- 1.
Obesity among children, adolescents, and adults is set to be one of the most important public health concerns of the 21st century.
- 2.
Over the last three decades, the incidence of obesity in childhood and adolescence has been a growing epidemic, with a rise by more than a half of overweight and a doubling of obesity.
- 3.
All around the world, 1 in 10 young people aged 5–17 years are overweight or obese, and most of them live in developing countries,
- 4.
More than 60% of children who are overweight before puberty will become overweight young adults.
- 5.
Globally, prevalence of childhood overweight and obesity increased from 4.25 in 1990 to 6.7% in 2010 with 8.5% in Africa and 4.9% in Asia.
- 6.
Data collected by WHO Europe show a prevalence of overweight/obesity ranging from 5% to more than 25%, with great variability among countries and a still growing incidence in more than half of them.
- 7.
In general, a greater proportion of overweight/obesity was found in boys than in girls, and more so in western and southern Europe as compared to Northern European countries.
- 8.
The prevalence rates are approximately double in Mediterranean nations than those of Northern European countries
- 9.
30% of North American children and adolescents are overweight or obese, with the highest rates among minorities and low-income families.
- 10.
Obesity rates of both genders are the highest in Mexican Americans (31%), followed by non-Hispanic blacks (20%), non-Hispanic whites (15%), and Asian Americans (11%).
1.1
Role of BMI charts
- 1.
In children and adolescents, obesity has not been as well defined as in adults, and therefore it is not a perfect measurement, but BMI is still considered to be a gold standard for diagnosis of overweight and obesity.
- 2.
Even by using a BMI percentile chart, different definitions of being overweight and obese have been described in different systems.
- 3.
Table 1.1 compares definitions for childhood and adolescent obesity as used by different organisations.
1.2
Aetiology
- 1.
Obesity is a multifactorial condition and involves both genetic and nongenetic factors but lack of physical activity and unhealthy eating habits are key determinants.
- 2.
Gungor has published a comprehensive list of possible aetiological factors of obesity in childhood and adolescence.
Genetic variations:
Rare genetic defects of leptin secretion, and more frequent genetic syndromes causing obesity, such as Prader-Willi syndrome.
Epigenetics:
In utero environments acting on DNA methylation which induce heritable changes in obesity expression ( Table 1.1 ).
| Definitions | CDC | WHO | IOTF | NCMP | SIGN |
|---|---|---|---|---|---|
| Overweight | 85th–95th | 85th–97th | 91st | >85th | 91st |
| Obesity | >95th | >97th | 99th | 95th | 98th |
| Severe obesity | >99.6th |
Endocrine disorders:
Hypothyroidism, growth hormone (GH) deficiency, and excess cortisol.
CNS diseases:
Congenital or acquired hypothalamic pathologies (Infiltrative diseases, tumours, or after treatment sequelae) that alter the hypothalamic regions in charge of hunger and satiety.
Intrauterine exposures:
Intrauterine exposures to gestational diabetes or extreme maternal adiposity (macrosomic and small for gestational age babies are at risk of childhood obesity).
BMI rebound:
An early postinfancy increase in weight before the age of 5.5 years is a risk factor for the development of obesity at later ages.
Diet:
- 1.
High energy intake food in infancy
- 2.
Excessive consumption of sweetened soft drinks in childhood
- 3.
Poor eating habits, such as inadequate intake of vegetables and fruits
- 4.
Skipping breakfast
- 5.
Eating out frequently
- 6.
Comfort eating
- 7.
Fast food with high calorie content
Low-energy expenditure:
- 1.
Poor physical activity
- 2.
Excessive time spent in sedentary activities (Television or other screen viewing activities)
Sleep pattern:
Shorter sleep duration in infancy and childhood
Infections:
- 1.
Microbial infections
- 2.
Composition of the gut flora
Iatrogenic:
- 1.
Cranial irradiation or surgery induced hypothalamic injury
- 2.
Psychotropic medication (Olanzapine and Risperidone)
- 3.
