restraint scores and energy intake or relative energy intake in the rest conditions only (r 0.54, P < 0.01). The decrease of relative energy intake between the rest and exercise conditions was higher in restrained than in unrestrained eaters (P < 0.01). These results confirm that a high-fat diet reversed the energy deficit due to exercise. There was no energy compensation in response to an acute bout of exercise during the following meal. In restrained eaters, exercise was more effective in creating an energy deficit than in unrestrained eaters. Exercise may help restrained eaters to maintain control over appetite.

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The effects of exercise and breakfast manipulations on mood and motivation to eat were assessed in 11 healthy females who were regular exercisers and habitual breakfast eaters. The study involved a two by two repeated-measures design, with exercise (or no exercise) and a high-energy breakfast (or low-energy breakfast) as the repeated measures. The exercise or no-exercise session (0800 h) was followed by consumption of the low- or high-energy breakfast (0900 h). An ad libitum lunch test meal was provided 4 hours after the beginning of the exercise session (1200 h). Mood and motivation to eat were continuously tracked from 0800 until 1700 h by an electronic appetite ratings system (EARS). In general, morning subjective mood states (e.g., contentment) were significantly lower in the low-energy breakfast condition, but exercise reversed this effect. Exercise also significantly decreased feelings of lethargy, independent of the breakfast condition. Desire-to-eat and fullness ratings were significantly increased in the low-energy breakfast and high-energy breakfast conditions, respectively. Impairments of mood disappeared in the afternoon after consumption of an ad libitum lunch. In these healthy young adults, the condition inducing the largest energy deficit (exercise and low-energy breakfast) was not associated with the lowest mental states.

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Ghrelin and obestatin are two peptides associated with appetite control and the regulation of energy balance in adults. It is intuitive that they have an important role in growth and development during puberty. Therefore, it is acknowledged that these peptides, in addition to others, form part of the substrate underlying energy homeostasis which in turn will contribute to body weight regulation and could explain changes in energy balance during puberty. Both peptides originate from the stomach; hence, it is intuitive that they are involved in generating signals from tissue stores which influence food intake. This could be manifested via alterations in the drive to eat (i.e. hunger), eating behaviors and appetite regulation. Furthermore, there is some evidence that these peptides might also be associated with physical activity behaviors and metabolism. Anecdotally, children and adolescents experience behavioral and metabolic changes during growth and development which will be associated with physiological changes.

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Over the years, approaches to obesity prevention and treatment have gone from focusing on genetic and other biological factors to exploring a diversity of diets and individual behavior modification interventions anchored primarily in the power of the mind, to the recent shift focusing on societal interventions to design ";temptation-proof"; physical, social, and economic environments. In spite of repeated calls to action, including those of the World Health Organization (WHO), the pandemic continues to progress. WHO recently projected that if the current lifestyle trend in young and adult populations around the world persist, by 2012 in countries like the USA, health care costs may amount to as much as 17.7% of the GDP. Most importantly, in large part due to the problems of obesity, those children may be the first generation ever to have a shorter life expectancy than that of their parents. This work presents the most current research and proposals for addressing the pandemic. Past studies have focused primarly on either genetic or behavioral causes for obesity, however today's research indicates that a strongly integrated program is the best prospect for success in overcoming obesity. Furthermore, focus on the role of society in establishing an affordable, accessible and sustainable program for implementing these lifestyle changes is vital, particularly for those in economically challenged situations, who are ultimately at the highest risk for obesity. Using studies from both neuroscience and behavioral science to present a comprehensive overview of the challenges and possible solutions, The brain-to-society approach to obesity prevention focuses on what is needed in order to sustain a healthy, pleasurable and affordable lifestyle.

