An interventional study of Satiating diet and Control diet in Obesity and Appetite Disorders, sponsored by Laval University. Completed at 2 sites in Canada. Open to male participants aged 30 Years to 50 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2017-04-26.
Sponsored by Laval University · Not applicable, Interventional, and Other
The global research project was organized as a clinical process starting with an evaluation aiming at the determination of a diagnosis pertaining to the degree of satiety signal capacity. It was extended by a phase of metabolic and behavioural characterization to better understand the clinical condition of the patients. The main part of the program was a weight loss intervention that was focused on high satiating foods. Finally, the process was completed by an evaluation allowing to determine the impact of the intervention on the metabolic and behavioural conditions of the patients.
Dietary restriction, being prescribed as low and very low calorie diets, has been largely used as a strategy of dietary management of obesity. Beyond the fact that these diets fully respect the first law of thermodynamics, they are also rather easy to supervise and they offer a guarantee of substantial weight loss to compliant patients. Dietary restriction strategies also carry important limitations which include their failure to take into account appetite sensations of the obese patient. This point is important since it dictates the extent to which the patient can tolerate his/her dietary regimen without hunger over time as well as its related body weight loss. In this regard, experimental and clinical data show that weight regain up to initial body weight and even more occurs over years after a diet-induced weight loss. Moreover, evidence also revealed that restraint behaviour is difficult to maintain over time and that a decrease in this behaviour is related to weight gain on a long term basis. The challenge thus becomes the search of a strategy that can promote a substantial spontaneous energy deficit without significantly altering hunger and satiety levels as well as their related well-being. Up to now, the only approach which emerges as having the potential to respect these two criteria is the design of functional foods, i.e. foods with sufficient satiety-promoting properties to compensate for the enhancing effect of body fat loss on appetite. The food specialists can rely on a catalogue of functional ingredients that can be used to prepare functional menus in order to improve the regulation of energy balance and body weight stability in individuals prone to obesity. As described above, this issue would be particularly relevant for obese individuals displaying a low satiety phenotype, i.e. individuals experiencing difficulty to match energy intake to expenditure in a context promoting excess food intake.
The objectives of this study were to characterize obese men displaying the low satiety phenotype (metabolic and behavioral characteristics) and to determine the impact of highly satiating foods on body weight loss, satiety feelings and compliance in this population.
EXPERIMENTAL DESIGN
Recruitment of subjects and satiety phenotype determination
Each patient referred by a physician was contacted by phone and a first screening interview was performed to validate the inclusion criteria. After recruitment, every subject was met to read and sign the letter of consent as well as to discuss every aspect of the program about which he might have some questions. We took advantage of this brief meeting to measure height, body weight and waist circumference to determine BMI and to estimate the level of abdominal fat.
This phase also included a 2-hour session of evaluation in order to determine satiety signal capacity (SQ). At the end of this session, each subject completed the Three-Factor Eating Questionnaire with the specific preoccupation to measure cognitive dietary restraint as an exclusion criterion. The information collected in this first phase of testing was used to subsequently classify subjects on the basis of their satiety signal capacity (low SQ vs normal/high SQ). Subjects not selected to participate in the next phase of the project received, in addition to their health report, a free dietary consultation focusing on the adoption of healthy behaviours. This first phase of testing allowed to rank order subjects on the basis of their score obtained with the satiety quotient. Seventy participants were selected to participate in the study
Initial metabolic and behavioural characterization (Time 0)
This phase of testing began by a standard medical examination performed by the physician of our research team several days before the main testing session. This permitted to identify potential illnesses influencing appetite control and to evaluate the general health condition of each subject. In order to evaluate the reproducibility over time of the satiety quotient determination and to ascertain the status of subjects determined at the initial evaluation, the standardized breakfast test meal was repeated. However, this test was performed in a session of longer duration that allowed to characterize metabolic and behavioural factors associated with a low/high satiety capacity. The measurements included in this phase of testing were used as baseline measurements for the next phase of this project.
Intervention study
The 70 participants were randomly assigned to either a weight loss program consisting of a highly satiating diet (n=35) (low to moderate in fat (30-35%), high in fibres (> 25g/day), high protein (20-25% of total energy intake) and including 45-50% energy as carbohydrate mainly provided by foods with low glycemic index and adequate to slightly increased vitamin and mineral intakes) which is expected to induce a spontaneous energy deficit or a diet supervision based on the guidelines concordant with the Canadian Food Guide (n=35) (10-15, 55-60 and 30% energy as protein, carbohydrate, and lipid, respectively). For statistical analysis, 4 subgroups have been created based on the SQ classification: 1) low SQ, high satiating diet 2) low SQ, conventional healthy diet, 3) normal/high SQ, high satiating diet, 4) normal/high SQ, conventional healthy diet. This experimental environment thus corresponded to a two by two factorial design in which the two independent variables are SQ and diet. Participants were encouraged to comply with the diets for a 16-week period even if a resistance to weight loss (i.e weight maintenance during one month) was observed during the protocol.
Final metabolic and behavioural characterization (Post-tests; week 16)
All the measurements performed at Time 0 were repeated immediately after the 16-week intervention period for each of the four subgroups of subjects.
