Is this the article you are referencing?
Effect of Prophylactic Supplementation with Grape Polyphenolics on Endotoxin-Induced Serum Secretory Phospholipase A2 Activity in Rats
It's no hidden secret that polypholics have poor bioavailability. In this article it's even stated:
The polyphenolics in GE are largely composed of polymeric polygalloyl polyflavan-3-ols41 that are poorly bioavailable when consumed orally.18,35,49
You incidentally didn't read the article in it's entirety or you would have noticed this next statement. Or you read the abstract only? This here alone is my deciding factor that GSE has no effect on lowering HH. Personally I don't buy into supplements lowering ones HH, especially if there is induced stimulus of EPO either be drug induced or by some underlying cause. Such as mentioned further down.
Take note:
The current study has several limitations. First, we did not measure additional markers of pathophysiologic status or perform organ histopathology, especially of the liver and kidney, that may have provided explanations for the body weight and hematocrit changes that we noted. For example, the continuous reduction of blood cell volume suggests that rats may have been overhydrated, presumably due to LPS-induced renal inflammation.2However, given the experimental design, the reduction in hematocrit may have resulted from the cumulative effects of the blood samplings from the animals.
Take notice of the adjuvant use of injection LPS (Lipopolysaccharide) with GSE. The intended provocation of LPS is to create a toxic environment in the rat models. LPS is what's consider an endotoxin.
The sole purpose of this study design, is to demonstrate the corrective or positive effects of GSE. Also to investigate the expression as well, the reversal implications of sPLA2 and CRP from LPS. Elevated levels of both sPLA2 and CRP are two contributing factors too atherosclerositic plaque. As I mentioned in my earlier post, I've taken GSE for a few years now. On two of my VAP cholesterol lab's there's indication that I have high levels of sPLA2 and I'm genetically predisposed to high levels of LP(a). Through my hormonal modulation and selective diet, I take several different supplements to counter the effects my genetics has handed me down. With the many supplements I take daily, I take 300mg per day of Jarrow OPC+95 GSE. Not one time have I noticed any fluctuations in my HH. I have lab's done every three months. The biggest thing that dropped my HH was treating my OSA. Certainly wasn't supplements.
Even if there was a possibility that GSE might lower ones HH. Aside from all the aforementioned, what a lot of people fail to realize is the HED (human equivalent dose). In this particular study if we used the 300mg/kg equivalency it would be:
Within the article:
The supplementation of the control diet with 100 or 300 mg/kg GE daily
We'll use an example of a 200lb person in kg which is 90.718kg
HED=300mgkg(6rat/37human)=48.64864865 x 90.718=4413.308108mg or 4.4g per day.
That's a lot of GSE!
Calculations based on these formulas from:
https://www.google.com/url?sa=t&sou...Gbm8gwaSEqhxQ3fAQ&sig2=Gv23VRKCq1oUaNmOCU226Q
And
Fasebj | Mobile
Mike I know you are looking for that magical supplement(s) that is going to reduce ones HH. Sorry to say, you are going to continue to run into dead in roads looking for this potion of magnificence. You or any one else that wants to lower your HH. Find the cause first, then treat. Aging in it of its self plays a role in ones HH to climb. AAS, GH, Ephedrine, OSA, right sided heart failure, ect ect. Even in severe cases of sinus congestion, this can induce hypoxic-hypoxia from habitual mouth breathing, resulting in mild elevation of HH, within physiological range, generally in the upper limits of normal. Add AAS and sleep apnea on top of that. Guess what happens?
One other thing to keep in mind. When our bodies are trying to fight off an infection. Depending on the severity of the acute onset as well the duration (as you stated, you waited awhile before going to see your physician/ER?) This will cause our spleen to destroy more RBC than normal therefore potentially causing splenomegaly (enlarged spleen) in which could potentially lead to hypersplenism further exacerbating of premature destruction of healthy RBC. Which all of this is secondary to the bacterial infection. You may not of even been aware that your spleen was enlarged. If you want to post up your labs, I could tell you rather quickly if your spleen was taking a hit.
Sorry Mike, I see no remotely close plausible effect on lowering ones HH.
.gif "IP Gear")
