What are the causes of varicose veins?

The return of blood from the lower limbs to the heart relies on a finely regulated venous system. The leg veins are fitted with unidirectional valves that prevent backflow and direct the flow upwards, against gravity. This mechanism is supported by the calf muscle pump, whose contractions facilitate the propulsion of venous blood. Under normal conditions, the majority of venous return is provided by the deep veins, whereas the superficial veins play a secondary role but are more vulnerable to dilatation phenomena.

When the wall of a superficial vein loses its tone — often linked to an inherent fragility of the connective tissue — its diameter gradually increases. The venous valves, unable to adapt to this distension, then no longer close properly. This leads to a reflux of blood into the distal segments of the leg, causing a stagnation of blood and a sustained elevation of venous pressure. This vicious cycle perpetuates the dilation of the vein and leads to the gradual appearance of varicose veins that are 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 provide the veins with elasticity and strength. In individuals with varicose veins, these proteins become disorganised or are quantitatively reduced. Moreover, venous smooth muscle cells lose their normal function and certain enzymes, known as matrix metalloproteinases (MMP-2, MMP-9), accelerate the degradation of venous tissue. As a result, the vein dilates, leading to an increase in 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 venous wall, alters the endothelium and induces structural remodelling.

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 arises from a complex interplay of genetic, hormonal, mechanical and environmental factors that progressively impair venous function.

1. Ageing.

Ageing is one of the main risk factors for varicose veins. With age, the venous wall and valves naturally lose elasticity and strength, while the effectiveness of the calf muscle pump diminishes. These changes make venous return to the heart more difficult, increase venous pressure and promote valvular dysfunction. Large population-based 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 data clearly indicate that ageing 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 affected individuals have a family history. When both parents are affected, about 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 the integrity of connective tissue and the development of venous valves have been identified. The most extensively studied gene is forkhead box protein C2 (FOXC2), which is 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 limbs, promoting venous reflux and the early onset of varicose veins.

Other genes associated with varicose veins influence connective tissue integrity and endothelial function. Variants of thrombomodulin (TM) can disrupt endothelial signalling and weaken the venous wall, while the polymorphism MTHFR C677T has been associated with less effective vascular remodelling and a higher prevalence of varicose veins in certain populations. These genetic alterations can disorganise the 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 oestrogen and progesterone, play a key role in venous dilatation, making women more susceptible to varicose veins. Progesterone induces relaxation of the venous smooth muscle, reducing its tone and facilitating vein enlargement under pressure. Oestrogen, on the other hand, modulates collagen and elastin remodelling, potentially softening connective tissue and weakening the veins’ structural support. This hormonal sensitivity explains why some women experience an increase in symptoms around menstruation, a time when hormonal fluctuations can temporarily reduce venous tone.

During pregnancy, these effects are greatly amplified. It is estimated that approximately 40% of pregnant women develop varicose veins. Progesterone levels then increase five- to tenfold, causing marked venous relaxation. Meanwhile, blood volume rises by 40 to 50%, and the expanding uterus exerts increased pressure on the pelvic veins and those of the lower limbs. Together, these changes create conditions favourable 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 everyday habits can gradually overload the venous system. The fact of remaining in the same position for extended periods, particularly when standing, exerts a continuous downward pressure on the leg veins. This increases hydrostatic pressure, slows venous return and heightens stress on the valves. Over time, this repeated strain can contribute to valve failure and the dilation of superficial veins.

Occupations that involve prolonged standing, such as teaching, nursing, security work, cleaning or retail, are strongly associated with an increased risk of varicose veins. Studies consistently show that individuals exposed to these demands develop varicose veins more frequently than those whose activities are more varied. Some research reports rates of up to 65% in these professions, rising to 73% among care assistants.

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

5. A history of deep vein thrombosis.

A history of deep vein thrombosis is one of the most important predictors of varicose vein development. A clot can cause permanent damage to venous valves, preventing them from closing properly. The resulting blood reflux leads to a chronic rise in pressure within the superficial veins, gradually stretching and weakening their walls. Deep vein thrombosis thus induces enduring structural alterations in the venous system, markedly 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-fibre diet may encourage chronic constipation, thereby increasing abdominal pressure and complicating venous return. Likewise, excessive salt intake can lead to fluid retention and leg swelling, heightening venous pressure. Nevertheless, despite these plausible physiological mechanisms, the scientific evidence recognising diet as a major risk factor remains limited.

7. Alcohol consumption and tobacco smoking.

Alcohol consumption may indirectly influence venous health, notably through its effects on hydration and inflammation, but its direct role in the development of varicose veins appears limited. Smoking, by contrast, is known to damage endothelial cells, increase oxidative stress and impair microcirculation. These effects compromise the venous wall and promote inflammation, accelerating venous remodelling. Some studies also suggest that tobacco reduces the availability of nitric oxide, which is essential for normal vessel relaxation, rendering veins less elastic and less capable of adapting to fluctuations in blood volume. Despite these deleterious effects, the direct link between smoking and the onset of varicose veins remains debated.

8. Chronic exposure to heat.

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

9. Certain environmental factors.

Some 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 evidence remains limited, and pollution is considered a possible factor rather than a definitively established cause.

10. Obesity.

Excess body weight increases the pressure exerted on the veins of the lower limbs, complicating venous return and promoting valvular failure. This increase in venous pressure can accelerate reflux and venous dilation. Epidemiological studies indicate that women with a high BMI have a 1.5 to 2 times greater 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 exacerbate pre-existing venous fragility. Chronic hyperglycaemia promotes oxidative stress and inflammation, damages the endothelium and reduces vascular elasticity. These changes slow blood flow and encourage stasis, gradually increasing venous pressure. Diabetes is also associated with slower healing and more frequent complications of chronic venous disease.

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