The environmental factors that have been implicated in childhood and adolescent obesity are myriad. Some of these issues include changes in family structure and meals, increased television and video games, and less physical activity. Medications, viruses, and environmental toxins have also been implicated. The best case can be made for those influences that increase caloric intake and decrease physical activity as those do directly contribute to obesity. More importantly, these are modifiable risk factors that can be adjusted to decrease rates of obesity.

Stimuli that are thought to increase caloric intake include increasing consumption of sugar-sweetened beverages, fast-food service, larger meal portions, school meals with poor nutritional content, and food with high glycemic indices as well as along with fewer meals with the family [9–11]. Of these causes, most evidence available suggests sugar-sweetened beverages can be a significant contributor to obesity in some patient populations [12]. Conversely, those environmental elements thought to decrease physical activity include increasing use of television and video games with decreasing structured physical activity, side walk availability, and playgrounds [9, 11]. The best-established environmental factor that contributes to childhood obesity is television viewing. Several studies have shown a direct correlation between the prevalence of childhood and adolescent obesity and the amount of time spent watching television [13–19].

The precise mechanism of genetics in the development of obesity is difficult to elucidate as there is an intimate relationship between genetic and environmental factors. There are rare childhood genetic abnormalities that lead to obesity such as Prader–Willi which are beyond the scope of this chapter. Current literature suggests genetic factors account for approximately 30–50 % of the variation in fat distribution [20]. In the general population, genetic polymorphisms likely lead to an individual’s susceptibility to the environmental factors that cause obesity; however, most genetic polymorphisms have yet to be isolated.

There is an emerging body of literature that conditions during the fetal and early postnatal period influence chronic disease through permanent effects on metabolic function. This concept is referred to as “fetal programming” [21–23]. Hales and Barker are directly linked to the concept of programming, or the Barker hypothesis whereby an insult or stimulus during a critical point in development has long-term consequences in the development of chronic disease [24, 25]. Fetal programming is thought to play a key role in the development of obesity as well as other metabolic disturbances such as type II diabetes, metabolic syndrome, and cardiovascular disease [26–32]. The proposed mechanism is that periods of undernutrition during fetal and early postnatal period result in changes in the metabolic milieu to slow down weight gain which permanently predisposes an infant to metabolic disturbances later in life [26, 29, 33–35]. This mechanism has been successfully validated in animal studies [27, 30, 31, 36–39].

Increased body weight in girls has been inconsistently associated with early onset of puberty [42–44]. Despite the inconsistency, it is definitively biologically plausible. Furthermore, obesity in childhood and adolescence has been associated with accelerated bone age and linear growth which may put obese girls at risk for short stature [45, 46]. It is not clear if early initiation of menses has a long-term effect on adult reproductive function.

Obesity increases adolescent’s risk of hyperandrogenism and polycystic ovary syndrome (PCOS). PCOS accounts for most cases of anovulation and hyperandrogenism in women and is the most common endocrine abnormality in obese females [47–49]. Given the possible long-term sequel, PCOS should be considered in adolescents with hirsutism, menstrual disturbances, acne which is resistant to treatment, or obesity. The long-term risks of PCOS include gynecological issues such as infertility and endometrial cancer as well as other endocrinopathies such as metabolic syndrome and type II diabetes mellitus.

Diagnosing PCOS during adolescence can be difficult as there are no formal diagnostic criteria for adolescents. Furthermore, given that it is a syndrome and not a disease, the clinical presentation can vary, especially in the adolescent population. Adolescent girls may present with menstrual disturbances, hirsutism, severe acne, hair loss, obesity, or acanthosis nigricans. The three sets of adult criteria are listed in Table 3.2. It is the current expert consensus that the diagnosis of PCOS can only be established 2 years after menarche in a female with hyperandrogenemia and menstrual irregularities [50].

PCOS has a great impact on reproductive function. This is primarily mediated by endocrine dysfunction. Girls with PCOS can experience abnormal pituitary function, abnormal steroidogenesis, and insulin-resistant hyperinsulinemia. All these factors culminate to create an endocrine milieu of hyperandrogenemia, elevated luteinizing hormone, and hyperinsulinemia with each factor acting independently and mutually to potentiate the others. Obesity exacerbates this endocrine dysfunction. Collectively these play a role in ovulatory dysfunction.

Most patients with PCOS, regardless of age, have symptoms of anovulation. Moreover, in adolescents regular menses does not ensure ovulation. During the first 2 years post menarche, roughly half of regular cycles are anovulatory [51]. Despite this, several girls with PCOS and regular menses do ovulate or have a minor ovulatory dysfunction that is revealed as unexplained infertility in adulthood [52, 53]. Ovulatory dysfunction in adolescence increases the risk of ovulatory dysfunction as an adult. The likelihood for prolonged dysfunction increases the longer these menstrual disturbances persist [54, 55].

Ovulatory dysfunction in adolescence increases the risk of ovulatory dysfunction as an adult. The association between obesity and decreased fertility in women can be linked to the association of obesity and PCOS but PCOS is not the only cause of decreased fertility in obese females. In obese females with regular menses increasing BMI is associated with decreasing pregnancy rates and decreasing time to pregnancy [56–58]. It is possible the endocrine environment in obese females has an unfavorable influence on ovarian function, oocyte quality, endometrial receptivity, or any combination of these factors.

