Peripheral signals arise from the sequence involving location, selection, ingestion, digestion, a... more Peripheral signals arise from the sequence involving location, selection, ingestion, digestion, and absorption of food. These signals can be anatomically localized to gastrointestinal signals, circulating factors, metabolic signals, nutrient stores, and the sensory capabilities of the nervous system. Since many of the physiologic signals thought to affect feeding are triggered by nutrient ingestion and feeding behavior is influenced by diet composition, it is useful to consider peripheral appetite signals in the context of energy and nutrient balance. Evidence suggests that nutrient metabolism is (directly or indirectly) related to postingestive satiety. Protein is the most satiating macronutrient and has the greatest detectable effect on qualitative intake. Carbohydrates (CHOs) exert potent effects on satiety. Inhibition of CHO metabolism stimulates intake, as do transient declines in plasma glucose. Inhibition of fat metabolism also stimulates intake, but fat is the least readily metabolized macronutrient, and therefore, joule for joule, is less satiating than CHO or protein. High-fat, energy-dense diets lead to excess energy intakes (EIs) and weight gain relative to lower-fat, less energy-dense diets, and fat intake is a risk factor for subsequent weight gain. Earlier models viewed peripheral control of feeding as due to one or more simple negative feedback loops. More recently research has focused on the multiple signalling systems involved in the maintenance of nutrient and energy balance (EB). While protein influences satiety at several levels, relatively little is known about “aminostatic” mechanisms. CHO status appears to be monitored in both the central nervous system (CNS) and periphery; signals relating to fat status largely appear to arise in the periphery. More progress has been made in identifying peripheral signals and some of their connections to the brain than in understanding their quantitative importance for normal feeding.
Obesity is commonly associated with a high incidence and prevalence of dyslipidaemia, cardiovascu... more Obesity is commonly associated with a high incidence and prevalence of dyslipidaemia, cardiovascular disease and Type II diabetes. Interestingly, studies have also reported decreased antioxidant levels in obese subjects. This may constitute an independent risk factor in the pathogenesis of coronary artery disease as obese subjects would have a decreased capacity to prevent the oxidative modification of low-density lipoproteins, which is a mechanism suggested as central to the development of atherogenesis. As part of a study to investigate responses to weight loss, we have assessed the effects on GSH status of a decrease in body mass of 5%, either after 6 days of complete starvation or 11 days of a very low calorie diet (2.55 MJ/day). There were significant differences between the two groups in the synthesis rate of erythrocyte GSH in response to weight loss. Both the fractional and the erythrocyte synthesis rate of GSH decreased significantly (P<0.01) in the starvation group by 22% and 16% respectively. In contrast, no change in synthesis rates was observed in the very low calorie diet group (P>0.05). Total erythrocyte concentration of GSH was unaffected by the weight loss within both groups. These results suggest that erythrocyte GSH synthesis is depressed in response to a very rapid weight loss induced by fasting. An acute reduction in GSH synthesis in response to a rapid weight loss may constitute a risk factor during periods of increased GSH demands.
An obesigenic environment is a potent force for promoting weight gain. However, not all people ex... more An obesigenic environment is a potent force for promoting weight gain. However, not all people exposed to such an environment become obese; some remain lean. This means that some people are susceptible to weight gain (in a weight-promoting environment) and others are resistant. Identifying the characteristics of appetite control and food motivation in these two groups could throw light on the causes of weight gain and how this can be either treated or prevented. We have investigated the issue experimentally by identifying people who habitually consume a high-fat diet (greater than 43% fat energy). These individuals have been termed high-fat phenotypes. We have compared individuals, of the same age (mean = 37 years old) and gender (male), who have gained weight (BMI = 34) or who have remained lean (BMI = 22). The susceptible individuals are characterised by a cluster of characteristics including a weak satiety response to fatty meals, a maintained preference for high-fat over low-energy foods in the post-ingestive satiety period, a strong hedonic attraction to palatable foods and to eating, and high scores on the TFEQ factors of Disinhibition and Hunger. The analysis of large databases suggests that this profile of factors contributes to an average daily positive energy balance from food of approximately 0.5 MJ. This profile of characteristics helps to define the symptomatology of a thrifty phenotype.
