Resveratrol combats ebv (study)...rituximab alternative?

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grandsons4
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by grandsons4 »

Orion98665, Hi: The article in Discovery had me on the edge of my seat like a good sci-fi movie. I wonder if infectious agents, such as the ones mentioned, contribute "missing pieces" of code to HERVs, enabling them to replicate?? Also, is it possible these HERVs exist in myelin, and are recognized there (more readily then elsewhere) by the immune system? I was attempting to read and understand the second article when my head exploded. I did manage to jump to the summary where they more precisely pinpointed the mechanism/s by which EBV persists, and thereby establish a potential target of future treatments. Thanks.
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by orion98665 »

grandsons4 wrote:Orion98665, Hi: The article in Discovery had me on the edge of my seat like a good sci-fi movie. I wonder if infectious agents, such as the ones mentioned, contribute "missing pieces" of code to HERVs, enabling them to replicate?? Also, is it possible these HERVs exist in myelin, and are recognized there (more readily then elsewhere) by the immune system? I was attempting to read and understand the second article when my head exploded. I did manage to jump to the summary where they more precisely pinpointed the mechanism/s by which EBV persists, and thereby establish a potential target of future treatments. Thanks.
Hi grandsons4, i'm not too sure about about HERVs existence in myelin, but i'm interested in how these viruses affects the endothelium or vascular system.. Theres just WAY TO MUCH EVIDENCE LINKING
MS AS JUST NOT AUTOIMMUNE DISEASE BUT ALSO A VASCULAR DISEASE.. Here is another thread that relates to ebv that was talked about on TIMS...

http://www.thisisms.com/forum/general-d ... 10536.html

I's still digging in my research papers but if i recall there is a paper that shows reactivation of EBV during a MS relapse...???

I still believe there are many factors that can contribute to MS that are NOT related to a virus... Such as car accidents (been talked about on this forum). Maybe this might explain why some therapies work
for some and not others..

edit: Here is a great link (MUST READ) of reactivation ebv during ms relapse..
In a new study published on April 11, investigators in Italy found that, in patients with relapsing-remitting multiple sclerosis (RRMS), the immune response to the Epstein-Barr virus (EBV) appeared to cycle simultaneously with their disease activity, meaning that when the virus was active, so was their MS./quote]

note: the date of article was just this last June...

http://www.healthline.com/health-news/m ... ion-061213

Last edit: Here is a link of the association of ebv and ccsvi
One of the most interesting findings of the present study was that subjects who had a history of infectious mononucleosis showed higher frequency of CCSVI diagnosis. It is known that the Epstein-Barr virus (EBV) infection has been associated with numerous cancers. There is also considerable evidence that EBV infection is the most important risk factor candidate for the development of MS [23]. MS risk is low in individuals who are EBV negative, but increases several fold following EBV infection. There is some evidence suggesting that EBV infection can act as a precipitating factor for venous thrombo-embolism in immuno-compromised patients [24]. The mechanisms by which EBV infection might trigger thrombosis are not fully understood, but include transient elevations of anti-phospholipid antibodies [25], and EBV-induced oxidative endothelial cell injury [26]. The EBV virus was also found to have caused venous thrombosis in a patient with hereditary thrombophilia [24]. Persistent EBV infection in the small vein vessel wall can directly promote a pro-inflammatory, pro-coagulant, and pro-atherogenic environment [24]. Whether EBV infection may damage the venous endothelium, causing venous thromboses and strictures in the cranial and spinal venous drainage system, is unknown at this time. It could also be hypothesized that an EBV-mediated autoimmune attack of the intra- and extra-cranial veins can cause chronic inflammation and scarring [27]. Further longitudinal studies should investigate the relationship between CCSVI and EBV infection./quote]

http://www.plosone.org/article/info%3Ad ... ne.0028062

Bob
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi,

I have no argument that Zinc depletion and Uric acid levels are correlated but correlation doesn't always explain the relationship.

