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Lottis
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Posted: Sun Jan 25th, 2009 10:43 |
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Amy is really doing some groundbreaking work! I am eagerly waiting for the paper to come out.  That is going to be very interesting!
 Back now to the iron.
http://www.jimmunol.org/cgi/reprint/178/10/6367
On page 3, at the right column in the journal of immunology, read the section that starts with this sentence;
LF levels in PMA-treated PMN supernatants from normal controls
and CGD patients were determined by ELISA.
There is a dysfunction of the ability to disable the pathogens by requesting their iron, in the CGD patients.
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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
Foundation Staff
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Posted: Sun Jan 25th, 2009 12:03 |
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Lottis,
You are trying to read too much into these in-vitro experiments, which at best are only a poor simulation of what happens in the diseased body.
It is well known that many bacterial strains accrete ferritin. No need to focus on fungus.
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Lottis
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Posted: Sun Jan 25th, 2009 12:22 |
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Sorry, I am not focus on fungus....that was a side topic.It is the neutrophiles function that caught my interest.
I know that pathogens rob us from our iron. That is why I do not want to give iron to my daughter, who has been diagnosed by a hematologist of being low in iron. This doctor suggested iron supplementation, I hesitated, because I knew this.
I am trying to find another solution for my daughter and her sick and tiredness.
http://curemyth1.org/view_topic.php?id=1072&forum_id=5&highlight=Little+My
No doctor wants to even discuss the MP treatment for her.
She is also low in her neutrophile counts, so I see a slight connection here. Her B12 is around 400, and I have no clue if B12 supplementation would be good for her.
She is in her final year at school, and she is aiming for high grades. That is why I need to understand this subject, you see.  -She has to get some help.
/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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Lottis
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Posted: Wed Feb 4th, 2009 09:06 |
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Curcumin in curry, might effect the levels of iron.
http://bloodjournal.hematologylibrary.org/cgi/content/abstract/113/2/462
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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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MarkN
Member in Phase 3
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Posted: Wed Feb 4th, 2009 19:19 |
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When I was researching lactoferrin, yes it keeps iron from the bacteria ... some say it also has a direct antibacterial effect, and I even found some references that it may send a chemical "message" that tells the bugs not to form biofilm.
So I don't know what it "really" does, except that it gives me very strong IP, especially where I need it, in the brain. It is also said to "modulate the immune system", which is generally a bad idea, so I don't take it very often. I do feel an anti-inflammatory effect for about 12 hours after taking it.
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General insanity (Aspergers ??), CFS, some joint paint ...
11/06:1,25D=37 25D=43, 12/09:25D=5.4 ... Avoid D 12/06 ... PhaseOne 1/07, PhaseTwo 3/07, PhaseThree 9/07
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cschifel
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Posted: Thu Mar 19th, 2009 18:52 |
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I have been using the tinted Kabana sunscreen. It is tinted with iron. Should I stop? I use it when I have to go out in the sun or heavy flourescent lighting. I don't now how much iron can be absorbed through the skin. I only put it on my face.
Carmen
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Lottis
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Posted: Sat Nov 28th, 2009 23:01 |
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Iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis
http://jrsm.rsmjournals.com/cgi/content/full/99/11/589
The findings suggest that iron deficiency provides protection from the development of EAE31 and also challenge traditional views on what constitutes a normal level of stored iron.14 The authors31 noted that, `The failure of iron-deficient mice to develop EAE is impressive. Many of the pharmaceutical approaches to inhibiting EAE are less effective than iron deficiency.'
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Lottis
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Posted: Sun Nov 29th, 2009 07:05 |
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The really interesting part about the findings in my last post, is the connection between iron overload and venous dysfunction.
The circulation problem here is not in the arteries, not in the capillaries, but in the venous system, which is malformed or clogged.
By doing angioplasty into the veins from the brain, the circulation were restored and many MS patients symptoms resolved. Not cured but with symptom relief.
So, my point is, the MP treatment is probably restoring the venous function, among all that is does, which seems to be the most important circulation problem in MS.
That MS is suggested to be more of a vascular disease, is interesting from the MP perspective.
The news from Nov 20th 2009 is here;
http://www.theglobeandmail.com/news/national/researchers-labour-of-love-leads-to-ms-breakthrough/article1372414/
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For the Italian professor, however, the quest was both personal and professional and the results were stunning.
