Obesity is a multifactorial disorder which is characterized by an increased accumulation of body fat. The interaction of genetic, metabolic, socio-economic and environmental factors plays a major role in the development of obesity.
The body weight is substantially influenced by genetic factors. It is estimated that 60-80% of the body mass index is the result of genetic background.
There exist solely genetically determined forms of obesity, either Mendelian inherited syndromes or monogenic forms of obesity. Both cases present with early-onset severe obesity.
In most of the syndromes there are congenital developmental defects of organs and various degree of mental retardation. On the contrary, monogenic forms of obesity in most cases do not present with a broad phenotypic characterization.
Endocrine disorders associated with weight gain constitute only a small proportion of all cases of childhood obesity. They should be considered if an individual presents with a slow growth rate.
A rapid increase in body weight, the presence of hyperphagia and other signs of central nervous system involvement are found in hypothalamic obesity. Several long-term used medications lead to an increased fat mass accumulation either by stimulation of center of hunger or by promoting adipogenesis.
Additionally, prenatal factors, including mother's pre-gestational body weight and nutrition, intrauterine programming and epigenetic factors may impact offspring's body weight later in life. Inadequate eating practices, inefficient degree of regular physical activity and sedentarism are associated with increased body weight.
More than eighty risk factors of obesity have so far been identified. This review aims at presentation both, the widely known etiopathogenetic factors as well as those less revealed.
There is not only an interaction among risk factors themselves but also with the individual genetic predisposition. Researchers and clinicians should therefore search for risk factors possibly associated with body weight gain in each obese patient.