The purpose of the study was to examine the effect of energy density and food weight (volume) on ... more The purpose of the study was to examine the effect of energy density and food weight (volume) on subsequent intake.Sixteen lean men were each studied four times during a 2-d protocol at the Rowett's Human Nutrition Unit. On day 1, subjects were fed a mandatory diet at 1.6 × resting metabolic rate (RMR). On day 2, during the mandatory morning period (08.30–12.30) subjects consumed a fixed breakfast (08.30) plus a snack (10.30) in one of four treatments [with values in weight (kg), ED (kJ/100 g), Energy (MJ)]: (i) zero intake, 0:0:0 (ii) low energy density (LED), 0.615: 400: 2.46; (iii) high energy density (HED), 0.615: 800: 4.92; (iv) 2 × LED, 1.225: 400: 4.91. From 12.30, throughout the remainder of the day, subjects had ad libitum access to 15 high-protein, 15 high-fat and 15 high-carbohydrate foods. Motivation to eat was tracked hourly using 100 mm line scales.ANOVA showed subjects were hungrier after the zero and LED treatments in the mandatory period (p < 0.001). Lunch time EI was 5.0, 3.1, 4.2 and 3.2 MJ on the zero, HED, LED and 2 × LED treatments, respectively (p < 0.001). Total ad libitum EI was 11.7, 9.6, 10.3 and 9.5 MJ/d, respectively (p = 0.033). Total ad libitum plus mandatory intakes amounted to 11.7, 14.5, 12.6 and 14.4 MJ/d, respectively (p = 0.001). Corresponding food intakes were 2.18, 2.39, 2.51 and 3.06 kg/d, respectively (p < 0.001).The present study showed that subjects respond to both the amount of food eaten in the morning and to the energy density of those foods. However, compensation was only partial and short-term. Subjects only compensated EI by ∼40% and that compensation only occurred at the next meal.
This paper considers the role of energy density (ED), diet composition and palatability in the co... more This paper considers the role of energy density (ED), diet composition and palatability in the control of energy intake (EI) in humans through several related considerations: (i) the relationship between ED and diet composition, (ii) the relationship between ED, diet composition and EI, (iii) the relationship between palatability and EI, (iv) the relationship between ED, palatability and EI, (v) the importance of postingestive factors in influencing palatability in the longer term, (vi) the contribution of sensory and nutritional factors to dietary hyperphagia and (vii) the implications these considerations have for people living their normal lives in their natural environment.The main factors influencing ED are the fat and water content of foods. Energy density does elevate EI, especially in short-term studies where it can account for >40% of the variance in EI. In real life, ED accounts for only approximately 7% of the variance in EI. This is because the determinants of EI are multifactorial and also because the short-term effects of ED on EI do not translate into the longer term. We argue that part of the longer term amelioration of short-term effects of ED on EI is due to learned compensation, based on the postingestive consequences of consuming familiar food that differ in ED. More energy-dense foods tend to be more palatable but we learn to consume them in smaller portion sizes. In the longer term, the perceived palatability of a food is strongly influenced by the postingestive consequences of eating it. This effect can override sensory factors alone. This implies that nutrient mimetics, if used continuously, would not be as efficacious as initially supposed and that their ad hoc use may undermine the stability of learned appetites and satieties for foods with different EDs and contribute to the poor weight control capability exhibited by consumers at large.
To examine the effects of a high dose (two high-intensity exercise sessions) of exercise on energ... more To examine the effects of a high dose (two high-intensity exercise sessions) of exercise on energy intake (EI) and subjective states (hunger and mood). Using a within subjects design, there were two treatment conditions, each of two consecutive days. The Human Appetite Research Unit at Leeds University Psychology Department. Eight lean males who were regular exercisers were recruited from the student/staff population of Leeds University. The effects of the high dose of exercise Ex1 were compared with the effects on the day immediately after exercise (Ex2) and two consecutive days of no exercise (R1 and R2). EI was monitored using self-record food diaries and subjective states were tracked using a new Electronic Appetite Rating System (EARS). Heart rate and physical activity were also measured. Feelings of hunger were not elevated by the high dose of exercise on Ex1 or on the day after exercise (Ex2). In fact, average daily feeling of hunger on Ex1 was significantly lower compared with the average daily feeling of hunger on Ex2 (t = 3.15, d.f. = 7, P &lt; 0.05), but not when compared with R1 or R2. EI and macronutrient intakes were not different on Ex1, Ex2, R1 or R2. Therefore, there were no increase in EI on Ex1 or Ex2 to account for the measured increase in exercise-induced energy expenditure (1200 kcal). Continuously monitored heart rate and activity profiles indicated that there was no difference in activity during the non-exercise periods between the four days. This study indicates that a high dose of exercise in one day failed to have any effect on EI within the same day or on the day immediately after exercise, compared with days of no exercise. These results demonstrate that an acute but substantial increase in energy expenditure (EE) due to intense exercise does not automatically increase hunger or EI within 48 h. This indicates the absence of any strong coupling between EE and EI in the short-term, probably as a result of food intake being held in place by environmental contingencies and short-term pre-absorptive physiological responses arising from eating itself.
