I imagine that the new aspirin study [JAMA (1)] will get a lot of media play, but I will post anyway.
A previous study concluded that the only people who benefit from low-dose aspirin are those who have already experienced a cardiovascular event. For everyone else, the risks obliterate any benefit.
Of course, for men with PCa, there is the added benefit of inhibiting microclots that might facilitate metastasis. PCa alters coagulation factors that make clots more likely. In fact, a deep-vein thrombosis increases the short-term risk of a PCa diagnosis in otherwise healthy men.
Also, men with PCa have an increased risk for cardiovascular disease. A risk that only increases with ADT.
The appeal of aspirin in PCa is the prevention of clots. However, I prefer to use nattokinase to clean-up any unwanted coagulation after the fact. I think it's safer. A periodic D-dimer test is needed to determine an appropriate nattokinase dose. (IMO, a D-dimer test should be performed even by aspirin users.)
The new study was confined to those who had no history of cardiovascular disease.
"This study found a significant increase in intracranial bleeding with daily low-dose aspirin but no significant reduction of ischemic stroke. These findings may have particular relevance to older individuals prone to developing intracranial bleeding after head trauma."
"To our knowledge, the ASPREE randomized clinical trial is the first large-scale trial to study the risks and benefits of aspirin in an exclusively older primary prevention population, in which an increased tendency to bleeding may alter the balance of risks and benefits of aspirin. This is particularly relevant to intracerebral events because intracranial hemorrhage is typically less treatable than ischemic events and more frequently fatal or disabling. With previous aspirin trials in mostly younger participants, an excess of intracerebral hemorrhagic events was frequently noted among individuals receiving active treatment, although numbers were small and in most cases did not approach statistical significance.
"The principal finding of this secondary analysis of a randomized clinical trial was an increase in intracerebral hemorrhagic events, which in absolute terms outweighed a smaller and nonsignificant reduction in ischemic strokes. Despite the older age of the cohort, incidences of both types of events were low, with an overall rate of 5.8 per 1000 person-years of follow-up. The incidence of ischemic stroke was 0.5 incidents per 1000 person-years of follow-up lower, which was not statistically significant, while that of intracranial hemorrhage was 0.7 incidents higher, which was statistically significant."
I've been doing the Natto-Serra thing since you and your neighbor put me on the research trail about the benefits of each. One of many Medical K9 Hat-Tips earned by both of you.
Stay Cool & Well,
Ciao - Kaptin K9
PS. Weatherwise, I guess we both would rather be in Leadville over the next week or so. K9 days of summer for sure>
I wish I had known more about coagulation from day one. I had been taking vitamin E and marine omega-3, & avoiding omega-6-rich cooking oils, & stupidly thought I was safe, but suddenly had a double DVT. Thankfully, not above the knee.
& so I was put on Warfarin & Heparin. I became familiar with the
INR (international normalized ratio), which is based on prothrombin time, at the "Coumadin Clinic".
The idea behind Warfarin is that it inhibits vitamin K reactivation & thereby decreases clotting factors II, VII, IX & X availability, leading to an increase in clotting time.
Warfarin does not dissolve fibrin clots. Plasmin does that - albeit slowly.
With a normal INR, a clot will continue to outgrow plasmin activity, but with the target INR it will accrue fibrin slowly - hopefully, slower than the rate at which plasmin is dissolving the clot. The process can take months . The danger is that with a longer clotting time, the patient might bleed-out following an accident.
Nattokinase is structurally similar to plasmin - but faster!
In the ER, I learned how to inject the proper dose of Heparin & why it was dangerous to inject more. Heparin was needed until the target INR was reached with Warfarin.
At the Coumadin Clinic, which I attended on Mon, Wed & Fri for numerous weeks, the INR was measured from a finger-prick drop of blood.
In my case, the normal Warfarin dose did not increase the INR. The dose was adjusted upward & I was told to use the full dose of Heparin. Later, I was told to inject a double dose. I was on high-dose Heparin for well over a month.
Eventually, a Warfarin dose was determined that brought the INR to within the target range.
However, the INR could jump around. Sometimes a bit below target & sometimes a bit above. When that happened, I was back to Mon/Wed/Fri visits. When I learned how to game the system, the reward was weekly visits. Two glasses of wine with lunch (before a test) would mess up the INR - but no-one cared if I drank a bottle of wine after the test. Spinach with dinner might result in a lower INR the next day. Adjusting the Warfarin dose accordingly would then mess up the next INR reading.
