on July 11, 2026
The classic paradigm of global public health has historically associated the concept of malnutrition with acute and chronic food deprivation, placing this phenomenon exclusively within the scope of developing countries and contexts of extreme poverty. However, modern pathophysiology and clinical epidemiology demand a radical revision of this conceptual model. Malnutrition does not only mean undernourishment or a quantitative lack of food, but more properly translates into a state of cellular and systemic imbalance between the intake of nutrients and energy and the biological needs required to ensure the growth, maintenance, and specific functions of the organism. This alteration manifests through two opposing but closely connected clinical polarities: undernutrition on one hand and qualitatively unbalanced overfeeding on the other, which results in the global epidemic of overweight and obesity.
The data published in the UNICEF report "Let's Weigh In: UNICEF's Commitment to Combat Malnutrition" outline a global nutritional transition with alarming contours, highlighting how childhood obesity is taking on the characteristics of a true endemic disease with global spread. It is estimated that approximately 38.3 million children and adolescents worldwide are overweight, exposing them to a significantly high relative risk of developing permanent obesity in adulthood. This trend is confirmed by World Health Organization monitoring, which attests that the prevalence of obesity has almost tripled over the last forty years. A data point of particular epidemiological relevance is the delocalization of the phenomenon: while in the past overweight and obesity were considered almost exclusively the lot of high-income nations, today an exponential growth is observed in low- and middle-income countries, especially in hotspots of rapid and uncontrolled urbanization. In Africa, the prevalence of overweight children under 5 years of age has increased by 50% in the last two decades, while more than half of overweight or obese pediatric patients reside permanently on the Asian continent. On a global scale, the combined prevalence between 5 and 19 years has gone from 4% in 1975 to 18% in 2016, without showing statistically significant variations between the sexes.
Clinical evidence demonstrates that the complications associated with excess weight and the accumulation of visceral adipose tissue exert a higher incidence on overall mortality compared to underweight conditions. Adipose tissue should not be considered a mere inert storage of triglycerides, but rather a highly active endocrine and immunological organ. The hypertrophy and hyperplasia of adipocytes determine an alteration of the secretory profile, characterized by a massive release of pro-inflammatory cytokines — such as tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and leptin — and by a simultaneous downregulation of adiponectin, a molecule with insulin-sensitizing and vasoprotective action. This state of low-grade chronic inflammation constitutes the primary pathogenetic substrate for the development of peripheral insulin resistance, which progressively evolves toward type 2 diabetes mellitus due to glucotoxicity and the functional exhaustion of pancreatic beta cells.
In parallel, the induction of atherogenic dyslipidemia — characterized by the elevation of low-density lipoproteins (LDL), the increase in blood triglycerides and the reduction of high-density lipoproteins (HDL) — accelerates the processes of endothelial atherosclerosis, exponentially increasing the incidence of ischemic heart disease, stroke and systemic arterial hypertension. No less relevant is the biological link between obesity, unbalanced dietary styles and oncogenesis. Chronic exposure to high levels of insulin and insulin-like growth factors (IGF-1), together with the hyperactivation of mitogenic pathways and the local action of estrogens resulting from the peripheral conversion of androgens in adipose tissue, promotes the stability and progression of several malignant neoplasms, particularly affecting the gastrointestinal tract, breast, and endometrium. The systemic consumption of red meats, animal-derived saturated fats, cheeses, and dairy products in quantities exceeding physiological needs directly correlates with the increase in such diseases, due to the accumulation of N-nitroso compounds and the pro-inflammatory alteration of the intestinal microbiota.
The roots of this metabolic drift lie in the profound transformations of contemporary social organization models, which have imposed frantic existential rhythms and a drastic reduction in the time dedicated to the preparation and consumption of meals. The culture of fast food and the systematic use of ultra-processed foods rich in simple sugars, trans fatty acids, and sodium chloride determine an alteration of the central mechanisms of hunger and satiety regulation at the hypothalamic level. The high caloric density of these foods, associated with a low satiety index, induces an unconscious excess energy intake. In pediatric and adolescent subjects, the constant availability of "junk food" and the establishment of fragmented eating habits overturn normal metabolic circadian rhythms, inducing a perennial insulinemic stimulation that promotes de novo lipogenesis and inhibits lipolysis, chronicizing the state of overweight from the early stages of ontogenetic development.
