Varicose veins have long been considered a condition that disproportionately affects women, and there are real biological reasons for this, particularly hormonal fluctuations and pregnancy. But the full picture is more complicated than most people assume. Some large population studies have found that men actually develop varicose veins at similar or even higher rates, suggesting that the gap between sexes may have less to do with biology alone and more to do with how hormones, pregnancy, genetics, and occupation interact.
How Female Hormones Affect Vein Walls
Progesterone, which rises dramatically during the second half of the menstrual cycle and throughout pregnancy, directly relaxes the smooth muscle cells in vein walls. It does this by activating specific receptors on muscle cells that trigger a chain of signals, ultimately reducing the tension that keeps veins firm and spring-like. When vein walls relax too much, the tiny one-way valves inside them can’t close properly. Blood pools instead of flowing upward toward the heart, and over time the vein stretches and becomes visible under the skin.
Estrogen also plays a role, though researchers understand less about its specific effects on vein structure. Varicose veins are associated with higher circulating estrogen levels, but estrogen also influences collagen formation throughout the body. Collagen and elastin are the structural fibers that give veins their shape and recoil. How estrogen remodels these fibers in vein walls specifically, rather than in skin or other tissues, is still not well mapped. What is clear is that the hormonal environment women experience monthly, and especially during pregnancy, puts repeated mechanical stress on leg veins in a way that men’s hormonal cycles do not.
Pregnancy Creates a Perfect Storm
Pregnancy is the single biggest risk factor unique to women. It combines nearly every condition that promote varicose veins at once. Blood volume increases by roughly 45% above pre-pregnancy levels, though it can rise anywhere from 20% to 100% depending on the individual. That surge begins within the first few weeks of gestation and climbs steadily until delivery. More blood circulating through the same veins means more pressure on vessel walls and valves, especially in the legs where blood has to fight gravity to return to the heart.
On top of this, the growing uterus physically compresses the inferior vena cava, the large vein that carries blood from the lower body back to the heart. This compression gets worse as the pregnancy progresses, and it’s most pronounced when lying on the back, where the weight of the uterus presses directly against the vein. The result is a backup of blood in the leg veins, with venous pressures that increase progressively throughout pregnancy. Combined with the high progesterone levels softening vein walls, it’s common for varicose veins to appear for the first time during pregnancy or worsen with each subsequent pregnancy.
Compression stockings are often recommended during pregnancy, but their ability to prevent new varicose veins from forming is limited. In a controlled study from the University Hospital of Zurich, compression stockings worn from early pregnancy to term did not prevent superficial varicose veins from appearing. They did, however, reduce deeper valve dysfunction at a key junction in the leg and improved symptoms like pain, discomfort, and cramps. So while they won’t necessarily stop visible veins from developing, they can protect deeper vein function and make pregnancy more comfortable.
Genetics With a Female Bias
Varicose veins run in families, and recent genetic research has uncovered some sex-specific wrinkles. A large Finnish population study identified one genetic region near the ERG gene on chromosome 21 that was associated with varicose vein risk only in women, along with two additional regions on the X chromosome. Since women carry two X chromosomes, genes on the X chromosome can sometimes escape the normal process that silences one copy, leading to higher expression in women than in men.
One gene of particular interest is TIMP1, located directly on the X chromosome. TIMP1 helps regulate the breakdown and remodeling of tissue, including vein walls. Because its silencing is inconsistent in women, some women may produce more of this gene’s protein than others, potentially predisposing them to changes in vein wall structure. Researchers have also found that several varicose vein-related genes contain numerous binding sites for estrogen and progesterone receptors, meaning these hormones can directly dial the activity of those genes up or down. This creates a feedback loop: the same hormones that soften vein walls may also be switching on genes that make the veins more vulnerable in the first place.
The Surprising Role of Occupation
Here’s where the conventional narrative gets complicated. A study examining prolonged standing and varicose vein symptoms in both sexes found that while women reported varicose veins more often than men, the type of standing work differed significantly between genders. When researchers added occupation into their statistical model, the effect of gender on varicose vein risk disappeared. In other words, prolonged standing at work may be a more important risk factor than biological sex itself.
Women are overrepresented in occupations that involve long hours on their feet: nursing, retail, teaching, food service, and hairdressing. Men in similar standing-heavy jobs, like factory work or security, develop varicose veins at comparable rates. This suggests that a meaningful portion of the perceived female predominance in varicose veins comes not from being female, but from what women are more likely to do for work.
Do Women Actually Get More Varicose Veins?
The assumption that varicose veins are overwhelmingly a women’s problem dates largely from studies conducted in the 1960s and 1970s. More recent and methodologically rigorous research tells a different story. The Edinburgh Vein Study, which examined over 1,500 people from the general population, found the age-adjusted prevalence of trunk varicose veins was actually 40% in men compared to 32% in women, a statistically significant difference in the opposite direction from what most people expect.
One explanation is that older studies relied on self-reported symptoms or clinic visits, and women are generally more likely to seek medical attention for visible vein changes, partly for cosmetic reasons and partly because pregnancy prompts awareness. Men may simply live with varicose veins without reporting them. Another clinical study on chronic venous insufficiency found that men tended to present with worse disease at the time of diagnosis, with higher severity scores, suggesting they delay seeking care until symptoms are more advanced.
So the real picture may be this: women are more likely to develop varicose veins during specific life stages (pregnancy, hormonal contraceptive use, perimenopause), and they seek treatment earlier. Men develop varicose veins at similar overall rates but are diagnosed later and with more severe disease. The visibility of varicose veins as a “women’s issue” reflects both real hormonal and pregnancy-related risks and a reporting bias that has shaped medical assumptions for decades.
Hormones After Menopause
After menopause, estrogen and progesterone levels drop sharply, which might seem like it would reduce varicose vein risk. But the cumulative damage from decades of hormonal cycling and any pregnancies doesn’t reverse. Veins that have been stretched and had their valves weakened don’t tighten back up when hormone levels fall. Additionally, women who take oral hormone therapy after menopause face a separate vascular risk: a roughly 35% increased chance of venous blood clots compared to non-users. For women who smoke and use hormone therapy, that risk climbs to about 70% higher than non-smoking, non-users. While blood clots and varicose veins are different conditions, they share the common thread of impaired venous function, and the hormonal exposures women accumulate over a lifetime leave a lasting mark on vein health.