Understanding Vein Disease

What Actually Causes Varicose Veins?

By Dr Johan Blignaut, Specialist Vein Surgeon · Vein Centres South Africa · Updated August 2026

Most people recognise a varicose vein when they see one — an enlarged, twisting vein that becomes visible beneath the skin. What is far less obvious is why it developed in the first place.

Patients often ask whether their veins were caused by standing too much, pregnancy, weight gain, exercise, getting older, crossing their legs or even wearing high heels.

The real explanation is more complex.

The short answer

Varicose veins develop when the normal system that returns blood from the legs towards the heart becomes abnormal. In most people this involves a combination of:

• changes in the vein wall
• failure of one-way venous valves
• backward blood flow, known as venous reflux
• increased pressure within the superficial veins
• an underlying genetic susceptibility

Over time, the affected vein may enlarge. As it enlarges, its valve leaflets may no longer meet properly. That allows more blood to fall backwards, which increases venous pressure and can stretch the vein further.

It can become a self-reinforcing cycle.

Importantly, researchers still debate exactly what starts this process in an individual patient. The evidence suggests that vein-wall changes, valve dysfunction and abnormal haemodynamics interact, rather than there being one single cause in every patient.^1–5

The bulging vein you see on your leg is therefore often the end result of a deeper problem within the venous system. That distinction matters when deciding whether — and how — a varicose vein should be treated.

First, how is blood supposed to get out of your legs?

The heart generates the pressure that sends blood through the arteries to your legs. Getting that blood back from your feet towards your heart is a different challenge, particularly when you are standing.

Your leg veins rely heavily on two mechanisms.

The calf muscle pump

When you walk, your calf muscles contract around the veins running through the leg. This compresses the veins and pushes blood upwards. When the calf muscles relax, the veins refill. Regular movement is therefore an important part of normal venous circulation.

One-way valves

Many leg veins contain small one-way valves. They open to allow blood to travel upwards and then close to limit blood falling backwards towards your feet. In a healthy venous system, the muscle pump and valves work together.

When a valve no longer closes properly, some blood can move in the wrong direction. This is called venous reflux.

Which comes first: the weak vein or the faulty valve?

For many years, varicose veins were explained very simply: the valve fails, blood flows backwards, pressure rises, and the vein becomes varicose.

That explanation is useful, but it is probably incomplete.

Studies of varicose veins show structural and biochemical abnormalities within the vein wall itself, including changes involving extracellular matrix, collagen, elastin, smooth muscle behaviour and inflammatory pathways.^3,5

This raises an important question: does the valve fail first, or does the vein wall begin to change and dilate first?

We do not yet have a definitive answer. There is credible evidence supporting both mechanisms.³

In some veins, progressive dilation may prevent previously normal valve leaflets from meeting in the middle. The valve then leaks. More blood flows backwards. Pressure increases. The vein dilates further. In other cases, valve dysfunction may be an important early event that contributes to the subsequent dilation.

Genetics: why varicose veins often run in families

One of the strongest clues to the cause of varicose veins is family history.

Large genetic studies have now confirmed that susceptibility to varicose veins is polygenic — meaning that many different genetic variants contribute to risk, rather than there being a single “varicose vein gene”.^4,5

A 2022 genome-wide study involving 810 625 individuals identified 49 significant genetic signals across 46 susceptibility loci. The biological pathways implicated included extracellular-matrix biology, inflammation, vascular smooth-muscle function and vascular development.⁵

That fits remarkably well with what is seen clinically. Some people appear to inherit veins whose walls, valves or supporting tissues are more susceptible to becoming abnormal over time.

Having a parent with varicose veins does not mean that you will definitely develop them. It means that your underlying susceptibility may be higher.

Risk factors are not necessarily causes

This distinction is important.

When research shows that varicose veins occur more frequently in people who are older, taller, overweight, pregnant or standing for prolonged periods, this does not necessarily mean that any one of those factors independently caused the veins.

