Classification and Degrees of Obesity
The assessment of overweight relies on several criteria. The primary tool is the body mass index (BMI), which is calculated as body weight in kilograms divided by height in meters squared.
There are four main classification criteria:
- By degree of weight increase (BMI): Normal values range from 18.5 to 24.9. Class I obesity is recorded at 25–29.9 (overweight). Class II obesity spans 30–39.9 (moderate obesity). Class III obesity is diagnosed at a BMI of 40 and above (morbid obesity).
- By adipose tissue distribution: A distinction is made between generalized and localized obesity. The latter is divided into the male type (android, with fat accumulation on the abdomen, chest, and back) and the female type (gynoid, with excess fat on the thighs and buttocks).
- By tissue morphology: The process can occur through an increase in cell size (hypertrophic), an increase in cell number (hyperplastic), or a combination of both paths (mixed).
- By etiology: Primary (synonym: hypothalamic) and secondary (symptomatic) obesity are distinguished.
Cellular Mechanisms and Body Weight Assessment
The morphological remodeling of adipose tissue determines the clinical course of the disease and the selection of therapeutic tactics.
- Hypertrophic obesity develops due to an increase in the mass and volume of pre-existing adipocytes.
- Hyperplastic obesity is associated with the predominance of cell division and an increase in their total number. This variant shows high resistance to conservative treatment methods and requires surgical intervention in severe cases.
- Hyperplastic-hypertrophic (mixed) obesity combines both mechanisms and is often observed in childhood.
To assess ideal body weight alongside BMI, the classical Broca index is used, which is calculated as height in centimeters minus 100.
Pathogenesis: Hypothalamic Variant and the Lipostat
The pathology is based on three main mechanisms: neurogenic, endocrine, and metabolic. The hypothalamic variant plays a key role in the neurogenic genesis, associated with damage to neurons in specific hypothalamic nuclei (ventromedial, paraventricular, and ventrolateral ventromedial).
A critical link in the pathogenesis is the dysfunction of the "Leptin–Neuropeptide Y" (lipostat) feedback loop, which sets the intensity of energy metabolism:
- Under normal conditions, adipose tissue produces the hormone leptin, which inhibits the synthesis of neuropeptide Y (NPY) in the ventrolateral ventromedial hypothalamic nucleus, thereby reducing the sensation of hunger.
- In pathology, leptin resistance or a gene mutation develops, causing NPY synthesis to rise, leading to constant hunger, increased appetite, and suppression of the body's energy expenditure.
Pathogenetic Significance and Complications
The disease is chronic with periods of exacerbations, leading to early disability and increased overall mortality, affecting children and adolescents as well. The resulting disorders are divided into several groups:
- Somatic and autonomic: Vegetovascular dystonia, gastrointestinal motility disorders (constipation, predisposition to irritable bowel syndrome), and respiratory failure caused by high diaphragmatic standing.
- Metabolic disorders: Insulin resistance, arterial hypertension, and type 2 diabetes mellitus.
- Impact on the central nervous system and development: In children, higher nervous activity (HNA) processes suffer due to restricted motor activity.
- Sexual development in children: Girls show premature appearance of secondary sexual characteristics and menstrual irregularities; boys may exhibit either accelerated or delayed puberty.