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Kas
Member in Phase 2
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Posted: Fri Jan 18th, 2008 05:20 |
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| Interesting. I wonder why so many doctors claim that being low in iron makes one fatigued and low in energy? Look at how many folk are swallowing those darn iron pills which give them gastric problems because medical people think it will make them feel much better.
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Sarc Dx by splenectomy 03- Lungs, lymph nodes, liver. Non MP meds: natural progesterone cream three weeks a month; cal/mag; probiotics; milk thistle daily; cranberry caps prn; quercetin prn.Noirs outdoors and under flourescent work lights, Spectra 3 cream
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Ruth Goold
Health Professional
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Posted: Fri Jan 18th, 2008 05:57 |
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Meg,
Is it possible that a person with (supposedly dangerously) high ferritin levels also suffers from Th1 inflammation?
Ruth
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03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
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Posted: Fri Jan 18th, 2008 06:17 |
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Serum ferritin may be high in chronic inflammation, especially if the liver is involved. This article lists the other tests done when a differential diagnosis is needed.
Anemia of chronic disease equals:
-ferritin normal or high
-iron low
-normal to low soluble transferrin receptor (sTfR)
-normal to low total iron-binding capacity (TIBC)
A high ferritin level suggests further investigation should be done with the D-metabolites tests.
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Ruth Goold
Health Professional
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Posted: Fri Jan 18th, 2008 07:20 |
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Thanks very much Meg. I'm working on yet another relative with likely Th1 problems. He's had the D tests done: certainly indicative of possible Th1 inflammantion with 25-D ~20 ng/ml and 1,25-D ~42 pg/ml (he's on no meds and does no supplementation of D or anything else). Of course, he's been told that both tests are 'perfectly normal'. He donates blood to bring his ferritin levels down but they have been very high for several years and I am concerned about him developing liver cancer.
He is currently waiting to see me improve on the MP (unfortunately, I am a spectacular case of one who seems to change very slowly). Before the MP, I was tired. Still tired. Can't honestly tell anyone that I think that I have changed (although I certainly hope that I have  ).
As always, I'll print out the info and pass it on. Thanks for your tireless efforts,
Ruth
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03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
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Claudia
Member in Phase 3
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Posted: Fri Jan 18th, 2008 18:02 |
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Periodic increases in ferritin which correlate with MP meds suggests liver inflammation.
aha! I knew my liver must be involved. But as for my "anaemia" - well, "it just gets curiouser and curiouser", as Alice said.
re:
Iron depletion (low serum ferritin) does not prove iron deficiency anemia. Anemia is common in chronic disease and iron deficiency anemia should be verified before an iron supplement is ordered. See My doctor says I'm anemic. What should I do?
in that thread suggested above, Belinda writes:
One of the potential 'benefits' of the anemia of chronic disease is that bacteria are being starved of the iron essential for their proliferation. Once CWD bacteria are killed off, iron stores will be available for your own body once again.
so, I think I am getting that:
1-anaemia, in chronic disease is a defensive move on the part of my body - to starve the bacteria.
2- that explains why iron supplementation (as I certainly experienced) will fail and even exacerbate the illness.
3- there is agreement with my statement that the MP frees up iron; but it is not clear where it is coming from; if that is what is showing up as ferritin levels rising or what. Can someone clarify why this is so, and how the liver is involved? Is the liver storing the iron to keep it from the bacteria?
I still wonder what happens to the iron/ferritin contained in the red blood cells when they are sacrificed during cell-death. Does it float around in the blood? End up in the liver? or elsewhere? hmmm...
Regarding my anaemia, I can recall my doctor telling me that at the time I first presented with hypothyroidism, I had Megaloblastic anaemia. I have no idea if iron supplementation is the correct treatment for that - perhaps not. (I think my body functions were all shutting down due to lack of thyroid hormone at the time.)
My ferritin at the time was 34 and my iron was 15. Iron supplementation seemed to temporarily boost these, but a month later both had dropped again - the iron dipping to its lowest, at 9. hmm.... rebounding due to flourishing CWD bacteria?
My Haemoglobin, Haematocrit, red cell count and white cell counts were all in normal range until I began the MP, more than a year later. In the course of the MP they all have dropped into "Low" levels, which I suppose indicates apoptosis, or programmed cell death of infected blood cells - would that be right? So that is my latest kind of anaemia. Does it have a name? Shall we dub it "Temporary Anaemia of MP Therapy"? 
