Chronic Microglial Activation in ME/CFS, And Its Possible Treatment Using Microglial Inhibitors

[Biarritz13]

Very interesting. That study contradicts the earlier study which found ganciclovir is a potent inhibitor of microglial proliferation and neuroinflammation.

And isn't Dr. Montoya who thinks that Valcyte inhibits microglia?

 

[Hip]

And isn't Dr. Montoya who thinks that Valcyte inhibits microglia?

Montoya suggests inhibition of microglial activation may be one of the possible mechanisms by which Valcyte helps ME/CFS.

Someone needs to examine these two contradictory studies, and figure out which one is likely to be correct.

 

[eljefe19]

@Hip have you heard of the drug Remicaid? It's a biologic that works against TNF-a. I just read an anecdote of a PWME who achieved long term improvements after using Remicaid for comorbid RA. If TNF-a is associated with TH1, maybe Remicaid would be a good adjunct to all the TH1 shifters we take.

 

[Hip]

I've tried some anti-TNF-alpha supplement and drug protocols. I find that inhibiting TNF-alpha reduces the irritability symptoms that can appear in ME/CFS.

Some Potent TNF-Alpha Inhibitors:

Cat's claw — a remarkably potent inhibitor of TNF-alpha production 1
Vinpocetine — potently inhibits TNF-alpha. 1
Taurine — significantly reduces TNF-alpha 1
Noopept — reduces TNF-alpha by half. 1
Wellbutrin (bupropion) — inhibits TNF-alpha, IL-1beta and gamma interferon. 1
Etanercept (Enbrel) — blocks the effects TNF-a by binding to it and stopping it from interacting with body’s cells. 1
Stinging nettle leaf — decreases LPS induced inflammatory mediators, triggering an 80% reduction in TNF-α and a 99% reduction in IL-1β 1
Four macrolides (roxithromycin, erythromycin, clarithromycin and azithromycin) — inhibit IL-1β, TNF-α, IL-6 LPS-stimulated J774 macrophages. 1 (full text). NOTE: Roxithromycin is the only macrolide antibiotic that crosses the blood-brain barrier.
Acetylcholine (neurotransmitter) — significantly inhibits the release of TNF.

 

[eljefe19]

@Hip wow great work my man. Seems like of the natural agents Stinging Nettle was a potent option. Might try this, as irritability is one of my worst symptoms. Especially when anxious or when my fibro is flaring. My symptoms are more or less controlled on high dose Oxymatrine and my efforts of late have been to further reinforce the Th shifting and preserve or heighten the effects, but I've definitely noticed increased irritability of late.

 

[Hip]

@eljefe19 The best treatment I found for the irritability symptoms is very low dose amisulpride. I've taken this every day at a 12.5 mg dose for a few years now.

 

[eljefe19]

@Hip what's your opinion on the theory that microglial activation is necessary, or useful, if we do in fact have a chronic CNS and brain enterovirus infection? I am taking almost every microglial activation inhibitor you listed, and I am feeling 50-60% better than when I switched from Valgancyclovir to Oxymatrine, and started designing my own regimen. I am looking for the best possible chance to clear the enterovirus into remission. I also take a number of the antiviral supps for Coxsackie and Echovirus, and a number of Th2>Th1 shifters, as well as numerous immune boosters of different mechanisms. I am not too concerned with microglial activation, because I think it is probably unlikely that I will be able to clear the enterovirus completely with supplementation and current medications, and therefore if inhibiting microglial activation lessens symptoms, its worth doing. But others have advised me otherwise.

 

[Hip]

I am taking almost every microglial activation inhibitor you listed,

Interesting!

and I am feeling 50-60% better than when I switched from Valgancyclovir to Oxymatrine, and started designing my own regimen.

I am not quite understanding your statement. Can you quantify your improvement in symptoms a bit more precisely please. Is it your brain fog that has improved, energy levels, PEM resistance?

I find that when talking about ME/CFS improvements, it is good to indicate those improvements on the ME/CFS severity scale of mild, moderate and severe. Any improvement that can move you up one level of that scale (eg, from moderate to mild) I consider a major improvement. Any improvement that moves you up a smaller amount, I view as a more minor improvement.

