Phillipa Caudwell

Bio: Phillipa Caudwell is an academic researcher from University of Leeds. The author has contributed to research in topics: Weight loss & Appetite. The author has an hindex of 24, co-authored 35 publications receiving 2426 citations.

Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss

Abstract: To identify and characterize the individual variability in compensation for exercise-induced changes in energy expenditure (EE). Twelve-week exercise intervention. Thirty-five overweight and obese sedentary men and women (body mass index, 31.8±4.1 kg m−2; age, 39.6±11.0 years) were prescribed exercise five times per week for 12 weeks under supervised conditions. Body weight, body composition, resting metabolic rate (RMR), total daily energy intake (EI) and subjective appetite sensations were measured at weeks 0 and 12. When all subjects' data were pooled, the mean reduction in body weight (3.7±3.6 kg) was significant (P<0.0001) and as predicted, which suggested no compensation for the increase in EE. However, further examination revealed a large individual variability in weight change (−14.7 to +1.7 kg). Subjects were identified as compensators (C) or noncompensators (NC) based on their actual weight loss (mean NC=6.3±3.2 kg and C=1.5± 2.5 kg) relative to their predicted weight loss. C and NC were characterized by their different metabolic and behavioural compensatory responses. Moderate changes in RMR occurred in C (−69.2±268.7 kcal day−1) and NC (14.2±242.7 kcal day−1). EI and average daily subjective hunger increased by 268.2±455.4 kcal day−1 and 6.9±11.4 mm day−1 in C, whereas EI decreased by 130±485 kcal day−1 and there was no change in subjective appetite (0.4±9.6 mm day−1) in NC. These results demonstrate that expressing the exercise-induced change in body weight as a group mean conceals the large inter-individual variability in body weight and compensatory responses. Individuals who experience a lower than predicted weight loss are compensating for the increase in EE.

Metabolic and behavioral compensatory responses to exercise interventions: barriers to weight loss.

Abstract: An activity-induced increase in energy expenditure theoretically disturbs energy balance (EB) by creating an acute energy deficit. Compensatory responses could influence the weight loss associated with the energy deficit. Individual variability in compensation for perturbations in EB could partly explain why some individuals fail to lose weight with exercise. It is accepted that the regulatory system will readily defend impositions that promote a negative EB. Therefore, a criticism of exercise interventions is that they will be ineffective and futile methods of weight control because the acute energy deficit is counteracted. Compensation for exercise-induced energy deficits can be categorized into behavioral or metabolic responses and automatic or volitional. An automatic compensatory response is a biological inevitability and considered to be obligatory. An automatic compensatory response is typically a metabolic consequence (e.g., reduced resting metabolic rate) of a negative EB. In contrast, a volitional compensatory response tends to be deliberate and behavioral, which the individual intentionally performs (e.g., increased snack intake). The purpose of this review is to highlight the various metabolic and behavioral compensatory responses that could reduce the effectiveness of exercise and explain why some individuals experience a lower than expected weight loss. We propose that the extent and degree of compensation will vary between individuals. That is, some individuals will be predisposed to compensatory responses that render them resistant to the weight loss benefits theoretically associated with an exercise-induced increase in energy expenditure. Therefore, given the inter-individual variability in behavioral and metabolic compensatory responses, exercise prescriptions might be more effective if tailored to suit individuals.

Body composition and appetite: fat-free mass (but not fat mass or BMI) is positively associated with self-determined meal size and daily energy intake in humans

Abstract: The idea of body weight regulation implies that a biological mechanism exerts control over energy expenditure and food intake. This is a central tenet of energy homeostasis. However, the source and identity of the controlling mechanism have not been identified, although it is often presumed to be some long-acting signal related to body fat, such as leptin. Using a comprehensive experimental platform, we have investigated the relationship between biological and behavioural variables in two separate studies over a 12-week intervention period in obese adults (total n 92). All variables have been measured objectively and with a similar degree of scientific control and precision, including anthropometric factors, body composition, RMR and accumulative energy consumed at individual meals across the whole day. Results showed that meal size and daily energy intake (EI) were significantly correlated with fat-free mass (FFM, P values < 0·02–0·05) but not with fat mass (FM) or BMI (P values 0·11–0·45) (study 1, n 58). In study 2 (n 34), FFM (but not FM or BMI) predicted meal size and daily EI under two distinct dietary conditions (high-fat and low-fat). These data appear to indicate that, under these circumstances, some signal associated with lean mass (but not FM) exerts a determining effect over self-selected food consumption. This signal may be postulated to interact with a separate class of signals generated by FM. This finding may have implications for investigations of the molecular control of food intake and body weight and for the management of obesity.

Role of resting metabolic rate and energy expenditure in hunger and appetite control: a new formulation

Abstract: A long-running issue in appetite research concerns the influence of energy expenditure on energy intake More than 50 years ago, Otto G Edholm proposed that "the differences between the intakes of food [of individuals] must originate in differences in the expenditure of energy" However, a relationship between energy expenditure and energy intake within any one day could not be found, although there was a correlation over 2 weeks This issue was never resolved before interest in integrative biology was replaced by molecular biochemistry Using a psychobiological approach, we have studied appetite control in an energy balance framework using a multi-level experimental system on a single cohort of overweight and obese human subjects This has disclosed relationships between variables in the domains of body composition [fat-free mass (FFM), fat mass (FM)], metabolism, gastrointestinal hormones, hunger and energy intake In this Commentary, we review our own and other data, and discuss a new formulation whereby appetite control and energy intake are regulated by energy expenditure Specifically, we propose that FFM (the largest contributor to resting metabolic rate), but not body mass index or FM, is closely associated with self-determined meal size and daily energy intake This formulation has implications for understanding weight regulation and the management of obesity

BRIEF COMMUNICATION ARISING: Gut hormone PYY3-36 physiologically inhibits food intake

Abstract: Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

‘Small Changes’ to Diet and Physical Activity Behaviors for Weight Management

Abstract: Obesity is associated with numerous short- and long-term health consequences. Low levels of physical activity and poor dietary habits are consistent with an increased risk of obesity in an obesogenic environment. Relatively little research has investigated associations between eating and activity behaviors by using a systems biology approach and by considering the dynamics of the energy balance concept. A significant body of research indicates that a small positive energy balance over time is sufficient to cause weight gain in many individuals. In contrast, small changes in nutrition and physical activity behaviors can prevent weight gain. In the context of weight management, it may be more feasible for most people to make small compared to large short-term changes in diet and activity. This paper presents a case for the use of small and incremental changes in diet and physical activity for improved weight management in the context of a toxic obesogenic environment.

Appetite control: methodological aspects of the evaluation of foods

Abstract: This report describes a set of scientific procedures used to assess the impact of foods and food ingredients on the expression of appetite (psychological and behavioural). An overarching priority has been to enable potential evaluators of health claims about foods to identify justified claims and to exclude claims that are not supported by scientific evidence for the effect cited. This priority follows precisely from the principles set down in the PASSCLAIM report. The report allows the evaluation of the strength of health claims, about the effects of foods on appetite, which can be sustained on the basis of the commonly used scientific designs and experimental procedures. The report includes different designs for assessing effects on satiation as opposed to satiety, detailed coverage of the extent to which a change in hunger can stand alone as a measure of appetite control and an extensive discussion of the statistical procedures appropriate for handling data in this field of research. Because research in this area is continually evolving, new improved methodologies may emerge over time and will need to be incorporated into the framework. One main objective of the report has been to produce guidance on good practice in carrying out appetite research, and not to set down a series of commandments that must be followed.