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Denes Molnar
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Molnar, D.; Erhardt, �. Prevention of Obesity in Prader–Willi Syndrome. Encyclopedia. Available online: https://encyclopedia.pub/entry/23340 (accessed on 10 July 2025).
Molnar D, Erhardt �. Prevention of Obesity in Prader–Willi Syndrome. Encyclopedia. Available at: https://encyclopedia.pub/entry/23340. Accessed July 10, 2025.
Molnar, Denes, Éva Erhardt. "Prevention of Obesity in Prader–Willi Syndrome" Encyclopedia, https://encyclopedia.pub/entry/23340 (accessed July 10, 2025).
Molnar, D., & Erhardt, �. (2022, May 25). Prevention of Obesity in Prader–Willi Syndrome. In Encyclopedia. https://encyclopedia.pub/entry/23340
Molnar, Denes and Éva Erhardt. "Prevention of Obesity in Prader–Willi Syndrome." Encyclopedia. Web. 25 May, 2022.
Prevention of Obesity in Prader–Willi Syndrome
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This entry is adapted from the peer-reviewed paper 10.3390/nu14091950

Prader–Willi syndrome (PWS) is a complex genetic disorder which involves the endocrine and neurologic systems, metabolism, and behavior. It is to summarize current knowledge on dietary management and treatment of PWS and, in particular, to prevent excessive weight gain. Growth hormone (GH) therapy is the recommended standard treatment for PWS children, because it improves body composition (by changing the proportion of body fat and lean body mass specifically by increasing muscle mass and energy expenditure), linear growth, and in infants, it promotes psychomotor and IQ development.

Prader–Willi syndrome nutritional phases obesity treatment prevention

1. Nutritional Aspects in Weight Gain Prevention

Nutritional management by nutritionists and gastroenterologists plays a major role in weight control in children with PWS, and specifically in terms of dietary intake. Appetite behavior in these children is a life-long challenge and can be life-threatening. The appetite of PWS patients changes [1][2] during the different phases of nutrition. In Phase 1a, children with PWS have no desire to eat and often will have FTT in infancy despite adequate calories (0–9 months). The nutritional goal in this period is to promote optimal growth without developing obesity. Decreased muscle mass and increased fat mass are present from infancy. Infants with PWS require less energy intake compared to healthy children. The physiologic background of this phenomenon is the reduced REE and reduced energy spent on physical activity than in healthy infants [1][3]. In the Phase 1b period, the appetite and weight return to normal, and generally continues up until the age of 36 months. Phase 2a begins at age 18–36 months, where weight increases without any change in appetite, and lasts until approximately age 4.5. During this period, appetite is appropriate for age. Gastric motility appears to slow down, and metabolism begins to change. Children with PWS will become obese if the recommended daily allowance (RDA) of calories is given at this age. The REE is decreased in these children and approximately 50–60% of the RDA is sufficient in this phase. An increasing interest in food begins between 4.5–8 years of age (in phase 2b). Appetite increases gradually and becomes insatiable [4][5]. The average onset of Phase 3 is around 8 years of age when an insatiable appetite develops. The weight gain can be rapid and life-threatening and may occur even on a low-calorie diet. The guidelines recommend 10–12 kcal/cm of height for weight maintenance and 6–8 kcal/cm for weight loss in pre-school- and school-aged children [6][7][8][9]. Children with PWS must be supervised where food is accessible at all times. In adulthood (Phase 4), the appetite is satiable and can decrease in rare situations.