@Hip what's your opinion on the theory that microglial activation is necessary, or useful,

Your guess is as good as mine on this. Some brain autopsies of ME/CFS patients have shown traces of enterovirus infection in the brain tissues (whereas none was found in the controls). So presumably some brain inflammation and the attendant microglial activation will be needed to keep this brain infection in check, assuming such brain infections are common in ME/CFS.

However, it possible that the brain inflammation and microglial activation are too ramped up, and are more fierce than is necessary to keep the brain infection in check. Brain inflammation can become ramped up when there is infection in other parts of the body (eg the gut), as when the vagus nerve senses infection in other parts of the body, it automatically signals to the brain, and the brain then ramps up brain inflammation. In this way, some gut dysbiosis (gut infection) might be increasing brain inflammation to higher than is necessary.

There is also the situation known as immune priming, where the immune system becomes oversensitive, and thus turns itself on too easily and too fiercely. Some researchers think immune priming may be involved in ME/CFS. See the posts here, here and here for more info on immune priming.

Autoimmunity (which the rituximab studies indicate is very likely involved in ME/CFS) may also be causing unnecessary brain inflammation.

In summary: it's possible that the microglial activation / brain inflammation is simply keeping a brain infection in check; but it is also possible that the brain inflammation is unnecessarily ramped up due to one or more of the factors detailed above.



By the way, in terms of reducing brain inflammation and the attendant microglial activation, you may want to look at the 29 supplements detailed in my thread here: Completely eliminated my severe anxiety symptoms with three supplements! These 29 supplements I found all helped reduce my anxiety levels; I believe my generalized anxiety disorder was underpinned by brain inflammation, and believe the reason most of these supplements worked to reduce anxiety is because they reduce brain inflammation. Supplements like turmeric are well known for their anti-neuroinflammation effects. I also think N-acetyl-glucosamine is likely a potent brain inflammation reducer.

Some of the 29 supplements, such as the probiotics and prebiotics, likely work to reduce brain inflammation indirectly, by reducing gut dysbiosis and gut inflammation. By the vagus nerve mechanism explained above, reducing gut inflammation can in turn reduce neuroinflammation.



Another important angle on brain inflammation is the connection between the dopaminergic system and neuroinflammation. Dr Andrew Miller's studies suggest low dopamine may increase the effects of inflammation: ie, low dopamine levels in the brain (in the basal ganglia) could cause a relatively benign mild inflammatory state to become something really problematic. See Cort's blog article on Dr Andrew Miller's dopamine research, and this second article also.

So if you can raise dopamine, you may lessen brain inflammation. This may be why very low dose amisulpride has been shown to have benefits for ME/CFS, as this drug works via stimulating the dopamine D2 and D3 receptors. See: Amisulpride — A Multipurpose Drug for ME/CFS I take 12.5 mg of amisulpride every day, and find it does help reduce some ME/CFS symptoms.

I posted a list of dopaminergic drugs and supplements here. However, most of these dopaminergic drugs probably will not work well in ME/CFS, because Dr Andrew Miller says ME/CFS may involve problems with the actual synthesis of dopamine, meaning there is a shortage of dopamine available. In the second Dr Andrew Miller article it says:

Stimulants such as amphetamines and dopamine reuptake inhibitors which increase dopamine release may be ineffective because innate immune activation is blocking dopamine synthesis.

Increasing dopamine synthesis (not enhancing dopamine release) is a more likely target in disorders like ME/CFS, and it’s to that we turn next.

Source: 1

As a result of reading about Dr Andrew Miller's work, I recently ordered the Russian drug bromantane, which works by up-regulating expression of the enzymes which synthesize dopamine. Ref: 1 Bromantane is quite unique in this respect, in that it increases dopamine by promoting the manufacture of dopamine. I am hoping bromantane will be beneficial not only for reducing ME/CFS neuroinflammation, but also for treating my anhedonia and depression, which may be due to low dopamine. I will be testing out bromantane in the coming months.

