Acute mental stress elicits blood hypercoagulability. Anticipatory cognitive appraisal determined the extent of coagulation activation to and recovery from stress in a study of 47 men. Particularly individuals who anticipated the stressor as more challenging and also more threatening had a greater fibrin stress response.
http://www.psychosomaticmedicine.org/cgi/content/full/68/6/851
In multiple regression analyses, body mass index (BMI) and life stress were the only significant predictors of fibrin D-dimer (increased levels of fibrin D-dimer are indicative of a hypercoagulable state). Together, BMI, hypertension status, gender, and depression accounted for 23% of the variance in fibrin D-dimer. After these variables had been controlled for, life stress explained an additional 9% of the variance in fibrin D-dimer. On the other hand, life stress did not significantly predict thrombin-antithrombin III complex (TAT) or von Willebrand factor (vWF) antigen.
http://www.psychosomaticmedicine.org/cgi/content/full/65/1/145
Obese women had significantly higher levels of leptin, von Willebrand factor, Factor VIIa, F1+2 compared with healthy women. Factor VIIa and von Willebrand factor were independently related to leptin levels. Reduction in adipose tissue after weight loss resulted in a decrease in both circulating leptin and endothelial and coagulative activation markers.
http://www.ncbi.nlm.nih.gov/pubmed/14629465
As compared to standard feeding, high fat diet feeding significantly increased plasma levels of coagulation factor VIII, combined factor II/VII/X , and plasminogen activator inhibitor-1 in mice, causing a prothrombotic shift of the coagulation profile.
In premenopausal women the important modulators of von Willebrand factor activity (plays a major role in blood coagulation) were: body mass, serum total cholesterol and sex hormone binding globulin (SHBG) levels.
http://www.ncbi.nlm.nih.gov/pubmed/11603175
After maximal exercise we found a significant reduction of activated partial thromboplastin time and thromboplastin time, a decrease in antithrombin III, von Willebrand factor-concentration, fibrinogen, plasminogen and alpha2-antiplasmin but an increase in fibrinolytic activity (the ability of some proteolytic enzymes to dissolve the fibrin in blood clots). After the physical conditioning program (12 weeks of aerobic conditioning) an increase in fibrinolytic activity at rest was noted in the training group. Opposed to that the fibrinolytic activity at rest decreased in the control group after abstinence of sports activity over this period.
http://www.ncbi.nlm.nih.gov/pubmed/11235004
Compared with control group, rats injected with a single dose of vitamin D(3) (600,000 U/kg) and fed with a high-fat diet had higher total cholesterol, low density cholesterol, plasma viscosity, whole blood viscosity, fibrinogen and malonaldehyde concentrations, and lower activated partial thromboplastin time, prothrombin time, thrombin time, erythrocyte deformation index, plasma nitric oxide, and total antioxidant capacity. After a 6-week high-fat diet, the rats in treatment group were treated with omega 3 polyunsaturated fatty acids at 250 mg×kg(-1)×d(-1). Compared with the high-fat diet group, omega 3 polyunsaturated fatty acids could reduce blood lipid levels, inhibit atherosclerotic plaque formation, decrease plasma viscosity (1.58 vs 1.81 mPa·s), whole blood viscosity [(4.76 vs 5.47 mPa·s),(4.24 vs 4.91 mPa·s), (4.04 vs 4.58 mPa·s)] and fibrinogen (2.45 vs 2.65 g/L), lower malonaldehyde content (10.1 vs 11.2 µmol/ml), prolong activated partial thromboplastin time, prothrombin time and thrombin time (29.04 vs 26.46 s), (13.86 vs 10.71 s), (23.05 vs 20.90 s), increase erythrocyte deformation index (0.35 vs 0.31), plasma nitric oxide (3.9 vs 2.8 nmol/ml) and total antioxidant capacity levels (8.0 vs 6.7 U/ml).
http://www.ncbi.nlm.nih.gov/pubmed/20979870
An increase in the fibrinogen level of the blood is largely caused by the lack of omega-3-alpha-linolenic acid in the diet. A high level of fibrinogen promotes the creation of thrombosis and maintains inflammation within the body. When the omega-3-alpha-linolenic acid level is too low, the body starts to manufacture more harmful omega-6-arachidonic acid out of the omega-6-linoleic acid, creating hormone-like compounds that cause thrombosis and inflammation. The study subjects replaced one-fourth of the food fat (margarine, cheese, butter) they used with rapeseed oil (canola oil). They took about a tablespoon of oil a day, for example, mixed with a salad. The rapeseed oil dose doubled the intake of omega-3-alpha-linolenic acid during the experiment period of six weeks. Due to the regime, all higher-than-average fibrinogen levels decreased by approximately 30 per cent.