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Objective: The evidence was reviewed on how physical activity could influence the regulation of food intake by either adjusting the sensitivity of appetite control mechanisms or by generating an energy deficit that could adjust the drive to eat. Design: Interventionist and correlational studies that had a significant influence on the relationship between physical activity and food intake were reviewed. Interventionist studies involve a deliberate imposition of physical activity with subsequent monitoring of the eating response. Correlational studies make use of naturally occurring differences in the levels of physical activity (between and within subjects) with simultaneous assessment of energy expenditure and intake. Subjects: Studies using lean, overweight, and obese men and women were included. Results: Only 19% of interventionist studies report an increase in energy intake after exercise; 65% show no change and 16% show a decrease in appetite. Of the correlational studies, approximately half show no relationship between energy expenditure and intake. These data indicate a rather loose coupling between energy expenditure and intake. A common sense view is that exercise is futile as a form of weight control because the energy deficit drives a compensatory increase in food intake. However, evidence shows that this is not generally true. One positive aspect of this is that raising energy expenditure through physical activity (or maintaining an active life style) can cause weight loss or prevent weight gain. A negative feature is that when people become sedentary after a period of high activity, food intake is not “down-regulated” to balance a reduced energy expenditure. Conclusion: Evidence suggests that a high level of physical activity can aid weight control either by improving the matching of food intake to energy expenditure (regulation) or by raising expenditure so that it is difficult for people to eat themselves into a positive energy balance.

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Exercise is known to cause physiological changes that could affect the impact of nutrients on appetite control. This study was designed to assess the effect of drinks containing either sucrose or high-intensity sweeteners on food intake following exercise. Using a repeated-measures design, three drink conditions were employed: plain water (W), a low-energy drink sweetened with artificial sweeteners aspartame and acesulfame-K (L), and a high-energy, sucrose-sweetened drink (H). Following a period of challenging exercise (70% VO2 max for 50 min), subjects consumed freely from a particular drink before being offered a test meal at which energy and nutrient intakes were measured. The degree of pleasantness (palatability) of the drinks was also measured before and after exercise. At the test meal, energy intake following the artificially sweetened (L) drink was significantly greater than after water and the sucrose (H) drinks (p < 0.05). Compared with the artificially sweetened (L) drink, the high-energy (H) drink suppressed intake by approximately the energy contained in the drink itself. However, there was no difference between the water (W) and the sucrose (H) drink on test meal energy intake. When the net effects were compared (i.e., drink + test meal energy intake), total energy intake was significantly lower after the water (W) drink compared with the two sweet (L and H) drinks. The exercise period brought about changes in the perceived pleasantness of the water, but had no effect on either of the sweet drinks. The remarkably precise energy compensation demonstrated after the higher energy sucrose drink suggests that exercise may prime the system to respond sensitively to nutritional manipulations. The results may also have implications for the effect on short-term appetite control of different types of drinks used to quench thirst during and after exercise.

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Serotonergic hypofunction is associated with a depressive mood state, an increased drive to eat and preference for sweet (SW) foods. High-trait anxiety individuals are characterised by a functional shortage of serotonin during stress, which in turn increases their susceptibility to experience a negative mood and an increased drive for SW foods. The present study examined whether an acute dietary manipulation, intended to increase circulating serotonin levels, alleviated the detrimental effects of a stress-inducing task on subjective appetite and mood sensations, and preference for SW foods in high-trait anxiety individuals. Thirteen high- (eleven females and two males; anxiety scores 45·5 (sd 5·9); BMI 22·9 (sd 3·0)kg/m2) and twelve low- (ten females and two males; anxiety scores 30·4 (sd 4·8); BMI 23·4 (sd 2·5) kg/m2) trait anxiety individuals participated in a placebo-controlled, two-way crossover design. Participants were provided with 40 g α-lactalbumin (LAC; l-tryptophan (Trp):large neutral amino acids (LNAA) ratio of 7·6) and 40 g casein (placebo) (Trp:LNAA ratio of 4·0) in the form of a snack and lunch on two test days. On both the test days, participants completed a stress-inducing task 2 h after the lunch. Mood and appetite were assessed using visual analogue scales. Changes in food hedonics for different taste and nutrient combinations were assessed using a computer task. The results demonstrated that the LAC manipulation did not exert any immediate effects on mood or appetite. However, LAC did have an effect on food hedonics in individuals with high-trait anxiety after acute stress. These individuals expressed a lower liking (P = 0·012) and SW food preference (P = 0·014) after the stressful task when supplemented with LAC.

