Discussion in 'Mast Cell Disorders/Mastocytosis' started by xchocoholic, Aug 25, 2012.
I love Quercitin. A safe supplement instead of meds.
I have to give the zyrtec a rest for a couple of weeks so I can get some IgE testing done, so it will be interesting to see how I go when I stop taking it. I am struggling a bit with the detachment it causes and subsequent anxiety.
Also, I found this from wikipedia about it's effects on HRV, IL6 and IL8 quite interesting, it's not just an antihistamine!
Interleukin 6 and interleukin 8 have been shown to be elevated in acute respiratory distress syndrome. Cetirizine contains L- and D-stereoisomers. Chemically, levocetirizine is the active L-enantiomer of cetirizine. In a recent study of airway epithelial cells the following was observed: Levocetirizine inhibits the production of intercellular adhesion molecule ICAM-1 and secretion of interleukin (IL)-6 and IL-8, which may have beneficial effects on the pathophysiologic changes related to human rhinovirus (HRV) infection. Levocetirizine treatment inhibited the HRV-induced increase in ICAM-1 mRNA and protein levels, as well as the HRV-induced expression of IL-6 and IL-8 mRNA and protein levels. Viral titer, as measured by culture in MRC-5 cells, was reduced by levocetirizine. Levocetirizine treatment also reduced the increased nuclear factor-kappa B (NF-κB) expression seen with HRV infection. Levocetirizine inhibited the expression of Toll-like receptor 3 (TLR3) mRNA and protein levels. These findings indicate that, in HNEC and A549 cells, levocetirizine inhibits HRV replication and HRV-induced upregulation of ICAM-1, IL-6, and IL-8, TLR3 expression and NF-κB activation. The results of this study suggest that levocetirizine may have a possible clinical application in the treatment of airway inflammation caused by HRV infection. Airway inflammation caused from a cytokine storm secondary to acute respiratory distress syndrome could also theoretically benefit.
One more thing; I'm wondering if there is any benefit in pulsing zyrtec, it seems to be advocated in a lot of other treatments.
I'm sorry, X. I didn't see your comment here.. I rediscovered this thread with a google search! My daughter has had some improvements in nausea with claritin and pepcid (the info I read indicated that Dr Afrin preferred to start with pepcid over zyrtek first so that's where we started).
I feel like some of my crazy symptoms have been better (skin crawling, gait going off, brain inflammation, and other wild symptoms like burning in nose and into gut, though I have had some flares lately and I do not take a stabilizer yet or more than twice a day with the h1 and h2 or more than 2 pills of each)
The CFS is not better and I also have found clonezepam, which I have taken for 7 years helps with symptoms. I thought I read somewhere.. read so much lately.. that mast cells share receptors with benzos, but could be wrong.
Neurotprotek is expensive and I am concerned about quercetin and my COMT++ status since it is a methy donor. I really feel boxed in by methlation genetics. I tried Neuroprotek for a while and then stopped because of the methyl donor issue and not sure how to proceed.
We did see a dysautonomia specialist who is pretty certain we have the POTS, EDS, Mast Cell trio. We have a slew of blood and urine tests to take and another tilt table test to line up, but have been sidetracked with dental work and subsequent crashes.
He actually prefers a mast cell stabilizer (gastrocrom) and singulair over h1 and h2 blockers. I have info as to why the h1 and h2 could present their own problems in my files somewhere.. I wish something would get easy.
I think I am an extreme leaker. Literally.. my legs just fill with pressure (and I think fluid leaking from veins) and are relieved by compression hose. I also adrenaline dump really badly and am wondering if this is adrenaline or adrenaline only or other by products of mast cell activation.
EDIT addition: I have noticed that when I eat histamine or histamine triggering foods, those crazy symptoms show up.. spine feels inflammed, gait goes off, brain weirdness that some have suggested might be brain anaphylaxis, and others.. just from the foods.
The pressure in my legs seems to be connected to fatigue in some way.. the pain and something else going on and I also recently read that exertion triggers mast cells (aerobic activity) which might explain some PEM? I have adrenaline surges and my legs go badly off when I exert too much.
You may want to try Histame and see if it helps. It's expensive, though.
This is what I think too. There is even people susceptible to exercise-induced anaphylaxis.
I think that PEM is likely caused by mast cell activation. This is anecdotal, but I have found that a lot of people I have spoken with used to break out in hives when they exercised way before they came down with ME/CFS. I had exercise-induced urticaria a full decade before any other symptoms started. Dr Afrin has found that most people can point to strange symptoms that went back years or even decades before their symptoms became disabling.
