2022-02-06, Sunday - 20%: MCAS… 
anti-(rib-)P (= lupus…)
v2 16:15 research on MCAS (and antibody anti-P) shows anyone with a whole load of inflammatory seeming symptoms should have a look at it.
v1: 14:15 managed some singing / recording, but aching, so needed quite a lot of rest, but had a few research ideas…
Triggers & resulting Symptoms
SLEEP (click for details): 8h46, up 5x (44') ✅, ➔ Feeling 90% well, Ache 2 of 7 ✅, getting up: 90%/2 ✅
No fw! lbu: belly tensing? No half-sitting on sofa! SUPPS & AIR 1st!
cold shower p0 Sleep 22:40- air
0:15 10’ 90%/2 p0 st1 drink fw2’
1:48 5’ 90%/2 p0 st1 drink fw2’ B1 air
3:51 15’ 90%/2 p0 st1 drink fw2’ B2 air - quite a bit of wind even now.
4:35 9’ 90%/2 p0 st1 drink fw2’ air HWB FCS (LBU - lying too long on it?)
7:15 5’ 90%/2 p0 st1 drink fw2’ B3 air
-8:10 air back ex
Sum: 1h20+8h10-(10+5+15+9+5=)44’ = 9h30-44’ = 8h46, up 5x (44’)
ACTIVITIES (aiming for 40% - well 20% - of pre-fibro) ➔ ACHE: singing recording ➔ 70%/3, resting ➔ 80%/2(?), errh, no, moving again turns out 70%/3, and after singing was ➔ 70%/4. After eating it’s still similar, not getting better. But still going out for a cycle-walk. Stays 70%/3 the whole day. Don’t know why.
“HOW DO I LOOK?” ?
ACTIONS ➔ PAINS: Clavicle , but trigger pointing helped. . Stiff after standing a long time is “normal”… . Hand pain while cycling slightly better than the days before .
Treatments
Docs: Preparing for GP and allergologist on Tuesday..
WHB (3 rounds) 
?
RIBOSE: ?
SELF-PHYSIO (click for details): 2h21... ✅.
airing 8x2’, cold shower 2x(10’), HWB 5x3’, teeth 1x2’, cream 2’, Timing, hunchback-pillow 15’, AuTr 3’, breath exercises 4’+10’, left foot on/under right knee/cross-legged 5’+5’+30’, palpate 4’, belly 3’, back 7’,
breath-hold 12’, neck 1+ 2’, neck 2 4’, plantar/calf stretch 5’, twist-stretch 5’, loins 5’, yoga/stretching 5’, jolt-jump 1’, marionette-hang 1’, mirror 2’, shaking dance 1’, workout 7’, hand-exerciser 3’, massage gun 20’, acupressure 6’, aloe vera 1’,
: calendula/tea tree 2x1’, foot bath 15’, gums 2x30’’, V ‘, RR x2’, temperature 5’, nux vomica 1’.
Supps (1st: 29): Supp costs: ~371€/m. CHANGE: Playing around with NAC vit. C in the early night? Carnitine's gone bad, get new. Srp is out, but stopping it for a while, it's so expensive, and I'm not at all sure of it. RIBOSE!? PLANNED/TAKEN TODAY: click for details:
Abbreviations resolved under blog references
ZERO: C 0x2x.5g, NAC Nc: 0x2.5g(5, incl. 2x1/night), Nd, Arg, B3, Rib, Pe, Ps, Se. (REGULAR (28): ALA .2g, B2 2x.1g, B12 5mg/2m, Cr 3x1g, DAO before meals, D3 1/w, EGCG: 250mg EllagicA: Fev/MSM: .2g Ga: ~2g+(4), 3Gi, Glu:~1.2g+(4), Hon, Luteolin .2g Mg Gly 2x2, Mg Ma1x2, Ω3, P5:1, Pf4, pine bark 2x.5g, Pq1, Q10 2x.1g/d, Qc !4x.5g/d, Rs2, Ro2, Sa1, Sily, 0 Sr 3x1x125k, The.2g, Zn1)
What-when-details: Updated Jan 20th (before: see the reference post)
/20:40 A1/2 “19:00” PF#1 Cr#1 mal#1+2 P5P/2Rho(0Se) PQQ Ω3 + 0Immun. DRINK! DAO! & Qc (slp! GI?)
/21:40? A3 “21:00” PF#2 .6 GABA&.4glu#1 (0NAC) & Lut (slp!) & Qc (slp! GI?)
Chamomile tea.