2. Pharmacologic Treatment Options

Growth Hormone Therapy

Patients with PWS have hypothalamic dysfunction, which may lead to several endocrinopathies such as hypothyroidism, hypogonadism, central adrenal insufficiency, and growth hormone deficiency (GHD). All individuals with PWS should be considered growth hormone (GH) deficient. The prevalence of GHD varies 40–100% based on different ones [10]. There was a 74% prevalence of GHD in the KIGS (Kabi International Growth Study) database [11]. This high discrepancy in prevalence is likely to be due to the variation of the testing methods, differences in GH assays, and the patients’ age at the time of testing. The exact pathogenesis of GHD is not clear. The aim of GH therapy is to improve body composition (decrease fat mass, increase muscle mass) and promote growth. However, IQ also improves with GH therapy, especially in children with severe cognitive delays. Carrel et al. [12] demonstrated that GH treatment in infants improves IQ and psychomotor development, so it is recommended to start GH therapy as soon as possible (often around 3–6 months of age). Miller et al. revealed [13] that children treated with GH before the first year of life had decreased fat mass and higher REE compared to those treated after one year of age, which may indicate that early treatment with GH may help ameliorate obesity in PWS. GH dosing needs to be individualized based on IGF-1, growth velocity, and body composition/height.
Short-term treatment with growth hormones for 1–2 years may not normalize body weight but significantly increases lean body mass and decreases fat mass. In addition, height in relation to age may increase and psychomotor development and behavior may improve in young children [14][15][16].
A 4-year-long, continuous GH treatment [17] in prepubertal children with PWS led to a pronounced improvement in body composition, but complete normalization could not be achieved. Why normalization could not be achieved may be due to the fact that the typical body composition in PWS is not only due to growth hormone deficiency but also a genetic defect affecting other pathways.
In another one, patients began GH therapy at the age of 3.7 years and continued to receive it for 8 years [18]. Body composition significantly changed in the first year of therapy, whereas this tendency slowed down in subsequent years and by the end of the 8-year treatment period, the body mass index (BMI) values of subjects with PWS remained higher than in normal children [19].
Contraindications of GH treatment in patients with PWS are severe obesity and severe obstructive sleep apnea [10][20].
PWS cannot be prevented, and there is no remedy for it. GH replacement treatment is the only Federal Drug Agency (FDA)-approved treatment for PWS [21]. Weight control is one of the most important goals in PWS therapy. However, it is a challenging task due to behavioral problems related to appetite control, decreased lean body mass, and reduced REE.
There are no widely accepted guidelines on the acceptability, safety, or efficacy for anti-obesity medication (AOM) in children with PWS.
Goldman et al. published  [22] on drugs used in children and adolescents with PWS. 14 articles (3 topiramate, 1 metformin, 4 liraglutide, 5 oxytocin, 1 naltrexone–bupropion) were yielded from the search. All were reported enhanced hyperphagia with variable BMI effects. No significant side effects were found.
Topiramate is an antiepileptic drug with off-label use for weight reduction. Its mechanism is not totally understood. Topiramate appears to block sodium and calcium channels, increasing the suppression effects of GABA. A double-blind, randomized placebo-controlled eight-week one was published [23] with a trend in reducing BMI without statistical significance, and a dose-dependent raise in hyperphagia among 62 patients (ages 12–45 years). An open-label one in seven patients with PWS demonstrated weight reduction or declined weight gain and improved mood [24]. An 11-year-old male with PWS was described whose aggression and ’demand for food’ decreased following treatment with topiramate [25].
Metformin is an oral drug classically used in type 2 diabetes to improve hyperglycemia and is also used off-label to treat obesity and prediabetes [26]. Effects of metformin are multi-factorial, including reduced glucose production in the liver and glucose absorption in the gastrointestinal tract; thus, insulin sensitivity increases. [27].
In a pilot one metformin treatment was started in 21 children and adolescents with PWS who had insulin resistance and glucose intolerance. Metformin treatment improved food-related distress and anxiety, evaluated by Hyperphagia Questionnaire; however, weight reduction did not occur. [27]. A total of 7 out of 10 males had to stop metformin due to a worsening behavioral condition.
Naltrexone-bupropion is a combined drug used to treat obesity and impulsive behavior. Naltrexone is an opioid receptor antagonist, and bupropion is a dopamine/norepinephrine reuptake inhibitor [22]. It has a role in the hypothalamus through the anorexigenic effect of the α-melanocyte-stimulating hormone from pro-opiomelanocortin neurons. [28][29]. The FDA has approved this drug for the treatment of obesity [22][26]. From the search, one was investigated the effect of this therapy in 13-year-old children with PWS. A decreased BMI with improved aggression was reported [28].
Glucagon-like peptide-1 (GLP-1) receptor agonist stimulates insulin release, inhibits glucagon secretion, and decreases plasma ghrelin levels. According to a systematic review on PWS patients, gastrointestinal tract motility decreased, and satiety increased after eating [30]. Liraglutide is the short-acting, daily preparation approved by the FDA and EMA for the treatment of obesity in patients older than 12 years [22][26].
In this [31], PWS patients who also had type 2 diabetes were treated with 1.2 to 1.8 mg/day of liraglutide (4 patients) and 20 mg/day of exenatide (2 patients). After 24 months of treatment, a tendency of reduction in BMI, HbA1c, waist circumference and improved glycaemia was seen [9][31]. A longitudinal study evaluated the efficacy of exenatide therapy (6 months) in overweight or obese young adults with PWS. Reduced appetite and an improvement in HbA1c were reported, whereas weight or BMI did not change. [32].
Oxytocin is a neuropeptide that has a wide range of indications. It induces weight reduction by increasing EE and lipolysis, as well as diminishing appetite, which can lead to decreased food intake [22]. Five were investigated the effect of the intranasal administration of an oxytocin analogue (carbetocin) in children with PWS. Three were showed improvement in social and food-related behaviors [33][34][35], whereas two could demonstrate only limited positive effects on behavior. [36][37].
Other drugs targeting weight control are under investigation as potential treatments for PWS. Tesofensine is a triple monoamine reuptake inhibitor of the neurotransmitter’s dopamine, norepinephrine, and serotonin that acts as an appetite reducer and has been connected with weight loss in a placebo-controlled trial of patients with obesity in Denmark [18][38].
Another drug is diazoxide, an ATP-sensitive K+ channel agonist that inhibits insulin secretion from the pancreas and modulates insulin-sensitive enzymes, leading to suppressed lipogenesis and increased lipolysis. It has been shown that diazoxide decreases fat mass, weight, and blood glucose levels in a mouse model with PWS [39]. A pilot one assessing the efficacy and safety of diazoxide choline found a significant decrease in fat mass and a significant reduction in hyperphagia among nine patients with PWS [40]. More extensive ones are in progress to substantiate the use of diazoxide choline in adolescents and young adults with PWS.
Setmelanotide (or RM-493) is an agonist of the appetite-regulating melanocortin-4 receptor, which is being examined for different forms of genetic obesity [6].
There is an unacylated ghrelin analog that has been shown to inhibit the orexigenic effect of unacylated ghrelin in animals, and it is assumed to have favorable metabolic effects in humans [41].

