What causes varicose veins?

The venous return of blood from the lower limbs to the heart depends on a finely tuned venous system. Leg veins are equipped with unidirectional valves that prevent blood reflux and channel it upward against gravity. This process is supported by the calf muscle pump, whose contractions facilitate the propulsion of venous blood. Under normal conditions, most of this venous return is managed by the deep veins, while the superficial veins play a secondary role but are more vulnerable to dilation phenomena.

When the wall of a superficial vein loses its tone — often related to an inherent fragility of the connective tissue — its diameter gradually increases. The venous valves, unable to adapt to this distension, then fail to close properly. This results in blood reflux toward the distal segments of the leg, causing a stagnation of blood and a sustained increase in venous pressure. This vicious cycle maintains the dilation of the vein and leads to the gradual development of varicose veins visible and tortuous.

One of the main causes of varicose veins is an abnormality in the structure of the venous wall. The collagen and elastin are two essential structural proteins that ensure the elasticity and strength of the veins. In individuals with varicose veins, these proteins become disorganized or are quantitatively reduced. Moreover, venous smooth muscle cells lose their normal function, and certain enzymes, the matrix metalloproteinases (MMP-2, MMP-9), accelerate the degradation of venous tissue. As a result, the vein dilates, leading to increased venous pressure. This rise in pressure also triggers endothelial activation, with elevated inflammatory markers (TNF-α, IL-6) within the vein. Gradually, this inflammation further weakens the vein wall, alters the endothelium, and induces structural remodeling.

The combination of these interdependent processes – structural weakness, valvular failure, reflux, increased pressure, and inflammation – contributes to the formation and progression of varicose veins.

The development of varicose veins results from a complex interaction of genetic, hormonal, mechanical, and environmental factors that gradually impair venous function.

1. Aging.

Aging is one of the primary risk factors for varicose veins. As people grow older, the venous wall and valves naturally lose elasticity and strength, while the efficiency of the calf muscle pump declines. These changes make it harder for blood to return to the heart, raise venous pressure, and promote valvular dysfunction. Large population studies suggest that the prevalence of varicose veins nearly doubles after age 65, with some cohorts reporting rates exceeding 80% among individuals aged 70 to 80. These findings clearly show that aging significantly increases susceptibility to varicose veins.

2. Genetic factors.

Genetics plays a major role in the development of varicose veins. Studies estimate that 50% to 80% of individuals with the condition have a family history. When both parents are affected, approximately 90% of their children also develop varicose veins. If only one parent is affected, the risk is estimated at 25% for men and 62% for women.

Several genes involved in connective tissue integrity and venous valve development have been identified. The most studied gene is forkhead box protein C2 (FOXC2), essential for the formation and maintenance of venous valves. A mutation in this gene leads to valve failure in the superficial and deep veins of the lower extremities, promoting venous reflux and the early onset of varicose veins.

Other varicose vein–associated genes affect connective tissue integrity and endothelial function. Variants of thrombomodulin (TM) can disrupt endothelial signaling and weaken the vein wall, while the polymorphism MTHFR C677T has been associated with less efficient vascular remodeling and a higher prevalence of varicose veins in certain populations. These genetic modifications can disorganize collagen and elastin architecture, reduce vessel elasticity, or compromise valve function.

Overall, current data indicate that varicose veins result from a polygenic mechanism, in which genetic factors interact with lifestyle habits and hormonal factors to determine the overall risk.

3. Hormonal factors.

Female hormones, particularly estrogen and progesterone, play a significant role in venous dilation, making women more prone to developing varicose veins. Progesterone induces relaxation of the smooth muscle in the venous wall, decreasing its tone and facilitating vein dilation under pressure. Estrogen, for its part, influences the remodeling of collagen and elastin, potentially softening connective tissue and weakening the structural support of veins. This hormonal sensitivity explains why some women experience a worsening of symptoms around menstruation, a period during which hormonal fluctuations can transiently reduce venous tone.