They may increase susceptibility, expose an existing weakness, or accelerate a disease process that was already developing. Several factors appear repeatedly in epidemiological and genetic studies.^4,6–9

Age

Varicose veins become more common with increasing age. Long-term population studies, including the Edinburgh Vein Study, demonstrate that chronic venous disease can develop and progress over time.^6,7 That is biologically plausible: the veins of the legs are exposed to gravitational and hydrostatic forces for decades, while the tissues making up the vein wall and valves also change with age.

Pregnancy

Pregnancy has a substantial effect on the venous circulation. During pregnancy:

• blood volume increases
• hormonal changes affect venous tone
• venous capacitance increases
• pressure within the abdomen and pelvis changes
• the enlarging uterus can influence venous return from the legs

Prospective ultrasound studies have demonstrated enlargement of superficial leg veins during pregnancy, with substantial reduction again after delivery.⁹ Large epidemiological studies also identify pregnancy as a risk factor for varicose veins.⁴

This helps explain why some women notice veins for the first time during pregnancy, and why some pregnancy-related veins improve considerably afterwards. Others persist. Repeated pregnancies may also reveal or worsen an underlying susceptibility to venous disease.

Weight

Higher body mass index is associated with chronic venous disease, and obesity has been identified as a risk factor in large population studies.^4,7 Excess body weight can increase abdominal and venous pressures and may worsen swelling and symptoms in established venous disease.

But again, weight is not the entire explanation. Lean, active people can develop severe superficial venous reflux. Conversely, many people who are overweight never develop prominent varicose veins.

Height

Height is one of the more interesting risk factors. The large UK Biobank analysis by Fukaya and colleagues found that greater height remained independently associated with varicose veins after adjustment for traditional risk factors.⁴ More importantly, Mendelian-randomisation analysis provided evidence suggesting that greater height itself contributes causally to the risk.

There is a plausible mechanical explanation. When you stand, a taller person has a longer vertical column of blood between the heart and ankle, which results in greater hydrostatic pressure in the lower-leg veins.

Height is obviously not something you can modify, but it demonstrates how anatomy and haemodynamics contribute to venous disease.

Does standing all day cause varicose veins?

This is particularly relevant to teachers, surgeons, nurses, pharmacists, hairdressers and other people who spend much of their working day on their feet.

Standing increases hydrostatic venous pressure in the lower leg, and prolonged occupational standing has been associated with an increased risk of clinically significant varicose veins. In a 12-year prospective Danish study, workers who spent most of their working time standing or walking had a higher risk of hospital treatment for varicose veins than other workers.⁸

But association is not the same as proof that standing alone creates varicose veins. Millions of people stand for prolonged periods without developing significant venous disease.

I therefore regard prolonged standing as an important contributing or aggravating factor, particularly in someone whose veins are already susceptible.

Walking is different from simply standing still. Walking repeatedly activates the calf muscle pump and assists venous return.

What about sitting?

Prolonged sitting reduces use of the calf muscle pump and allows more venous pooling than regular movement. That is one reason it is sensible to get up and walk periodically if you spend many hours at a desk or travelling.

However, the evidence that sitting itself is an independent primary cause of varicose veins is less convincing than the evidence for age, genetics, pregnancy, obesity, height and prolonged occupational standing. So I would not tell a patient, “you have varicose veins because you sit too much.” The biology is rarely that simple.

Can a previous DVT cause varicose veins?

Yes — and this represents a different mechanism.

Most ordinary varicose veins are primary varicose veins, arising from disease within the superficial venous system.

A previous deep vein thrombosis (DVT) can damage valves in the deep veins or leave residual venous narrowing or obstruction. This can produce post-thrombotic venous disease. The superficial veins can then be exposed to abnormal pressures and, in some patients, may become important collateral pathways carrying blood around a deeper obstruction.¹

That has practical consequences. A superficial vein that appears abnormal should not automatically be assumed to be disposable. Understanding the deep venous circulation can sometimes change the appropriate treatment completely.

