Criteria of diagnosing childhood obesity

It is strongly believed that the diagnosis of obesity is not a difficult task. This article will tell you about the chosen criteria of diagnosing, which is more convenient for an adequate therapy for the disease. In addition, we will answer the question of what is childhood obesity of the first, second, and third degree. Also, we will tell about the role of leptin in the pathology inheritance.


  1. Classification
  2. Clinical symptoms of individual forms
  3. Sequela


Obesity can be noted already at the first examination of the child. But children with advanced forms of pathology are still admitted to clinics. The initial degrees of obesity do not bother parents and the child himself up to a certain time. This fact is sad.

Better than others, the problem was emphasized by French pediatricians, who classified obesity as follows:

  • 1st degree — causes a feeling of tenderness in infancy and envy in parents of young children;
  • 2nd degree — surprise;
  • 3rd degree — makes people laughter;
  • 4th degree — causes a feeling of regret.

In general, there are a number of gradations of childhood obesity. Practitioners get used to classify childhood obesity according to the scheme proposed ten years ago by V. A. Peterkova and O. V. Vasyukova. This is the division of obesity by triggers.

Etiologically can be distinguished:

  • idiopathic or simple weight gain;
  • neuroendocrine;
  • hypothalamic;
  • as a result of a medical error;
  • syndromal and genetic.
  • According to the presence of sequela, obesity is also distinguished as:
  • a result of an imbalance in carbohydrate metabolism;
  • a consequence of non-alcoholic fatty liver disease;
  • a result of dyslipidemia;
  • a consequence of hypertension;
  • a result of type 2 diabetes.

According to the degree of obesity or according to BMI (body mass index):

  • 1st degree — BMI up to 2.5;
  • 2nd degree — BMI up to 3.0;
  • 3rd degree — BMI up to 4.0;
  • 4th degree — BMI > 4 means morbid or extreme degree of obesity.

Normally, BMI in boys and girls ranges from 15 to 85 percentiles. BMI is up to 95 means overweight, everything above is obesity.

In terms of genetics, we can distinguish:

  • monogenic obesity;
  • genetic syndromes associated with obesity;
  • simple obesity, which occurs in 85-90% of cases with a polygenic type of inheritance. More than 80% of the inheritance of excess weight by children is expected in families with obese parents. Only 15% of the children are overweight with healthy parents.

According to the nature of the course, obesity can be:

  • rapidly progressive: +8 -10 kg per year;
  • slowly progressive: +5-6 kg per year;
  • stable: the same increase in body weight for a long time;
  • regressive.

Excess fat can be:

  • evenly accumulated, which is inherent in alimentary obesity;
  • variously accumulated: gynoid obesity — fat is deposited mainly on the buttocks, lower abdomen, and android obesity — fat is on the shoulders, chest and abdomen;
  • selectively accumulated, which is typical for endocrine pathology.

The pathology trigger is a factor associated with central dysregulation of the energy balance, an increase in the number of lipocytes, and their metabolic activity in any obesity type. The number of fat cells is correlated with heredity, and the size of these cells is a nutritional factor. There are many peptides and receptors in the center and at the periphery that increase or decrease appetite. Their destruction provokes perverted eating behavior.

A simple form of obesity is diagnosed at the age of up to a year. More often this is obesity of 1-2 degrees, with a uniform distribution of the subcutaneous fat layer and slow progression. In summer, everyone loses weight, but in puberty, as a rule, only boys lose weight, and girls, on the contrary, gain weight. At the same time, everyone’s state of health remains satisfactory.

Hypothalamic obesity begins during puberty most often. Its hallmark is the reversibility of violations. Many triggers play a role in the development of this form of obesity: chronic infections, intoxication, craniocerebral, and mental trauma, stress, conflicts in the family anD children’s team, gluttony, and hence the amount of leptin in the blood. But the basis is changes in puberty, when the hypothalamus grows and the hypothalamic-pituitary-adrenal system is activated. As a result of its imbalance, there is an excess production of tropic hormones (ACTH, TSH, gonadotropin hormone, somatotropic hormone) and complaints of headaches, obesity, fatigue, pain in the heart, thirst, insomnia, and a feeling of constant hunger. Leptin imbalance plays the first role here.

