Clinical Evaluation to Improve Obesity Intervention Prescription: Functional Foods as a Potential Solution for Individuals With a Low Satiety Quotient Phenotype?
试验速览
- 阶段
- 不适用
- 状态
- 已完成
- 入组人数
- 70
- 试验地点
- 4
- 主要终点
- Change from baseline satiety responsiveness (satiety quotients) at 16 weeks
研究概览
简要总结
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.
详细描述
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.
研究设计
- 研究类型
- Interventional
- 分配方式
- Randomized
- 干预模型
- Parallel
- 主要目的
- Other
- 盲法
- None
入排标准
- 年龄范围
- 30 Years 至 50 Years（Adult）
- 性别
- Male
- 接受健康志愿者
- 是
入选标准
- •aged between 30 and 50 years
- •obese (BMI between 30 and 40 kg/m2)
- •overall good health
排除标准
- •Participants taking medication which could influence appetite sensations (hormones, tranquillizers such as chlorpromazine and benzodiazepin, lithium carbonate for bipolar disorders, cyproheptadine, antihistaminic, serotonin antagonist, sulfonylurea and glucocorticoids)
- •Type 2 diabetic patients treated with insulin
- •Large body weight fluctuations (>4 kg over the last two months)
- •High level of restraint behaviour (score > 10 as measured with the Three Factor Eating Questionnaire)
- •Performing more than 3 x 30 minutes/week of physical activity.
结局指标
主要结局
Change from baseline satiety responsiveness (satiety quotients) at 16 weeks
时间窗: Pre- and post-intervention (week 0 and 16)
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)
Change from baseline body weight at 16 weeks
时间窗: Pre (Week 0)- and post-intervention (after 16 weeks)
Body weight (kg)
次要结局
- Change from baseline susceptibility for hunger at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline diet quality (macronutrient composition) at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline rigid restraint at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline level of stress at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline waist circumference at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline binge eating tendencies at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline depression symptoms at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline resting blood pressure at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline percent fat mass at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline distress-related body esteem at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood cortisol at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline BMI at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline resting heart rate at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline resting energy expenditure at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline lean body mass at 16 weeks(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)(Pre- and post-intervention (week 0 and 16))
- Change from baseline cognitive restraint at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline flexible restraint at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline sleeping quality at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fat mass at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline spontaneous energy intake at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline daily energy intake at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline disinhibition at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline anxiety symptoms at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood insulin at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood glucose at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood LDL-apolipoprotein at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline awakening cortisol response at 16 weeks (T15min)(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood leptin at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood free T4 at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline awakening cortisol response at 16 weeks (T60min)(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood total cholesterol at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood LDL-cholesterol at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood total T3 at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline awakening cortisol response at 16 weeks (T0)(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood HDL-cholesterol at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood phospholipids at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline fasting blood triglycerides at 16 weeks(Pre- and post-intervention (week 0 and 16))
- Change from baseline awakening cortisol response at 16 weeks (T30min)(Pre- and post-intervention (week 0 and 16))