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Objective: To examine exercise-induced changes in the reward value of food during medium-term supervised exercise in obese individuals. ---------- Subjects/Methods: The study was a 12-week supervised exercise intervention prescribed to expend 500 kcal/day, 5 d/week. 34 sedentary obese males and females were identified as responders (R) or non-responders (NR) to the intervention according to changes in body composition relative to measured energy expended during exercise. Food reward (ratings of liking and wanting, and relative preference by forced choice pairs) for an array of food images was assessed before and after an acute exercise bout. ---------- Results. 20 responders and 14 non-responders were identified. R lost 5.2 kg±2.4 of total fat mass and NR lost 1.7 kg±1.4. After acute exercise, liking for all foods increased in NR compared to no change in R. Furthermore, NR showed an increase in wanting and relative preference for high-fat sweet foods. These differences were independent of 12-weeks regular exercise and weight loss. ---------- Conclusion. Individuals who showed an immediate post-exercise increase in liking and increased wanting and preference for high-fat sweet foods displayed a smaller reduction in fat mass with exercise. For some individuals, exercise increases the reward value of food and diminishes the impact of exercise on fat loss.

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Prostate cancer is the second most common cause of cancer-related deaths in Western males. Current diagnostic, prognostic and treatment approaches are not ideal and advanced metastatic prostate cancer is incurable. There is an urgent need for improved adjunctive therapies and markers for this disease. GPCRs are likely to play a significant role in the initiation and progression of prostate cancer. Over the last decade, it has emerged that G protein coupled receptors (GPCRs) are likely to function as homodimers and heterodimers. Heterodimerisation between GPCRs can result in the formation of novel pharmacological receptors with altered functional outcomes, and a number of GPCR heterodimers have been implicated in the pathogenesis of human disease. Importantly, novel GPCR heterodimers represent potential new targets for the development of more specific therapeutic drugs. Ghrelin is a 28 amino acid peptide hormone which has a unique n-octanoic acid post-translational modification. Ghrelin has a number of important physiological roles, including roles in appetite regulation and the stimulation of growth hormone release. The ghrelin receptor is the growth hormone secretagogue receptor type 1a, GHS-R1a, a seven transmembrane domain GPCR, and GHS-R1b is a C-terminally truncated isoform of the ghrelin receptor, consisting of five transmembrane domains. Growing evidence suggests that ghrelin and the ghrelin receptor isoforms, GHS-R1a and GHS-R1b, may have a role in the progression of a number of cancers, including prostate cancer. Previous studies by our research group have shown that the truncated ghrelin receptor isoform, GHS-R1b, is not expressed in normal prostate, however, it is expressed in prostate cancer. The altered expression of this truncated isoform may reflect a difference between a normal and cancerous state. A number of mutant GPCRs have been shown to regulate the function of their corresponding wild-type receptors. Therefore, we investigated the potential role of interactions between GHS-R1a and GHS-R1b, which are co-expressed in prostate cancer and aimed to investigate the function of this potentially new pharmacological receptor. In 2005, obestatin, a 23 amino acid C-terminally amidated peptide derived from preproghrelin was identified and was described as opposing the stimulating effects of ghrelin on appetite and food intake. GPR39, an orphan GPCR which is closely related to the ghrelin receptor, was identified as the endogenous receptor for obestatin. Recently, however, the ability of obestatin to oppose the effects of ghrelin on appetite and food intake has been questioned, and furthermore, it appears that GPR39 may in fact not be the obestatin receptor. The role of GPR39 in the prostate is of interest, however, as it is a zinc receptor. Zinc has a unique role in the biology of the prostate, where it is normally accumulated at high levels, and zinc accumulation is altered in the development of prostate malignancy. Ghrelin and zinc have important roles in prostate cancer and dimerisation of their receptors may have novel roles in malignant prostate cells. The aim of the current study, therefore, was to demonstrate the formation of GHS-R1a/GHS-R1b and GHS-R1a/GPR39 heterodimers and to investigate potential functions of these heterodimers in prostate cancer cell lines. To demonstrate dimerisation we first employed a classical