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Health Protocols

Blood Clot Prevention

Risk Factors for Thrombosis

The risk factors for thrombosis are believed to increase clotting through one or more of these three mechanisms: 1) altering or damaging the blood vessel lining (endothelium); 2) impairing or slowing the flow of blood; or 3) promoting a state that favors excess coagulation (hypercoagulation).

Alteration of the blood vessel lining (endothelium). Alteration of the endothelium produces areas of disturbance that are not necessarily tears, but may nonetheless mimic the physiology of vascular injury, thus encouraging the recruitment of platelets and the clotting process. Factors that pose a risk to endothelial cell health include:

  • Abnormal blood lipids. Abnormal blood lipids, particularly elevated total cholesterol, LDL (low-density lipoprotein) cholesterol, triglycerides, and low HDL (high-density lipoprotein) cholesterol, pose a risk to endothelial cell health. Blood lipid values outside of optimal ranges (see Table 2) are one of the risk factors for atherosclerosis, which causes arterial plaques on blood vessel walls. Clots can form on or near the lipid-rich arterial plaques in vessel walls, disrupting blood flow and increasing heart attack or stroke risk. Scientific strategies for cholesterol risk reduction are available in Life Extension's “Cholesterol Management” protocol.
  • Elevated high-sensitivity C-reactive protein (hs-CRP). hs-CRP is an indicator of inflammation and blood vessel injury; high levels are predictive of future risk of heart attack or stroke.10 CRP also exerts several pro-thrombotic activities, and may be associated with risk of venous thrombosis.11
  • Hypertension. Sustained high blood pressure compromises the integrity of the endothelium, and can cause endothelial activation and initiation of clotting.12 For optimal endothelial protection and blood clot prevention, a target blood pressure of 115/75 mmHg is suggested. Those with blood pressure higher than the optimal range are encouraged to read Life Extension's “High Blood Pressure” protocol.
  • Elevated glucose. Elevated blood glucose levels, even those that remain in the lab-normal range, may significantly increase the risk of developing a blood clot. In fact, a clinical study involving patients with coronary artery disease (CAD), found that patients with fasting glucose levels above 88 mg/dL had greater platelet dependent thrombosis than those with levels below 88 mg/dL. The authors of this study remarked: "The relationship is evident even in the range of blood glucose levels considered normal, indicating that the risk associated with blood glucose may be continuous and graded. These findings suggest that the increased CAD risk associated with elevated blood glucose may be, in part, related to enhanced platelet-mediated thrombogenesis."13 Life Extension suggests fasting glucose levels be kept between 70–85 mg/dL to limit glucose-induced platelet aggregation and promote optimal overall health.
  • Excess abdominal body fat. Abdominal obesity, also known as android obesity, consists of excessive deposition of fat tissue around the trunk of the body (eg, the belly). The fatty tissue around the trunk is prone to secrete inflammatory chemicals and cause high blood sugar and hypertension, all factors that pose dire risk to the health of the endothelial cells. Maintaining an ideal body weight is critical to reducing thrombosis risk.
  • Elevated homocysteine. Elevated homocysteine has been associated with a 60% increase in venous thrombosis risk for each 5 µmol/L increase in concentration.14 Homocysteine damages the endothelium, increases endothelial cell and platelet activation, and lowers fibrinolytic (clot breakdown) activity.15 Life Extension recommends keeping homocysteine levels below 7‒8 µmol/L for optimal health (Table 2); guidelines for doing so are discussed in the “Homocysteine Reduction” protocol.
  • History of stroke, transient ischemic attack, heart attack, or coronary artery disease. These all indicate a susceptibility to arterial thrombosis and are among the strongest predictors of future thrombotic events.

Note: In addition to these factors listed above, additional discussion of risk factors that compromise endothelial health (and therefore increase risk for thrombosis) can be found in the Life Extension Magazine article entitled "How to Circumvent 17 Independent Heart Attack Risk Factors."

Interrupted blood flow. Interrupted blood flow stimulates thrombosis by allowing the localized accumulation of circulating platelets and clotting factors and by increasing the probability of clotting reactions. Risk factors include:

  • Sedentary behavior. Sedentary behavior, either as inactive lifestyle or due to extended immobilization such as during hospitalization or long-distance travel,16 increase thrombosis risk. According to the CDC, adults aged 18+ should engage in at least 2.5 hours of moderate intensity aerobic exercise each week, and full-body strength training at least twice a week. Even greater health benefits are available through five hours of moderate-intensity aerobic exercise each week combined with full-body strength training two or more days a week.
  • Surgeries of the lower extremities (hip, knee, ankle). Surgeries of the lower extremities increase thrombosis risk either due to trauma to the veins during surgical manipulation, or immobilization during recovery.17 Without treatment, the incidence of DVT following total hip or total knee replacement surgery is as high as 40­–60%.18
  • Atrial fibrillation. Atrial fibrillation, the most common type of abnormal heart rhythm, can lead to blood pooling in the heart and subsequent clot formation in the left atrium, increasing stroke risk 5-fold.19