POTENTIAL OUTCOME AND FUTURE PERSPECTIVES
The main conceptual outcomes of this were: 1) the characterization of factors implicated in different satiety signal capacities; 2) the investigation of the role of individual capacity of satiety signal in body weight loss and diet compliance, and 3) the determination of the impact of functional menus promoting satiety to compensate for the low spontaneous satiety level in some obese individuals. In addition, this project provided clinical and economical outcomes. Indeed, it represented the first study documenting the weight-reducing impact of a healthy diet based on foods whose functionality have been upgraded by food design. If this project confirms that such a diet can promote weight loss without restriction, but while rather being associated with well-being, this will be a major gain for clinical nutritionists who have up to now unsuccessfully try to counteract the obesity epidemic and who have to deal with consumers who primarily request palatable foods instead of a priori focusing on healthy food. From an economical standpoint, this program will be a reference source of validation for the industry seeking justifications and claims to promote healthy foods facilitating body weight control.
6,296 studies on the registry are indexed under Obesity; 1,692 are open to participants now.
This study's enrollment of 70 is below the median of 78 across 4,878 interventional studies indexed under Obesity.
Browse Obesity studies →Laval University is the lead sponsor of 371 studies on the registry; 68 are open to participants now.
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Exclusion Criteria:
Low satiety phenotype subjects who were submitted to the experimental diet (satiating diet) for a 16-week period.
Behavioral: Satiating diet
High satiety phenotype subjects who were submitted to the experimental diet (satiating diet) for a 16-week period.
Behavioral: Satiating diet
Low satiety phenotype subjects who were submitted to the control diet (based on the Canadian Food Guide) for a 16-week period.
Behavioral: Control diet
High satiety phenotype subjects who were submitted to the control diet (based on the Canadian Food Guide) for a 16-week period.
Behavioral: Control diet
Change from baseline body weight at 16 weeks
Body weight (kg)
Time frame: Pre (Week 0)- and post-intervention (after 16 weeks)
Change from baseline satiety responsiveness (satiety quotients) at 16 weeks
Measured by a standardized breakfast test meal using visual analogue scales for 4 appetite sensations (hunger, desire to eat, fullness and prospective food consumption) (mm/100kcal)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline BMI at 16 weeks
kg/m2
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline waist circumference at 16 weeks
cm
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline resting blood pressure at 16 weeks
mmHg
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline resting heart rate at 16 weeks
beat/min
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline resting energy expenditure at 16 weeks
kcal/day
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fat mass at 16 weeks
kg
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline lean body mass at 16 weeks
kg
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline percent fat mass at 16 weeks
percent (%)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline spontaneous energy intake at 16 weeks
Measured following an ad-libitum buffet-type meal (kcal)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline daily energy intake at 16 weeks
Three-day dietary record (kcal/day)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline diet quality (macronutrient composition) at 16 weeks
Three-day dietary record (% carbohydrates, proteins and lipids)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline appetite sensations at 16 weeks (desire to eat, fullness, hunger and prospective food consumption)
Measured following an ad-libitum buffet-type meal (0-150 mm).
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline binge eating tendencies at 16 weeks
Binge Eating Scale (possible score between 0-46)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline distress-related body esteem at 16 weeks
Body Esteem Scale (possible score between 0-92)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline cognitive restraint at 16 weeks
Three Factor Eating Questionnaire (possible score between 0-21)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline flexible restraint at 16 weeks
Three Factor Eating Questionnaire (possible score between 0-7)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline rigid restraint at 16 weeks
Three Factor Eating Questionnaire (possible score between 0-7)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline disinhibition at 16 weeks
Three Factor Eating Questionnaire (possible score between 0-16)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline susceptibility for hunger at 16 weeks
Three Factor Eating Questionnaire (possible score between 0-14)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline depression symptoms at 16 weeks
Beck Depression Inventory (possible score between 0-63)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline anxiety symptoms at 16 weeks
State-Trait Anxiety Inventory (possible score between 20-80)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline level of stress at 16 weeks
Perceived Stress Scale (possible score between 0-40)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline sleeping quality at 16 weeks
Pittsburgh Sleep Quality (possible score between 0-21)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood glucose at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood insulin at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood leptin at 16 weeks
ng/ml
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood cortisol at 16 weeks
nmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood total cholesterol at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood HDL-cholesterol at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood LDL-cholesterol at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood phospholipids at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood triglycerides at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood LDL-apolipoprotein at 16 weeks
mmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood free T4 at 16 weeks
nmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline fasting blood total T3 at 16 weeks
nmol/L
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline awakening cortisol response at 16 weeks (T0)
Determined from salivary samples taken at the time of awakening (ug/dl)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline awakening cortisol response at 16 weeks (T15min)
Determined from salivary samples taken 15 minutes after the awakening (ug/dl)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline awakening cortisol response at 16 weeks (T30min)
Determined from salivary samples taken 30 minutes after the awakening (ug/dl)
Time frame: Pre- and post-intervention (week 0 and 16)
Change from baseline awakening cortisol response at 16 weeks (T60min)
Determined from salivary samples taken 60 minutes after the awakening (ug/dl)
Time frame: Pre- and post-intervention (week 0 and 16)
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Laval University