 

[eljefe19]

@Hip So looking at the NICE guidelines, I was heading into solidly into severe CFS from moderate, at the time of ditching Valgancyclovir and starting Equilibrant. I believe I would have stayed at severe level had it not been for the changes I made. Muscle pain was unbearable at times, severe IBS stomach cramps, severe PEM, feeling flu-like like all the time, brain fog and anxiety at severe levels (I begged my doctor for a Clonazepam script because I was starting to have panic attacks, exacerbated by my ever declining health and ability to take care of myself. After starting Equilibrant I immediately felt even sicker. It seemed like some symptoms like pain, anxiety, depression, and the flu-like symptoms got worse. It took every ounce of strength and mental fortitude, but I was determined to carry on. I ramped up to 6 tablets of Equilibrant every day, did that for a month, but then my research into Oxymatrine, Astragalus, Olive Leaf Extract, Shiitake Mushroom, and Licorice, and each of their unique benefits to people with an enterovirus infection, led me to pursue high doses of each individually.
I ramped up to:
1200mg Oxymatrine (Alternative Medicine Solutions)
3g Astragalus
50mg Hydroxytyrosol (From Powdercity.com, The more beneficial compound in OLE due to its long half life)
2g OLE
900mg Shiitake Mushroom Extract

Compared to the 1.5g proprietary blend of Equilibrant this was a much more aggressive approach. It was not easy as the herx reaction combined with Th1 dominance depression side effects almost broke me. I started at this point to pursue a robust anti depressive and anti anxiety stack, consisting of both supplements and medications.
I used your 29 Anti-anxiety supplements as a reference.

Also, your pro Dopamine supplements and medications was another stack I've referenced. I tried Memantine, Bromantane, Low Dose Amisulpride, and soon to try Amantadine (I have an EV7 infection, I have no specific research showing Amantadine is effective against EV7, but your work indicated it was effective against a couple strains of EV, and Dr Chia uses it so I'm going to give it a try. Bromantane is the only other pro dopamine medication I'm taking at the moment, waiting for more Amisulpride to come in, and I also was fascinated with its seemingly panacea of effects for CFS. Not only up regulates tyrosine into dopamine synthesis but also is anti IL6, and has other immune boosting effects. I take 200mg a morning, have tried both Ladasten and Nootropicssource.com's batch. I want to try ceretropics as I trust them greatly. It has very subtle acute effects, and any assessment of chronic effects is tough as I do feel better in terms of energy and mood from when I started Bromantane, but even with so many Th2-Th1 shifters, and endogenous interferon boosters, not to mention some cholinergic substances (DMAE for Inosine potentiation for instance), that any attempt to gauge individual supplements effects on mood are tough. I do feel like Oxymatrine and other Th2-Th1 shifters did induce a surge of anxiety and depression.

I've been looking for a good phosphatydil(sp?)serine source and saw you use 400mg for anti anxiety, do you mind providing that?

Also, yes in addition to using almost all your listed microglial activation inhibitors, I've also used your work to develop an NK booster stack, Th2-Th1, Endogenous interferon boosters, STAT1 promotion and STAT3 inhibiton, as well as some misc. immune boosters. Combined all these with gcmaf. According to gcmaf.se, LDN decreased gcmaf effectiveness in MECFS and that's something to consider in the, inhibit microglia or not debate. I can't express how much your work has influenced my current well being. Even after my doctors proposed Equilibrant over Valgancyclovir, it took your work on these forums to convince me the science was there. And that just started me down the rabbit hole, as I think I've seen every stack you've posted on this website. I'd be incredibly interested in helping you research any new stacks you might be envisioning. I have became totally passionate with researching my own condition and advancing my health through any means possible.

 

[Hip]

I've been looking for a good phosphatydil(sp?)serine source and saw you use 400mg for anti anxiety, do you mind providing that?

I buy my phosphatidylserine here. It's the cheapest source I've found.

I'd be incredibly interested in helping you research any new stacks you might be envisioning.