co-immunoprecipitation technique. Using cells co-overexpressing FLAG- and Myc- tagged GHS-R1a, GHS-R1b and GPR39, we were able to co-immunoprecipitate these receptors. Significantly, however, the receptors formed high molecular weight aggregates. A number of questions have been raised over the propensity of GPCRs to aggregate during co-immunoprecipitation as a result of their hydrophobic nature and this may be misinterpreted as receptor dimerisation. As we observed significant receptor aggregation in this study, we used additional methods to confirm the specificity of these putative GPCR interactions. We used two different resonance energy transfer (RET) methods; bioluminescence resonance energy transfer (BRET) and fluorescence resonance energy transfer (FRET), to investigate interactions between the ghrelin receptor isoforms and GPR39. RET is the transfer of energy from a donor fluorophore to an acceptor fluorophore when they are in close proximity, and RET methods are, therefore, applicable to the observation of specific protein-protein interactions. Extensive studies using the second generation bioluminescence resonance energy transfer (BRET2) technology were performed, however, a number of technical limitations were observed. The substrate used during BRET2 studies, coelenterazine 400a, has a low quantum yield and rapid signal decay. This study highlighted the requirement for the expression of donor and acceptor tagged receptors at high levels so that a BRET ratio can be determined. After performing a number of BRET2 experimental controls, our BRET2 data did not fit the predicted results for a specific interaction between these receptors. The interactions that we observed may in fact represent ‘bystander BRET’ resulting from high levels of expression, forcing the donor and acceptor into close proximity. Our FRET studies employed two different FRET techniques, acceptor photobleaching FRET and sensitised emission FRET measured by flow cytometry. We were unable to observe any significant FRET, or FRET values that were likely to result from specific receptor dimerisation between GHS-R1a, GHS-R1b and GPR39. While we were unable to conclusively demonstrate direct dimerisation between GHS-R1a, GHS-R1b and GPR39 using several methods, our findings do not exclude the possibility that these receptors interact. We aimed to investigate if co-expression of combinations of these receptors had functional effects in prostate cancers cells. It has previously been demonstrated that ghrelin stimulates cell proliferation in prostate cancer cell lines, through ERK1/2 activation, and GPR39 can stimulate ERK1/2 signalling in response to zinc treatments. Additionally, both GHS-R1a and GPR39 display a high level of constitutive signalling and these constitutively active receptors can attenuate apoptosis when overexpressed individually in some cell types. We, therefore, investigated ERK1/2 and AKT signalling and cell survival in prostate cancer the potential modulation of these functions by dimerisation between GHS-R1a, GHS-R1b and GPR39. Expression of these receptors in the PC-3 prostate cancer cell line, either alone or in combination, did not alter constitutive ERK1/2 or AKT signalling, basal apoptosis or tunicamycin-stimulated apoptosis, compared to controls. In summary, the potential interactions between the ghrelin receptor isoforms, GHS-R1a and GHS-R1b, and the related zinc receptor, GPR39, and the potential for functional outcomes in prostate cancer were investigated using a number of independent methods. We did not definitively demonstrate the formation of these dimers using a number of state of the art methods to directly demonstrate receptor-receptor interactions. We investigated a number of potential functions of GPR39 and GHS-R1a in the prostate and did not observe altered function in response to co-expression of these receptors. The technical questions raised by this study highlight the requirement for the application of extensive controls when using current methods for the demonstration of GPCR dimerisation. Similar findings in this field reflect the current controversy surrounding the investigation of GPCR dimerisation. Although GHS-R1a/GHS-R1b or GHS-R1a/GPR39 heterodimerisation was not clearly demonstrated, this study provides a basis for future investigations of these receptors in prostate cancer. Additionally, the results presented in this study and growing evidence in the literature highlight the requirement for an extensive understanding of the experimental method and the performance of a range of controls to avoid the spurious interpretation of data gained from artificial expression systems. The future development of more robust techniques for investigating GPCR dimerisation is clearly required and will enable us to elucidate whether GHS-R1a, GHS-R1b and GPR39 form physiologically relevant dimers.

