Varicose veins develop when the one-way valves inside your leg veins stop working properly, allowing blood to pool and stretch the vessel walls. The underlying causes range from genetics and hormonal changes to everyday habits like prolonged standing. About 1 in 5 adults will develop them, and women are roughly four times more likely to be affected than men.
How Vein Valves Fail
Your leg veins carry blood upward against gravity, back toward the heart. Tiny flap-like valves inside these veins open to let blood through, then snap shut to prevent it from sliding back down. When those valves weaken or are damaged, blood flows backward (called reflux), and the resulting pressure causes the vein to bulge, twist, and become visible under the skin.
Valve failure can start in a few different ways. Sometimes the vein wall itself is structurally weak from the beginning, which stretches the valve leaflets apart so they no longer seal tightly. Other times, inflammation from a blood clot or injury directly damages the valve. There’s also a cascade effect: when valves in the deep veins or the “perforator” veins that connect deep and surface systems fail, high-pressure blood gets forced outward into the superficial veins near the skin. The muscle pump in your calf, which normally helps push blood upward, instead drives blood backward through these broken connections, dilating surface veins and wrecking their valves too.
Over time, this elevated pressure doesn’t just affect the large veins you can see. It filters down into the tiniest blood vessels, causing capillary beds to elongate, dilate, and become tortuous. Basement membranes thicken, gaps open between cells lining the vessels, and fluid leaks into surrounding tissue. That’s what produces the swelling, skin changes, and heaviness that often accompany visible varicose veins.
Family History Is the Strongest Predictor
Genetics plays an outsized role. A French study of 134 families found that when both parents had varicose veins, their children faced a 90% chance of developing them. A UK case-control study reported that 85% of people with varicose veins had a positive family history, compared with just 22% of people without them. Patients with the condition were 21.5 times more likely to report affected family members than controls.
Researchers have identified several genetic factors that contribute. Smooth muscle cells in incompetent varicose veins show reduced activity of a gene called desmuslin, which helps maintain the structural integrity of the vein wall. Mutations affecting blood clotting proteins, iron metabolism, and the growth of lymphatic valves have all been linked to venous disease or its complications. A specific mutation in thrombomodulin, a protein involved in blood clotting regulation, has been directly associated with a history of varicose veins. These aren’t genes you’d typically be tested for, but they help explain why some people develop severe varicosities while others with the same lifestyle never do.
Pregnancy Creates a Perfect Storm
Pregnancy combines nearly every risk factor for varicose veins at once. The growing uterus physically compresses the large iliac veins and the inferior vena cava in the pelvis, partially blocking the return of blood from the legs. This mechanical compression is most pronounced in the third trimester and also explains why vulvar varicose veins sometimes appear late in pregnancy.
On top of that compression, total blood volume increases substantially during pregnancy to support the growing fetus. Hormonal shifts (particularly rising progesterone) relax the smooth muscle in vein walls, making them more distensible. The vein wall itself undergoes structural changes. All of these factors combine to increase the pressure on leg vein valves, promoting distention and reflux. Varicose veins that appear during a first pregnancy often worsen with subsequent pregnancies, though some improve after delivery once the mechanical and hormonal pressures ease.
Excess Weight Raises Venous Pressure
Carrying significant extra weight increases intra-abdominal pressure, which in turn raises the pressure inside the pelvic and upper leg veins. The mechanism is straightforward: abdominal fat, both within the abdomen and in the abdominal wall, presses on the veins that drain the legs. Research on morbidly obese patients found that increases in sagittal abdominal diameter (the front-to-back depth of the belly) correlated directly with rising intra-abdominal pressure.
This elevated pressure in the pelvic veins transmits downward through the femoral veins into the lower leg, especially when the femoral valves are already incompetent. The result is greater venous reflux, wider vein diameters, and higher venous pressures throughout the leg. In severely and morbidly obese patients, this process causes chronic venous stasis, where blood essentially stagnates in the lower limbs, accelerating both the development of varicose veins and the progression to more serious complications like skin changes and ulcers.
Prolonged Standing and Sitting
When you stand still for long stretches, your calf muscles aren’t contracting and relaxing the way they do when you walk. That muscle pump action is what normally squeezes blood upward through your leg veins. Without it, blood pools in the lower legs, and the sustained hydrostatic pressure gradually weakens valve function. The same principle applies to prolonged sitting, which compresses the veins at the hip and knee and limits the muscle pump’s effectiveness.
Occupations that involve hours of standing, such as teaching, nursing, retail, and factory work, consistently show higher rates of varicose veins. The risk isn’t from a single long day but from years of cumulative pressure. Regular movement breaks, calf raises, or walking periodically can help activate the muscle pump and reduce venous pooling.
Age, Sex, and Hormones
Varicose veins become more common with age, though the increase is gradual rather than sudden. Vein walls lose elasticity over decades, and valves that have been opening and closing millions of times eventually wear down. Studies show slightly higher prevalence in adults between 35 and 60 compared with younger groups, even if the increase doesn’t always reach statistical significance in smaller studies.
Women are disproportionately affected. Research estimates that women are more than four times as likely as men to develop varicose veins, a gap that reflects the combined influence of pregnancy, hormonal contraceptives, and hormone replacement therapy. Estrogen and progesterone both relax vein walls, and fluctuations across the menstrual cycle, pregnancy, and menopause all influence venous tone. This doesn’t mean men are exempt. Male varicose veins are common and driven by the same valve failure mechanisms, just at lower overall rates.
Other Contributing Factors
A history of deep vein thrombosis (DVT) is one of the most direct causes of valve damage. When a blood clot forms in a deep leg vein, it can physically destroy the valve leaflets as it resolves. The resulting incompetence in the deep venous system forces high-pressure blood into the superficial veins, often producing varicose veins months or years after the original clot. This is sometimes called post-thrombotic syndrome.
Chronic constipation and heavy lifting can both transiently spike intra-abdominal pressure in a way similar to obesity, though the effect is intermittent rather than constant. Tight clothing that restricts blood flow at the waist or groin may contribute in rare cases. Leg injuries, previous vein surgeries, and episodes of superficial vein inflammation (phlebitis) can all damage valves directly and set the stage for varicose veins in the affected area.