During pregnancy, these effects are significantly amplified. It is estimated that approximately 40% of pregnant women develop varicose veins. Progesterone levels then increase five- to tenfold, leading to marked venous relaxation. Simultaneously, blood volume rises by 40 to 50%, and the expanding uterus exerts increased pressure on the pelvic veins and those of the lower limbs. All of these changes create conditions conducive to venous stasis and valvular dysfunction, contributing to the development of varicose veins during pregnancy.

4. Mechanical stress and lifestyle-related factors.

Repeated mechanical stresses and certain daily habits can gradually overload the venous system. The act of remaining in the same position for extended periods, particularly standing, exerts a continuous downward pressure on the leg veins. This increases hydrostatic pressure, slows venous return, and heightens the strain on the valves. Over time, this repeated stress can contribute to valve failure and the dilation of superficial veins.

Occupations that require prolonged standing—such as teaching, nursing, security, janitorial work, or retail—are strongly linked to an increased risk of varicose veins. Studies consistently show that individuals exposed to these conditions develop varicose veins more frequently than those with more varied physical activities. Some research reports prevalence rates of up to 65% in these occupations and even 73% among nursing aides.

Wearing very tight clothing and physical inactivity can also increase venous pressure. The garments compressing the waist, groin, or thighs can obstruct blood flow back to the heart, promoting blood stasis. Moreover, insufficient muscle activity reduces the effectiveness of the muscle pump, allowing blood to pool in the lower limbs and raising pressure in the superficial veins.

5. History of deep vein thrombosis.

A history of deep vein thrombosis is one of the most significant predictors of varicose vein development. A clot can cause lasting damage to the venous valves, preventing them from closing properly. The resulting venous reflux leads to a chronic rise in pressure within the superficial veins, gradually stretching and weakening their walls. Deep vein thrombosis thus induces lasting structural changes in the venous system, significantly increasing the risk of varicose veins.

6. Dietary factors.

The role of diet in the development of varicose veins remains uncertain. Some hypotheses suggest that a low-fiber diet may promote chronic constipation, increasing abdominal pressure and impairing venous return. Similarly, excessive salt intake may encourage fluid retention and leg swelling, heightening venous pressure. However, despite these plausible physiological mechanisms, scientific evidence designating diet as a major risk factor remains limited.

7. Alcohol consumption and tobacco use.

Alcohol consumption can indirectly influence venous health, notably through its effects on hydration and inflammation, but its direct role in the development of varicose veins appears limited. In contrast, smoking is known for damaging endothelial cells, increasing oxidative stress and impairing microcirculation. These effects weaken the venous wall and promote inflammation, accelerating venous remodeling. Some studies also suggest that tobacco reduces the availability of nitric oxide, which is essential for normal vessel relaxation, making veins less elastic and less adaptable to changes in blood volume. Despite these deleterious effects, the direct link between smoking and the onset of varicose veins remains debated.

8. Chronic heat exposure.

Frequent exposure to intense heat sources, such as hot baths or saunas, leads to a dilation of superficial veins, linked to thermoregulatory mechanisms. When this vasodilation is repeated or prolonged, it can exert mechanical stress on the venous wall and its valves. Over time, this may reduce venous tone and promote blood stasis, aggravating symptoms such as heaviness, swelling, or visible varicose veins, especially in predisposed individuals.

9. Some environmental factors.

Certain studies suggest that environmental factors, notably air pollution, could contribute to venous disorders. Pollutants such as fine particulate matter or nitrogen dioxide can induce oxidative stress and low-grade inflammation, which may impair the endothelium and weaken the venous wall. However, the data remain limited, and pollution is regarded as a potential factor rather than a definitively established cause.

10. Obesity.

Excess weight increases the pressure exerted on the veins of the lower limbs, complicating venous return and promoting valvular insufficiency. This increase in venous pressure can accelerate reflux and vein dilation. Epidemiological studies show that women with a high BMI have a 1.5- to 2-fold higher risk of developing varicose veins, whereas this association is less pronounced in men.

11. Diabetes.

Diabetes does not directly cause varicose veins, but it can worsen preexisting venous fragility. Chronic hyperglycemia promotes oxidative stress and inflammation, damages the endothelium, and reduces vascular elasticity. These changes slow blood flow and promote stasis, progressively increasing venous pressure. Diabetes is also associated with a slower healing and more frequent complications of chronic venous disease.

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