I am always trying or retrying things, usually 2 or 3 experiments every week, but most of the time the benefits are so small it's not even clear that there are any benefits. However, every now and then I find something that has a significant effect that you can obviously notice, and then I post of thread about it.



I am still not clear about the benefits you are getting specifically from taking these microglial activation inhibitors (rather than oxymatrine, etc). Is that you are taking so many different things that you are not sure what is causing what?

 

[eljefe19]

I buy my phosphatidylserine here. It's the cheapest source I've found.





I am always trying or retrying things, usually 2 or 3 experiments every week, but most of the time the benefits are so small it's not even clear that there are any benefits. However, every now and then I find something that has a significant effect that you can obviously notice, and then I post of thread about it.



I am still not clear about the benefits you are getting specifically from taking these microglial activation inhibitors (rather than oxymatrine, etc). Is that you are taking so many different things that you are not sure what is causing what?

Yes its muddied because I never made decisions based on the scientific method, I acted out of emotion. The emotion of slipping into the severe category, and massive anxiety about becoming a Whitney Dafoe level CFS patient. So once I started researching, using your stacks I expanded from Equilibrant (which made me sicker at first, I'd say for 6 weeks after starting it) to over the weeks 50-60 supplements, which I've then since replaced and refined constantly. I was absolutely desperate to get a strong effect because I didn't believe I would be able to take care of myself if I remained in the severe category. Hope that helps to settle the confusion. I do know that I didn't start feeling better until I had implemented much of my current regimen. It was a solid six weeks of constantly adding supplements, and absolutely horrible and persisting herxing and side effects that persisted for weeks on end. I can only speculate based on the theoretical benefits of these stacks which is causing which. I do believe Oxymatrine to be an essential component, as I value Dr. Chia's work above all other doctors on this subject.

I believe that I am doing everything I possibly can (with the exception of interferon itself) to treat the infections I've tested positive for (Coxsackie A(4 strains), Echovirus 7, HHV-6) with the exception of Mycoplasma Pneumonia. (As an aside what is your opinion about taking an antibiotic for Mycoplasma? I know with my body in Th1 dominance now I leave myself more vulnerable to bacteria) The point I'm trying to get to here is that I am keenly interested in any possible but within reason way to continue to make progress. I'm still moderate level in that I probably should not work, because my PEM is nowhere close to gone, and work has always exacerbated my symptoms in the past. I don't have to work at the moment, I am being supported, and therefore I have 100% freedom to explore, research, and invest in my ongoing treatment. Do you mind teaching me how you do research? I would love to discover more antiviral options specifically EV7.

 

[Hip]

@eljefe19 I understand why you are trying everything all at once, and have no problem with your approach. But that then means that you will not really be able to make statements about which things are helping, as you cannot really know at this stage.

That might be something you can figure out later though. For example, you can drop one protocol for a month, and see if you feel worse. If you don't then that protocol was probably not helping. I'd be cautious about dropping oxymatrine though, as sometimes this does not work again the second time.

I don't have to work at the moment, I am being supported, and therefore I have 100% freedom to explore, research, and invest in my ongoing treatment. Do you mind teaching me how you do research?

It took me many years to learn, just by reading lots of medical science articles and discussion on forums like this one, and learning as I go along. Longecity.org is another useful forum. I did have the advantage of a scientific educational background (my degree was in mathematics and physics), and a prior interest in health supplements; but apart from that, my understanding of medicine and biology was very limited. I started the learning process in 2003, when I first caught my virus. So I have been at it for 13 years.

I also had a lot of time on hand, because I was not able to work due to severity of symptoms.

As an aside what is your opinion about taking an antibiotic for Mycoplasma?

See the roadmap of chronic fatigue syndrome treatment (drugs and supplements) regarding Mycoplasma pneumoniae treatment.

Don't you have access to a good ME/CFS doctor, by the way?

I believe that I am doing everything I possibly can

Have you looked into rituximab treatment? According to Kolibri Medical, rituximab treatment cures ⅓ of ME/CFS patients, makes an improvement in another ⅓ of patients, and has no effect in the final ⅓ of patients. Ref: 1 There is a whole sub-forum on PR dedicated to rituximab.

