Multiple Myeloma an incurable disease, but I have spent the last 25 years in remission using a blend of conventional oncology and evidence-based nutrition, supplementation, and lifestyle therapies from peer-reviewed studies that your oncologist probably hasn't told you about.
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Choose between conventional blood thinner therapies such as coumadin, plavix, aspirin, or non-conventional therapies such as green tea extract, omega 3 fatty acids or curcumin-
I am a long-term multiple myeloma survivor. As a result of high-dose chemotherapy, I developed chronic atrial fibrillation in late 2010. . My 91 year old mother also has chronic a-fib. Both mom and I have an increased risk of stroke. Both mom and I employ therapies to reduce our increased risk of stoke.
Mom takes one of the standard-of-care, FDA approved blood thinners linked and excerpted below. I do not take a conventional blood thinner. I learned about the laundry list of potential side effects that come with conventional blood thinners and I decided to lower my risk of stroke by supplementing:
I decided to supplement with these three antioxidants for their anti-multiple myeloma action as well. The stroke risk lowering properties were a bonus for me.
Yes, there are possible risks with supplementing with fish oil, green tea extract and curcumin. While my gut is not really evidence-based, I think that my blood thinning therapy is better, safer and cheaper than my mom’s.
I am a multiple myeloma survivor and MM cancer coach. Please scroll down the page, post a question or comment and I will reply to you ASAP.
“Prevention of atrial fibrillation-related stroke is an important part of atrial fibrillation management. However, stroke risk is not homogeneous and varies with associated morbidities and risk factors. Risk stratification schemes have been developed that categorize patients’ stroke risk into classes based on a combination of risk factors. According to the calculated level of risk, guidelines recommend patients with atrial fibrillation receive antithrombotic therapy either as a vitamin K antagonist or aspirin. Despite recommendations, however, many patients with atrial fibrillation do not receive adequate thromboprophylaxis. We will discuss some of the underlying reasons, in part related to the drawbacks associated with vitamin K antagonists. These highlight the need for new anticoagulants in atrial fibrillation. The novel oral anticoagulants in development may overcome some of the limitations of vitamin K antagonists and address their underuse and safety concerns.”
“Clopidogrel, sold as the brandname Plavix among others, is a medication that is used to reduce the risk of heart disease and stroke in those at high risk. It is also used together with aspirin in heart attacks and following the placement of a coronary artery stent (dual antiplatelet therapy). It is taken by mouth. Onset of effects is about 2 hours and lasts for 5 days…
Serious adverse drug reactions associated with clopidogrel therapy include:
In the CURE trial, people with acute coronary syndrome without ST elevation were treated with aspirin plus clopidogrel or placebo and followed for up to one year. The following rates of major bleed were seen:
The CAPRIE trial compared clopidogrel monotherapy to aspirin monotherapy for 1.6 years in people who had recently experienced a stroke or heart attack. In this trial the following rates of bleeding were observed.
In CAPRIE, itching was the only adverse effect seen more frequently with clopidogrel than aspirin. In CURE, there was no difference in the rate of non-bleeding adverse events.
“Atrial fibrillation- Apixaban is recommended by the National Institute for Health and Clinical Excellence for the prevention of stroke and systemic embolism in people with non-valvular atrial fibrillation and at least one of the following risk factors: prior stroke or transient ischemic attack, age 75 years or older, diabetes mellitus, or symptomatic heart failure.
Apixaban and other newer anticoagulants (dabigatran and rivaroxaban) appear equally effective as warfarin in preventing non-hemorrhagic stroke in people with atrial fibrillation and are associated with lower risk of intracranial bleeding.
Premature discontinuation of any oral anticoagulant, including apixaban, increases thrombotic event risk. This is not due to any rebound effect from discontinuation. To reduce this risk, administering another anticoagulant is advised.
Apixaban can increase the risk of bleeding and may cause serious, potentially fatal, bleeding. Concurrent use with drugs affecting hemostasis (e.g. other anticoagulants, heparin, aspirin and other antiplatelet drugs, selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors, and nonsteroidal anti-inflammatory drugs (NSAIDs) can further increase the risk of bleeding.
One concern with the use of apixaban and the other newer anticoagulants is the absence of well-established protocol for reversal of their activity (no antidote is available). This is an important disadvantage relative to warfarin when bleeding complications occur or when people taking the drugs require emergency surgery.
When spinal/epidural anesthesia or puncture is utilized, patients who are being treated with anti-thrombotic agents for the prevention of thromboembolic complications are at risk for developing a hematoma, which can cause long-term or permanent paralysis. The risk of this may be increased by using epidural or intrathecal catheters after a surgical operation or from the concurrent use of medicinal agents that affect hemostasis.