This may have been mentioned earlier in the thread, but I saw somewhere that one old treatment for mast cell disorders was to exercise several times a day so that you spread out the degranulation. Obviously it is better to find a way to stabilize the mast cells and I suspect most people with ME/CFS can't exercise once a week, let alone multiple times a day. It is best to exercise on an empty stomach if you can as that can lessen the chances of a reaction.
I would make sure your dysautonomia specialist knows about the study from Vanderbilt about POTS and mast cell disorders (http://hyper.ahajournals.org/content/45/3/385.full)
Mast cells release norepinephrine. Your feeling of an adrenaline dump could be due to that. And you are remembering correctly- there is a benzo receptor on mast cells and some mast cell experts prescribe it.
Allergies have accompanied me since I was a baby, accumulated over the years, and became bizzare with ME/CFS and MCS. As I've shared in posts here, for the first 2 years after my ME/CFS became severe there were many times I lierally ran out of foods I could eat, resorting to fasting, synthetic "feed tube" powder, and finally I.V. nutrition. Surviving that, I stabilized to a select 5 particular kinds fo food from particular sources prepared a particular way and lived on that for several years. Even so, I've had to take allergy meds at least 3 times a week for severe reactions, had no bedding due to reactions (slept on bare wood) and developed an anaphylactic response to the active ingredient in benedryl.
Treatments I've tried:
- Homeopathic treament protocol, which included lots of tests. Went through the program twice as a kid. No improvement. Naturopathic doctor was perplexed and said "it just doesn't work on some people"
- Growing out of it. Every doctor told my parents I would, so it's a legitimate treatment, right?
- Allergy shots. This was when my ME/CFS was still "mild". I began reacting to the shots with extreme exhaustion, (different than my PENE because it was physical exhaustion only and mental groggyness from being so sleepy) would sleep 18 hours at a time directly after the appointment receiving the shot. It was worsening in length and severity each time. The allergy doctor insisted there was no possible way the shots could be causing it, but eventually I decided I knew better since it never happened otherwise. The symptoms stopped. I later heard from another allergy specialist that my symptoms describe a sort of low-level extended type of anaphylaxis and was quite dangerous.
- Taking Benedryl before every meal. This approach was recommended by a doctor so that I could get enough to eat. It seemed to make things worse, but I couldn't figure out why and continued with it for several weeks. I kept changing the form of the Benedryl, thinking it was the inactive ingredients causing issues. Years later I discovered i have a true allergy to the single active ingredient - yes, allergic to an antihistamine. Note that prior to ME/CFS I had taken benedryl as needed for about a decade to relieve reactions and had no problem with it.
- Nambutripad's Allergy Elimination Technique (NAET). NAET is a method utilizing acupressure points to try to "reset" a body's abnormal reaction to specific allergens. This was attempted when my ME/CFS was at its worst, I was very unstable and fighting to find anything I could eat at all. At first, the treatment seemed to be helping, but when we hit my oldest allergy (dairy) I reacted nonstop for weeks, barely able to get enough air and liquid food with the throat restriction, and started acquiring new allergies rapidly. They actually determined the treatment was giving me new allergies, and the doctor was not comfortable continuing.
- Heparin injections. An MCS and allergy specialist mentioned that if epinephrine is contraindicated, he uses heparin to relieve anaphylaxis in patients reacting to allergy treatment. He said in 30 years of practice he has never seen it fail, though it works *slightly* less quickly. Its effect has been proven in animal studies but is not in mainstream use. Despite the inevitable bruising, heparin is still my treatment of choice for relieving reactions due to its lack of side effects and the slight temporary improvement it sometimes gave me.
Compounded Loratadine is the other tool in my toolbox that is used to relieve reactions.
I once read that onions had a lot of quercitine which was an antihistamine, so I thought those should help. I reacted very badly to them.
Cranial osteopathy. I didn't intend this treatment to address my allergies, but after a few months of cranial osteopathic treatment by a D.O. board-certified in neuromusculoskeletal medicine, I noticed I hadn't needed my allergy meds in a while. This after several years straight of needing them several times a week despite avoiding all known problematic items. I'm now approaching 9 months of no allergy meds whatsoever, and have begun expanding my diet to previously untolerated foods. My ME/CFS is also dramatically improved and my recovery is an ongoing process.