 

[eljefe19]

@Hip I do have a CFS doctor but he is ultra cautious. He has not recommended any treatments outside of LDN and salt tablets. I will bring up Rituximab at our next meeting, but isn't this considered a high risk treatment? He probably will not be game for it but I will try.

Thanks for the research help. I also like the longecity forums. I was asking more specifically though how do you do your research as far as finding treatments for EV7 specifically, let's say. Just pubmed searches?

 

[eljefe19]

@Hip http://www.globalsciencebooks.info/Online/GSBOnline/images/0906/IJBPS_3(SI1)/IJBPS_3(SI1)1-25o.pdf

Found this resource off google. For echovirus 7 it says they found grape, Apple, and strawberry juice to be antiviral. Huh...who would have guessed?

 

[knackers323]

Interesting!
no



I am not quite understanding your statement. Can you quantify your improvement in symptoms a bit more precisely please. Is it your brain fog that has improved, energy levels, PEM resistance?

I find that when talking about ME/CFS improvements, it is good to indicate those improvements on the ME/CFS severity scale of mild, moderate and severe. Any improvement that can move you up one level of that scale (eg, from moderate to mild) I consider a major improvement. Any improvement that moves you up a smaller amount, I view as a more minor improvement.





Your guess is as good as mine on this. Some brain autopsies of ME/CFS patients have shown traces of enterovirus infection in the brain tissues (whereas none was found in the controls). So presumably some brain inflammation and the attendant microglial activation will be needed to keep this brain infection in check, assuming such brain infections are common in ME/CFS.

However, it possible that the brain inflammation and microglial activation are too ramped up, and are more fierce than is necessary to keep the brain infection in check. Brain inflammation can become ramped up when there is infection in other parts of the body (eg the gut), as when the vagus nerve senses infection in other parts of the body, it automatically signals to the brain, and the brain then ramps up brain inflammation. In this way, some gut dysbiosis (gut infection) might be increasing brain inflammation to higher than is necessary.

There is also the situation known as immune priming, where the immune system becomes oversensitive, and thus turns itself on too easily and too fiercely. Some researchers think immune priming may be involved in ME/CFS. See the posts here, here and here for more info on immune priming.

Autoimmunity (which the rituximab studies indicate is very likely involved in ME/CFS) may also be causing unnecessary brain inflammation.

In summary: it's possible that the microglial activation / brain inflammation is simply keeping a brain infection in check; but it is also possible that the brain inflammation is unnecessarily ramped up due to one or more of the factors detailed above.



By the way, in terms of reducing brain inflammation and the attendant microglial activation, you may want to look at the 29 supplements detailed in my thread here: Completely eliminated my severe anxiety symptoms with three supplements! These 29 supplements I found all helped reduce my anxiety levels; I believe my generalized anxiety disorder was underpinned by brain inflammation, and believe the reason most of these supplements worked to reduce anxiety is because they reduce brain inflammation. Supplements like turmeric are well known for their anti-neuroinflammation effects. I also think N-acetyl-glucosamine is likely a potent brain inflammation reducer.

Some of the 29 supplements, such as the probiotics and prebiotics, likely work to reduce brain inflammation indirectly, by reducing gut dysbiosis and gut inflammation. By the vagus nerve mechanism explained above, reducing gut inflammation can in turn reduce neuroinflammation.



Another important angle on brain inflammation is the connection between the dopaminergic system and neuroinflammation. Dr Andrew Miller's studies suggest low dopamine may increase the effects of inflammation: ie, low dopamine levels in the brain (in the basal ganglia) could cause a relatively benign mild inflammatory state to become something really problematic. See Cort's blog article on Dr Andrew Miller's dopamine research, and this second article also.

So if you can raise dopamine, you may lessen brain inflammation. This may be why very low dose amisulpride has been shown to have benefits for ME/CFS, as this drug works via stimulating the dopamine D2 and D3 receptors. See: Amisulpride — A Multipurpose Drug for ME/CFS I take 12.5 mg of amisulpride every day, and find it does help reduce some ME/CFS symptoms.

