Anemia is a common blood disorder characterized by a decrease in hemoglobin concentration or insufficient red blood cell count, leading to impaired oxygen supply to tissues. The causes behind this condition are complex and varied, potentially related to genetic factors, environmental exposures, nutritional intake, and chronic diseases. Understanding the causes of anemia is crucial for prevention and treatment; the following will delve into its pathogenic mechanisms from different perspectives.
From a pathological standpoint, anemia can be classified into three main types: insufficient erythropoiesis, excessive destruction, or rapid loss of red blood cells. The causes behind each type are interwoven; for example, nutritional deficiencies may lead to abnormal erythropoiesis, while genetic defects may exacerbate cellular metabolic abnormalities. Environmental and behavioral factors are likely to amplify the effects of congenital defects, forming a complex pathogenic pattern. This article will systematically analyze the key causes and explore their interactions.
Genetic defects are key factors leading to congenital anemia. β-thalassemia is caused by impaired synthesis of the hemoglobin β chain, resulting in premature destruction of red blood cells. This genetic disorder has a prevalence of up to 5%-15% in specific populations along the Mediterranean and in Asia, highlighting the influence of genetic background. α-thalassemia can lead to abnormal red blood cell morphology, and in severe cases, can cause fetal edema or even miscarriage.
Another typical hereditary anemia is aplastic anemia, which arises from gene mutations in hematopoietic stem cells in the bone marrow, preventing the differentiation and maturation of red blood cell precursors. About 30% of cases are associated with genetic syndromes such as Fanconi anemia, where patients often have defects in the chromosome repair system. The X-linked inheritance pattern dominates in certain types, with males having a risk of disease several times higher than females due to the characteristics of their sex chromosomes.
Recent genomic studies have found specific single nucleotide polymorphisms (SNPs) associated with susceptibility to iron deficiency anemia. For example, mutations in the HFE gene can interfere with the regulation of iron ion metabolism, leading to abnormal iron absorption. This genetic predisposition may interact with environmental factors, forming a complex pathogenic network. Genetic counseling is significant for high-risk families, as genetic testing can predict the likelihood of disease.
Environmental exposures are important external factors that can trigger acquired anemia. Chronic infections such as tuberculosis or HIV can suppress bone marrow hematopoietic function, with viruses directly damaging hematopoietic stem cells or inducing excessive secretion of inflammatory cytokines (such as IL-6), leading to impaired erythropoiesis. Parasitic infections like hookworm disease can create a dual mechanism of anemia through chronic blood loss and nutritional absorption disorders.
Chemical exposure has direct toxic effects; benzene solvents and chemotherapy drugs can directly damage the hematopoietic microenvironment of the bone marrow. Organophosphates in pesticides can interfere with the synthesis pathway of heme, leading to the accumulation of hemoglobin precursors. Occupational groups with long-term exposure to these substances have anemia incidence rates 2-4 times higher than the general population.
Geographical environment also has a significant impact, with the prevalence of iron deficiency anemia being 20-30% higher in rural areas than in urban areas, primarily due to a monotonous diet and soil depletion of iron. Residents in high-altitude areas may develop secondary anemia due to prolonged exposure to low-oxygen environments, which can exacerbate the metabolic burden on red blood cells.
Dietary habits are key triggers for acquired anemia. Long-term vegetarians who do not supplement with vitamin B12 may develop megaloblastic anemia. Studies show that the incidence of this type of anemia is five times higher among vegetarians than omnivores. Phytates and oxalates in the diet (such as excessive intake of unfermented legumes) can interfere with iron absorption, increasing the risk of iron deficiency anemia.
Smoking exacerbates anemia through various pathways. Carbon monoxide in tobacco binds to hemoglobin to form carboxyhemoglobin, reducing the blood's oxygen-carrying capacity. Nicotine-induced arterial constriction reduces blood supply to the bone marrow, further inhibiting erythropoiesis. Smokers have a 37% higher rate of abnormal iron metabolism compared to non-smokers, indicating the interaction between behavioral factors and metabolic abnormalities.