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Intrusive thoughts about food may play a role in unhealthy eating behaviours. Food-related thoughts that capture attention can lead to craving and further intrusive thoughts (Kavanagh, Andrade, & May, 2005). We tested whether diverting attention to mental images or bodily sensations would reduce the incidence of intrusive thoughts about snack foods. In two experiments, participants reported their thoughts in response to probes during three 10 min periods. In the Baseline and Post-task period, participants were asked to let their mind wander. In the middle, Experimental, period, participants followed mind wandering (Control), thought diversion, or Thought Suppression instructions. Self-directed or Guided Imagery, Mindfulness-based Body Scanning, and Thought Suppression all reduced the proportion of thoughts about food, compared to Baseline. Following Body Scanning and Thought Suppression, food thoughts returned to Baseline frequencies Post-task, rather than rebounding. There were no effects of the interventions upon craving, although overall, craving and thought frequency were correlated. Thought control tasks may help people to ignore thoughts about food and thereby reduce their temptation to snack.

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This paper seeks to link anthropological and economic treatments of the process of innovation and change, not only within a given ‘complex system’ (e.g. a cosmology; an industry) but also between systems (e.g. cultural and economic systems; but also divine and human systems). The role of the ‘Go-Between’ is considered, both in the anthropological figure of the Trickster (Hyde 1998) and in the Schumpeterian entrepreneur. Both figures parlay appetite (economic wants) into meaning (cultural signs). Both practice a form of creativity based on deception, ‘creative destruction’; renewal by disruption and needs-must adaptation. The disciplinary purpose of the paper is to try to bridge two otherwise disconnected domains – cultural studies and evolutionary economics – by showing that the traditional methods of the humanities (e.g. anthropological, textual and historical analysis) have explanatory force in the context of economic actions and complex-system evolutionary dynamics. The objective is to understand creative innovation as a general cultural attribute rather than one restricted only to accredited experts such as artists; thus to theorise creativity as a form of emergence for dynamic adaptive systems. In this context, change is led by ‘paradigm shifters’ – tricksters and entrepreneurs who create new meanings out of the clash of difference, including the clash of mutually untranslatable communication systems (language, media, culture).

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The present study tested the utility of an extended version of the theory of planned behaviour that included a measure of planning, in the prediction of eating foods low in saturated fats among adults diagnosed with Type 2 diabetes and/or cardiovascular disease. Participants (N = 184) completed questionnaires assessing standard theory of planned behaviour measures (attitude, subjective norm, and perceived behavioural control) and the additional volitional variable of planning in relation to eating foods low in saturated fats. Self-report consumption of foods low insaturated fats was assessed 1 month later. In partial support of the theory of planned behaviour, results indicated that attitude and subjective norm predicted intentions to eat foods low in saturated fats and intentions and perceived behavioural control predicted the consumption of foods low in saturated fats. As an additional variable, planning predicted the consumption of foods low in saturated fats directly and also mediated the intention–behaviour and perceived behavioural control–behaviour relationships, suggesting an important role for planning as a post-intentional construct determining healthy eating choices. Suggestions are offered for interventions designed to improve adherence to healthy eating recommendations for people diagnosed with these chronic conditions with a specific emphasis on the steps and activities that are required to promote a healthier lifestyle.