Peripheral signals arise from the sequence involving location, selection, ingestion, digestion, a... more Peripheral signals arise from the sequence involving location, selection, ingestion, digestion, and absorption of food. These signals can be anatomically localized to gastrointestinal signals, circulating factors, metabolic signals, nutrient stores, and the sensory capabilities of the nervous system. Since many of the physiologic signals thought to affect feeding are triggered by nutrient ingestion and feeding behavior is influenced by diet composition, it is useful to consider peripheral appetite signals in the context of energy and nutrient balance. Evidence suggests that nutrient metabolism is (directly or indirectly) related to postingestive satiety. Protein is the most satiating macronutrient and has the greatest detectable effect on qualitative intake. Carbohydrates (CHOs) exert potent effects on satiety. Inhibition of CHO metabolism stimulates intake, as do transient declines in plasma glucose. Inhibition of fat metabolism also stimulates intake, but fat is the least readily metabolized macronutrient, and therefore, joule for joule, is less satiating than CHO or protein. High-fat, energy-dense diets lead to excess energy intakes (EIs) and weight gain relative to lower-fat, less energy-dense diets, and fat intake is a risk factor for subsequent weight gain. Earlier models viewed peripheral control of feeding as due to one or more simple negative feedback loops. More recently research has focused on the multiple signalling systems involved in the maintenance of nutrient and energy balance (EB). While protein influences satiety at several levels, relatively little is known about “aminostatic” mechanisms. CHO status appears to be monitored in both the central nervous system (CNS) and periphery; signals relating to fat status largely appear to arise in the periphery. More progress has been made in identifying peripheral signals and some of their connections to the brain than in understanding their quantitative importance for normal feeding.
Obesity is commonly associated with a high incidence and prevalence of dyslipidaemia, cardiovascu... more Obesity is commonly associated with a high incidence and prevalence of dyslipidaemia, cardiovascular disease and Type II diabetes. Interestingly, studies have also reported decreased antioxidant levels in obese subjects. This may constitute an independent risk factor in the pathogenesis of coronary artery disease as obese subjects would have a decreased capacity to prevent the oxidative modification of low-density lipoproteins, which is a mechanism suggested as central to the development of atherogenesis. As part of a study to investigate responses to weight loss, we have assessed the effects on GSH status of a decrease in body mass of 5%, either after 6 days of complete starvation or 11 days of a very low calorie diet (2.55 MJ/day). There were significant differences between the two groups in the synthesis rate of erythrocyte GSH in response to weight loss. Both the fractional and the erythrocyte synthesis rate of GSH decreased significantly (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt;0.01) in the starvation group by 22% and 16% respectively. In contrast, no change in synthesis rates was observed in the very low calorie diet group (P&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;gt;0.05). Total erythrocyte concentration of GSH was unaffected by the weight loss within both groups. These results suggest that erythrocyte GSH synthesis is depressed in response to a very rapid weight loss induced by fasting. An acute reduction in GSH synthesis in response to a rapid weight loss may constitute a risk factor during periods of increased GSH demands.
An obesigenic environment is a potent force for promoting weight gain. However, not all people ex... more An obesigenic environment is a potent force for promoting weight gain. However, not all people exposed to such an environment become obese; some remain lean. This means that some people are susceptible to weight gain (in a weight-promoting environment) and others are resistant. Identifying the characteristics of appetite control and food motivation in these two groups could throw light on the causes of weight gain and how this can be either treated or prevented. We have investigated the issue experimentally by identifying people who habitually consume a high-fat diet (greater than 43% fat energy). These individuals have been termed high-fat phenotypes. We have compared individuals, of the same age (mean = 37 years old) and gender (male), who have gained weight (BMI = 34) or who have remained lean (BMI = 22). The susceptible individuals are characterised by a cluster of characteristics including a weak satiety response to fatty meals, a maintained preference for high-fat over low-energy foods in the post-ingestive satiety period, a strong hedonic attraction to palatable foods and to eating, and high scores on the TFEQ factors of Disinhibition and Hunger. The analysis of large databases suggests that this profile of factors contributes to an average daily positive energy balance from food of approximately 0.5 MJ. This profile of characteristics helps to define the symptomatology of a thrifty phenotype.