This is a reasonable explanation of the relationship between zinc and Nitric Oxide Synthase (all forms)- http://proteopedia.org/wiki/index.php/N ... e_Synthase

"In order for NOS to be active it has to dimerize and bind H4B. The dimer is structurally stabilized by a zinc ion. which is situated at the oxygenase domain interface of the dimer[8]. The zinc ion is tetrahedrally coordinated by four cysteins (two from each monomer - Cys109 and Cys104). The zinc ion is found at a region which connects the N-terminal hook and the subunit core. The coordination of zinc arranges the N-terminal hooks so that they interact with their own subunit. However, when there is no zinc ion present, two of the thiolate ligands (cysteines) form a disulfide bond connecting the two subunits".

In terms of Peroxynitrite this article may be of use - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150913/

"ONOO– or SIN-1, but not decomposed ONOO–, H2O2, NO, or O2.–, promoted the release of zinc from the zinc-thiolate cluster of eNOS. .... Because iNOS and nNOS often function under oxidative conditions such as inflammation where they may be uncoupled , it is conceivable that ONOO– also causes zinc loss from both iNOS and nNOS by a similar mechanism. Finally, the fact that high concentrations of exogenous reduced thiols did not block the oxidation by ONOO– of zinc-thiolate complexes in eNOS dimer suggests that the zinc-thiolate complex rather than free thiols in eNOS is the primary target for ONOO–. "

Peroxynitrite clearly impacts NOS unbinding zinc but it will also impact on other pathways leading to low uric acid. I think the relationship between zinc and uric acid is coincident not cause and effect. The relationship is between peroxynitrite and other elements rather than Zinc and Uric acid.

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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi Anonymoose,

Rituxumab is a monoclonal antibody that targets B cells. I tried to get my doctor to give it to me but he has a blind spot about them as his own sister died from an adverse reaction to one of them. A monoclonal antibody is a designer antibody that has been optimised to perform a certain function by binding exclusively to one domain in a V shaped vector. If it does more than that then it may do something disastrous.
Without going into detail I think two things are going wrong. The precondition relates to endothelial dysfunction. This gives rise to iNOS where eNOS or nNOS should exist. I suspect this goes right back to birth and relates to an adrenal malfunction (which we may grow out of) but is obviously slow to manifest as a problem. The health of the mother may be an issue but how will we ever know. I am suspicious that something is awry with the retinoids and Vitamin A way back at that stage which set us on the wrong path. (My pet idea which lacks sufficient research based evidence). This endothelial dysfunction is metabolic.
The second element involves a viral trigger. The most obvious candidate is EBV but it could be something else that is persistent and promotes Superoxide. EBV stays resident in B cells and "breeds up" as we make new B cells. Again this takes time. It is not really autoimmune as it is not the immune system attacking the host, it is the B cell being altered. Rituxumab should address this but it won't be looking at the accumulation of damage from endothelial dysfunction. Adding Arginine will help the endothelium to recover but it won't stop the permanent damage already done by Peroxynitrite or stop the replication of EBV.
Many people have EBV without symptoms but they don't have low uric acid or endothelial dysfunction as well. Elevating Uric acid (by diet or medication) helps scavenge Peroxynitrite. High Uric acid tops out with gout symptoms so MS symptoms lessen as the peroxynitrite is mopped up.
My approach is aimed at doing several things 1) lower Peroxynitrite by limiting Superoxide and 2) repair the endothelium.
The Valtrex and now the Resvesterol are all about disrupting the EBV to lower the viral load and hence lower superoxide. The Arginine is all about repairing the endothelium to lower iNOS. Carrot juice is about retinoids to elevate RXR and hopefully heal the gut at the same time. Olive leaf extract is to elevate PPAR to help the lipids. The probiotic helps the mucked up gut flora. The coenzyme Q10 is to boost ATP as I assume this step permanently damaged and can't help cell function properly any more.
I'm not sure what to suggest about the oestrogen issue. I haven't looked at that issue in any detail. Someone else may have a better idea. Can you provide more colour around that topic? Is it based on what you have read or how you feel? Can there be contraindications with other things you are taking?
I'm sure there are many ways to skin a cat but the structure of what I do is working very well for me.