Currently, I'll still sometimes get hives, violent sneezing, and a runny nose. I seem to have narrowed it down to the combination of overdoing and my nervous system being in sympathetic mode - if either one of these is removed from the equation then it immediately settles down. Before beginning this treatment my nervous system was sympathetic all the time, even when I was as relaxed as I'd ever been in my life, and my fatigue and PENE was not relieved by rest. Now that my body is eased enough that rest relieves my fatigue, and I've worked out how to manually bring my nervous system down, managing this apparent mast cell response without drugs is a relatively simple matter whereas it would have been impossible previously. As my body improves, this reaction is becoming more rare - several months ago it was happening about once a week for 24-48 hours, and now it's more like once a month for 30 mins. At this rate I expect it will someday disappear completely as I continue to improve, but we'll see.
I do sometimes get itchyness and hives over an area where structural shifting is occurring in the fascia. It is always localized, and does not get out of hand unless the other two factors mentioned above are present. The location is never suprising to me, since generally the area will have been tight for days if not an entire week before this symptom appears.
I've heard NAET and similar treatments of a different name seem to help several ME/CFS people's widespread allergy issues, and suspect that in my current state it would bring about improvement rather than making things worse. If I finish cranial osteopathic treatment and still have allergies I intend to revisit this possibility.
I'm so glad things are improving for you Dainty. Could you say a bit more about how you manually bring your nervous system down please?
Wow, that is quite story! Are you planning on being tested for mast cell activation disorders? If you ask me, you do fit the mastocytosis profile quite nicely!
Have you seen this: Mastocytosis - Fabio's Story?
Hi ... I'm feeling way too groggy nowadays and was thinking of switching to natural treatments. Are these less likely to make us drowsy ?
I'm ok off and on throughout the day. My brain is just getting tired easily. And I'm taking a nap almost everytime I lay down.
My cognitive problems may not be related to these meds of course. This happens to me a lot esp if I take too many sleep meds or supplements. Or if I eat poultry. Or eat too much fruit. I'm a pita.
I saw where nano recommended trying quercitin and rutin before buying neuroprotek. That was in the pheonix rising mast cell article by cort. Do you still recommend this ? Tx.
I vaguely remember quercitone being mentioned too.
If there's an inexpensive way to do this that would be great.
I've been trying supps and caffeine but nothing has unscrambled my brain yet.
Tx .. X
You are not taking H2 blockers, right? Something for you to chew on:
Cell Mol Neurobiol. 2000 Apr;20(2):131-47.
Inflammatory mediators and modulation of blood-brain barrier permeability.
Division of Physiology, GKT School of Biomedical Sciences, King's College London, UK. firstname.lastname@example.org
1. Unlike some interfaces between the blood and the nervous system (e.g., nerve perineurium), the brain endothelium forming the blood-brain barrier can be modulated by a range of inflammatory mediators. The mechanisms underlying this modulation are reviewed, and the implications for therapy of the brain discussed. 2. Methods for measuring blood-brain barrier permeability in situ include the use of radiolabeled tracers in parenchymal vessels and measurements of transendothelial resistance and rate of loss of fluorescent dye in single pial microvessels. In vitro studies on culture models provide details of the signal transduction mechanisms involved. 3. Routes for penetration of polar solutes across the brain endothelium include the paracellular tight junctional pathway (usually very tight) and vesicular mechanisms. Inflammatory mediators have been reported to influence both pathways, but the clearest evidence is for modulation of tight junctions. 4. In addition to the brain endothelium, cell types involved in inflammatory reactions include several closely associated cells including pericytes, astrocytes, smooth muscle, microglia, mast cells, and neurons. In situ it is often difficult to identify the site of action of a vasoactive agent. In vitro models of brain endothelium are experimentally simpler but may also lack important features generated in situ by cell:cell interaction (e.g. induction, signaling). 5. Many inflammatory agents increase both endothelial permeability and vessel diameter, together contributing to significant leak across the blood-brain barrier and cerebral edema. This review concentrates on changes in endothelial permeability by focusing on studies in which changes in vessel diameter are minimized. 