I posted a list of dopaminergic drugs and supplements here. However, most of these dopaminergic drugs probably will not work well in ME/CFS, because Dr Andrew Miller says ME/CFS may involve problems with the actual synthesis of dopamine, meaning there is a shortage of dopamine available. In the second Dr Andrew Miller article it says:


As a result of reading about Dr Andrew Miller's work, I recently ordered the Russian drug bromantane, which works by up-regulating expression of the enzymes which synthesize dopamine. Ref: 1 Bromantane is quite unique in this respect, in that it increases dopamine by promoting the manufacture of dopamine. I am hoping bromantane will be beneficial not only for reducing ME/CFS neuroinflammation, but also for treating my anhedonia and depression, which may be due to low dopamine. I will be testing out bromantane in the coming months.

very interested in this

 

[flitza]

Interesting!

How did it work out with the Bromantane?


I am not quite understanding your statement. Can you quantify your improvement in symptoms a bit more precisely please. Is it your brain fog that has improved, energy levels, PEM resistance?

I find that when talking about ME/CFS improvements, it is good to indicate those improvements on the ME/CFS severity scale of mild, moderate and severe. Any improvement that can move you up one level of that scale (eg, from moderate to mild) I consider a major improvement. Any improvement that moves you up a smaller amount, I view as a more minor improvement.





Your guess is as good as mine on this. Some brain autopsies of ME/CFS patients have shown traces of enterovirus infection in the brain tissues (whereas none was found in the controls). So presumably some brain inflammation and the attendant microglial activation will be needed to keep this brain infection in check, assuming such brain infections are common in ME/CFS.

However, it possible that the brain inflammation and microglial activation are too ramped up, and are more fierce than is necessary to keep the brain infection in check. Brain inflammation can become ramped up when there is infection in other parts of the body (eg the gut), as when the vagus nerve senses infection in other parts of the body, it automatically signals to the brain, and the brain then ramps up brain inflammation. In this way, some gut dysbiosis (gut infection) might be increasing brain inflammation to higher than is necessary.

There is also the situation known as immune priming, where the immune system becomes oversensitive, and thus turns itself on too easily and too fiercely. Some researchers think immune priming may be involved in ME/CFS. See the posts here, here and here for more info on immune priming.

Autoimmunity (which the rituximab studies indicate is very likely involved in ME/CFS) may also be causing unnecessary brain inflammation.

In summary: it's possible that the microglial activation / brain inflammation is simply keeping a brain infection in check; but it is also possible that the brain inflammation is unnecessarily ramped up due to one or more of the factors detailed above.



By the way, in terms of reducing brain inflammation and the attendant microglial activation, you may want to look at the 29 supplements detailed in my thread here: Completely eliminated my severe anxiety symptoms with three supplements! These 29 supplements I found all helped reduce my anxiety levels; I believe my generalized anxiety disorder was underpinned by brain inflammation, and believe the reason most of these supplements worked to reduce anxiety is because they reduce brain inflammation. Supplements like turmeric are well known for their anti-neuroinflammation effects. I also think N-acetyl-glucosamine is likely a potent brain inflammation reducer.

Some of the 29 supplements, such as the probiotics and prebiotics, likely work to reduce brain inflammation indirectly, by reducing gut dysbiosis and gut inflammation. By the vagus nerve mechanism explained above, reducing gut inflammation can in turn reduce neuroinflammation.



Another important angle on brain inflammation is the connection between the dopaminergic system and neuroinflammation. Dr Andrew Miller's studies suggest low dopamine may increase the effects of inflammation: ie, low dopamine levels in the brain (in the basal ganglia) could cause a relatively benign mild inflammatory state to become something really problematic. See Cort's blog article on Dr Andrew Miller's dopamine research, and this second article also.

So if you can raise dopamine, you may lessen brain inflammation. This may be why very low dose amisulpride has been shown to have benefits for ME/CFS, as this drug works via stimulating the dopamine D2 and D3 receptors. See: Amisulpride — A Multipurpose Drug for ME/CFS I take 12.5 mg of amisulpride every day, and find it does help reduce some ME/CFS symptoms.