It often felt like I was taking part in a fiasco, and that tampering with the normal (safe) clotting time was a protocol that belonged to an earlier time.
Anyway, the take home message for me was that (a) increasing clotting time for 3 or 6 months was dangerous, and (b) did nothing to dissolve the clot, except passively & very slowly, and (c) the fastest intervention would be to boost plasmin activity with nattokinase.
Warfarin is too dangerous to use preemptively. And so, clots are allowed to develop until, perhaps, a life-threatening event occurs - a pulmonary embolism or ischemic stroke. A deep vein thrombosis might develop unnoticed, but if verified via ultrasound would probably result in a trip to the ER. Basically, one needs an ER visit to get a Warfarin script. There is no preemptive protocol.
The D-dimer test measures a fibrin degradation product caused by fibrinolysis due to plasmin acting on a clot. If someone goes to the ER with chest pain, s/he will first get a D-dimer test. A low number will rule out a blood clot. A high number isn't proof of a clot.
My own experience is that I can always get D-dimer to <0.20 mg/L FEU (the lowest LabCorp reading) by increasing daily nattokinase intake.
If D-dimer is non-specific, what weight should one give it? IMO, for someone with PCa, one should act as though an elevated D-dimer is due to a clot.
Is it OK for D-dimer to be in the reference range (0 - 0.49)? I have a zero-tolerance for D-dimer results above 0.20 mg/L FEU, but it looks like ER use numbers above 0.49 mg/L FEU for suspected DVT, pulmonary embolism & ischemic stroke.
See (1) for more D-dimer info.
There are now a number of alternatives to Warfarin, but they typically inhibit a coagulation factor, such as Xa, in order to increase clotting time. Same concept, just a better mousetrap (than rat poison. lol).
From Wiki:
Edoxaban, sold under the brand name Lixiana among others, is an anticoagulant medication and a direct factor Xa inhibitor.
Rivaroxaban, sold under the brand name Xarelto among others, is an anticoagulant medication. ... Rivaroxaban inhibits both free and bound Factor Xa in the prothrombinase complex.
Apixaban, sold under the brand name Eliquis, is an anticoagulant medication ... through directly inhibiting factor Xa.
D-dimer is a by-product of the degradation of cross-linked fibrin by plasmin [1, 2]. It is mainly produced by secondary fibrinolysis after thrombus formation and elevated D-dimer levels reflect ongoing or potential thrombus formation:[1,2,3,4] therefore, D-dimer has been used in the clinical diagnosis of various thromboembolic diseases [5, 6]. The most representative diseases are deep vein thrombosis or pulmonary embolism, and D-dimer is widely used in conjunction with clinical scales to exclude these diseases in patients with low clinical probability [7, 8]. D-dimer has been also proposed as a diagnostic tool for various cardiovascular, cerebrovascular, and aortic diseases, but has not gained as much consensus as venous thromboembolism yet [9,10,11].
D-dimer has also been used as an indicator in patients with ischemic stroke [2]. Its level is closely related to the size or severity of stroke lesions and short-term and long-term prognosis [12,13,14,15,16,17]. Additionally, the D-dimer level indicates the etiological mechanism of stroke [3, 18, 19]. D-dimer levels are higher in cardiogenic strokes that form fibrin-rich clots than in strokes caused by other mechanisms 18–21]. In strokes caused by large artery disease that form a platelet-rich thrombus or small vessel occlusion based on lipohyalinosis, D-dimer elevation was relatively insignificant [4, 20, 21]. Further, hidden malignancy has recently been suggested as one of the major etiologies of cryptogenic stroke, especially Embolic Stroke of Undetermined Source (ESUS), and its frequency can go up to 6.5% 22]. In these patients, D-dimer was found to be the most potent diagnostic marker and plays an important role as a predictor of early neurological deterioration (END), recurrence, and mortality [21, 23, 24].
I didn't know that low dose aspirin could be a threat for intra-cranial bleeds. What about the 'industrial strength' blood thinners like Xarelto, are they a bigger threat? I've been taking low dose aspirin to reduce stroke threats associated with atrial fibrillation. A-fib ablation surgery has pretty much ended my a-fib episodes so I am wondering if I should continue the aspirin regimen.
If you are over 70 years old than it is better for you to stop low dose aspirin as it can cause increased incidents of bleeding in older people and bleeding stroke would rise also and you really don't want that.
I also stopped aspirin as I believe (maybe I am wrong) that it could causes diverticulitis.
Aspirin is maybe OK if you are under 70. I am 65 now and I don't believe that I will start again.
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