Obesity is a risk factor for endometrial hyperplasia and type I endometrioid carcinoma. In addition, chronic anovulation, such as that experienced in females with PCOS, is a risk factor as well. Both obesity and chronic anovulation increase endogenous estrogen exposure, the main risk factor for endometrial cancer [59]. In both conditions peripheral adipose tissue converts androgens to estrogens via aromatase which leads to continued proliferation of the endometrium and ultimately to endometrial hyperplasia or carcinoma. What’s more is that obesity and PCOS commonly coexist but it is unclear if together they increase the risk of endometrial pathology. Regardless, endometrial hyperplasia and cancer are both presenting at younger ages in those girls with obesity and there is a clear association between BMI and early development of endometrial cancer [60]. A meta-analysis of 19 prospective studies in 2008 which included over three million women demonstrated that as BMI increased, the risk of developing endometrial carcinoma increased as well [61]. This is exacerbated by the fact that other associated factors of endometrial cancer such as nulliparity, infertility, type II diabetes mellitus, and hypertension are generally more prevalent in obese women.

Studies estimate that approximately 10 % of adolescents have metabolic syndrome [62–64]. The prevalence increases as the severity of obesity increases among adolescents. The adult criteria for metabolic syndrome were outlined previously in this chapter. Presently it is debated if adolescents should be diagnosed by the same adult criteria given that several physiologic pubertal changes mirror the changes in metabolic syndrome. Some suggested diagnostic criteria are listed in Table 3.3. As a consequence of this diagnostic quandary, it is difficult to compare pediatric studies of metabolic syndrome. Thus, the long-term consequence of metabolic syndrome in children and adolescents remains unclear.

Impaired glucose tolerance is a frequent sequelae of childhood and adolescent obesity. The prevalence ranges from 7 to 25 % in obese adolescents and children [65–67]. It can present independently or as a component of PCOS or metabolic syndrome. Moreover, impaired glucose can suggest an increased risk of developing type II diabetes mellitus.

Type II diabetes mellitus (T2DM) is an “adult disease” that is often seen in obese children and adolescents. The prevalence is approximately 4 % in obese adolescents and children [65]. The development of T2DM in childhood is not without added risk. Individuals who develop T2DM in childhood or adolescents are noted to have more rapid progression of diabetes-associated complications [68].

Hyperinsulinemia can be the initial defect prior to impaired glucose tolerance as well as type II diabetes mellitus. Obesity increases the risk of insulin resistance and thus hyperinsulinemia. Hyperinsulinemia can have multiple effects on the female reproductive system primarily by potentiating or initiating hyperandrogenemia [69]. Hyperinsulinemia is known to impact ovarian and adrenal function to increase androgens. It can also lower sex hormone binding globulin leading to increased amounts of free bioavailable testosterone. These factors can lead to PCOS or a PCOS-like phenotype.

There are several psychosocial repercussions to childhood and adolescent obesity. The most punitive is discrimination from peers in the form of bias and bullying [70, 71]. Girls have more lasting effects from these experiences than boys. Adolescent girls exposed to such behaviors are more likely to have negative self-images during adulthood [70, 71]. Additionally, obese adolescent females are noted to complete fewer years of advanced education, decreased incomes, lower marriage rates, and higher poverty rates compared to nonobese counterparts in adulthood [72, 73].

As previously mentioned, childhood and adolescent obesity is associated with abnormalities in a multitude of organ systems. Here we touch on other systems for completeness. Cardiovascular risks in obese children include hypertension and dyslipidemia, previously noted as components of metabolic syndrome, as well as abnormal cardiac structure and function and adult coronary artery disease. Hypertension is by far the most common comorbidity associated with obesity. Pulmonary issues include obstructive sleep apnea (OSA) and obesity hyperventilation syndrome. It should be noted that PCOS and obesity are independent risk factors for OSA, thus providers should prudently screen obese girls with PCOS for OSA. Gastrointestinal problems include nonalcoholic fatty liver disease (NAFLD), the most common cause of liver disease in children, and cholestasis [71, 74]. Orthopedic concerns consist of slipped capital femoral epiphysis, tibia vara, fractures, and musculoskeletal pain. Dermatologic comorbidities include hidradenitis suppurativa, intertrigo, and furunculosis. Lastly, neurologically obese children are at risk for idiopathic intracranial hypertension.

Lifestyle changes, eating a healthy diet and regular exercise, are of the utmost importance when managing childhood and adolescent obesity. This category merits clinicians’ well-spent time. The key principles are decreasing caloric intake, avoiding fad diet, and increasing the level of exercise. Ideally support and encouragement emanates from parent or guardian; this includes three meals a day that are well designed with regard to protein, carbohydrate, and fat content. Avoiding excessive amounts of sugars and fatty foods, limiting sugar-sweetened beverages, skim milk in place of whole milk are to be suggested. Excellent diets such as Weight Watchers^® have proven to be successful long term.

Medications need to be carefully selected in teens and young adult females as the bottom line remains, “life style modification”. Medications are listed in Table 3.4. Increased satiety and appetite suppression result from this medical treatment [75].