Fighting for his wife's health, Dr. Zamboni looked for answers in the medical literature. He found repeated references, dating back a century, to excess iron as a possible cause of MS. The heavy metal can cause inflammation and cell death, hallmarks of the disease. The vascular surgeon was intrigued – coincidentally, he had been researching how iron buildup damages blood vessels in the legs, and wondered if there could be a similar problem in the blood vessels of the brain.
Using ultrasound to examine the vessels leading in and out of the brain, Dr. Zamboni made a startling find: In more than 90 per cent of people with multiple sclerosis, including his spouse, the veins draining blood from the brain were malformed or blocked. In people without MS, they were not.
He hypothesized that iron was damaging the blood vessels and allowing the heavy metal, along with other unwelcome cells, to cross the crucial brain-blood barrier. (The barrier keeps blood and cerebrospinal fluid separate. In MS, immune cells cross the blood-brain barrier, where they destroy myelin, a crucial sheathing on nerves.)
More striking still was that, when Dr. Zamboni performed a simple operation to unclog veins and get blood flowing normally again, many of the symptoms of MS disappeared. The procedure is similar to angioplasty, in which a catheter is threaded into the groin and up into the arteries, where a balloon is inflated to clear the blockages. His wife, who had the surgery three years ago, has not had an attack since...
...The researchers theory is simple: that the underlying cause of MS is a condition he has dubbed “chronic cerebrospinal venous insufficiency.” If you tackle CCSVI by repairing the drainage problems from the brain, you can successfully treat, or better still prevent, the disease.
Last edited on Sun Nov 29th, 2009 07:27 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
Foundation Staff
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Posted: Sun Nov 29th, 2009 09:18 |
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Lottis,
We have discussed this specious MS concept elsewhere:
http://www.marshallprotocol.com/forum11/13520.html
We already know that postural hypotension (vascular dysfunction) disappears with a few years on the MP, and we have preliminary data that Arterial IMT actually decreases during the course of the MP. One of my clinical colleagues is collecting controlled data to compare the arterial IMT progress of his patients on the MP and his patients on Statins.
Preliminary results are showing that MP is curative, wall thickness actually decreases, while statins, at best, only maintain current thickness.
Ten years ago I myself had terminal pulmonary hypertension. My cardiovascular system now shows no signs of disease, in particular, my carotid arteries are free of any artifact visible to ultrasound. A data set of size one, but there are many others in the cohort who are reporting similar progress.
It sure looks like all chronic disease can be laid back at the feet of the Th1 metagenomic microbiota...
ps: I assume you have read this thread:
http://www.marshallprotocol.com/view_topic.php?id=10090&forum_id=39
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Lottis
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Posted: Mon Nov 30th, 2009 05:56 |
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Forgive me, I am sorry I did not do a search before I posted. I usually do.
That discussion went by me since I was without computer, in the countryside, for a few months last summer. There were just too much for me to catch up with. Thank you for your answer, pointing this out.
I have personal reasons to be overly focused on iron and blood dysfunctions.
We have in our family a rare form of blood cancer, my mother is now within her last month of life, diagnosed with CMML that entered the acute phase a few weeks ago, AML.
My daughter shows signs of blood disease as well, not yet being cared for or diagnosed. She too, is losing color, being low in iron and in neutrophiles since a few years back.
I am still a little confused about this iron accumulation.
High levels of ferritin come and go during the immune pathology process of the bacterial killing. In those situations iron levels are low, but ferritin is high.
Does this align or fit in with Dr. Zambonis theories?
Zamboni writes:
| Macrophages take up iron accumulated in the tissue and store it in intracellular ferritin-like structures (Figure 3B). Intra- and extra-cellular overload of iron in the tissue could potentially be dangerous for generation of free radicals due to possible release of free iron from deposits.4-9,13,14 Wenk et al.7 and Yeoh-Ellerton13 found increased iron levels in exudates from chronic leg ulcers as compared to acute wounds. They also observed significant concentrations of metabolites from oxidative stress.7,13 |
Last edited on Mon Nov 30th, 2009 06:30 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
Foundation Staff
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Posted: Mon Nov 30th, 2009 06:59 |
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Dr Zamboni is entitled to his concepts, but they appear to be extremely limited and simplistic to me, incapable of helping him fully understand the disease process.
In the human body, iron performs one of its primary functions in a complex called 'heme' which lies at the heart of many of our P450 enzymes. It can be displaced from this task by other bivalent, and event multivalent metals. That is not really the problem, however.