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MP Phase1 23Mar_06; Phase2 July 10_06; Phase3 Nov 4_06. Dx Thyroiditis (Thyroxine); arthritis; glaucoma; CFS (1988-92);Kidney & bladder probs. Feb06 1,25D=43.3; Aug07 1,25D=27.5; Feb06 25D=44; Aug07 25D=28; Nov07 25D=36; Mar08 25D=16.4
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ndodd
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Posted: Fri Jan 25th, 2008 09:56 |
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Megaloblastic anaemia means reduction in numbers of red cells but an overall increase in their size, ie they are abnormally large. Can be associated with B12 deficiency, alcoholism, or for no known reason. Iron deficiency aneamia has small cells with reduced haemoglobin content (low MCV and low MCHC), so these two aneamias are quite different.
An 'anaemia of chronic disease' does seem to be common to phase 3 patients. Personally I dont think its cell death. Red cells are replaced every 3 months, and white cells every 4 months I think. So your body has slowed down the replacement of them, IMO because its caught up in a much bigger fight and is 'tired'. Therefore the importance of ramping cautiously.
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Mild RA 9 yrs: Nov07 125D 38, 25D 18; Ph1 Dec07; Ph2 Jan08, 25D 8; Ph3 May08, 25D7; NoIRs outdoors,hat,gloves
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P.Bear R.N.
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Posted: Fri Jan 25th, 2008 11:24 |
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I also think that the Benicar may be boosting renal blood flow and renal tissue oxygenation enough that the production of erythropoietin is down regulated and there is some consequent reduction in the stimulus to produce red cells (that is not too profound). I do think that herx/immunopathology can at times either wipe out red cells or effect their production in certain people due to endotoxin effects.
http://ajplegacy.physiology.org/cgi/content/abstract/231/1/73
best, P.B.
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Caitiegirl
Member in Phase 2
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Posted: Wed Jan 30th, 2008 20:08 |
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I feel like my life has just traveled in a circle. Twenty something years ago I was in Grad school studying Vibrio cholera and Vibrio vulnificus. While almost everyone has heard of Cholera, V. vulnificus is a particuarly nasty food borne illness. It can also be contracted by swimming in infected waters with an open wound. The research in our lab at that time was showing that the bacteria's ability to obtain iron from the host was one of the major, if not the major determining factor in mortality. I remember the case of an alcoholic with cirrhosis of the liver who was standing on an ant hill. He ran into the ocean to wash the ants off his legs. The bacterium entered through the ant bites and he was dead in days. Only people with high serum ferritin levels responded this way to this infection. I am sure the research into the mechanism of siderophores in this species of bacterium has continued and progressed since I was there. Sadly I have not kept up with the science and this was not my area of expertise. I was supposed to develope a probe which would find "viable but non-recoverable" V. vunificus in seafood and the environment. Sounds a little like CWD? It was later found that in the VBNR state bacteria had significant changes in their cell wall structure and became coccoid (vibrio is rod shaped normally).
To get back on subject, it is very easy for me to believe that low iron levels is the body's adaptive response to prevent the bacterial infection from thriving. I think this is just another example of doctor's having test results but viewing them in a two dimensional, simplistic fashion. Maybe it's not the cause of the fatigue but the result of the disease process causing the fatigue.
JMHO, Mindy
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Caitlin(18) lyme, seizures, myoclonus, dystonia, digestive, chronic headache, mental fog: 10/23/07 25D 36 1,25D 58, 1/12/09/5.7, 1/18/08 25D 9.9 Cut sun/D 9/26/07 Benicar 10/25/07, NoIRs 10/29/07
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schesche
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Posted: Fri Mar 7th, 2008 19:53 |
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Belgian Rickettsial researcher and pioneer for occult infections Dr JAdin allready cited low iron as a consequence of chronic rickettsial infection--in 1955 along with paul giroud ,paul Legag
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CFS, Lyme/neuro,joint pain,brain fog, insomnia,rage 125D56, MP 10/07, Triazep, zolpid, bvi, NoIRs, low lux home, lite exp. r/t work, covered up, 25D16
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Cocoa
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Posted: Sat Oct 25th, 2008 16:13 |
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I was watching an Australian science program this week. It focussed on the resurgence in TB due to the bugs developing abx resistance.
The program was fascinating stating that TB eschews the immune system by hiding in the macropages and, more relevant to this topic, that a new drugs is being developed to combat TB by preventing the bugs from getting access to the host's iron which is fundamental to their survival.
Very interesting! You can watch it at: http://www.abc.net.au/catalyst/stories/2395725.htm
Does anyone think that this could be applied to others suffering from CWD infection... by the way I wonder if TB gets into the macrophages by converting to the L-form?
Best, Cocoa.
