her 2+ and flaxseed oil

[RobinP]

Clinical Summary From MSK website:

(RB, see bold italics below)

Derived from plant oils and various foods. Patients use vitamin E to prevent and treat heart disease, cancer, diabetes, and Alzheimer's disease. Natural food sources include plant oils, wheat germ, eggs, green leafy vegetables, and whole grains (3). Vitamin E acts as an antioxidant, preventing the propagation of free-radical reactions and protecting polyunsaturated fatty acids within membrane phospholipids. Although sold in a variety of formulations, only the d-isomer is considered active (1). A recent analysis of seven brands of commercially available vitamin E revealed actual content to vary considerably from the labeled dosage (5). Most research describes vitamin E in terms of milligrams, but most products are sold in international units (IU). The conversion is 1 IU natural vitamin E equals 0.67 mg d-alpha-tocopherol and 1 IU of synthetic vitamin E equals 0.45 mg d-alpha-tocopherol. Studies evaluating vitamin E supplementation suggest that it may reduce the risk of some cancers (19) (20), improve immune response in the elderly, and slow the progression of Alzheimer's disease (9) (15) (16) (18). However, 200mg of vitamin E per day has no effect on reducing the incidence of acute respiratory tract infection (12). In addition, a meta-analysis of seven randomized trials showed that Vitamin E provided no benefit in mortality, nor reduced the risk of cardiovascular death or cerebrovascular accident when compared with control treatment (26). Nor was it effective in arresting the development or progression of macular degeneration (14) and Early Parkinson's Disease (21). Vitamin E supplementation also has been shown to reduce the incidence of cisplatin induced neurotoxicity (22). One clinical trial shows that vitamin E is more effective than a placebo in reducing hot flashes in breast cancer survivors (27). There are no significant adverse effects associated with vitamin E, although toxicity may occur with chronic supplementation of doses greater than 800 IU. Daily supplementation over 400 IU may increase all-cause mortality (29). A recent review of 14 clinical trials shows that supplementation with antioxidants beta-carotene, vitamins A, C, and E does not seem to prevent gastrointestinal cancer and may actually increase overall mortality (28). Data from a large, multicenter Prostate, Lung, Colorectal, and Ovarian Cancer Screening trial also suggests that antioxidant supplementation may not lower the risk of prostate cancer (31). Vitamin E was recently found in a study to increase the risk of a second primary cancer in the first few years following supplementation. Researchers also suggest that it may interfere with radiation therapy (30). Vitamin E may also enhance the activity of warfarin, but data are inconsistent (7) (8). PT and INR should be monitored when vitamin E supplementation is initiated or discontinued in patients receiving warfarin. A clinical trial in women on HRT with coronary artery disease shows an increased risk of death and nonfatal myocardial infarction in patients who took Vitamin C and Vitamin E supplements (13).
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Food Sources

Plant-derived oils (wheat germ, soybean, sunflower, almond, safflower, corn), wheat germ, liver, eggs, nuts and seeds, green leafy vegetables, whole grains (1) (2)
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Purported uses

[R.B.]

I have seen a lot of the suggestions in the trail you post in a variety of other similar trials looking at vitamin E.

Vit E can help but it is not the answer in a very rough summary.

Vit E is generally reported as an antioxidant.

I have seen arguments that antioxidants may interfere with chemo radiation etc.

My questions was effectively - was it the blood thinning or something else that was causing spread. It could be the blood thinning but I would guess is more likely to be something else, and this article does not seem to be suggesting that it is blood thinning - it just posts a caveat.

This is all hugely complex, and very great deals remain unknown, but there are suggestions that long chain omega threes particularly increase oxidation ( which can kill rougue cells). The mitochondrial membrane has it own type of lipid that shows a predisposition to take up high levels of DHA when available. DHA has particular properties and may have a special role both as fuel and source of controlled oxidation which enables rougue cell destruction.

Vitamin E helps protects fats from unwanted oxidation but I GUESS and no more where people have insufficient omega 3 / blocked fats pathways / deficiences in long chain fats may be it has a negative effect by blocking weaker oxidiation paths?

In conclusion I have no problem with a suppostion that in certain circumstances excess Vit E may be related to spread - I dont know the answer but can see in very vague terms possibilities why - but I do not think the article would support your concerns on blood thinning and spread re the omega threes. ( Omega threes and warfarin)

There are anumber of trials suggesting synergies for long chain omega threes and various chemos and indeed in animals radiation.

Please do come back if you disagree - I struggle with all this too - and thank you for the post, and obviously always talk to your advisors as I am only trying to report what I read but claim no particular expertise.


RB

[RobinP]

I don't know why vit E in some studies has promoted cancer spread. Perhaps it isn't related to blood thinning as I was told! In fact, I just googled these articles that actually have some positive things to say about blood thinners, decreasing thrombin, used in cancer tx.

Tissue factor, thrombin, and cancer.

Rickles FR, Patierno S, Fernandez PM.

Department of Medicine, George Washington University, Washington, DC, USA.

In addition to its primary role in hemostasis and blood coagulation, thrombin is a potent mitogen capable of inducing cellular functions. Therefore, it should come as no surprise that thrombin has proved to be of importance in the behavior of cancer. In this review, we focus on the ability of tissue factor (TF) and thrombin to influence tumor angiogenesis. Both exert their influence on angiogenesis through clotting-dependent and clotting-independent mechanisms: (1). directly affecting signaling pathways that mediate cell functions, and (2). mediating clot formation, thereby providing a growth media for tumor cells. Therefore, anticoagulant drugs may prove efficacious in cancer treatment due to their ability to reduce the characteristic hypercoagulability of cancer and alter the fundamental biology of cancer.

Effects of thrombin/thrombosis in angiogenesis and tumour progression.

Maragoudakis ME, Tsopanoglou NE, Andriopoulou P, Maragoudakis MM.

University of Patras, Medical School, Department of Pharmacology, 261 10 Rio, Patras, Greece. maragoud@med.upatras.gr

Laboratory, histopathological, pharmacological and clinical evidence support the notion that a systemic activation of blood coagulation is often present in cancer patients. On the other hand, epidemiological studies provide evidence of an increased risk of cancer diagnosis following primary thromboembolism. Moreover, the metastatic ability of human breast cancer cells is correlated with the number of thrombin receptors of these cells, and thrombin treatment of B16 melanoma cells dramatically increases the number of lung metastases in rats. We have proposed that these tumour-promoting effects of thrombin can be explained by the ability of thrombin to activate angiogenesis, an essential requirement for tumour progression. Many of the cellular events involved in the angiogenic cascade can be activated by thrombin. At the molecular level, brief exposure of endothelial cells to thrombin causes an upregulation of the receptors (KDR and Flt-1) of VEGF, the key angiogenic mediator. This results in a synergistic effect of thrombin and VEGF in the activation of angiogenesis. In addition, thrombin activates cancer cells to secrete VEGF, thus causing a mutual stimulation between EC and CA cells. Cancer cells exposed to thrombin secrete metalloproteinase 92 KD and overexpress the integrin a(v)b(3), all of which are involved in tumour metastasis.

[R.B.]

You are thorough!

Interesting.

Thanks for acknowledging my slightly random thoughts.

RB