The issue is that a body sick with Th1 disease is to a great extent under the control of its metagenomic microbiota. Those species which require iron, get it by scavenging from their host. The proteins, mRNA, etc, that these species secrete to do this are likely to cause a range of problems in the host cells, problems I wouldn't dare to try and quantify at this point.
I wouldn't necessarily expect the levels of ferritin or the levels of iron to correlate as is implied in the text you cite. I use the word "imponderable" in some of my presentations. We can understand the root cause of the disease process, but the totality of ways in which the body can be affected by the microbiota are complex beyond definition, at least at this point in time.
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Phillyguy
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Posted: Mon Nov 30th, 2009 18:04 |
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I read this about a month ago and thought it may be of interest to the discussion. It relates to the selective modulation of TLR4-activated inflammatory responses by altered iron homeostasis (in mice).
From the introduction:
Conditions of iron overload have been shown to predispose to infections such as salmonellosis and tuberculosis (2–6). Similarly, iron deficiency confers relative resistance to infection, whereas iron supplements can reverse this effect (7–10). The effects of altered iron metabolism on infectious disease have been attributed to changes in the host immune response, as well as direct effects of iron on microbial growth (1, 11), but the underlying mechanisms remain poorly understood.
From the discussion:
The results reported here demonstrate a surprising specificity for the effect of Hfe deficiency and the associated reduction of intramacrophage free iron levels on TLR-activated responses. The data indicate that the abnormality in TLR function in the Hfe KO macrophages not only is specific to TLR4, but also appears to affect only 1 of the 2 signaling pathways activated by this receptor, namely, that dependent on the TRAM and TRIF adaptor proteins. Furthermore, based on what is known about TLR signaling and on our finding that upregulation of IFN-β in the Hfe KO macrophages was impaired in response to LPS but not poly(I:C), the simplest interpretation of the data is that Hfe deficiency and the associated decrease in intramacrophage iron levels negatively impact the MyD88-independent signaling pathway at a step unique to TLR4, that is, proximal to TRIF (Figure 8). Such an abnormality would also explain the reduction in Salmonella- and LPS-induced production of TNF-α and IL-6 in the Hfe KO macrophages reported here and in our earlier work (25), because both TRAM and TRIF are required for expression of these cytokines (28, 29).
http://www.jci.org/articles/view/39939?key=4fae98a76d788644e09d
So this may be yet another example of a persistence mechanism whereby certain pathogens sequester intracellular iron in an effort to not only assist their own metabolism but also inhibit TLR4 signalling. I suppose that the body may also independently downregulate iron in an effort to block microbial metabolism.
Interestingly,the Mal/MyD88-dependent signaling is intact in iron deficient cells so TLR4 signalling appears to remain partially intact (TRAM/TRIF knocked out) so if the body downregulates iron stores in response to infection, the pathogens' metabolism would be impacted but TLR4 would still be able to signal via the Mal/MyD88 pathway?
On a related note, I just read that bartonella quintana LPS is being studied as a potential anti-inflammatory in auto-immune disease as it is apparently an especially effective TLR4 antagonist. I'm beginning to really appreciate how the totality of multiple pathogens synergistically and putatatively interfere with the innate immune system. Some hit the TLR's directly, some indirectly hit intracelluler signalling pathways, some hit the VDR, etc....Put them all together in one cell and you have a real problem.
Last edited on Mon Nov 30th, 2009 18:05 by Phillyguy
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NickBowler
Member in Phase 3
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Posted: Thu Dec 3rd, 2009 09:24 |
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Lottis this MS ‘revelation’ is not new either. When I first got noticeably sick in 1994 my research led me to consult with Dr. Patrick Stortebecker, who was a retired neurologist from the Karolinska in Stockholm. At the time I thought I was developing ALS and he espoused an interesting (and thus vilified) theory outlined in his book ‘Motor Neuron Disorder. Deficiency of Arterial Blood Supply to Spinal Cord and Brain Stem’
http://jnnp.bmj.com/content/47/8/896.3.full.pdf
He had documented case studies demonstrating a greater than doubling in average survival rates by treating his patients with high dose niacin and vitamin E. The book also discusses microbes as a possible causative factor. He has also written on microbial causes of cancer :
http://catalogue.nla.gov.au/Record/1589225
So it is a great pity that he has passed away now as he would surely have greatly added to debate on the MP. The VDR is important in both iron sequestration (through the AMP hepcidin) and calcium deposition (the traditional role of vitamin D) so it seems that seizing control of it back from the microbiota by the MP is probably the best strategy yet devised for postponing the aging process:
http://www.longevinex.com/resveratrol.asp?story=The%20Unifying%20Theory%20of%20Aging%20PART%201
Apologies for the link to a D pusher but I couldn’t find a better description of this interesting idea. The references are extensive anyway.