The purpose of the study was to examine the effect of energy density and food weight (volume) on ... more The purpose of the study was to examine the effect of energy density and food weight (volume) on subsequent intake.Sixteen lean men were each studied four times during a 2-d protocol at the Rowett's Human Nutrition Unit. On day 1, subjects were fed a mandatory diet at 1.6 × resting metabolic rate (RMR). On day 2, during the mandatory morning period (08.30–12.30) subjects consumed a fixed breakfast (08.30) plus a snack (10.30) in one of four treatments [with values in weight (kg), ED (kJ/100 g), Energy (MJ)]: (i) zero intake, 0:0:0 (ii) low energy density (LED), 0.615: 400: 2.46; (iii) high energy density (HED), 0.615: 800: 4.92; (iv) 2 × LED, 1.225: 400: 4.91. From 12.30, throughout the remainder of the day, subjects had ad libitum access to 15 high-protein, 15 high-fat and 15 high-carbohydrate foods. Motivation to eat was tracked hourly using 100 mm line scales.ANOVA showed subjects were hungrier after the zero and LED treatments in the mandatory period (p < 0.001). Lunch time EI was 5.0, 3.1, 4.2 and 3.2 MJ on the zero, HED, LED and 2 × LED treatments, respectively (p < 0.001). Total ad libitum EI was 11.7, 9.6, 10.3 and 9.5 MJ/d, respectively (p = 0.033). Total ad libitum plus mandatory intakes amounted to 11.7, 14.5, 12.6 and 14.4 MJ/d, respectively (p = 0.001). Corresponding food intakes were 2.18, 2.39, 2.51 and 3.06 kg/d, respectively (p < 0.001).The present study showed that subjects respond to both the amount of food eaten in the morning and to the energy density of those foods. However, compensation was only partial and short-term. Subjects only compensated EI by ∼40% and that compensation only occurred at the next meal.
This paper considers the role of energy density (ED), diet composition and palatability in the co... more This paper considers the role of energy density (ED), diet composition and palatability in the control of energy intake (EI) in humans through several related considerations: (i) the relationship between ED and diet composition, (ii) the relationship between ED, diet composition and EI, (iii) the relationship between palatability and EI, (iv) the relationship between ED, palatability and EI, (v) the importance of postingestive factors in influencing palatability in the longer term, (vi) the contribution of sensory and nutritional factors to dietary hyperphagia and (vii) the implications these considerations have for people living their normal lives in their natural environment.The main factors influencing ED are the fat and water content of foods. Energy density does elevate EI, especially in short-term studies where it can account for >40% of the variance in EI. In real life, ED accounts for only approximately 7% of the variance in EI. This is because the determinants of EI are multifactorial and also because the short-term effects of ED on EI do not translate into the longer term. We argue that part of the longer term amelioration of short-term effects of ED on EI is due to learned compensation, based on the postingestive consequences of consuming familiar food that differ in ED. More energy-dense foods tend to be more palatable but we learn to consume them in smaller portion sizes. In the longer term, the perceived palatability of a food is strongly influenced by the postingestive consequences of eating it. This effect can override sensory factors alone. This implies that nutrient mimetics, if used continuously, would not be as efficacious as initially supposed and that their ad hoc use may undermine the stability of learned appetites and satieties for foods with different EDs and contribute to the poor weight control capability exhibited by consumers at large.
To examine the effects of a high dose (two high-intensity exercise sessions) of exercise on energ... more To examine the effects of a high dose (two high-intensity exercise sessions) of exercise on energy intake (EI) and subjective states (hunger and mood). Using a within subjects design, there were two treatment conditions, each of two consecutive days. The Human Appetite Research Unit at Leeds University Psychology Department. Eight lean males who were regular exercisers were recruited from the student/staff population of Leeds University. The effects of the high dose of exercise Ex1 were compared with the effects on the day immediately after exercise (Ex2) and two consecutive days of no exercise (R1 and R2). EI was monitored using self-record food diaries and subjective states were tracked using a new Electronic Appetite Rating System (EARS). Heart rate and physical activity were also measured. Feelings of hunger were not elevated by the high dose of exercise on Ex1 or on the day after exercise (Ex2). In fact, average daily feeling of hunger on Ex1 was significantly lower compared with the average daily feeling of hunger on Ex2 (t = 3.15, d.f. = 7, P &lt; 0.05), but not when compared with R1 or R2. EI and macronutrient intakes were not different on Ex1, Ex2, R1 or R2. Therefore, there were no increase in EI on Ex1 or Ex2 to account for the measured increase in exercise-induced energy expenditure (1200 kcal). Continuously monitored heart rate and activity profiles indicated that there was no difference in activity during the non-exercise periods between the four days. This study indicates that a high dose of exercise in one day failed to have any effect on EI within the same day or on the day immediately after exercise, compared with days of no exercise. These results demonstrate that an acute but substantial increase in energy expenditure (EE) due to intense exercise does not automatically increase hunger or EI within 48 h. This indicates the absence of any strong coupling between EE and EI in the short-term, probably as a result of food intake being held in place by environmental contingencies and short-term pre-absorptive physiological responses arising from eating itself.
Uploads
Papers by james stubbs