Regards
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by grandsons4 »

Scott1: In the article you recommended (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150913/), the case is made that peroxynitrite targets eNOS, the reason being the zinc at the center. One reason they used to substantiate their conclusion was the fact that "the effects of ONOO– were mimicked by the zinc chelator TPEN," implying the similar pulling of zinc from the dimer. (Interesting connection: In another article I read the following, "Peroxynitrite toxicity is a major cause of neuronal injury in stroke and neurodegenerative disorders. The mechanisms underlying the neurotoxicity induced by peroxynitrite are still unclear. In this study, we observed that TPEN, a zinc chelator, protected against neurotoxicity induced by exogenous as well as endogenous peroxynitrite." TPEN apparently steals the zinc from the peroxynitrite.) Question: Near the end of the article they state, "The zinc-thiolate cluster represents a selective target for ONOO–. The reaction of ONOO– with zinc-thiolate clusters is at least 1,000 times faster than its reaction with cysteine-thiols.", and "Thus, zinc will attract anionic oxidants, resulting in the loss of zinc followed by disulfide bond formation within the metal binding site." So, peroxynitrite ignores the antioxidant cysteine, but gobbles up zinc. Question: Wouldn't supplementation with zinc help to satisfy its appetite? (P.S. What does peroxynitrite do with the zinc?)
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi,

I'll defer to Jimmylegs greater knowledge on Zinc but I don't think "gobbles up" is quite the right way of describing it.

I'm not anti zinc. There is plenty of evidence that it is disturbed in MS but I'm not really comfortable with saying a Zinc deficiency is the cause of things. It can be in some circumstances but I think it is often (not exclusively though) coincident rather than the cause. Certainly it is a marker that something not right and I don't doubt supplementing can help. What causes the zinc depletion interests me.
Peroxynitrite doesn't have a plan for the Zinc. It is a very short lived volatile radical. It's more like a wrecking ball in a china shop. It just goes around stuffing things up. It exists in normal healthy humans but if the ingredients (superoxide and iNOS) are abundant then all hell breaks loose.

If you want to read more about Peroxynitrite then google "Csabo Szabo" + "peroxynitrite". He is the man. You will be reading for weeks.

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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Anonymoose »

Scott1 wrote:Hi Anonymoose,

Rituxumab is a monoclonal antibody that targets B cells. I tried to get my doctor to give it to me but he has a blind spot about them as his own sister died from an adverse reaction to one of them. A monoclonal antibody is a designer antibody that has been optimised to perform a certain function by binding exclusively to one domain in a V shaped vector. If it does more than that then it may do something disastrous.
Without going into detail I think two things are going wrong. The precondition relates to endothelial dysfunction. This gives rise to iNOS where eNOS or nNOS should exist. I suspect this goes right back to birth and relates to an adrenal malfunction (which we may grow out of) but is obviously slow to manifest as a problem. The health of the mother may be an issue but how will we ever know. I am suspicious that something is awry with the retinoids and Vitamin A way back at that stage which set us on the wrong path. (My pet idea which lacks sufficient research based evidence). This endothelial dysfunction is metabolic.
The second element involves a viral trigger. The most obvious candidate is EBV but it could be something else that is persistent and promotes Superoxide. EBV stays resident in B cells and "breeds up" as we make new B cells. Again this takes time. It is not really autoimmune as it is not the immune system attacking the host, it is the B cell being altered. Rituxumab should address this but it won't be looking at the accumulation of damage from endothelial dysfunction. Adding Arginine will help the endothelium to recover but it won't stop the permanent damage already done by Peroxynitrite or stop the replication of EBV.
Many people have EBV without symptoms but they don't have low uric acid or endothelial dysfunction as well. Elevating Uric acid (by diet or medication) helps scavenge Peroxynitrite. High Uric acid tops out with gout symptoms so MS symptoms lessen as the peroxynitrite is mopped up.
My approach is aimed at doing several things 1) lower Peroxynitrite by limiting Superoxide and 2) repair the endothelium.
The Valtrex and now the Resvesterol are all about disrupting the EBV to lower the viral load and hence lower superoxide. The Arginine is all about repairing the endothelium to lower iNOS. Carrot juice is about retinoids to elevate RXR and hopefully heal the gut at the same time. Olive leaf extract is to elevate PPAR to help the lipids. The probiotic helps the mucked up gut flora. The coenzyme Q10 is to boost ATP as I assume this step permanently damaged and can't help cell function properly any more.
I'm not sure what to suggest about the oestrogen issue. I haven't looked at that issue in any detail. Someone else may have a better idea. Can you provide more colour around that topic? Is it based on what you have read or how you feel? Can there be contraindications with other things you are taking?
I'm sure there are many ways to skin a cat but the structure of what I do is working very well for me.