6. Bradykinin (Bk) increases blood-brain barrier permeability by acting on B2 receptors. The downstream events reported include elevation of [Ca2+]i, activation of phospholipase A2, release of arachidonic acid, and production of free radicals, with evidence that IL-1 beta potentiates the actions of Bk in ischemia. 7. Serotonin (5HT) has been reported to increase blood-brain barrier permeability in some but not all studies. Where barrier opening was seen, there was evidence for activation of 5-HT2 receptors and a calcium-dependent permeability increase. 8. Histamine is one of the few central nervous system neurotransmitters found to cause consistent blood-brain barrier opening. The earlier literature was unclear, but studies of pial vessels and cultured endothelium reveal increased permeability mediated by H2 receptors and elevation of [Ca2+]i and an H1 receptor-mediated reduction in permeability coupled to an elevation of cAMP. 9. Brain endothelial cells express nucleotide receptors for ATP, UTP, and ADP, with activation causing increased blood-brain barrier permeability. The effects are mediated predominantly via a P2U (P2Y2) G-protein-coupled receptor causing an elevation of [Ca2+]i; a P2Y1 receptor acting via inhibition of adenyl cyclase has been reported in some in vitro preparations. 10. Arachidonic acid is elevated in some neural pathologies and causes gross opening of the blood-brain barrier to large molecules including proteins. There is evidence that arachidonic acid acts via generation of free radicals in the course of its metabolism by cyclooxygenase and lipoxygenase pathways. 11. The mechanisms described reveal a range of interrelated pathways by which influences from the brain side or the blood side can modulate blood-brain barrier permeability. Knowledge of the mechanisms is already being exploited for deliberate opening of the blood-brain barrier for drug delivery to the brain, and the pathways capable of reducing permeability hold promise for therapeutic treatment of inflammation and cerebral edema.
Lol. What part of feeling groggy didn't you understand ? Thanks anyway tho. I'll try to read this.
Fwiw tho .. I was just thinking
today that I may want to try betaine hcl, stomach acid, to see if it helps me digest hard to digest meats like beef, shrimp
and pork. So far, my digestive enzymes, creon, aren't enough. I'm working on increasing my dose tho.
It would be just my luck that creon is making me groggy.
Can others digest these meats ?
Tc .. X
That's why I bolded the important stuff!
I found it but got lost after the second "and". Lol. The date on this is 2000. right ? Fwiw, I've seen some interesting new research on brain function recently. I "think" the one I'm thinking of disputed earlier findings on how the bbb worked. Ok, I'll have to look for it now. Brb.. X
Eta. I can't find it in my favorites. I googled sciencedaily blood brain barrier and couldn't find it either.
Regardless ... we know allergies and antihistamines affect our brains. Second generation meds are less likely to cause drowsiness than first but they still can cause drowsiness.
I'm just not sure if all the mc meds I'm on could be making my cfs brain fog worse. I can only take a small amount of Klonopin (.125) without becoming a zombie. And I'm taking mega doses of mc meds.
Everyday I'm taking 25 - 30 mg wal-zyr + 90 mg Allegra + tsp Liq Benadryl.
Tc .. X
I'm having some luck with Quercetone from Thorne. It's water soluble, so better absorbed than typical quercetin. Theoharides did a study on this and 2 grams a day performed better than cromolyn. It's giving a bit of a boost to my mood and energy, and I'm not quite as itchy. Nothing real dramatic though.
There's a group on facebook for those attempting a more holistic approach to treating mast cell activation, although I notice that most are still on zyrtec and a few other meds. Here's the link if you want to check them out: https://www.facebook.com/groups/287752947987652/
Thanks camas. I'll look at this. Do I have to join that facebook group ? I've sworn off joining anymore
internet groups. Lol. Tc .. X
Well I've been off the 2.5 mg of Zyrtec for 2 days now and I have declined significantly.
Yep, it's a closed group so you have to join to see the posts, but I've found it pretty informative. The U.S. Mastocytosis Society also has a facebook group that's open, but if you post there the whole world can see it. https://www.facebook.com/groups/155824303735/
I hear you. I tried to go off zyrtec for a day to get tryptase testing done, and was so weak I couldn't get out the house to get a blood draw. Kind of a dilemma.
That's not good. Thankfully I'm still able to get about, just much more slowly. I'd love to know if it's the histamine reduction or the anti HRV effect that is the benefit.
I've only briefly skimmed this http://www.orthomed.com/unprimed.htm , but the author talks about reducing disulphide bonds as a way to reduce allergy. It's interesting that DMSA helps me a great deal, and it is a powerful disulphide bond reducer. NAC also helps me(albeit temporarily) - another disulphide bond reducer.
You can also try a Google Site Search
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