/00:20 A4 “23:00” PF#3 .6 GABA&.3glu#2 & Ellagic acid,
/01:50 B1 “01:00” PF#4 0SRP#1
/03.:50 B2 “03:00” +ALA+2x pine bark, (teeth) (+1NAC)
/07:20 B3 “07:00” (-30’) Q10#1 Qc#1 Rs#1 SAM-e
/08:35 B4 “07:00” EGCg + Fev/MSM
/10:50 MEAL! C1/2 “+30’=Meal” 2Cr#2 .6GAB#3, (C2:) .1gB2, gink#1, Zn (0NAC) 1xHONOKIOL! DRINK! DAO!
/10:50 C3 “08:00” 0x.5gC#1 2The2 (0NAC), taking Qc#2 to 19:00
/14:15 C4 “11:00” (+2h/) gi#2 gly#1+2 0SRP#2. Nd#? & Ellagic acid
1 DAO (D1) “13:00” 0psyllium
/16:15 D2/3 “15:00” 0x.5gC#2,Cr#3,!.6GA#4/0glu#3,gink#3,gly#3+4, 0NAC#5 DRINK! Taking Qc#3 to 21:00
/18:00 D4 “17:00” (“meal/acids+2h”) Nd#?.Qc#4.Q10#2.Rs#2, 0SRP#3.
eve:
“18:00” Prepare: 1) Complete & C changed supps. 3) Complete ##. 4) Tally irreg. 5) Remove “v” 6) Cut template 7) Save this 8) Paste 1x & unhide & paste 2nd (+1 to date and ##). BATCHES OK? Close 2nd TAB!
(Nov 4th: 18:00 vitamin B12 5mg methylcobalamin s.c.; next: Jan 4th.)
The day's 16 compartments (10', plus 5' making capsules)
Arg: Capsules? Pf: A1+3+4+B1, B2:A1+C2 2Cr: A1+C1+D2, Ell: A4,C4. Ga: A3,A4,C1,D2, Glu: A3,a4,0D3, Gi: C2,C4,D3 2Gly: C4+D3, 2Mal: A2 Qc: A2.A3.B3.D4 (not C3.D2) Q1&Rs:B3,D4 Sr0x: B1,0C4,0D4. SINGLE: A2:P5/Ro/0Immun., B2: ALA+0x2! pine, A3: Luteolin, B3:Sa B4: EGCG&Fev/MSM&Sily C2:Zn&Hon. C3:2Th (A2:Ω/Pq:meal) DAO before every meal.
(0x2C:C2,D3) (A2:0Se), (B2:0mu), (B4: 5NADH if nec.) (D1:0Pe). (0 Nia+) (0Nc: A3, B1,C1,C3,D2)
Development
Jab-sfx: 14:15: Sinuses histaminey-aching..
Research-search today:
At this point of the Afrin-video on MCAS he mentions “substance P, which is a neuropeptide, docks with the substance P receptor on the mast cell” making a mast cell release tons of mediators…
which reminds me of a blood donor pass I have which says I have antibody anti-P = anti--P/anti-ribose-P/anti-rib-P, which spawned loads of research (click for details) and checking my doc papers which all say: no ANAs.
I does start slow and I was wondering whether I wanted these deep fundaments on MCAS before I’m even quite sure I have it. But at https://youtu.be/lrKqlv6VK_w?t=2211 shows the impressive “explosively degranulating” mast cell. Now what exploded in me even more at that moment was him mentioning substance P. It reminded me of my blood donor pass of 40 years back, which notes I have a complicated blood type including “antibody anti P” (which isn’t the same thing tho). I was told nothing really to worry about at the time (but how would they’ve known?). OTOH I’ve had antinuclear antibodies screened by 2 rheums, a centre for rare diseases and a rheum clinic, and anti-(ribose-)P seems to be a regular one to look for. But maybe it has to be more specific or something different was meant… If it’s true, it’d point me in the direction of autoimmune/lupus/nephritis/hepatitis…
-
Brazil 2014 review The clinical utility of anti-ribosomal P autoantibodies in systemic lupus erythematosus - PubMed
https://www.tandfonline.com/doi/abs/10.1586/1744666X.2014.966692
Anti-P (if it’s the same one as mine) seems a biomarker (present in 10-13%) in SLE (lupus) - which I don’t have much symptoms of, but still an exciting indication: "Anti-ribosomal P protein (anti-Rib-P, anti-P) antibody, described in the 1980s, is a serological marker for SLE that is present in 13-20% of cases. ".