Hypercoagulable states. Hypercoagulable states (sometimes called thrombophilias) are conditions in which the nature or composition of the blood encourages coagulation. Some hypercoagulable states are inherited disorders that increase the activity of clotting factors or reduce the activity of natural anticoagulants. Some of the more common non-genetic hypercoagulable states include:

  • Thyroid disorders. Thyroid disorders, which alter the balance of clotting factors and anticoagulants, can increase the risk of thrombosis. Hyperthyroidism (high thyroid function) increases the risk of thrombosis due to disruption of the clotting process, such as increased production of clotting factors, increased thrombin activity, and reduced rate of fibrinolysis (clot breakdown).20 Hyperthyroidism also can increase blood volume, which can lead to high blood pressure and cardiac arrhythmias, both of which are risk factors for thrombosis.21 In hyperthyroid patients, the incidence of arterial thrombosis, especially cerebral thrombosis, is between 8% and 10%.22 Hypothyroidism (low thyroid function) also increases the risk of thrombosis. Hypothyroid patients cannot clear clotting factors from the blood as quickly, have elevated levels of fibrinogen, and have reduced rates of fibrinolysis.23
  • Elevated plasma fibrinogen. Elevated plasma fibrinogen, the main coagulation protein, may result from a variety of conditions such as smoking, thyroid disorders, or infection. A comprehensive review of observational studies estimated that a 98 mg/dL reduction in fibrinogen concentration would lead to a relative risk reduction of 80% in coronary heart disease.24
  • Pregnancy. Pregnancy shifts the balance of hemostatic factors towards coagulation and enhances the activation of platelets, especially in pre-eclampsia (pregnancy-associated hypertension), which may affect 2–4% of pregnancies.25
  • Cancer. Cancer can increase risk of venous thrombosis 4- to 7-fold, especially in metastatic cancers or those where the infiltration of tumors or compression of blood vessels disrupt blood flow.26 Pancreatic, brain, and gastric cancers especially increase the risk of thrombosis.26

Blood clots may be predictive of cancer risk as well. In a case-control study involving nearly 60,000 patients, the likelihood of developing any cancer within six months of diagnosis of venous thromboembolism (VTE) was 420% higher than that of the general population.27 Particularly, cancer of the ovary was more than 700% more likely, while non-Hodgkin’s lymphoma and Hodgkin’s disease were 500–600% more likely within a year of VTE.

Tumors exert a number of pro-thrombotic effects on the blood, as does chemotherapy itself.28 Unfortunately, once cancer has progressed sufficiently to cause a blood clot, it is usually in an advanced stage, and the survival rate of patients diagnosed with cancer within one year of VTE is poor.29

Alarmingly, the close link between cancer and thrombogenesis appears to be underappreciated by conventional physicians. A small survey of oncologists revealed that 27% believed cancer patients were not at increased risk for clotting.28 Similarly, another survey found that the majority of oncologists utilize thromboprophylaxis in cancer patients very rarely, despite the fact that VTE is a leading cause of death in this population.30

Additional risk factors include age, female sex, smoking, and obesity; additionally, surgery can increase thrombosis risk.

Table 1 shows the standard reference ranges and optimal levels recommended by Life Extension for blood parameters associated with risk of thrombosis or its complications.

Table 1. Recommended Blood Values and Pressure to Reduce Thrombosis Risk*

Blood Test

Standard Reference Range

Optimal

Total cholesterol

100‒199 mg/dL

160‒180 mg/dL

LDL cholesterol

0‒99 mg/dL

under 70‒100 mg/dL

HDL cholesterol

over 39 mg/dL

over 50‒60 mg/dL

Fasting Triglycerides

0‒149 mg/dL

under 80 mg/dL

Fasting Glucose

65‒99 mg/dL

70‒85 mg/dL

Homocysteine

0‒15 µmol/L

under 7‒8 µmol/L

Fibrinogen

150‒450 mg/dL

295‒369 mg/dL

TSH

0.45‒4.5 μIU/mL

1.0‒2.0 μIU/mL

CRP

0‒3.0 mg/L

Men: under 0.55 mg/L
Women: under 1.0 mg/L

Blood Pressure

Hypertension: over 139/89 mmHg

115 /75 mmHg31

*TSH=thyroid-stimulating hormone; LDL=low-density lipoprotein; HDL=high-density lipoprotein; CRP=C-reactive protein; μU/dL=microunits per deciliter; mg/dL=milligrams per deciliter; µmol/L=micromoles per liter; mg/L=milligrams per liter; mmHg: millimeters of mercury.

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