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Vitamin Deficiency – Causes, Symptoms and Consequences of Avitaminosis

Wojciech Wiśniewski

Wojciech Wiśniewski

2026-03-23
4 min. read
Vitamin Deficiency – Causes, Symptoms and Consequences of Avitaminosis
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Certainly, everyone knows that vitamins should be ingested, though not everyone is aware of precisely what they are. The first vitamin was discovered by a distinguished Polish researcher who unknowingly contributed to this discovery. He observed that dogs fed with plant-based protein were losing weight and weakening, and when meat was added to their diet, these animals regained strength. Indisputably, this was one of the stimuli that prompted Kazimierz Funk to carry out further research. In 1910, he started investigations that led to the official discovery of vitamin B1 in 1913. Upon examining beri-beri patients, he observed that patients consuming polished rice were more prone to the disease than patients consuming rice with a lower degree of processing.

Avitaminosis – complete absence of essential vitamins in the human body

Vitamins constitute an indispensable component of daily nutrition, a fact reflected in their very nomenclature—the term "vita," coined by a Polish scientist, derives from the Latin word for "life." From a chemical standpoint, they represent a diverse array of bioactive compounds whose primary classification hinges on solubility: water-soluble (hydrophilic) or fat-soluble (lipophilic). While nearly all food products contain trace amounts of at least one vitamin, meeting daily requirements necessitates a meticulously balanced diet. Disruptions in vitamin equilibrium manifest as hypovitaminosis (partial deficiency) or avitaminosis (complete absence), with the latter posing far more severe health risks and directly endangering essential physiological functions.

Vitamin deficiency: origins and developmental mechanisms of avitaminosis

The primary etiological factor underlying a specific vitamin deficiency within the human body is its insufficient dietary intake or complete absence from consumed foods. A notable exception in this context is fat-soluble vitamin D, whose natural occurrence in food sources is minimal. However, the human organism possesses the intrinsic capacity to synthesize this compound endogenously through exposure to ultraviolet radiation—thus, a chronically inadequate diet combined with persistent avoidance of sunlight may precipitate a gradual depletion of vitamin D reserves and consequent severe health complications. Certain vitamins may also be generated internally from dietary precursors; for instance, retinol (vitamin A) is metabolically derived from the provitamin beta-carotene. Another critical yet frequently overlooked contributor is impaired gastrointestinal absorption, which can affect a broad spectrum of vitamins, with cobalamin (vitamin B12) being particularly vulnerable—its deficient uptake, when compounded by a diet devoid of animal-derived products, poses a substantial threat to physiological equilibrium. Biotin (vitamin H) is distinctive in that it is produced by intestinal microbiota, though this biosynthetic process may likewise become dysfunctional. The causes of malabsorption are multifaceted, ranging from intestinal pathologies to the presence of dietary inhibitors that may impede nutrient assimilation.

Severe vitamin deficiency: Recognizing avitaminosis and its associated pathological conditions

Complete avitaminosis—the absolute absence of essential vitamins in the body—rarely presents abruptly, as most symptoms emerge during the milder stage of hypovitaminosis. This condition arises from chronic insufficient intake or malabsorption, ultimately leading to severe pathological states. Consequently, it is more informative to examine the specific diseases correlated with deficiencies of individual vitamins. Among the initial indicators of profound deficiencies in fat-soluble vitamins (A, D, E, K) are: impaired vision and nyctalopia (vitamin A), bone demineralization and rickets (vitamin D), reproductive dysfunction and infertility (vitamin E), and coagulopathy with heightened bleeding tendency (vitamin K). Meanwhile, deficiencies in water-soluble vitamins—including thiamine (B1), riboflavin (B2), niacin (PP), pantothenic acid, pyridoxine (B6), biotin (H), folic acid, cobalamin (B12), and ascorbic acid (C)—manifest clinically as: peripheral neuropathy and cognitive decline, glossitis and angular cheilitis, inflammatory dermatoses and seborrheic dermatitis, paresthesia and numbness, chronic fatigue and muscle weakness, hyperseborrhea, megaloblastic or hemolytic anemia, neural fiber degeneration, and—in cases of extreme vitamin C deficiency—scurvy characterized by gingival hemorrhage and tooth loss.

Apavitaminosis: Severe repercussions of profound vitamin depletion and high-risk demographic groups

Apavitaminosis represents one of the most severe metabolic disorders, characterized by the complete depletion of vitamin reserves within the human body, often leading to critical conditions that are challenging to reverse without immediate medical intervention. Profound deficiencies in individual vitamins can trigger disturbances of varying severity—ranging from mild functional impairments to irreversible organ damage and, in the most extreme cases, life-threatening complications. The demographic groups at heightened risk of severe consequences include pregnant women, infants, children, and adolescents undergoing rapid growth phases, elderly individuals with compromised immune systems, patients suffering from chronic debilitating illnesses, as well as adults exposed to chronic physical or psychological stress, such as those subjected to excessive workloads. Vitamins serve as indispensable cofactors in myriad biochemical processes, and their absence disrupts the proper functioning of the nervous, immune, circulatory, and metabolic systems. While a balanced and diverse diet forms the cornerstone of prevention, it does not always ensure adequate intake—additional risk factors for apavitaminosis include poor lifestyle habits, comorbid conditions impairing absorption, drug interactions, genetic predispositions, and environmental influences that disrupt the biological activity of vitamin compounds.
Wojciech Wiśniewski

Wojciech Wiśniewski

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