In the fuller text it adds stuff about kidneys, liver and often starting early, plus: “Anti-Rib-P may identify a subgroup of overlap syndromes that is particularly associated with lupus.” -
Croatia 2021 review Assessment of antinuclear antibodies (ANA): National recommendations on behalf of the Croatian society of medical biochemistry and laboratory medicine - PubMed
full: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8047791/
Here it says 10-35% in SLE (High specificity for SLE) -
France 2019 case report
Chronic hepatitis associated with antiribosomal-P autoantibodies in a 14-year-old girl - PubMed and full:
full: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6787851/
It’s also occasionally associated with chronic hepatitis
“mainly known to be lupus‐specific and have shown little association with autoimmune hepatitis. Only one study has reported the presence of these autoantibodies in 10% of adults with AIH. From diagnosis until 1‐year follow‐up, no other clinical manifestations of lupus occurred.” “this could be the first reported case of pediatric AIH with negative common laboratory investigation results but positive antiribosomal‐P autoantibodies.” -
study from 2021 Clinical aspects and risk factors of lupus nephritis: a retrospective study of 156 adult patients - PubMed
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6833424/
“anti-ribosomal P protein antibody positivity rates were all significantly increased in patients with active LN compared with inactive LN.” LN = lupus nephritis. But again - hardly any of those symptoms. in Table 1 of “Clinically most relevant ANA specificities in inflammatory connective tissue diseases” ANA = antinuclear antibodies,
Significant as in 54% as opposed to 3%, where renal damage is not necessary (40% as opposed to 52% with renal damage(?)) -
China 2018 The Predictive Value of Autoantibody Spectrum on Organ Damage in Patients With Systemic Lupus Erythematosus - PubMed
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6719570/
evaluated retrospectively: positive anti-Rib antibodies in renal damage. -
2018 Paris Detection in whole blood of autoantibodies for the diagnosis of connective tissue diseases in near patient testing condition - PubMed
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6116987/
A novel technology to measure antibodies, photonic ring immunoassay (PRI) is good & faster.
Anti-Rib-P: https://www.orgentec.com/de/produkte/alegria/Autoimmundiagnostik/Rheumadiagnostik/ORG+217.html
https://www.labor-und-diagnose-2020.de/k27.html Anti-P und Anti-Tja (Anti-P, Anti-P1, Anti-Pk): Diese Antikörper kommen extrem selten vor, da nur wenige Menschen diese Antigene nicht selbst besitzen (Tab. 27-11 – P-System).
Die Alloimmunisierung erfolgt in diesen seltenen Fällen meist schon in früher Kindheit, da es sich um ubiquitäre Antigene handelt. Die Antikörper sind dann zwar Kälte reaktive, natürliche Alloantikörper (IgM), zeigen aber auf Grund ihrer breiten Temperaturamplitude und ihrer Fähigkeit, Komplement zu aktivieren, starke hämolytische Aktivität.
%%title%% %%page%% - Arktis BioPharma Schweiz AG
Podcast Histamin Kyra Kaufmann %%title%% %%page%% - Arktis BioPharma Schweiz AG, amazon reviews Amazon Sign In
Incidentally, here https://youtu.be/lrKqlv6VK_w?t=2324 Afrin says “rare” disease, but isn’t he the one who says something like 17%? get it?
https://youtu.be/lrKqlv6VK_w?t=2438 What a BRILLIANT cartoon, using the old Indian analogy of 5 blind people (in this case doctors) describing an elephant from the part they see - and whaddyaknow - my fibromyalgia, GERD and praps CFS are in there too…
Here the “typical presentation” Afrin focuses on MCAS patient journeys https://youtu.be/lrKqlv6VK_w?t=3112
Nice little allergy joke:
Thinks that "UTI"s without inflammation, lipids, esp. triglycerides high…
Interesting thought of Afrin here in the video of his talk using Occam’s razor: “No, the patient probably is not so uniquely unlucky as to have coincidentally acquired so many different problems all of them independently of one another and it is much more likely that they have one problem that is biologically capable of causing directly or indirectly most or all of the issues that have shown up.”
Treatment: 1) Identify (as precisely as possible) and avoid triggers. 2) Inhibit mediator production. (antihistamines) 3)-6) Trying loads of different medications. State of the science is so immature that only trial & error is possible.
Bottom line for me after this video is, which Afrin also specifies on this slide: Anyone with many more inflammatory seeming symptoms than might be expected in fibromyalgia should have a look at MCAS.
Lessons in self-care #215 Singing despite more pain = “singing in the rain”!
Reasons to be cheerful #222 Learning is fun and helps understand.
- Jab-sfx-summary, being edited, major edit Jan 10th 12:35
- My blog references, e.g. abbreviations, supp chart/overview
- My “How to symptom track & trigger hunt”
- Next up…: Summaries & finishing off treatment list…