3. Prevention of Obesity in Prader–Willi Syndrome

In general, the prevention of obesity in childhood is a major task for pediatricians. In children with PWS, it is important to introduce preventive programs as early as possible to control caloric intake, which is very difficult due to the low compliance of these children.
Preventive methods for weight management in PWS must be performed simultaneously by using dietary, physical activity and behavioral interventions. The role of a multidisciplinary team is mandatory to treat these children. During the first months, the main task of nutritionists is to ensure the appropriate caloric intake of children with PWS [6][42]. After the first year of life, a low-calorie but well-balanced diet is required, and close supervision is needed to minimize food-stealing [9]. Physical activity and the encouragement of muscle mass training has to be a daily routine in subjects with PWS at all ages. [43]. PA level is decreased in PWS patients due to low (skeletal) muscle mass and muscle hypotonia compared to healthy children [43]. Complex and early interventions are recommended to promote skill acquisition and improve motor development [9].
Bellicha et al. published [44] a systematic review on habitual PA and sedentary behavior and the effects of PA in children with PWS. The effect of eight different interventions were explored. The summarized benefit of PA interventions was due to the improvement of physical fitness, such as improved walking capacity, muscle strength, and gait parameters. In contrast, only one was showed a significant weight reduction after PA intervention, whereas the others did not find significant weight and/or fat loss. In subjects with PWS, PA interventions seem to have a beneficial effect on lean body mass [45] and bone mineral density [46]. Observational ones have also reported a positive relation between habitual PA and lean body mass [44][45] or bone parameters [47].
GH treatment could also have an important role in the prevention of obesity, when initiated during infancy. Patients with PWS greatly require behavioral programs in which, besides medical personnel, teachers, friends, parents, and other family members are also to be included. Supervised PA programs are feasible in children with PWS and these programs should be arranged individually and should offer a variety of enjoyable activities [9][44].

References

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