Clinical symptoms of individual forms

Many babies have round cheeks and cute fullness. But during the period of growing up, they suddenly gain weight sharply and begin to look older than their years. This is due to the rapid formation of secondary sexual characteristics and a tendency to tallness. At the same time, the distribution of fat is uniform, sometimes it is slightly more on the abdomen, pubis, chest, on the back of the neck, and buttocks. Cushingoid obesity is less common, and in young men it is feminine (false gynecomastia). There is little facial hair, tender skin, sexual development is slightly delayed. Muscles are normal. Secondary sexual characteristics in girls are formed on time and very quickly: the face is round, full, ruddy. Skin with cyanosis, there are striaes.

Signs of vegetative-vascular dystonia especially interfere with well-doing: labile pressure, subfebrile condition, muffled heart sounds, bradycardia. In addition, psychopathic disorders are also may be happened: fear, anxiety, insomnia, depression, asthenia. Alimentary obesity is rare. Latrogenic obesity is a consequence of incorrect tactics of the doctor and errors in therapy.

Separately, there is monogenic obesity, in which the dominant is a phenotypic trait. Mutation of the gene that controls leptin and its receptors leads to the development of obesity. These genes code for the hypothalamus and its appetite-regulating hormones. Congenital proopiomelanocortin deficiency is characterized by rapidly progressive obesity and ACTH deficiency in the blood with the development of adrenal insufficiency. Newborns with a similar diagnosis are born absolutely normal and on time. But by 4 months they develop paratrophy with symptoms of hypoglycemia.

Some babies are red-haired with pale skin. A combination of extra pounds, insulin resistance, high linear growth is typical for this type of obesity. Congenital leptin deficiency is a rare syndrome. Mutated leptin cannot affect the hypothalamus, but today there is a way to replace it with a recombinant hormone.

The syndromes that accompany obesity are quite common. They include pathologies with numerous malformations: Ahlstrom, Lawrence-Moon-Biedl, Prader-Willi syndrome. Epigenetics is a new direction in medicine, it deals with the correction of gene mutations. Epigenetic mechanisms do not change the structure of DNA, but they work with RNA, or other markers of obesity. All these interventions are strictly individual. In other words, the external factors of obesity are able to control the activity of the child’s genes without damaging the genetic code.


Patients are concerned about weakness, fatigue, sweating, and thirst at the beginning of an obesity. They also can feel fluctuations in blood pressure. But it is precisely at the beginning of the disease that it is most effectively treated. Sequela can be developed with the progression of obesity and the maturation of children. This is an imbalance of carbohydrate metabolism, fatty infiltration of the liver, secondary damage to the hypothalamus, hypertension, sexual infantilism, especially in boys, or, on the contrary, ultra-fast puberty. Girls are at risk of hyperandrogenemia. Concomitant pathologies are: flat foot, degenerative changes in the musculoskeletal system, Blount’s disease. Striae, hyperpigmentation, folliculitis are visualized from the dermis.

Insulin activates genes that control obesity with prolonged high energy potential. They increase the activity of the iconic catalysts of the biochemical processes involved in the accumulation of fat reserves. These genes lead to an increase in the size of fat cells and their number. A long-term high concentration of fatty acids in the bloodstream changes the susceptibility of cells to pancreatic hormones, and disrupts the algorithm of insulin synthesis by pancreatic cells. The severe course of obesity provokes psychological or even mental discomfort in young patients.

Recently, it has become fashionable to believe that obesity is accompanied by metabolic syndrome. It is based initially on insulin resistance and the concomitant high concentration of the hormone in the blood of children with excess visceral fat. This provokes a violation of all metabolic processes, high hypertension. The common, comprehensive signs of the metabolic syndrome include type 2 diabetes mellitus, perverse tolerance to glucose, insulin, high blood sugar. Concomitant sequela include hypertension, abdominal-visceral obesity, atherogenic dyslipidemia, microalbuminuria. There are additional criteria: the level of leptin, other lipoproteins, fibrinolytic factors, and blood clotting.

In childhood, the criteria for diagnosing the metabolic syndrome are not clear. In adolescence, they are guided by the corrected diagnostic signs of adults. However, there are still disputes about the validity of the separation of the metabolic syndrome into an independent nosology affiliated with leptin. Metabolic manifestations are correlated with the phases of the course of simple and hereditary obesity. They are also can be a part of their sequelas.


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