JayCS’s Fibro Blog

JayCS · February 25, 2022, 1:45pm

2022-02-25, Friday 5% - food triggered? PEA for FM & MCAS & lipids & bp & IBS.

Activity down again: cos of 1) slivers of cheese or 2) 3 slices of spelt bread, 3) too much (100g) raisins or 4) (200ml) soy yoghurt
Wondering if palmitoylethanolamide (PEA) might help get my mast cells under control. (Only slight evidence, but it also seems to decrease triglycerides, blood pressure and IBS, so I’ve ordered it.)

Triggers & resulting Symptoms

SLEEP (click for details): 8h45, up 3x (15') ✅, and ➔ Feeling 90% well, Ache 1 of 7 ✅, getting up: 80%/2 🧐. Taking a 4th 350mg passiflora at 6 was possibly too late, didn't help much either, so next I'll try taking whichever last one at 4.

cold shower p0 Sleep 23:00-
3:05! 5’ 90%/1 p0 st1 drink fw2’ air Slight skin itch-turnburn
3:25 5’ 90%/1 p0 st1 drink fw2’ LBU: phoenix, cold wash, HWB.
6:15 5’ 90%/1 p0 st1 drink fw1’ air
20’’ 2nd shower cold and/or warm (nostrils)! HWB! Chatter: GABA-speck? SUPPS & AIR 1st!
7:00: Heating on!
-8:00
Sum: 1h+8h-(5+5+5=)15’ = 8h45, up 3x (15’)

ACTIVITIES (aiming for 40% - well 20% - physical activity of pre-fibro) ➔ ACHE: Stool ➔ 70%/3 (quite often the case).
(e.g. cycle , TT , meetings/social , mask , kids , work ➔ ?80%/2) ?
"HOW DO I LOOK?" 10:20 Same as ever, white and tired. At doc’s not bad, and O2 95-98%.
ACTIONS ➔ PAINS: Bit of elbow → stretches & massage gun. Painfully sudden cramping stool → rest (food trigger?)
(e.g. lie, stand, loins, sit, arms up, neck, stiff, walk, cycle, 0xp1-2, GI, talk, mask.)

Treatments

Docs:

GP prescribed more of the antihistamine, couldn’t help with the Factor VIII or white lips.
Factor VIII up: MCAS and CVD? Cardiologist. Hyperlipidemia from MCAS?? White Lips?
N-methylhistamine normal. So: Prostaglandin D2 or 2,3-Dinor-11beta-prostaglandin F2 alpha or Leukotriene-E4? I think I’d better check that with my allergologist. (This German site) seems to suggest that only the Leukotriene-E4 needs to be frozen, here that the 11-β-PGF2α is best refrigerated, but frozen or with the preservatives acetic acid, boric acid or sodium carbonate are acceptable.

WHB (3 rounds)
RIBOSE:

SELF-PHYSIO (click for details): 59' ✅ (Oooooh: getting lax?! O.o ;-)). Combine. List-prioritize: next.

Supps (Feb 25th: 27): Supp costs: ~344€/m. CHANGE: Passionflower, now pure, .350mg: 3/d? 19:00 and 21:00 was enough to sleep from 23:00 to 3:00! Cu, pine bark, rhodiola (& Zn) arrived. Look for better honokiol. Arg 0 since praps bad for lp(a)! RIBOSE!? PLANNED/TAKEN TODAY: click for details:

ZERO now: Arg, B3/Nia, Mum, Mg Gly 50mg, Mg Mal 45mg, Nc 1*.5g, (Nd), (Rib), Pe, Ps, Se, Sr 31125k, Zn.
REGULAR as of Feb 25th (27, next: 28 incl. Cu, pine, Pf, Rho & Zn have arrived; leaving Zn for a time, while I get Cu up again): ALA .2g, B2 2*.1g, B12 5mg/2m, C 2*.5g, Cr 31g, DAO before meals, D3 1/w, EGCG (50%, incl. theanine?).5g, EllagicA .2g (+43mg vit. C), Fev/MSM .4g (+.2g MSM), Ga: 4*.6g+.4g=~2.8g, Gi 3*?, Glu:~0.8g, Hon (2%).4g=8mg, Luteolin .2g, Ω3 5mg, P5 27mg, Pf 3-4.35g, pine bark 2*.5g, Pq 1, Q10 (ubq) !1*.1g/d, Qc 4*.5g/d, Rs (50%) 2*.4g, Ro 2*.2g(+B1 1.4mg), Sa .1g, Sily (80%)*.5g (+83mg L-cholin) , The .2g (+.15g polyphenols).
What-when-details: Updated Feb 15th (before: see the reference post)
/20:30 “17:00” - whoopsy…
/21:33 A1/2 “19:00” PF#1 Cr#1 0mal#1+2 P5P/2Rho(0Se) PQQ Ω3 & Qc. Meal: DAO.
/23:00 A3 “21:00” PF#2 .6 GABA&.4glu#1 & Lut (slp!) & Qc +0NAC!
/23:00 Chamomile tea.
/03:05 ! A4 “23:00” PF#3 .6 GABA&.3glu#2 & Ellagic acid + Rupafin
/06:15 B1 “01:00” PF#4
Heating on! Warm shower?
/08:05 B2 “07:00” +ALA+2x pine bark, (teeth)
/08:05 B3 “07:00” (-30’) Q10#1 Qc#1 Rs#1 SAM-e
/08:05 B4 “07:00” EGCg + Fev/MSM + Sily
/09:30 C1/2 “MEAL!” 2Cr#2 .6GAB#3, (C2:) .1gB2, gink#1, Zn 1xHon! DAO?
/09:30 C3 “MEAL” .5gC#1 2The2 (0NAC)
/14:00 11:30 C4 “11:00” (+2h/) gi#2 gly#1. Nd#? & Ellagic acid
/14:00 1 DAO (D1) “13:00” 0psyllium
/16:15 D2/3 “15:00” .5gC#2,Cr#3,!.6GA#4,gink#3,0gly#3+4, 0NAC#5 DRINK!
/18:50 D4 “17:00” (“meal/acids+2h”) Qc#4.Rs#2, Nd#?
eve:
“18:00” Prepare: 1) Cpl & chk/C supp-chg. 2) Remove “v”, cut, save, paste 1x & unhide & paste 2nd (+1 to date and ##). Close 2nd TAB!
(Nov 4th, Jan 10th: B12 5mg methylcobalamin s.c.; next: Mar 10th.)

The day's 16 compartments (10', plus 5' making capsules)

Pf: A1+3+4+B1, B2:A1+C2 C:C3+D2 3x2Cr: A1+C1+D2, Ell: A4,C4. Ga: A3,A4,C1,D2, Glu: A3,a4 Gi: C2,C4,D3 Qc: A2.A3.B3.D4 Rs:B3,D4 SINGLE: A2:P5/Ro A3: Luteolin A4: Rup! B2: ALA+0x2 pine B3:Sa+Q1 (->ubiquinone <150mg/d!) B4: EGCG&Fev/MSM&Sily C2:0Zn&Hon C3:2Th (A2:Ω/Pq:meal) DAO before every meal.
(A2:0Se), (B2:0mu), (5NADH if nec.) (D1:0Pe). (0Mg:C4.D3.A2) (0 Nia) (0Nc: A3, B1,C1,C3,D2) (0Sr: B1,C4,D4)

Development
Jab-sfx/MCAS/antihistamine:
20:00 Slightly burnt tongue feeling. Again at 23:00 but maybe after (cold) chamomile tea. Slight skin itch-turnburn at 23:00 and 3:05. Deep sleep without “23:00”-batch (so no antihistamine, maybe the new passiflora 2x?) Hard moving today, at the doc’s I needed minutes to get up, I was so stiff and exhausted. 16:15 Burning skin (after eating red cabbage with fennel, a little wholemeal rice, a little dark chocolate).

’Research’ today:
Ending yesterday’s stint on mast cells this letter to the editor by Cassisi, 2014/5, in answer to Pollack’s supporting comments on their article mentions neuro-inflammation, mast cells connecting nerve fibres & blood vessels, whilst microglia can contribute to and maintain pain by responding to (non-neuronal) CNS mast cells). These might be kept under control with cannabinoid receptor antagonists like the cannabimimetic palmitoylethanolamide reducing histamine-overreactions.
This makes me wonder what palmitoylethanolamide is, as “non-pharmaceutical” makes it sound like a supp.