Regards
Thanks scott1! Great summary and it totally makes sense. The vitamin A also suppresses th17 which can have the effect of down regulating cd8+ T cells that are needed to kill ebv and are usually lower in msers than in healthy controls. I think I need a juicer. :)

As for the estrogen issues, I think the sweet potato based phytoceramide supplement I am taking might be combining with the resveratrol to double whammy my hormone balance. Stopping resveratrol hasn't stopped the spotting (you asked for colour!). But even that is now further complicated as I've started a bcp to eliminate the nuisance of my monthly tragedy during my rituximab infusions. I'll retry resveratrol at a low dose when things are back under control.

Now you and gs4 are going far more into technical details than I can stand with the zinc/uric acid discussion. I prefer the fruit on the ground or the lower branches. Since jimmylegs seems to be enjoying life much as you have (granted for a longer period of time), could it be that her supplement and diet program have gotten the ebv and all fallout like low uric acid levels and altered gut flora/permiability under control. Maybe there aren't any residual deficits so long as you take care of your immune system and its nutritional needs.
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by grandsons4 »

Scott1: It was late and my writing was slipping. I was trying to ask if zinc actually binds to the peroxynitrite, rendering it inert and able to be safely eliminated. While simultaneously looking to restore balance (which will take time), I consider, in the interim and in order to minimize presently occurring damage, a "band-aid" approach to be wholly acceptable, if not mandatory. Zinc would present another low-risk/high-reward option (again, inosine one of the others) for eliminating excess peroxynitite. So, I'll rephrase: In your opinion, would zinc, introduced via supplementation, present a viable alternative "target" for peroxynitrite, thereby preserving functioning eNOS?
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by jimmylegs »

on causality vs correlation..

low zinc intakes or diets/regimens/meds that are hard on zinc absorption can lead to poor zinc status and consequently low uric acid.

I've had this question before re correlation vs causation (that was in relation to nutrient status and disease state, after a presentation on applying restoration practice to human illness) and my out loud answer was, it can be both - but everything I have seen leads me to believe that nutrient status can certainly be causal. my less diplomatic facetious answer might have been that we can decide that scurvy causes vit c deficiency or is perhaps correlated with low vit c, or that rickets causes vit d deficiency or is merely correlated with low vit d. when of course we know that these conditions are caused by nutrient deficits.

anyway back on the zinc/ua track. I fought low uric acid for years with no success until identifying and correcting zinc deficiency. after working on zinc, I later made the zinc-uric acid connection. it's not the easiest thing in the world to sniff out a causal link in the literature, but this was my first hint - in this study they put women (no disease process) on a low zinc diet and watched the uric acid levels fall, whether or not they were taking oral contraceptive drugs:

Effect of Low Zinc Intake and Oral Contraceptive Agents on Nitrogen Utilization and Clinical Findings in Young Women
jn.nutrition.org/content/107/12/2219.full.pdf
"Serum uric acid, «-2-and /8-glob- ulin changed significantly in both groups. Clinical problems developed in all the subjects with serum zinc levels below 50 ug/dl during the study; three of the six with serum zinc levels above 50 ug/dl also complained of clinical symptoms. The results suggest that zinc deficiency through depletion of accessible body zinc stores developed during the 35-day study."