In the face of this health and metabolic emergency, the analysis of reference nutritional models takes on a crucial therapeutic role. The classic Mediterranean diet, validated by over six decades of epidemiological research, has changed profoundly compared to its original configuration. The historical model was based on a clear prevalence of foods of plant origin, such as legumes, whole grains, fresh fruit, and seasonal vegetables, with a sporadic and limited consumption of animal proteins and an elective use of extra virgin olive oil as the main lipid source. The current food industrialization has instead determined a saturation of the market with accessible and ready-to-use products of animal origin, overturning the biochemical balance of the contemporary Mediterranean diet. A rational return to the origins of this model, focused on restricting the animal-derived portions and increasing the plant-based fraction, not only proves optimal for the modulation of anthropometric and metabolic parameters, but also guarantees a significantly reduced environmental impact, reducing the carbon footprint and the consumption of the planet's water resources.
In this context of nutritional transition, vegetarian and vegan diets should not be interpreted as trends lacking clinical basis, but rather as dietary regimens with solid scientific validation. The Italian Society of Human Nutrition (SINU) has extensively documented that plant-based diets, when accurately and balanced planned, prove nutritionally adequate and capable of providing significant benefits in the prevention and treatment of chronic degenerative diseases. Such regimens are completely safe in every stage of the life cycle, including childhood, adolescence, old age, pregnancy, and breastfeeding. The body's protein requirement is defined by the need to recruit essential amino acids, which can be entirely derived from plant matrices through the synergistic combination of cereals and legumes. To compensate for the lower digestibility and the different amino acid profile of some plant proteins, the guidelines suggest a cautious 10% increase in total protein intake compared to omnivorous subjects, maintaining the target intake within the physiological range of approximately 0.9 grams of protein per kilogram of ideal body weight per day.
The only critical element that requires mandatory and constant exogenous supplementation in both the vegan and vegetarian regimen is vitamin B12 (cyanocobalamin), due to the absence of biologically active and bioavailable sources in the plant kingdom. The correct structuring of these dietary plans by nutrition professionals allows to avoid micronutrient deficiencies and to exclude the adoption of unbalanced high-protein diets, often promoted in non-medical contexts for purposes of rapid weight loss or muscle hypertrophy. Protein excesses, in fact, since they cannot be stored by the body in the form of amino acids, require a process of hepatic deamination with a consequent production of urea and a drastic increase in renal glomerular filtration. This chronic functional overload on the renal and hepatic excretory system can compromise organ functionality in the long term.
The integrated management of malnutrition in its two manifestations therefore requires structured interventions in dietary and health education starting from school age. The early acquisition of nutritional awareness, based on the predominant consumption of whole plant-based foods, the drastic limitation of ultra-processed foods, and the respect for metabolic physiology, represents the only preventive therapeutic strategy capable of halting the progression of childhood obesity, eradicating at the root the pathogenetic bases of adult cardiovascular and metabolic diseases.
Bibliographic references and clinical studies
· UNICEF. (2018). Let's Weigh In: UNICEF's Commitment to Combat Malnutrition. Global report on the pediatric nutritional transition.
· World Health Organization (WHO). (2016). Global report on obesity and overweight trends (1975-2016). Geneva: WHO.
· Italian Society of Human Nutrition (SINU). (2017). Guidelines for a Healthy Italian Diet and Position Paper on vegetarian diets.
· Hotamisligil, G. S. (2006). Inflammation and metabolic disorders. Nature, 444(7121), 860-867. Study on the molecular mechanisms of low-grade inflammation induced by adipocyte hypertrophy.
· Willett, W., et al. (2019). Food in the Anthropocene: the EAT-Lancet Commission on healthy diets from sustainable food systems. The Lancet, 393(10170), 447-492. Clinical and ecological validation of plant-based dietary regimens.
· Velasquez, M. T., & Bhathena, S. J. (2007). Role of dietary soy protein in obesity. International Journal of Medical Sciences, 4(2), 72-82. Analysis of the impact of plant proteins on the lipid and metabolic profile.
