Varicose veins develop when one-way valves inside your leg veins stop working properly, allowing blood to flow backward and pool instead of returning to the heart. This pooling increases pressure inside the vein, stretching the walls outward until the vein becomes the swollen, rope-like bulge visible under the skin. The condition affects 10 to 30 percent of the global population, and while it can be partly cosmetic, the underlying cause is a real mechanical failure in how your circulatory system moves blood against gravity.
How Vein Valves Fail
Your leg veins contain small flap-like valves spaced along their length. These valves open to let blood flow upward toward the heart, then snap shut to prevent it from sliding back down. When a valve becomes “leaky,” blood reverses direction (a process called reflux) and collects in the vein segment below. The extra volume of blood increases pressure on the vein wall, which forces it to stretch wider.
That stretching triggers a damaging cycle. As the vein wall is pulled outward, the body produces enzymes that break down the structural proteins holding the wall together. This further weakens the vein, allowing even more dilation, which in turn damages the next valve down. Over months or years, the problem cascades from one valve to the next, producing the long, winding varicose veins that run down the calf or thigh.
Whether the process starts with the valves themselves or with weakness in the vein wall is still debated. Some people appear to have structurally defective valves that leak first, causing the wall to stretch secondarily. In others, the wall may weaken and widen first, pulling the valve leaflets apart so they can no longer meet in the middle. Either way, the result is the same: rising venous pressure, progressive dilation, and visible varicose veins.
Genetics and Body Height
Family history is one of the strongest predictors. If both your parents had varicose veins, your risk is substantially higher than someone with no family history. Several genes have been linked to the condition, including FOXC2 (involved in valve development), thrombomodulin (related to blood clotting regulation), and desmuslin (a structural protein in vein walls). Mutations in any of these can alter how veins function from a relatively young age.
A large genetic study of roughly 500,000 people also identified variants in genes connected to connective tissue structure, including one linked to a Marfan-like syndrome. This makes sense: varicose veins are fundamentally a connective tissue problem, so genes that influence the strength and elasticity of tissue throughout the body can predispose you to weaker vein walls.
One of the more surprising findings from that same study is a causal link between height and varicose veins. Taller people face about a 26 percent higher risk per unit increase in genetically predicted height. The explanation is straightforward physics: the taller you are, the longer the column of blood your leg veins must push upward, and the greater the hydrostatic pressure on valves near the ankle and calf. There is roughly 16 percent genetic overlap between height and varicose veins, meaning some of the same gene variants that make you tall also raise your risk.
Prolonged Standing and Sitting
When you stand still for long periods, your calf muscles aren’t contracting. Those muscles normally act as a pump, squeezing veins with every step to push blood upward. Without that pumping action, blood sits in the lower legs under the full force of gravity, and venous pressure climbs. Professions that require hours of standing, such as nursing, teaching, retail work, and military service, carry notably higher rates of varicose veins. Healthcare workers, for example, have a pooled prevalence of about 25 percent.
Prolonged sitting creates a similar, though less intense, problem. Bent knees can partially compress veins, slowing return flow and raising pressure in the lower leg. Long-haul flights and desk jobs both contribute, though the risk is lower than with standing because sitting at least removes the full gravitational column from ankle to heart.
Pregnancy and Hormones
Varicose veins frequently appear during pregnancy for several overlapping reasons. Blood volume increases by roughly 40 to 50 percent to support the developing baby, putting more strain on vein walls that were previously coping fine. At the same time, the growing uterus compresses the large veins in the pelvis, partially blocking the return of blood from the legs and raising pressure downstream.
Hormonal shifts add a third layer. Progesterone, which rises dramatically during pregnancy, relaxes smooth muscle throughout the body, including the smooth muscle in vein walls. This makes veins more distensible and more prone to the stretching that pulls valve leaflets apart. The combination of higher blood volume, physical compression, and hormonally softened vein walls explains why varicose veins often appear in the second trimester and worsen through the third. Many improve after delivery, but with each subsequent pregnancy the damage accumulates and veins are less likely to fully recover.
Hormonal influence also helps explain why women are affected more than men overall. A meta-analysis found that female sex carries about 3.3 times the odds of developing varicose veins compared to male sex, even after accounting for pregnancy. Fluctuations in estrogen and progesterone across the menstrual cycle and during menopause likely contribute to this gap.
Obesity and Abdominal Pressure
Carrying excess weight, particularly around the abdomen, raises the pressure inside your abdominal cavity. That elevated pressure pushes down on the veins that drain your legs, making it harder for blood to flow upward and increasing the load on every valve below. Studies have found that higher body weight is associated with greater venous reflux, wider vein diameters, and higher venous pressures in the legs.
The effect is mechanical and dose-dependent: the more weight pressing on those pelvic veins, the greater the backpressure transmitted to the legs. This is one reason why varicose veins can improve with weight loss, though veins that are already significantly stretched and valve-damaged won’t fully reverse.
Blood Clots and Secondary Causes
Not all varicose veins start with a genetic predisposition or lifestyle factor. A deep vein thrombosis (DVT), a blood clot in one of the deep leg veins, can directly cause varicose veins as a secondary consequence. After a clot forms, the body gradually breaks it down through a combination of natural clot-dissolving processes and the growth of new tiny blood vessels through the blockage. This recanalization is often incomplete, leaving behind residual obstruction and scarred, incompetent valves.
The resulting condition, called post-thrombotic syndrome, produces sustained high pressure in the veins during walking. That chronic pressure damages vein walls and valves in the superficial system, leading to visible varicose veins along with skin changes like brownish discoloration, eczema, and in severe cases, open ulcers near the ankle. Between 20 and 50 percent of people who experience a DVT develop some degree of post-thrombotic syndrome within two years.
How Severity Progresses
Varicose veins exist on a spectrum. Clinicians grade chronic venous disease on a scale from C0 (no visible signs) through C6 (an active skin ulcer). The stages in between mark a predictable progression:
- C1: Small spider veins or faint blue reticular veins, generally cosmetic.
- C2: True varicose veins, defined as 3 millimeters or wider, raised and often palpable.
- C3: Swelling (edema) in the ankle or lower leg, usually worse at the end of the day.
- C4: Skin changes, including darkening of the skin near the ankle, eczema, or hardening of the tissue beneath the skin.
- C5 and C6: Venous ulcers, either healed or actively open.
Not everyone progresses through every stage. Many people stay at C1 or C2 for decades without complications. But the underlying venous pressure doesn’t resolve on its own, and without intervention, the general trend is toward worsening over years. Symptoms like heaviness, aching, and leg fatigue often appear well before visible skin changes do, particularly after long days on your feet.
Why Multiple Factors Overlap
In practice, varicose veins rarely have a single cause. A tall woman with a family history who works a standing job and goes through two pregnancies is stacking multiple risk factors, each one independently raising venous pressure or weakening vein walls. Someone with none of those risk factors can still develop varicose veins purely from age-related wear on their valves, since decades of gravity and billions of valve cycles take a cumulative toll on even healthy veins.
Understanding which factors apply to you can guide realistic expectations. You can’t change your genetics or your height, but you can address the modifiable contributors: maintaining a healthy weight, breaking up long periods of standing or sitting with movement, wearing compression stockings during high-risk activities, and staying physically active to keep your calf muscle pump working effectively. These won’t eliminate genetic risk, but they reduce the additional venous pressure that accelerates valve failure.