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Hematological Disorders

Thrombophilia

Thrombophilia testing clarifies your blood’s tendency to clot, revealing pro-thrombotic physiology. At Superpower, we assess Homocysteine, CRP, Platelets, and the neutrophil-to-lymphocyte ratio (NLR) to map inflammation, endothelial stress, and hemostatic balance—key drivers of venous and arterial thrombosis risk.

With Superpower, you have access to a comprehensive range of biomarker tests.

Test for Thrombophilia
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Key Benefits

  • Understand your clotting risk from inflammation and metabolism using homocysteine, CRP, platelets, NLR.
  • Spot elevated homocysteine tied to clot risk and B‑vitamin or renal issues.
  • Flag systemic inflammation that can tip blood toward clotting using CRP and NLR.
  • Check platelet count to detect overproduction or low levels affecting clot and bleed risk.
  • Guide personalized prevention and referrals, from B‑vitamin repletion to hematology evaluation when indicated.
  • Protect fertility and pregnancy by identifying inflammation–clot patterns linked to complications and loss.
  • Track trends over time to confirm improvement after treatment, illness, or pregnancy.
  • Best interpreted with a full thrombophilia panel and your clinical history, including clots.

What are Thrombophilia

Thrombophilia biomarkers are signals that reveal how your body’s clot-control system is tuned—whether it is more prone to form clots than it should. They reflect the balance between clot promoters (coagulation) and the body’s built‑in brakes and cleanup crew (anticoagulation and fibrinolysis). Testing can uncover inherited shifts that push the system toward clotting, such as Factor V Leiden or a prothrombin gene change, and shortfalls in natural inhibitors like protein C, protein S, and antithrombin. It also checks for acquired immune drivers, notably antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti–beta‑2 glycoprotein I), which disrupt cell surfaces and tip blood toward clot formation. Some panels include broader signals of vessel and thrombin activity (homocysteine, thrombin–antithrombin complexes) that indicate a prothrombotic environment. Together, these markers map your personal clotting set‑point and help explain unexplained clots, pregnancy losses, or heightened risk during hormones, surgery, or immobility. Knowing this biology enables targeted prevention—deciding when to use blood thinners, modify hormones, or add precautions at high‑risk times.

Why are Thrombophilia biomarkers important?

Thrombophilia biomarkers are clues to how “sticky” your blood is—how platelets, clotting proteins, vessel lining, and inflammation interact to form or prevent clots. Because clots can affect veins, arteries, the brain, lungs, and placenta, these markers matter across cardiovascular, neurologic, and reproductive systems.

Homocysteine typically sits around 5–15; lower-in-range tends to align with healthier endothelial function, while higher values suggest impaired methylation or renal handling and correlate with arterial and venous clot risk. CRP is best near the low end (below 1), with 1–3 being average inflammation and above 3 signaling a prothrombotic inflammatory milieu. Platelets usually fall near 150–450; mid-range is optimal, as higher counts amplify platelet-driven clotting and lower counts impair primary hemostasis. The neutrophil-to-lymphocyte ratio is commonly around 1–3; nearer 1–2 reflects balanced immunity, while higher values point to inflammation and neutrophil activity that can promote thrombosis (including NETs).

When values run low, homocysteine and CRP generally indicate favorable vascular biology and are symptom-free. A low NLR likewise reflects calm immune tone. Low platelets, however, can bring easy bruising, nosebleeds, gum bleeding, or heavy periods; despite bleeding risk, rare conditions can pair low platelets with clotting. In pregnancy, platelets often drift lower and homocysteine tends to drop, yet overall clot risk rises; CRP can be modestly higher. Children may show a slightly higher NLR in early years without thrombosis.

Big picture: these biomarkers integrate metabolism, inflammation, platelet kinetics, and vessel health to forecast events like deep vein thrombosis, pulmonary embolism, stroke, placental complications, and post-thrombotic syndrome. Patterns over time, combined with age, sex, genetics, comorbidities, and imaging, sharpen risk assessment and guide how closely to watch the clotting system.

What Insights Will I Get?

Thrombophilia is a tendency to form clots that disrupts oxygen delivery, energy production, cardiovascular and brain function, fertility, and recovery from illness. Biomarkers that map coagulation, inflammation, and endothelial health reveal risk before events. At Superpower, we test Homocysteine, CRP, Platelets, and Neutrophil-to-Lymphocyte Ratio (NLR).

