Concerned with ursa major?

Pjunior22

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I saw some supporting studies that say ursolic acid can promote blood clottage and artery blockage? Should this be a concern
 
cheftepesh1

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At the end of the day it is important to look at who Funded the study. Many times they have a vested interest in a certain out come.
 
Iwilleattuna

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OP, I think you're confusing ursolic acid with arachidonic acid lol
 
nostrum420

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No, the studies referred to in the OP do exist. I have my concerns with the methodology but I'm not a research hematologist. 🤷‍♂️
 
Marne40

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I honestly didn’t look at all the studies referenced in this article, but this was the only thing I could find (didn’t spend much time looking lol) that referenced blood becoming “sticky.” I’m also a UA fanboy so I’m admittedly biased and only saw what I wanted to see. It’s been mentioned a couple times already, but you really have to take some of these studies lightly since the motives behind them are sometimes biased (think palm vs coconut oil). You also have to take into account that everyone’s body chemistry is a little different and we’re eating different things that may or may not interact with a supplement. In the end, you never really know how something will affect you until it’s in your body.
 
nostrum420

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"In this study, the effect of UA and OA on platelet aggregation was examined on the basis that alteration of platelet activity is a potential process contributing to cardiovascular events."

Translation: they created pro-clotting conditions in this study because some people have pro-clotting conditions.

"Treatment of UA enhanced platelet aggregation induced by thrombin or ADP, which was concentration-dependent in a range of 5–50 μM."

Translation: they administered drugs to rat blood to make it more prone to clotting and that only happened once certain blood levels of those drugs was achieved.

"UA and OA did not affect plasma coagulation assessed by measuring prothrombin time and activated partial thromboplastin time."

Translation: even with the goal of this study in mind, one of the experiments showed no effect on one of the most important factors in clot formation.

"Preparation of washed platelets
Washed platelets (WP) were prepared as described previously (Liu et al., 2013). Briefly, blood was collected from the abdominal aorta of rats anesthetized with ether using acid-citrate-dextrose (ACD; 85 mM trisodium citrate, 66.6 mM citric acid, and 111 mM glucose) as an anticoagulant (ACD: blood =1:6). After centrifugation at 250×g for 15 min, platelet-rich plasma (PRP) was obtained from the supernatant. Platelets were centrifuged at 500×g for 10 min, and washed once with a buffer comprised of 138 mM NaCl, 2.8 mM KCl, 0.8 mM MgCl2, 0.8 mM NaH2PO4, 10 mM HEPES, and 5 mM EDTA (pH 7.4) by suspension and centrifugation. WP were prepared by resuspending the platelet pellets in suspension buffer solution (138 mM NaCl, 2.8 mM KCl, 0.8 mM MgCl2, 0.8 mM NaH2PO4, 10 mM HEPES, 5.6 mM dextrose, and 1mM CaCl2, pH 7.4). The number of cells was adjusted to 2×108 cells/ml.
Platelet aggregation
Platelet aggregation experiments were performed using a four-channel aggregometer (Chrono-log) as described previously (Liu et al., 2013). WP were treated with the indicated concentrations of UA or OA for 5 min, and were stimulated with either thrombin, ADP, or collagen. Aggregation was assessed by measuring the changes in light transmission with the aggregometer.
Whole blood aggregation
Blood was collected from the abdominal aorta of ether-anesthetized rats using 3.2% sodium citrate as an anticoagulant (sodium citrate:blood=1:9) and diluted with normal saline (1:1). Blood was incubated with UA or OA for 5 min and was stimulated with thrombin. Aggregation was assessed by measuring the impedance change with a whole blood aggregometer (Chrono-log).
Plasma coagulation
Plasma coagulability was tested by measuring prothrombin time (PT) and activated partial thromboplastin time (aPTT) using a Coagulator2 analyzer (Behnk Elektronik, Norderstedt, Germany) with thromboplastin-D or CaCl2 and APTT-XL re-agents (Fisher Diagnostics) respectively, according to the manufacturer’s instructions."

This ^^^ is long and complicated but basically, they did the testing in a sort of combination of in vitro and in vivo methodology... Again, I'm not a research hematologist. Maybe this is the standard for these types of studies but it seems far removed from in vivo conditions in living humans.

Additionally, the plasma test was the one done with the least of these pro-clotting conditions in play and low and behold: no clotting.


 

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