Occasionally, the problem is higher up

Not every abnormal vein pattern originates in the superficial veins of the thigh or calf. Less commonly, venous obstruction or abnormal venous anatomy within the pelvis or abdomen can contribute to lower-limb venous hypertension and unusual varicose-vein patterns.¹

These patients may require additional investigation. This is another reason why an unusual distribution of veins should not simply be treated according to what can be seen on the skin.

What does not appear to be a major cause?

Several persistent myths deserve clarification.

Crossing your legs

Crossing your legs occasionally has not been established as a cause of chronic superficial venous reflux.

Exercise

Normal exercise does not cause ordinary varicose veins. Walking and other activities that repeatedly activate the calf muscles generally assist venous return.

Running

Runners can certainly develop varicose veins. They still have genetics, vein walls and venous valves. Running itself is not recognised as a usual cause of primary varicose veins.

High heels

High heels can alter ankle movement and calf-pump mechanics while being worn. But footwear alone does not adequately explain the development of chronic superficial venous reflux.

Why is the vein you can see often not the source of the problem?

This is one of the most important concepts to understand.

Common sources of that backward flow include the:

• great saphenous vein
• small saphenous vein
• accessory saphenous veins
• perforating veins
• other non-saphenous venous pathways

The pattern varies considerably from person to person.

One common pattern is reflux beginning around the saphenofemoral junction, where the great saphenous vein joins the deep venous system in the groin, and extending down the great saphenous vein.

But this is not the only pattern. Not all great saphenous reflux begins at the saphenofemoral junction, and not all visible varicose veins originate from the great saphenous vein.^1,2 That is why looking at the leg alone cannot reliably identify the source.

This is why duplex ultrasound matters

A venous duplex ultrasound does much more than look for a blood clot. It combines conventional ultrasound imaging with Doppler assessment of blood flow.

This allows us to examine the superficial and deep venous systems and determine:

• which veins are anatomically normal
• which veins have reflux
• where the reflux begins
• how far the reflux extends
• which visible veins are connected to it
• whether the deep veins are patent
• whether there is evidence of previous thrombosis
• whether obstruction or unusual anatomy may be relevant

In other words, duplex ultrasound creates a functional map of the venous circulation. Two people can have remarkably similar-looking varicose veins but completely different underlying anatomy.

Current European and American venous guidelines recommend duplex ultrasound as the principal investigation for defining superficial venous reflux when clinically significant disease is being evaluated and treatment is being considered.^1,2

That is why, in my view, the diagnosis should come before the procedure.

Can you prevent varicose veins?

Probably not completely. You cannot change your genetics, your height, your age, your previous pregnancies or a history of DVT. And there is limited evidence that lifestyle measures can reliably prevent genetically susceptible veins from eventually developing reflux.

That does not mean lifestyle is irrelevant. Regular walking and exercise maintain calf-pump function. Avoiding very prolonged immobility reduces venous pooling. Maintaining a healthy weight has broader health benefits and may reduce the haemodynamic burden associated with obesity. Leg elevation and compression stockings can also reduce symptoms in selected patients.

These measures can improve venous function and symptoms. What they generally cannot do is make an established, structurally incompetent venous valve permanently normal again.

Does having reflux mean you need treatment?

No — and this is equally important.

A duplex scan showing venous reflux does not automatically mean that the vein requires treatment. Likewise, simply having visible varicose veins does not automatically mean that you need a procedure.

Some patients have surprisingly large veins and very few symptoms. Others have less dramatic visible veins but experience aching, heaviness, itching, swelling, inflammation, skin pigmentation, eczema or progressive skin changes — the changes that, left long enough, can end in a venous leg ulcer.

Treatment decisions should take into account the patient's symptoms, clinical examination, ultrasound findings, disease severity, expectations and individual circumstances. When treatment is indicated, the options range from compression through ultrasound-guided foam sclerotherapy to endovenous radiofrequency ablation, which seals the refluxing vein from the inside under local anaesthetic in our office operating rooms.