Last edited on Sat Oct 25th, 2008 16:16 by Cocoa
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CFS, POTS, rickettsia, tachycardia, 125D46, MP 8/07, ModPh211/07, florinef for BP, Lamictal, clonazepam, melatonin, NoIRs, limited outings covered up, low lux home, 25D12 Sept 07
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Dr Trevor Marshall
Research Team
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Posted: Sat Oct 25th, 2008 16:24 |
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Mycobacteria use a different mechanism to evade the immune system than the metagenomic microbiota (biofilm) which causes Th1 disease.
The resurgence of TB is actually due to a surge in Th1 disease, which knocks out the innate immune system. The 'experts' will figure this out, eventually. I did have a sentence or two about this in my Bioessay:
http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf
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Rico
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Posted: Sat Oct 25th, 2008 16:48 |
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So, TB mycobacteria are co-infections? Boy, it's been one deception after another...it's incredible to see how medicine has been side-tracked all these years ... and all of the suffering and gazillions of dollars spent on studies, all the while the root cause was just continuing to strive and making things worse ... sigh ... food for thought.
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No diagnosis/some symptoms; wife with Sarc on MP; Olm 40mg q6h| avoid D| 1,25D=63 25D=32 (May 2006) 1,25D=44; 25D=10(Dec 2006)PhaseI(May06) PhaseII(Aug06) PhaseIII(Aug07)
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Dr Trevor Marshall
Research Team
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Posted: Sat Oct 25th, 2008 18:45 |
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The microbiota have been around since Neolithic times, so, as a civilization we have come to expect nothing except what they deal us.
Just today there was news that the same mutation caused several, apparently unrelated cancers, it has been tough to put 2 and 2 together until we started to really understand the metagenome.
http://www.reuters.com/article/healthNews/idUSTRE49N83D20081024
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NickBowler
Member in Phase 3
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Posted: Sun Oct 26th, 2008 01:48 |
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Here are a couple of articles I posted back in Feb in another thread. Hepcidin is an AMP which is regulated by the VDR. When the VDR is blocked, hepcidin levels drop and serum iron rises because hepcidin is a major controller of the iron withholding system in the body. The TH1 bacteria can then thrive. Just another piece in the puzzle!
I had high transferrin saturationand serum iron for quite a while before I found the MP, but a few months after starting I had developed megaloblastic anemia.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=308925
http://bloodjournal.hematologylibrary.org/cgi/content/full/102/3/783
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Sarcoirodis CIDP, MP start 11/07, NoIRs, 02/08 25D-8, Ph3 since 07/08|
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geirf
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Posted: Sun Dec 21st, 2008 20:45 |
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And we get them as a birth present , at least some of them ?
The infection route is rather difficult for most of them I guess if they don`t get help from Ticks or mosquitos ??
Or blood transfusions and vaccinations ??
what about eating raw meat or fish ??
My main patient population are autists..
Have there been any look into how many of the autists having Th1 disease - or intracellular metagenome as a cause ?
TO my knowledge that have not been looked at, and causes are mainly stated to be viral, and or toxicological combined with genetic susceptibility .
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Geir Flatabø
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Dr Trevor Marshall
Research Team
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Posted: Sun Dec 21st, 2008 21:35 |
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Geirf,
Yes, all of the above sources. Please take the time to look at the new videos of my two presentations in China over the Holidays. This exact question of where the bugs come from was canvassed in my presentations and in the question and answer sessions (the seminar at West China Hospital will be put online later today, my Keynote at the Gene 2008 conference is already online).
We have several 'autistic' ADHD and ASD children. We have not been recruiting for a number of reasons, but I can tell you that they respond with Immunopathology just as the adults with the rheumatic diseases do, and the kids on the MP have started on their paths to recovery, by, at least, getting back to school - and their classmates
Although Matt was primarily beset by 'tics' and not true ASD, you can read his recovery story here:
http://bacteriality.com/2007/10/28/interview6/
A Very Merry Christmas and many Happy New Years to you and yours
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Lottis
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Posted: Fri Jan 23rd, 2009 08:31 |
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Dr Inger Mattsby-Baltzer at the clinical bacteriology department of Sahlgrenska,
is doing some interesting research from Goteborg, Sweden.
Peptides taken from a large molecule in human maternal milk, Lactoferrin, has been indicating to inhibit the fibrosis that often appears in scarring and especially in the abdomen connected to IBD (inflammatory bowl diseases).
http://www.google.com/patents?hl=en&lr=&vid=USPAT7253143&id=-86AAAAAEBAJ&oi=fnd&dq=Inger+Mattsby-Baltzer
Testing on patients, with these peptides will begin at the end of 2009.
http://www.nyteknik.se/nyheter/bioteknik_lakemedel/lakemedel/article497055.ece
I dug a little bit futher into lactoferrin, and found this paper from 2007, that studies cases of iron depletion in prolonged neutropenia and cases of chronic granulomatous disease (CGD).