I posted a list of dopaminergic drugs and supplements here. However, most of these dopaminergic drugs probably will not work well in ME/CFS, because Dr Andrew Miller says ME/CFS may involve problems with the actual synthesis of dopamine, meaning there is a shortage of dopamine available. In the second Dr Andrew Miller article it says:


As a result of reading about Dr Andrew Miller's work, I recently ordered the Russian drug bromantane, which works by up-regulating expression of the enzymes which synthesize dopamine. Ref: 1 Bromantane is quite unique in this respect, in that it increases dopamine by promoting the manufacture of dopamine. I am hoping bromantane will be beneficial not only for reducing ME/CFS neuroinflammation, but also for treating my anhedonia and depression, which may be due to low dopamine. I will be testing out bromantane in the coming months.

 

[tango]

Thank you @Hip for this wonderful analysis

I find estrogen and phytoestrogens very helpful for my health

I also find progesterone and magnesium problematic and wonder if this is linked to the NMDA receptors?

I have a couple of questions

• Silymarin is helpful but so are phytoestrogens. Silymarin detoxes estrogen so would taking both be counterproductive? Silymarin itself has estrogenic properties I believe so I would like to understand this better - especially as I am post-menopausal and trying to support healthy estrogen
• Where do the normal dietary guidelines (eg reduced sugar and alcohol fit into this)? In all honesty I am fine with both so long as I don't overdo it but I'm wondering about their impact on LPS. Also, the latest research showing that even small amounts of alcohol kill brain cells
• Is beetroot helpful given it's effect on nitric oxide? I'm not sure if it would be helpful or harmful
• Is GLA helpful given its effect on prostaglandins?
• What about DHA from fish oil or EPA from fish oil because they are meant to build healthy brains. Do they affect the microglial activation?

Any other dietary ideas would be welcomed as I have maxed out on supplements!

Lycopene is one I'm interested in. I've tried to get lycopene from

 

[Hip]

@tango I don't know the answers to most of these questions. Though I believe DHA and EPA do have anti-inflammatory effects in the brain.

 

[Gondwanaland]

Silymarin is helpful but so are phytoestrogens. Silymarin detoxes estrogen so would taking both be counterproductive? Silymarin itself has estrogenic properties I believe so I would like to understand this better - especially as I am post-menopausal and trying to support healthy estrogen

I am on estrogen replacement and my personal feeling is it works best when it is properly eliminated rather than reabsorbed and recycled. I feel that things that help with that are beneficial (e.g., silymarin, B6, B2 etc ).

Having said that, I am extremely sensitive to estrogen antagonizers like flax seeds, soy, zinc, chia seeds, and progesterone promoters (since I can't make my own estrogen - B3 deficiency?) like Evening Primrose Oil, avocadoes and per extension choline :thumbdown:

I think there might be a very individual response.

 

[tango]

I am on estrogen replacement and my personal feeling is it works best when it is properly eliminated rather than reabsorbed and recycled. I feel that things that help with that are beneficial (e.g., silymarin, B6, B2 etc ).

Having said that, I am extremely sensitive to estrogen antagonizers like flax seeds, soy, zinc, chia seeds, and progesterone promoters (since I can't make my own estrogen - B3 deficiency?) like Evening Primrose Oil, avocadoes and per extension choline :thumbdown:

I think there might be a very individual response.

I am on bioidentical estrogen. I also take a supplement with soy isoflavones and black cohosh. I'm hoping milk thistle only eliminates the bad estrogen as my symptoms are so much better with estrogen. Mood, pain and energy all improve. They also improve with isoflavones and chia. I'm not so sure on linseed. I think that's a negative for me although LSA is okay. Maybe the almonds or sunflower counteract linseed???

Soy isn't really an estrogen antagonist. It's simpler a weaker form of estrogen. So it should be helpful. Have you tried isoflavones supplements?

Progesterone and zinc I understand as zinc supports progesterone and lowers copper