Extreme manifestations of exercise habits can also induce anemia. Endurance athletes commonly experience exercise-induced anemia, caused by mechanical destruction of red blood cells due to repeated foot impact, along with increased iron ion excretion induced by exercise. Female athletes have a 2.3 times higher incidence of anemia than males due to the combined effects of menstrual blood loss and exercise-related depletion.
Chronic diseases often accompany anemia, with patients suffering from renal failure experiencing decreased erythropoietin secretion, leading to chronic disease-related anemia in about 50% of cases. Patients with inflammatory bowel disease may experience a complex impact of nutritional deficiencies and metabolic abnormalities due to intestinal absorption disorders and chronic inflammation. Anemia caused by these diseases typically has a slow progression and requires a multi-system assessment for detection.
Adverse drug effects are increasingly recognized, with non-steroidal anti-inflammatory drugs (NSAIDs) potentially inducing chronic gastrointestinal bleeding, leading to iron deficiency anemia. Certain antiepileptic drugs may interfere with folate metabolism, indirectly affecting DNA synthesis. Chemotherapy drugs, such as antifolates, directly inhibit the division of bone marrow precursor cells.
Age factors exhibit a bimodal distribution: infants aged 6 months to 2 years have an anemia incidence rate of 15%-20% due to rapid growth and insufficient iron reserves. In contrast, the anemia detection rate in individuals over 70 years old exceeds 30% due to declining digestive absorption functions and the accumulation of chronic diseases. This age-related correlation suggests differences in prevention strategies at various stages.
The network of causes of anemia involves the interplay of genetic factors, environmental stimuli, behavioral patterns, and underlying diseases. From congenital genetic defects to acquired nutritional imbalances, from occupational exposures to chronic disease complications, these factors often exacerbate the severity of anemia through additive effects. Modern medicine has developed treatment strategies targeting different mechanisms, but prevention still requires a multifaceted approach, including improving dietary structures, avoiding harmful exposures, and early genetic screening. Understanding these causal networks aids in formulating personalized health management plans to fundamentally reduce the long-term impact of anemia on health.
Excessive intake of tea, coffee, or milk may affect iron absorption, as the tannins and calcium in these beverages can interfere with non-heme iron absorption. It is recommended to avoid consuming these drinks simultaneously with iron-rich foods and to pair them with vitamin C (such as citrus fruits) to enhance iron absorption.
Why do some people not see improvement in anemia symptoms after taking iron supplements?The causes of anemia are diverse; if iron supplementation is ineffective, it may involve other types of anemia, such as folate or B12 deficiency, anemia related to chronic diseases, or absorption disorders (such as after gastric resection). It is advisable to track changes in hemoglobin and further examine indicators such as ferritin and hemolysis indices to determine the cause.
What side effects should be noted when receiving erythropoiesis-stimulating agent (ESA) treatment?ESA may lead to elevated blood pressure, increased risk of thrombosis, or abnormal iron metabolism. During treatment, regular monitoring of hemoglobin levels, blood pressure, and ferritin levels is necessary to avoid excessive elevation of hemoglobin and to supplement iron to reduce the risk of cardiovascular events.
Why are patients with chronic diseases prone to anemia?Chronic diseases (such as renal failure and rheumatoid arthritis) may suppress bone marrow hematopoietic function and interfere with iron metabolism, leading to elevated ferritin levels but ineffective hemoglobin production. This type of anemia is usually mild and difficult to fully correct, requiring treatment targeting the underlying disease.
What common medications may induce drug-induced anemia?Long-term use of non-steroidal anti-inflammatory drugs may lead to gastrointestinal bleeding and result in iron deficiency anemia; certain antiepileptic or antitumor drugs may inhibit bone marrow hematopoietic function. Regular blood tests should be conducted during medication, especially when gastrointestinal symptoms or unexplained fatigue are present.
%201.svg)
Copyright © 2025 MedFrontiers. All Rights Reserved.
