You bruise from nothing. Your genes may explain why.

Factor V is one of the body’s primary clotting factors, a protein that sits in your blood ready to jump into action the moment a blood vessel is damaged. When you get a cut, Factor V helps weave fibrin strands that form the scaffold of a clot. Without it, you’d bleed uncontrollably. The system is elegantly balanced so clots form quickly but not too quickly.

The Factor V Leiden variant, carried by roughly 5% of people with European ancestry, changes a single amino acid in this protein. This small change makes the clotting cascade much harder to turn off once it starts. People with the Leiden variant have 4 to 8 times higher risk of venous thromboembolism (blood clots in veins), and the risk climbs 80-fold if they also take oral contraceptives. But here’s what most people don’t realize: this overactive clotting doesn’t just create clots in veins. It also shifts your entire clotting balance, making your blood stickier and your vessels more reactive to minor injury.

You bruise easily because your blood is primed to clot too aggressively. Minor trauma that shouldn’t trigger clotting in someone else triggers it in you. Blood pools under the skin more readily. The bruise develops faster and often lasts longer because the clot isn’t dissolved as efficiently.

Prothrombin is the inactive form of thrombin, the enzyme that actually converts fibrinogen into the fibrin strands that make up a blood clot. It sits dormant in your blood, waiting for a signal to spring into action. The moment a blood vessel is damaged, a cascade of proteins activates prothrombin into thrombin, and the clotting process explodes forward.

The F2 G20210A variant is present in approximately 2 to 3% of people with European ancestry. This variant increases the amount of prothrombin circulating in your blood, making your blood literally more likely to clot. People with this variant have 2 to 3 times higher clotting risk on its own. When combined with Factor V Leiden (many people carry both), the risk multiplies dramatically.

With elevated prothrombin, your body treats minor vessel damage as an emergency requiring maximum clotting response. A small bump causes a bigger clot than it should. Blood accumulates under the skin more readily. You develop bruises from contact so light you barely remember it happening.

MTHFR catalyzes one of the most important reactions in your body: converting folate into methylfolate, the active form your cells can use. This isn’t just about energy or mood. Methylfolate is essential for regulating homocysteine, an amino acid that, when elevated, damages blood vessel walls and makes blood clots more likely to form.

The MTHFR C677T variant, carried by roughly 40% of people with European ancestry, reduces this enzyme’s efficiency by 40 to 70%. You can eat a perfect diet rich in folate and still accumulate dangerously elevated homocysteine because your cells cannot convert the folate into the active form they need. Elevated homocysteine is an independent cardiovascular risk factor; it damages endothelial cells (the inner lining of blood vessels) and makes clotting more likely.

When your vessel walls are damaged by elevated homocysteine, they become more fragile and reactive to trauma. Minor bumps cause disproportionate clotting responses. Blood pools under the skin more readily because the vessels themselves are weaker. You bruise easily partly because your clotting is overactive and partly because your vessels are more vulnerable.

Your body doesn’t want clots to last forever. The moment a blood vessel heals, you need a system to dissolve the clot and restore normal blood flow. That system is led by a protein called plasminogen, which is converted into plasmin, the enzyme that cuts up fibrin and dismantles clots. PAI-1 is the regulator that controls how aggressively this clot-dissolving process happens.

The PAI1 4G/5G polymorphism is extremely common; the 4G/4G genotype, which shows the strongest effect, is carried by roughly 25% of the population. People with the 4G/4G variant produce more PAI-1, which means their clots dissolve slower. A normal clot might be reabsorbed in days. Yours lingers. The longer a clot sits under your skin, the more dramatic the bruise, and the longer it takes to fade.

You bruise easily and bruise darkly because once a clot forms under your skin from minor trauma, your body is slow to clean it up. The blood sits there longer, oxidizing from red to purple to yellow-green. Your bruises are not just common; they’re more severe and more persistent than they should be.

Nitric oxide is a signaling molecule your blood vessel walls use to stay relaxed and open. When endothelial cells (the inner lining of your vessels) produce nitric oxide, blood vessels dilate, blood pressure drops, and blood flows freely without turbulence. NOS3 is the enzyme that produces this critical molecule. Without adequate nitric oxide, your vessels remain constricted, blood pressure rises, and blood cells slam against vessel walls with more force.

The NOS3 Glu298Asp variant, carried by roughly 30 to 40% of the population, reduces nitric oxide production. Lower nitric oxide means your blood vessels stay slightly constricted and stiffer than they should be, making them more vulnerable to damage from normal blood pressure and physical trauma. Blood cells circulate under higher pressure and with more mechanical stress.

You bruise easily because your vessels are less flexible and less effective at protecting themselves. When you bump your arm, the vessel wall tears more readily because it lacks the cushioning effect of optimal nitric oxide signaling. Blood spills into the surrounding tissue. The bruise forms faster and appears darker because vessel damage is more extensive relative to the trauma.

Vitamin K is famous for clotting, but few people understand how it works. Vitamin K doesn’t make clots directly. Instead, it activates clotting factors like Factor II, Factor VII, Factor IX, and Factor X by adding carboxylic acid groups to them. Without this activation step, these factors cannot function. VKORC1 is the enzyme that recycles vitamin K so your cells can use it repeatedly. When VKORC1 function is normal, vitamin K works efficiently and clotting factors are optimally active.

VKORC1 variants, present in roughly 10 to 50% of the population depending on ancestry, alter how efficiently this recycling works. Certain variants make your clotting factors more resistant to anticoagulation, meaning they remain active even in the presence of vitamin K antagonists like warfarin. But beyond warfarin response, VKORC1 variants also affect how sensitive your clotting is to dietary vitamin K. If your variant makes you more dependent on vitamin K, fluctuations in intake directly shift your clotting balance.

You bruise easily because your clotting factors remain activated even when circumstances should dial them down. Dietary vitamin K variation causes your clotting to fluctuate unpredictably. A week of eating more leafy greens shifts your clotting baseline. Missing them shifts it back. Your vessels respond to this unstable environment with bruising.