Chemotherapeutics
- 4.
Hormonal contraception—medroxy progesterone acetate
Ethnic origin:
More frequent in Hispanic and South Asian children and adolescents.
Country of birth:
Children from developing countries, who are born underweight, are at higher risk.
Residence in urban versus rural areas:
There is higher incidence of obese children in urban area globally.
Socioeconomic level:
Children of the lowest socioeconomic groups living in high income countries.
There is a complex interplay between an obesogenic environment and the individuals’ predisposition to adiposity.
It involves a number of appetite stimulating hormones, such as ghrelin, the anorexigenic peptide YY, the pancreatic polypeptide, glucagon, and others.
Onset of puberty:
- 1.
An adequate nutritional status is a prerequisite for the central onset of puberty
- 2.
At puberty there is an increase in BMI and subcutaneous adiposity.
- 3.
Fat acts as metabolic trigger for initiation of puberty.
- 4.
Obesity may lead to premature activation of the gonadotrophin-releasing hormone pulse generation.
- 5.
Obese children frequently show a tall stature for their age, associated with an accelerated epiphyseal growth plate maturation and early puberty in both sexes, but mainly in girls.
- 6.
Chronic malnutrition delays the onset of puberty.
Puberty is a developmental process during which a child becomes a young adult, characterised by the secretion of gonadal hormones and the development of secondary sexual characteristics that lead to sexual maturation and reproductive capability.
The age of onset of puberty ranges from 8 to 13 years old (average age of 10 years in White Americans and at 8.9 years in African-Americans).
Main physiological events include:
Although the physical sequelae of gonadarche and adrenarche occur concomitantly, a discordance of the two processes may also occur in normal development.
Adrenarche:
- 1.
Involves the increased production of androgens by the adrenal cortex.
- 2.
Typically precedes gonadarche.
- 3.
There is increased secretion of dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), and androstenedione.
- 4.
Leads to the appearance of sexual hair (pubarche).
- 5.
Absence of adrenarche does not prevent Gonadarche or the attainment of fertility.
Pubarche: is the appearance of pubic hair, primarily due to the effects of the androgens from the adrenal gland. It also refers to the appearance of axillary hair
Gonadarche:
- 1.
It comprises growth and maturation of the gonads with increased secretion of gonadal sex steroids by the pituitary hormones FSH and LH,
- 2.
Gonadarche leads to thelarche and menarche.
Thelarche: is the appearance of breast bud under the areola under the influence of oestrogen,
Menarche:
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Is the onset of the menstrual cycle, caused by the action of oestradiol on the endometrium and is usually not associated with ovulation;
- 2.
Menarche arrives on average at age 12.5 years, regardless of ethnicity, generally occurs 2–3 years after the onset of breast development;
- 3.
Following thelarche on average by 2.5 years (range 0.5–3 years);
- 4.
Menarche occurs in Tanner stage three or four;
- 5.
Peak height velocity occurs at Tanner stage 2–3.
Precocious puberty:
When signs of puberty develop before 8 years of age in girls.
Delayed puberty:
The absence of thelarche or menarche by age 13 and 16 years, respectively.
Pubic hair scale
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Stage 1: No hair
- 2.
Stage 2: Downy hair
- 3.
Stage 3: Scant terminal hair
- 4.
Stage 4: Terminal hair that fills the entire triangle overlying the pubic region
- 5.
Stage 5: Terminal hair that extends beyond the inguinal crease onto the thigh
Female breast development scale
- 1.
Stage 1: No glandular breast tissue palpable
- 2.
Stage 2: Breast bud palpable under areola (1st pubertal sign in females)
- 3.
Stage 3: Breast tissue palpable outside areola; no areolar development
- 4.
Stage 4: Areola elevated above contour of the breast, forming “double scoop” appearance
- 5.
Stage 5: Areolar mound recedes back into single breast contour with areolar hyperpigmentation, papillae development, and nipple protrusion