Cassisi's full reply

Although many of the mechanisms and characteristics of fibromyalgia are well defined, its pathophysiology is still far from being fully understood (2). Mast cells probably play an important role in chronic pain (and therefore fibromyalgia) not only on the grounds of the histological evidence referred to by Dr Pollack (3, 4), but above all because of their importance in neuro-in- flammation. Neuro-endocrine immune stimuli can induce an increasing number of local mast cells and further the extent of their degranulating activity (5). Mast cells have a close anatomo-functional relationship with nerve fibres and blood vessels, and produce and rapidly release nerve growth factor (6). Microglia respond to the pro-inflammatory signals released by other non-neuronal cells, such as CNS resident mast cells, and it has been suggested that activated glial cells can contribute to spreading the sensation of pain and maintain its chronic status (7). The growing evidence of mast cell-glia communication opens up new perspectives for developing therapies that target neuro-inflammation by differentially modulating the activation of the non-neuronal cells that normally control both peripheral and central neuronal sensitisation (8).
The data concerning palmitoylethanolamide, a non-pharmacological analgesic, are promising insofar as its cannabimimetic action on mast cell receptors may reduce histamine-induced responses and modulate the onset and maintenance of pain (9, 10). We hope that further scientific contributions will clarify the relationship between mast cells and chronic pain, and the potential therapeutic role of cannabinoid receptor agonists in the treatment of fibromyalgia.

Continuing on palmitoylethanolamide

it seems good for pain: Biomarkers of response to alpha-lipoic acid ± palmitoiletanolamide treatment in patients with diabetes and symptoms of peripheral neuropathy - PubMed
The suggestion it might interact with lipid-lowering drugs on wikipedia made me look for its effect on lipids, blood pressure, and that seems good too, according to 1) neuroscientists at the Alzheimer’s Drug Discovery Foundation and 2) Pai et al. 2021, Am J Nephrol 2021;52:59–68.
Alzdiscovery: “PEA (300 mg twice daily) for 3 months …led to significantly improved flow-mediated vasodilation compared to placebo. This effect appeared to be due to improved peripheral endothelial function and its positive effect lasted longer than the duration of PEA intake. In spontaneously hypertensive rats, PEA treatment (30 mg/kg/day) for 5 weeks significantly reduced blood pressure by downregulating the angiotensin receptor 1 and angiotensin-converting enzyme (ACE)” and
Pai et al 2021: “However, while these lipid-derived mediators may counteract the effect of inflammation, they also activate fatty acid oxidation, resulting in reduced serum triglycerides, increased energy expenditure, and decreased body mass.”
Also good for IBS: Does Palmitoylethanolamide (PEA) Have Health Benefits? - SelfHacked
Now what about MCAS? Well, up to now I’ve found quite a few German sites saying: Yes. As far as English sites go, this one Palmitoylethanolamide for Neuro Inflammation - Sophia Health Institute came up which makes very offhand statements about using it in fibromyalgia and MCAS, altho it belongs to one Dr. Dietrich Klinghardt, who seems internationally renowned as a functional doc (but also in Germany etc.):

“Mast Cell Activation Syndrome (MCAS) is a very common symptom in chronic illnesses, and PEA supplementation can be of great benefit for reducing symptoms. PEA supplements are often combined with the plant pigment luteolin in a 10:1 ratio. Luteolin on its own is also used to calm mast cells, but the combination of PEA and luteolin has been shown to be more effective than either substance by itself (5).”
Firstly, MCAS (like any syndrome) is of course not a symptom . Whether it is common is still matter of debate, I think Afrin likes to assume it will be recognized that more and more. The referenced article (5) is not about MCAS, the abstract contains no reference to it, the full article costs 51$.
Then “PEA is popularly used for fibromyalgia”: Not true; if it had even been mentioned anywhere I’d’ve tried it; no reference given.
Bryant Rubright is the author of this misrepresentation, not Klinghardt himself.
Checking the fibromylgia track on healthrising about PEA “A recent study suggests it could be helpful in fibromyalgia.” and “Reduced PEA levels in the trapezius muscles of women with chronic widespread pain suggest PEA supplementation might be helpful in Fibromyalgia.” This paragraph explains the ‘search’-situation tho: “Why is PEA not better known in the West? PEA appears to been used in Italy and Spain for quite some time. Interest picked up in the Netherlands and Germany when a Netherlands distributor came on the scene. It’s hardly known in the U.S., although Palmitoylethanolamide For Pain reports that “many people” on the West coast of the U.S. as well as Australia and Canada are using it.”
I’ve decided to try PEA anyway. Anyone else?

Lessons in self-care #233 Lax on the self-physio today, praps better try tomorrow…
Reasons to be cheerful #240 Finding a “new” supp, PEA, let’s see

1st Jab-sfx-summary, last edit: Feb 7th.
My blog references, e.g. abbreviations, supp chart/overview
My “How to symptom track & trigger hunt”
Next up…: Summaries & finishing off treatment list…

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JayCS’s Fibro Blog

2022-02-25, Friday 5% - food triggered? PEA for FM & MCAS & lipids & bp & IBS.

Triggers & resulting Symptoms

Treatments

Related topics