Human Polymorphonuclear Leukocytes Inhibit Aspergillus fumigatus
Conidial Growth by Lactoferrin-Mediated Iron Depletion
http://www.jimmunol.org/cgi/reprint/178/10/6367
Very interesting!
We show that human PMN (polymorphonuclear leukocytes)from both normal controls and CGD (chronic granulomatous disease) patients are equipotent at arresting the growth of Aspergillus conidia in vitro, indicating the presence of a reactive oxygen species-independent factor(s).
Cell-free supernatants of degranulated normal and CGD neutrophils both suppressed fungal growth and were found to be rich in lactoferrin, an abundant PMN secondary granule protein.
Purified iron-poor lactoferrin at concentrations occurring in PMN supernatants (and reported in human mucosal secretions in vivo) decreased fungal growth, whereas saturation of lactoferrin or PMN supernatants with iron, or testing in the presence of excess iron in the form of ferritin, completely abolished activity against conidia.
These results demonstrate that PMN lactoferrin sequestration of iron is important for host defense against Aspergillus. |
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HTN,LVH,CHF,arrhythmia,hypercholesterol,IBS? fibromyalgia?salivarystones,gallstones,ect...|15feb-07 init. 1,25D 37,5,|25-D 7,8(latest 15/2-07)| Ph1 29/7-08| Palliativ Meds. at the present; |Zoloft|NoIR's|covered up|disabled|
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Lottis
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Posted: Fri Jan 23rd, 2009 09:45 |
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Professor Kjell Olmarkers findings was the driving force, to find the peptides for preventing the fibrosis.
http://journals.lww.com/spinejournal/pages/articleviewer.aspx?year=2004&issue=11150&article=00002&type=abstract
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HTN,LVH,CHF,arrhythmia,hypercholesterol,IBS? fibromyalgia?salivarystones,gallstones,ect...|15feb-07 init. 1,25D 37,5,|25-D 7,8(latest 15/2-07)| Ph1 29/7-08| Palliativ Meds. at the present; |Zoloft|NoIR's|covered up|disabled|
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Lottis
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Posted: Sun Jan 25th, 2009 09:08 |
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Lottis wrote: Dr Inger Mattsby-Baltzer
http://www.google.com/patents?hl=en&lr=&vid=USPAT7253143&id=-86AAAAAEBAJ&oi=fnd&dq=Inger+Mattsby-Baltzer
Human Polymorphonuclear Leukocytes Inhibit Aspergillus fumigatus
Conidial Growth by Lactoferrin-Mediated Iron Depletion
http://www.jimmunol.org/cgi/reprint/178/10/6367
Both of the discussions at those sites, refer mostly to fungus.
I wonder if maybe fungus require more iron than many other pathogens.
That could mean that if somebody has more fungus pathogens, the less levels of iron will be detected in the persons blood. More fungus = Less iron? 
Pregnant women often get infected with fungus, since the pH in the mucus often go more basic during pregnancy. Many other factors has made fungus infection quite common among young girls, as well. And also iron deficiency.
To heal the imbalance of fungus and other pathogens, breast feeding will supply the child with the weapons to balance and normalize the little baby. We know this, but maybe, now we know even more...
/LottisLast edited on Sun Jan 25th, 2009 09:11 by Lottis
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HTN,LVH,CHF,arrhythmia,hypercholesterol,IBS? fibromyalgia?salivarystones,gallstones,ect...|15feb-07 init. 1,25D 37,5,|25-D 7,8(latest 15/2-07)| Ph1 29/7-08| Palliativ Meds. at the present; |Zoloft|NoIR's|covered up|disabled|
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Dr Trevor Marshall
Research Team
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Posted: Sun Jan 25th, 2009 10:00 |
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Lottis said "Pregnant women often get infected with fungus"
I have several comments about this. Firstly, it is common for physicians to diagnose "fungus" based just on what the inflammation 'looks like'.
Second, the acute inflammation of Th1 dysfunction weakens the immune system to the point where an actual fungus may be able to take hold, and even become strong enough to be cultured.
The $64,000 question is, of course, whether it is Th1 inflammation or fungus-induced inflammation at the heart of what occurs in pregnant women.
Amy just wrote a peer-reviewed paper about Th1 in women, but it is still "in press." meanwhile you might like to look at her Porto transcript at:
http://AutoimmunityResearch.org/transcripts/ICA2008_Transcript_AmyProal.pdf
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