What does this mean for you?

If you have varicose veins, the most useful question is usually not “how do I get rid of this vein?” It is “why is this vein there?”

That change in question is important. If the visible vein is simply the downstream result of reflux somewhere else, treating only what can be seen may fail to address the underlying problem — one of the reasons veins sometimes come back, which I deal with separately on recurrent varicose veins.

Conversely, not every abnormal-looking vein requires intervention. The objective should be to understand the venous anatomy first, and then decide whether anything actually needs to be done.

So, what actually causes varicose veins?

If I had to reduce the evidence to one paragraph, it would be this:

And perhaps the most important practical point is this: the vein you can see is not necessarily the vein causing the problem. Before deciding what should be done about a varicose vein, it helps to understand why it is there.

When should you have your veins assessed?

Consider an assessment if your varicose veins are associated with:

• persistent aching or heaviness
• swelling
• itching or eczema around the lower leg
• brown pigmentation around the ankle
• hardening or inflammation of the skin
• recurrent superficial vein inflammation
• bleeding from a varicose vein
• ulceration

If you are unsure whether your veins warrant further assessment, our free online vein screening is a sensible first step.

Frequently asked questions

References

1. De Maeseneer MG, Kakkos SK, Aherne T, et al. European Society for Vascular Surgery (ESVS) 2022 Clinical Practice Guidelines on the Management of Chronic Venous Disease of the Lower Limbs. Eur J Vasc Endovasc Surg. 2022;63(2):184–267. doi:10.1016/j.ejvs.2021.12.024
2. Gloviczki P, Lawrence PF, Wasan SM, et al. The 2022 Society for Vascular Surgery, American Venous Forum, and American Vein and Lymphatic Society clinical practice guidelines for the management of varicose veins of the lower extremities. Part I: Duplex Scanning and Treatment of Superficial Truncal Reflux. J Vasc Surg Venous Lymphat Disord. 2023;11(2):231–261.e6
3. Jacobs BN, Andraska EA, Obi AT, Wakefield TW. Pathophysiology of varicose veins. J Vasc Surg Venous Lymphat Disord. 2017;5(3):460–467. doi:10.1016/j.jvsv.2016.12.014
4. Fukaya E, Flores AM, Lindholm D, et al. Clinical and Genetic Determinants of Varicose Veins: Prospective, Community-Based Study of Approximately 500,000 Individuals. Circulation. 2018;138(25):2869–2880. doi:10.1161/CIRCULATIONAHA.118.035584
5. Ahmed WUR, Kleeman S, Ng M, et al. Genome-wide association analysis and replication in 810,625 individuals with varicose veins. Nat Commun. 2022;13:3065
6. Robertson LA, Evans CJ, Lee AJ, Allan PL, Ruckley CV, Fowkes FGR. Incidence and Risk Factors for Venous Reflux in the General Population: Edinburgh Vein Study. Eur J Vasc Endovasc Surg. 2014;48(2):208–214. doi:10.1016/j.ejvs.2014.05.017
7. Robertson L, Lee AJ, Evans CJ, et al. Incidence of chronic venous disease in the Edinburgh Vein Study. J Vasc Surg Venous Lymphat Disord. 2013;1(1):59–67. doi:10.1016/j.jvsv.2012.05.006
8. Tüchsen F, Hannerz H, Burr H, Krause N. Prolonged standing at work and hospitalisation due to varicose veins: a 12 year prospective study of the Danish population. Occup Environ Med. 2005;62(12):847–850. doi:10.1136/oem.2005.020537
9. Boivin P, Cornu-Thenard A, Charpak Y. Pregnancy-induced changes in lower extremity superficial veins: an ultrasound scan study. J Vasc Surg. 2000;32(3):570–574. doi:10.1067/mva.2000.107991