Homocysteine is a sulfur amino acid from one‑carbon metabolism; when high, it injures endothelium, increases oxidative stress, and tilts blood toward clotting. CRP is an acute‑phase protein reflecting systemic inflammation that amplifies coagulation and impairs fibrinolysis. Platelets are the cells that build the initial clot; higher counts or reactivity raise thrombotic potential. NLR gauges innate–adaptive immune balance; a higher ratio signals neutrophil‑driven inflammation linked to thrombosis.

For stability, physiologic homocysteine supports endothelial nitric oxide and balanced coagulation; higher values mark a procoagulant, pro‑oxidative milieu. Low, steady CRP signals quiet cytokine activity and more predictable clot dynamics; elevated CRP indicates an inflammatory tilt toward hypercoagulability. A platelet count in the usual range implies adequate hemostasis without excess thrombotic drive; persistent thrombocytosis or activation increases risk. A balanced NLR reflects coordinated immunity; a high NLR flags stress‑inflammation that can initiate and propagate clots.

Notes: Pregnancy and postpartum, age, acute infection, surgery, trauma, cancer, and chronic inflammation can transiently raise CRP, platelets, and NLR. Estrogens, corticosteroids, and chemotherapies alter counts; anti‑inflammatory drugs lower CRP. Homocysteine rises with renal impairment and certain medications, and may vary by fasting status and assay. Coexisting inherited thrombophilias also modify risk.

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Frequently Asked Questions About Thrombophilia

What is Thrombophilia testing?

It looks for signals that your blood is more prone to clot. Superpower measures Homocysteine, C‑reactive protein (CRP), Platelets, and the Neutrophil‑to‑Lymphocyte Ratio (NLR). Together they reflect vascular stress, inflammation, and clotting readiness (hypercoagulability). These are physiologic risk markers, not genetic thrombophilia tests, and they do not diagnose a current clot.

Why should I get Thrombophilia biomarker testing?

It helps uncover hidden pro‑clotting biology before an event occurs. Elevated homocysteine, CRP, high platelets, or a high NLR point to endothelial strain, inflammation, or platelet‑driven risk that can compound with surgery, immobility, pregnancy, or hormones. A baseline clarifies your systemic terrain and can explain past events or guide future risk discussions.

How often should I test?

There’s no one schedule. Get a baseline, then retest when your risk context changes. Many people repeat annually, and again after major illness, surgery, pregnancy, a new estrogen therapy, or new unexplained symptoms. Persistent abnormalities matter more than a single spike.

What can affect biomarker levels?

Acute infection, injury, surgery, pregnancy/postpartum, and vigorous exercise can raise CRP, NLR, and platelets. Smoking, stress, poor sleep, and chronic inflammation shift NLR and CRP. Low B12/folate or reduced kidney function elevates homocysteine. Iron deficiency can raise platelets. Medications (estrogens, steroids) and age also influence results.

Are there any preparations needed before Thrombophilia biomarker testing?

Fasting is not typically required for homocysteine, CRP, platelets, or NLR. Test when you’re well and hydrated, not during an acute illness if possible. Avoid strenuous exercise immediately beforehand. Do not stop prescribed medicines for testing unless your clinician has told you to.

Can lifestyle changes affect my biomarker levels?

Yes. Tobacco exposure, excess adiposity, inactivity, psychosocial stress, and poor sleep tend to push CRP and NLR up. Micronutrient status (B12/folate) and kidney function affect homocysteine. Intercurrent infections and inflammation can transiently raise most of these markers. These influences are real but variable across individuals.

How do I interpret my results?

Normal values suggest low current inflammatory and platelet‑driven clotting tone, but they do not rule out inherited thrombophilia. High homocysteine signals endothelial stress and prothrombotic potential. High CRP or NLR indicates systemic inflammation that tilts blood toward clotting. High platelets (thrombocytosis) can add clot risk; very low platelets raise bleeding risk, not thrombophilia. Trends over time and your history determine significance.

How do I interpret my results?

Normal values suggest low current inflammatory and platelet‑driven clotting tone, but they do not rule out inherited thrombophilia. High homocysteine signals endothelial stress and prothrombotic potential. High CRP or NLR indicates systemic inflammation that tilts blood toward clotting. High platelets (thrombocytosis) can add clot risk; very low platelets raise bleeding risk, not thrombophilia. Trends over time and your history determine significance.

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Superpower Chief Longevity Officer, Harvard MD & MBA

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Clinician & Founder of The Centre for New Medicine

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Founder & Medical Director of Concierge MD

Dr Robert Lufkin

UCLA Medical Professor, NYT Bestselling Author

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