after reading that study I started measuring zinc and ua together. finally with improved zinc status my urea cycle had begun to function properly, the zinc levels and the uric acid levels were both up. I shudder to think what my ammonia levels must have been when my zinc was deficient - research on zinc levels and their inverse relationship with ammonia makes me wish I had known enough at the time to ask for ammonia testing. certainly my cognitive function at the time was a disaster. if we found a case where uric acid was low and zinc replete, then we'd be looking for something else. but when uric acid marches in lockstep with zinc status AND intake, as supported in research and in personal practice, you start to gain certainty re causality. check out these patient results.. by sept 2012 you can really see the zinc ua connection: https://sites.google.com/site/brmnutrients/ the vit d3 connection is visible too.

across the board I prefer to ensure optimal status of essential nutrients before looking to non-essential products such as inosine (by non-essential i mean it is synthesized endogenously in humans if the biochemistry is functioning properly). unfortunately the pathway is complex enough that I can't name the specific nutrients involved off the top of my head.. on that subject, I am having trouble getting a handle on the difference between adenosine deaminase, which appears to be zinc-dependent, and adenosine deaminidase.. i digress.

the relevant action of inosine in ms appears (if murine eae studies can be considered applicable) to be via conversion to ua..

Therapeutic intervention in experimental allergic encephalomyelitis by administration of uric acid precursors
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC138606/
"We have assessed the effects of inosine, as well as inosinic acid, on parameters relevant to the chemical reactivity of peroxynitrite and the pathogenesis of EAE. Both had no effect on chemical reactions associated with peroxynitrite, such as tyrosine nitration, or on the activation of inflammatory cells in vitro. ... the mode of action of inosine and inosinic acid in EAE is via their metabolism to UA."

leaving aside whether inosine does one or two or ten different things, and really regardless of whether these eae research conclusions are in fact transferable to human ms, i would definitely come down on the side of optimizing zinc first and letting it do its hundreds if not thousands of jobs - known and documented jobs.. (which definitely include virus-fighting, ensuring membrane (eg endothelium, intestinal, BBB) impermeability, being a requirement for the utilization of vitamin A, and possibly including supporting endogenous inosine synthesis)- rather than choosing an inosine supplement to do one or even several of zinc's many jobs (i may not have been looking in the right places, but i have yet to see any hint that inosine is specifically antiviral).

another issue i have with inosine is the lack of information on reference or target serum inosine levels. my full text access is still pending and there don't appear to be any easily accessible abstracts that actually give numbers and units for healthy control vs patient inosine levels. here's one study i came across the other day, in which inosine levels seem to have been in excess:

Purine metabolites in fibromyalgia syndrome.
http://www.ncbi.nlm.nih.gov/pubmed/23000315
"Significantly higher serum inosine, hypoxanthine and xanthine levels (p<0.001) and significantly lower serum adenosine (p<0.05) were detected in the FMS patients vs healthy controls... purines, in particular adenosine and inosine, may be involved in pain transmission in fibromyalgia"

that 2013 study was actually done in humans, but doesn't seem to have anything to do with supplementation. there's just not enough data :S

anyway. excess can be a danger for anything, but with zinc we can research what those numbers are quite easily. with inosine i am not finding this to be the case. we also have a pretty decent handle on how zinc supplementation can affect other nutrients. i have yet to see research on how inosine supplementation might affect internal balance of related systems. we're seeing the outcome of action without full comprehension of interactions, with the increase in mortality after years (decades?) of being urged to supplement calcium without considering impacts on magnesium balance... or zinc status for that matter.
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi,

I absolutely agree with the concept that the relationship can be both causal and coincidental.