http://www.sciencedaily.com/releases/2010/11/101108072258.htm
Our data support the notion that low molecular weight heparin is efficacious in patients with recurrent abortions and thrombophilia. 82 pregnancies in 79 women with a history of recurrent miscarriage were treated with subcutaneous heparin, independently of thrombophilia. Overall, 83.8% (67/80) of pregnancies resulted in live births. In 22/79 women (27.8%), thrombophilia markers were positive. Most noteworthy, patients with thrombophilia markers had live births at a similar frequency as patients without those parameters. We demonstrated the same effect of heparin in women with unexplained miscarriage without thrombophilia. The potential mechanism of action of heparin in early and late miscarriage warrants further study.
http://www.ncbi.nlm.nih.gov/pubmed/19666941
22 patients with persistent antiphospholipid syndrome associated with recurrent miscarriage (defined as three or more miscarriages) were treated with fish oil, equivalent to 5.1 g eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) at a ratio of 1.5 EPA to DHA. Twenty-two patients had 23 pregnancies (one patient had two pregnancies) over a period of 3 years. There was only one intrauterine fetal death at the 27th week associated with pre-eclampsia. Twenty-one pregnancies, 19 of which ended after the 37th week, produced a baby. Two pregnancies ended with cesarean section for pre-eclampsia at 30th and 35th week of gestation and one is ongoing at 32nd week. All babies are well. The weight at birth of babies delivered at term was always > 2500 g.
http://www.ncbi.nlm.nih.gov/pubmed/8305926
In a case-control study, we found no significant increase in risk of first venous thromboembolism in patients with low vitamin B12 or folate levels. However, levels of pyridoxal-5'-phosphate (PLP), the coenzyme form of vitamin B6, < 21.7 nmol/L gave a two-fold higher thrombotic risk. This was independent of folate, vitamin B12 and homocysteine levels. We hypothesized that low vitamin B6 levels may give an increased risk of recurrent venous thromboembolism.
http://www.haematologica.org/cgi/content/full/92/9/1250
The optimal level of vitamin B6, in the form of pyridoxal-5-phosphate, on the antithrombotic effect was investigated in the platelet function and blood coagulation of rabbits. Platelet aggregations induced with different agonists were assessed in platelet-rich plasma with vitamin B6 from 0 to 3.0 mM. Vitamin B6 significantly inhibited platelet aggregation to different agonists at the final concentration of
0.6 mM and reached the plateau of inhibition at 1.8mM. These results suggested that vitamin B6 displayed antiplatelet and anticoagulation action in rabbits at around 0.36 to 1.8 mM plasma level.
http://linkinghub.elsevier.com/retrieve/pii/S0271531798001729
Calcium supplements linked to 30% increased risk of heart attack
Eligible studies were randomised, placebo controlled trials of calcium supplements (>or=500 mg/day), with 100 or more participants of mean age more than 40 years and study duration more than one year. In the five studies contributing patient level data, 143 people allocated to calcium had a myocardial infarction compared with 111 allocated to placebo (hazard ratio 1.31). Non-significant increases occurred in the incidence of stroke (1.20), the composite end point of myocardial infarction, stroke, or sudden death (1.18), and death (1.09). The meta-analysis of trial level data showed similar results: 296 people had a myocardial infarction (166 allocated to calcium, 130 to placebo), with an increased incidence of myocardial infarction in those allocated to calcium (pooled relative risk 1.27). CONCLUSIONS: Calcium supplements (without coadministered vitamin D) are associated with an increased risk of myocardial infarction. As calcium supplements are widely used these modest increases in risk of cardiovascular disease might translate into a large burden of disease in the population. A reassessment of the role of calcium supplements in the management of osteoporosis is warranted. (Calcium is required for blood clotting; previous studies have found no increased cardiovascular risks with higher dietary calcium intake, suggesting that the risks are restricted to supplements).
http://www.natap.org/2010/newsUpdates/081110_05.htm
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