Varicose veins form 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 it outward until it becomes the swollen, twisted, bluish cord visible beneath the skin. About 23% of U.S. adults have varicose veins, with women affected roughly twice as often as men.
How Blood Normally Moves Through Your Veins
Your veins carry blood back to your heart, working against gravity when you’re standing upright. To keep blood flowing in the right direction, veins contain small one-way valves that open to let blood pass upward, then snap shut to prevent it from sliding back down. Your calf and thigh muscles act as a pump: every time you walk or flex, they squeeze the veins and push blood toward the heart. Between squeezes, the valves hold blood in place so it doesn’t fall back under its own weight.
This system works well when the valves seal tightly and the muscles pump regularly. Problems start when either component fails.
Valve Failure and Blood Reflux
The core event behind varicose veins is valve incompetence. When a valve no longer closes completely, blood leaks backward through the gap. This backward flow is called reflux, and it increases the pressure bearing down on the section of vein below.
That elevated pressure stretches the vein wall outward. As the vein widens, the valve flaps are pulled further apart, making the leak worse. The next valve down now faces more pressure than it was designed for, and it can fail too. This creates a cascade: one damaged valve leads to another, progressively extending the stretch and pooling down the length of the vein.
There’s also a connection between your deep veins (the large vessels buried within your leg muscles) and your superficial veins (the ones closer to the skin). Short connector veins called perforators link the two systems. When perforator valves fail, the high pressures generated by your calf muscle pump get forced backward into the superficial veins, which have thinner walls and are less equipped to handle it. This is why varicose veins almost always appear near the surface.
What Happens to the Vein Wall Itself
A healthy vein wall is flexible. It can stretch slightly under pressure and spring back. This ability depends on two types of structural fibers: collagen, which controls how far the wall can stretch, and elastin, which provides the snap-back. When a vein is under chronically high pressure, the balance between these fibers shifts. The body produces enzymes that break down the structural matrix of the vein wall, weakening it over time. The wall loses its ability to recoil, becoming permanently dilated.
As the vein stretches further, the surrounding tissue also changes. High pressure forces fluid, proteins, and red blood cells out through the increasingly leaky capillary walls into the surrounding tissue. This is what causes the aching, heaviness, and swelling that often accompany visible varicose veins. Over months or years, leaked red blood cells break down and deposit iron pigments in the skin, producing the brownish discoloration some people notice around their ankles.
Why Some People Get Them and Others Don’t
Genetics plays the largest role. A study of 134 families found that the risk of developing varicose veins was 90% when both parents were affected, compared to just 20% for people whose parents had no vein problems. Researchers have identified a gene called FOXC2 as the first gene strongly linked to primary valve failure in both the deep and superficial veins of the lower leg. Mutations in FOXC2 cause a hereditary condition involving lymphatic dysfunction, and a significant number of those patients develop varicose veins.
But genetics sets the stage. Several other factors push the process along:
- Pregnancy. Progesterone binds to receptors in the vein wall, relaxing the smooth muscle and inhibiting collagen production. This causes the vein to dilate and may trigger valve reflux. On top of that, blood volume rises significantly during pregnancy, and the growing uterus compresses the large veins in the pelvis, making it harder for leg blood to drain upward. These factors combined explain why varicose veins often appear during pregnancy, particularly in the second and third trimesters.
- Prolonged standing or sitting. When you stand still for extended periods, gravity keeps a continuous column of blood pressing down on the valves in your legs, and your calf muscles aren’t pumping to relieve that pressure. Sitting for long stretches has a similar effect because the muscle pump stays inactive. Over years, this sustained pressure can weaken valves that might otherwise hold up.
- Age. Vein walls and valves naturally lose elasticity as you get older. Between the ages of 40 and 80, varicose veins affect an estimated 22 million women and 11 million men in the U.S.
- Obesity. Extra body weight increases abdominal pressure, which in turn raises pressure in the leg veins, accelerating valve wear.
What Crossing Your Legs Does Not Do
Despite its reputation, crossing your legs does not cause varicose veins. The external pressure from crossing is minimal and nowhere near enough to damage a valve or vein wall. It can, however, temporarily worsen symptoms like swelling or discomfort if you already have compromised veins. The same applies to tight pants or compression from clothing: these don’t create the problem, though they can aggravate existing symptoms depending on where and how long the pressure is applied.
How the Condition Progresses
Varicose veins don’t always stay the same. In many people, they remain a cosmetic issue, causing only mild heaviness or aching after a long day on their feet. In others, the underlying venous pressure continues to worsen over time.
The earliest visible signs are often spider veins, the small red or purple webs near the skin’s surface. When you factor in spider veins and reticular veins (slightly larger blue-green veins), up to 80% of men and 85% of women show some form of superficial venous change. Not all of these progress to true varicose veins, but they reflect the same underlying issue of pressure and reflux on a smaller scale.
When the condition advances, you may notice persistent swelling in the lower legs, especially by evening. Skin changes follow: the area around the ankle can become dry, itchy, and discolored as trapped red blood cells leave iron deposits in the tissue. In the most severe cases, the skin breaks down entirely, forming venous ulcers that are slow to heal. This full progression from valve failure to skin ulceration can take years or decades, and not everyone reaches the later stages.
What Keeps the Cycle Going
Once varicose veins form, they tend to sustain themselves. A stretched vein can’t return to its original diameter on its own, so the valves inside it remain incompetent. The calf muscle pump also becomes less effective when veins are dilated, because the muscles can’t compress widened vessels as efficiently. This means the immediate pressure after walking stays nearly as high as the pressure after prolonged standing, removing one of the body’s main relief mechanisms.
Compression stockings work by externally narrowing the veins, helping the valves close more fully and restoring some of the muscle pump’s effectiveness. They don’t reverse the structural damage, but they reduce the pressure that drives the cycle forward. Treatment options that close or remove the damaged vein, whether through heat, chemical injection, or surgery, reroute blood through healthier veins where the valves still function.