Pathophysiology, comorbidities, and interventions related to childhood obesity

In a recent study published in Frontiers in Pediatrics, researchers discuss the psychological and physiological impacts of obesity on pediatric populations, as well as possible intervention strategies that could help in preventing problems accompanying obesity.

Study: Childhood and adolescent obesity: A review. Image Credit: Africa Studio /


Childhood obesity is a growing concern worldwide and has been classified as an epidemic. Research indicates that obesity cannot be narrowed down to one specific cause; rather, it is a result of complex interactions between genetic, behavioral, environmental, developmental, and biological factors.

Recent studies have also found that the gut microbiome, epigenetic factors, intrauterine environment, small size at gestational age, early incorporation of protein in the infant’s diet, and the reliance on formula rather than breast milk are associated with a higher probability of childhood obesity.

Various concomitant problems have been associated with childhood obesity and present a growing public health burden.

For example, children with obesity are at a higher risk of early puberty development, sleep disorders, menstrual complications in female children, prediabetes, complications associated with high cholesterol, metabolic syndrome, hypertension, type 2 diabetes, and non-alcoholic fatty-liver disease. Childhood obesity also results in psychological issues such as body-image issues, eating disorders, anxiety, depression, and low self-esteem.

Despite the various behavioral, lifestyle, pharmacological, dietary, and surgical interventions being practiced, childhood obesity continues to have detrimental impacts on the psychological and physiological health of adolescents and children.

The pathophysiology of obesity

Obesity is the result of complex interactions between various factors on the societal and individual levels, with biological, genetic, behavioral, and environmental influences on the individual. Socioeconomic factors, as well as familial and community-related influences, can also contribute to weight gain.

Hormonal and neural systems regulate feelings of satiety and hunger, with the hypothalamus regulating appetite under the control of various hunger-stimulating or orexigenic and appetite-suppressing or anorexigenic hormones. Stress and disruptions in sleep cycles due to emotional upheavals associated with psychiatric disorders can also dysregulate the balance between anorexigenic and orexigenic hormones, thus resulting in emotional eating.

Another major biological factor that can contribute to weight gain is the gut microbiome, which is similarly affected by a wide range of factors such as the environment, genetics, lifestyle, diet, gestational age at birth, use of formula during the neonatal and infant stages, feeding practices, age of solid food introduction, and antibiotic use. Dysbiosis, which is defined as an imbalance in the proportion and diversity of gut microbiota, can influence energy dynamics and fat production.

The genetic factors of obesity can be classified as monogenic or polygenic, the latter of which are more common. Monogenic factors include mutations in specific genes, such as the leptin and tyrosine kinase receptor genes, or genetic disorders such as Prader-Willi Syndrome.

Polygenic factors involve an interaction between the environment and gene variants that increase an individual’s susceptibility to obesity. Behaviors that increase the risk of obesity during the developmental stages include eating larger portions, consumption of high-energy and processed foods, as well as sedentary lifestyles with limited physical exercise, which are also linked to cultural and parenting pressures.


In children, obesity is associated with various comorbidities such as hyperinsulinemia, leptin resistance, precocious puberty, and obstructive sleep apnea with associated neurocognitive dysfunction and behavioral abnormalities. Non-alcoholic fatty liver disease and slipped capital femoral epiphysis are other comorbidities observed in obese children.

Obesity in adolescent girls can cause irregularities in their menstrual cycle, thus increasing the risk of polycystic ovarian disorder. The risk of metabolic syndrome involving hypertension, central adiposity, hypertriglyceridemia, and hyperglycemia, as well as sleep disorders, is also higher in obese adolescents.


Preventative measures include anticipatory guidance to children and their families about avoiding unhealthy eating practices and sedentary habits and increasing physical activity levels. Involving the family in the weight-loss process is particularly effective in treating obesity in children between the ages of two and six. An interdisciplinary approach to weight management involving a psychologist, dietician, and physician has also been associated with positive outcomes.

Other interventions include pharmacological options such as Orlistat, Metformin, and glucagon-like peptide 1 agonist, as well as interventions such as Hydrogel technology to target different levels of the gut-liver axis. The roles of docosahexaenoic acid (DHA), vitamin E, and probiotics in tackling obesity are also being explored.

Bariatric surgery comprising procedures such as Roux-en-Y gastric bypass, gastric banding, and laparoscopic sleeve gastrectomy, along with prolonged care from a mental health provider, are also effective options for children with severe obesity.


Obesity is a complex disorder that is influenced by a multitude of biological, genetic, environmental, and lifestyle-associated factors. While anticipatory guidance and the involvement of families in the weight-loss process, along with a multidisciplinary approach that addresses dietary, physiological, and mental health, have shown promise, cases of severe obesity continue to require pharmacological and surgical interventions.

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