Etiology
Obesity in children is multifactorial. Interactions among factors such as genetic predisposition, behavioral and cultural practices, biologic factors, and environmental influences lead to discordant energy balance. Energy intake in excess of energy expenditure eventually leads to overweight and obesity in predisposed people.
Rapid weight gain during infancy and preschool years has been associated with an increased risk of childhood and adolescent obesity.[14][15][16] Preschool children who are overweight (BMI >85th percentile) between the ages of 24 and 54 months have a fivefold greater likelihood of being overweight at 12 years of age.[17] Children with obesity at age 8 years will tend to have more severe obesity, as well as increased morbidity, as adults.[18][19]
Behavioral, environmental, and socioeconomic changes must play an important role even in genetically predisposed children, as the prevalence of obesity in children has increased dramatically over the last 30 years despite a low likelihood of a rapid change in the genetic makeup of the population.
Many factors typically coexist in an individual person, making it difficult to determine the impact of any one factor independently of the others on the development of obesity.
Genetic predisposition[20]
A child's risk of obesity is increased with ≥1 parents with obesity.
Twin studies have demonstrated that BMI and obesity are highly heritable.
Epidemiologic studies have shown that Hispanic and African-American children have a higher incidence of obesity, compared with white and Asian-American children.[5]
Associations between BMI, physical activity, and TV/video viewing vary according to sex and race.[21]
In-utero environment[22][23][24][25]
Maternal pre-pregnancy obesity and gestational weight gain are associated with fetal macrosomia and childhood obesity.
Maternal gestational diabetes is associated with increased newborn fat mass, higher BMI, and higher prevalence of overweight/obesity in children.
Poor nutrition in utero has been correlated with obesity in childhood and adulthood.
Behavioral practices[26][27][28][29]
Sub optimal dietary habits leading to increased energy intake, including energy-dense foods, large portion sizes, fast food, and sugary beverages, are thought to play a role in the development of obesity.
Children who get less exercise are at higher risk of obesity.
Obesity risk is increased in children who have screen time (e.g., television, video games, internet) >2 to 3 hours per day.
Epidemiologic studies show a link between short sleep time and development of obesity in infants, children, and adolescents.
Environmental and social influences[25]
Technological advances have led to a decrease of physical activity.
In addition, energy-dense foods and high-sugar beverages are easily available both in schools and in the community, and are often less costly than healthier alternatives.[30]
Children raised in poor families have a higher risk of obesity.
Medical and pharmacotherapeutic factors[31][32]
Include endocrine disorders (e.g., hypothyroidism, Cushing syndrome, pseudohypoparathyroidism, and hypothalamic obesity following surgery for a craniopharyngioma) and genetic syndromes (e.g., Prader-Willi syndrome, Bardet-Biedl syndrome) and mood disorders such as depression, anxiety, etc.
Exposure to long-term corticosteroids increases the risk of obesity.
Exposure to antibiotics or acid-suppressing medication at age <2 years has been associated with increased risk of obesity in later childhood.
Pathophysiology
Several physiologic systems control how the body regulates weight. The arcuate nucleus, located in the hypothalamus, serves as the master center of weight regulation by integrating hormonal signals that direct the body to adjust its food intake and energy expenditure.
The arcuate nucleus contains two major types of neurons with opposing actions. Activation of the peptide neurotransmitters neuropeptide Y (NPY) and agouti-related peptide (AgRP) leads to stimulation of appetite and decrease in metabolism. In contrast, activation of pro-opiomelanocortin (POMC)/cocaine and amphetamine-regulated transcript neurons causes release of melanocyte-stimulating hormone, which inhibits eating.
Short-term feeding has been linked to two peptide hormones produced in the digestive tract, ghrelin and peptide YY, which control how much and how often we eat on a given day. Ghrelin is a potent appetite stimulator that is produced in the stomach and activates the NPY/AgRP neurons. Increased ghrelin levels are associated with meal initiation. Peptide YY may play an important role in satiety, as it activates the POMC neurons while inhibiting the NPY/AgRP neurons.
Longer-term weight regulation, over months to years, is linked to leptin and insulin.[33] Leptin is released from adipocytes and normally promotes satiety. When fat stores and leptin levels decrease, NPY/AgRP neurons are activated and POMC neurons are inhibited, thereby stimulating weight gain. The opposite occurs with increased fat mass and increased leptin levels. However, some people with obesity develop leptin and insulin resistance, reducing satiety and disrupting the homeostatic mechanisms affecting body weight.[34]
A diet high in sugar and saturated fat may induce hypothalamic inflammation and leptin resistance.[35] Visceral adipose tissue can induce and maintain local and systemic inflammation.[36] The triggers for this inflammation and its contribution to metabolic changes in obesity have not been fully elucidated.
Gut microbiota variations have been associated with weight gain and adiposity.[37]
Hedonic signals from overeating can override weight-regulating physiologic mechanisms. Procuring and eating palatable food activates dopaminergic signaling in the corticolimbic system, giving a sense of reward and pleasure. This causes people to continue eating, even in the presence of satiety signals.[38][Figure caption and citation for the preceding image starts]: 3T3-L1 adipocytes stained with Oil Red O (ORO). ORO stains lipid droplets redFrom the collection of Dianne Deplewski; used with permission [Citation ends].
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