I don't think it's wise to think of NOS as a Zinc substrate (although I guess it is along with many other things). Binding Peroxynitrite and Zinc is not the answer. You need to prevent the excess formation of Peroxynitrite in the first place. That means limit superoxide formation and iNOS formation. Promote eNOS and nNOS. The best answer is use Arginine for the NOS and follow an anti EBV protocol.
Peroxynitrite has a short life. It keeps breaking down and reassembling. It's not going to remain stable enough to transport anything by binding to it. that process helps it to expand very rapidly.

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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by jimmylegs »

throwing nutrition and Superoxide Dismutase into the equation here...

three kinds of SOD: SOD1 and 3 need copper and zinc. SOD2 needs manganese.
http://en.wikipedia.org/wiki/Superoxide_dismutase#Human

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis
http://www.sciencedirect.com/science/ar ... 770091051X
"... The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. ... Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. ... Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD."

Impact of superoxide dismutase on nitric oxide and peroxynitrite levels in the microcirculation--a computational model.
http://www.ncbi.nlm.nih.gov/pubmed/18002134
"Interactions of free radicals such as superoxide (O2-), nitric oxide (NO), and peroxynitrite (ONOO-) are important in pathophysiological conditions such as hypertension, atherosclerosis, diabetes and the resulting cardiovascular diseases. Excessive levels of superoxide during oxidative stress cause a reduction in NO bioavailability by forming peroxynitrite and resulting in endothelial dysfunction. Superoxide dismutase (SOD) competes with NO for superoxide, and reduces the formation of peroxynitrite. ... The model predicts that a reduction in SOD levels results in increased superoxide and peroxynitrite concentrations and decreased NO concentration in the vessel. The results also suggest a role of SOD in the amelioration of oxidative stress and NO bioavailability in microcirculation. This model will help in furthering our knowledge of endothelial dysfunction in pathological conditions and the impact of specific SODs on free radical interactions."
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi,
That all makes sense but don't forget we need Superoxide to kill bacteria and SOD helps to keep the level appropriate so we don't have superoxide running out of control. The Superoxide from EBV infected B cells is over and above that. We are asking a lot of SOD to do all the lifting.

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Re: Resveratrol combats ebv (study)...rituximab alternative?

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particularly if zinc status is suboptimal, and therefore insufficient zinc is allocated to the production of cu-zn sod in the first place.
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Scott1 »

Hi Anonymoose,

I am clearly not on firm ground but your symptoms sound to me that they are triggered by falls in Progesterone levels. That should happen in a normal cycle at the appropriate time. I can't find a reference that suggests Resvesterol causes that so it may be something else.
Some things I read suggested Progesterone deficiency could also be described as an Estrogen dominance . Other references noted adrenal malfunction.
I'm not sure where I can go with this as I'm not strong in this area. Maybe there is a medication or other factor at play and Resvesterol is an coincidental involvement.

Just a suggestion.

Regards
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Re: Resveratrol combats ebv (study)...rituximab alternative?

Post by Anonymoose »

Scott1 wrote:Hi Anonymoose,

I am clearly not on firm ground but your symptoms sound to me that they are triggered by falls in Progesterone levels. That should happen in a normal cycle at the appropriate time. I can't find a reference that suggests Resvesterol causes that so it may be something else.
Some things I read suggested Progesterone deficiency could also be described as an Estrogen dominance . Other references noted adrenal malfunction.
I'm not sure where I can go with this as I'm not strong in this area. Maybe there is a medication or other factor at play and Resvesterol is an coincidental involvement.

Just a suggestion.

Regards
Thanks for diving in to foreign territory on my behalf. Who knew you would one day be exploring the intricacies of female hormones? :P I am pretty sure the resveratrol and sweet potato powder combo threw me into estrogen dominance. I stopped the sweet potato powder (sometimes used to treat estrogen shortage) yesterday et voila...spotting gone. I know the resveratrol contributed because the spotting became stronger with resveratrol and even more so as I increased the dose. I think I may be able to handle just resveratrol so I will retry once I am certain I am back to normal.

Oh the joys of self guinea-pigdom! Btw, got a juicer yesterday...carrot juice is clearly an acquired taste! Throwing in some apple and ginger today.

Thanks again. :)
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