“Warfarin, sold under the brand name Coumadin among others, is a medication that is used as an anticoagulant (blood thinner). It is commonly used to treat blood clots such as deep vein thrombosis and pulmonary embolism and to prevent strokein people who have atrial fibrillation, valvular heart disease or artificial heart valves…”
The only common side effect of warfarin is bleeding. The risk of severe bleeding is small but definite (a typically yearly rate of 1-3% has been reported) and any benefit needs to outweigh this risk when warfarin is considered. All types of bleeding occur more commonly, but the most severe ones are those involving the brain (intracerebral hemorrhage/hemorrhagic stroke) and the spinal cord. Risk of bleeding is increased if the INR is out of range (due to accidental or deliberate overdose or due to interactions). This risk increases greatly once the INR exceeds 4.5.
A number of risk scores exist to predict bleeding in people using warfarin and similar anticoagulants. A commonly used score (HAS-BLED) includes known predictors of warfarin-related bleeding: uncontrolled high blood pressure (H), abnormal kidney function (A), previous stroke (S), known previous bleeding condition (B), previous labile INR when on anticoagulation (L), elderly as defined by age over 65 (E), and drugs associated with bleeding (e.g. aspirin) or alcohol misuse (D). While their use is recommended in clinical practice guidelines, they are only moderately effective in predicting bleeding risk and do not perform well in predicting hemorrhagic stroke. Bleeding risk may be increased in people on hemodialysis. Another score used to assess bleeding risk on anticoagulation, specifically Warfarin or Coumadin, is the ATRIA score, which uses a weighted additive scale of clinical findings to determine bleeding risk stratification. The risks of bleeding are increased further when warfarin is combined with antiplatelet drugs such as clopidogrel, aspirin, or nonsteroidal anti-inflammatory drugs.
A rare but serious complication resulting from treatment with warfarin is warfarin necrosis, which occurs more frequently shortly after commencing treatment in patients with a deficiency of protein C. Protein C is an innate anticoagulant that, like the procoagulant factors that warfarin inhibits, requires vitamin K-dependent carboxylation for its activity. Since warfarin initially decreases protein C levels faster than the coagulation factors, it can paradoxically increase the blood’s tendency to coagulate when treatment is first begun (many patients when starting on warfarin are given heparin in parallel to combat this), leading to massive thrombosis with skin necrosis and gangrene of limbs. Its natural counterpart, purpura fulminans, occurs in children who are homozygous for certain protein C mutations.
After initial reports that warfarin could reduce bone mineral density, several studies have demonstrated a link between warfarin use and osteoporosis-related fracture. A 1999 study in 572 women taking warfarin for deep venous thrombosis, risk of vertebral fracture and rib fracture was increased; other fracture types did not occur more commonly.A 2002 study looking at a randomly selected selection of 1523 patients with osteoporotic fracture found no increased exposure to anticoagulants compared to controls, and neither did stratification of the duration of anticoagulation reveal a trend towards fracture.
A 2006 retrospective study of 14,564 Medicare recipients showed that warfarin use for more than one year was linked with a 60% increased risk of osteoporosis-related fracture in men; there was no association in women. The mechanism was thought to be a combination of reduced intake of vitamin K, which is necessary for bone health, and inhibition by warfarin of vitamin K-mediated carboxylation of certain bone proteins, rendering them nonfunctional.
Another rare complication that may occur early during warfarin treatment (usually within 3 to 8 weeks of commencement) is purple toe syndrome. This condition is thought to result from small deposits of cholesterol breaking loose and causing embolisms in blood vessels in the skin of the feet, which causes a blueish purple colour and may be painful.
It is typically thought to affect the big toe, but it affects other parts of the feet as well, including the bottom of the foot (plantar surface). The occurrence of purple toe syndrome may require discontinuation of warfarin.
Several studies have also implicated warfarin use in valvular and vascular calcification. No specific treatment is available, but some modalities are under investigation.
“The CHADS2 score and its updated version, the CHA2DS2-VASc score, are clinical prediction rules for estimating the risk of stroke in patients with non-rheumatic atrial fibrillation (AF), a common and serious heart arrhythmia associated with thromboembolic stroke. Such a score is used to determine whether or not treatment is required with anticoagulation therapy or antiplatelet therapy, since AF can cause stasis of blood in the upper heart chambers, leading to the formation of a mural thrombus that can dislodge into the blood flow, reach the brain, cut off supply to the brain, and cause a stroke…”
A high score corresponds to a greater risk of stroke, while a low score corresponds to a lower risk of stroke. The CHADS2 score is simple and has been validated by many studies.[
My risk of ischemic stroke- based on the CHA2DS2–VASc score is 2.8% risk-
My 85 year old mom’s risk of stroke based on the CHA2DS2–VASc score is 8.5% risk-