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Sarcoirodis CIDP, MP start 11/07, NoIRs, 02/08 25D-8, Ph3 since 07/08|
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scooker48
Member in Phase 3
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Posted: Thu Dec 3rd, 2009 20:49 |
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I post these questions from a colleague. Possible to answer? Thank you.
The ultimate cause in this case IS physical. However, the researchers prior to this have been looking in the wrong places.
What will an excessive amount of Iron in the blood do?
Could it be the underlying cause for MS, a deterioration of the myelin sheath around the nerves.
Could excess iron be causing malformation of major blood vessels in the neck and thus starve the nerves? (No one knows if the myelin sheath is more susceptible to oxygen deprivation than the actual nerves themselves.)
Could excessive iron poison the myelin sheath itself?
Everything revolves what happens at the boundary layer, those few layers of atoms actually touching another substance. A level we can’t see and are just now beginning to understand. See chaos theory, quantum mechanics, physical chemistry, electronics theory, etc.
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Necrotizing granulomas biopsy 10/88; Dx 12/04 Sarcoid liver spleen. 2/2/05: VitD 25/VitD125 62. 11/7/09 D25 at 6, Liver function normal 4/08; Wear NoIRs outside. No K creme used. 5/09 Liver and kidneys normal. ACE still high at 113 on 11/7/09.
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Dr Trevor Marshall
Foundation Staff
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Posted: Fri Dec 4th, 2009 17:49 |
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Sherry,
When somebody starts with "The ultimate cause in this case IS physical" then there is no point for any further discussion, That is a closed mind.
I would even dispute that the myelin sheath is the root of the problem - it is much deeper than that. Many have attempted to understand the brain with neurons functioning as storage and decision elements - like a digital computer - but it is far more complex than that. Wave theory is involved in some yet-to-be-determined manner... Probably a conjunction between partly-ordered chaos and waves. Imponderable at this point in time.
Anybody who thinks they can quantify how the body works in simplistic terms is deluded. Yes, the atomic boundary layer is key, but more important is the way molecules move around to give that boundary layer a chance to come into play.
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scooker48
Member in Phase 3
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Posted: Fri Dec 4th, 2009 19:18 |
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My colleague's reply:
Sir, I believe we are on the same page. As I said to my colleague, “if I had known that the questions would be posted to a medical audience possessing expertise at the post-doc level and beyond I would have framed my questions much more narrowly and paid considerably more attention to how they were phrased”. Please do not allow my clumsy phrasing and overly broad construction of my response to detract from my underlying point… “we are on the boundary of knowledge here”.
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Necrotizing granulomas biopsy 10/88; Dx 12/04 Sarcoid liver spleen. 2/2/05: VitD 25/VitD125 62. 11/7/09 D25 at 6, Liver function normal 4/08; Wear NoIRs outside. No K creme used. 5/09 Liver and kidneys normal. ACE still high at 113 on 11/7/09.
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Limburg
Member in Phase 2
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Posted: Fri Dec 4th, 2009 22:25 |
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Zamboni says in an interview CCVSI is
possibly not the rootcause of MS, but his (temporary)solution of ballooning/stenting is good news for many patients whose MS already lead to handicaps.
http://www.corriere.com/viewstory.php?storyid=94433
Unfortunately it is in Italian.....
Annemarie
Last edited on Fri Dec 4th, 2009 22:31 by Limburg
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MS,DX 1997,Auto-immune hepatitis,DX 2008, MP start jan.2009. 25D: 20.4 (october 7,2009)25D: 12.5 (november 23,2009)
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Diesel
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Posted: Mon Jan 11th, 2010 17:44 |
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Hi all,
From the site irondisorders:
Anemia of Chronic Disease
http://www.irondisorders.org/anemia-of-chronic-disease
There is no treatment for anemia of chronic disease except to address the underlying condition. Iron supplementation is inappropriate in these patients because the added iron can become free to nourish bacteria and cancer cells
http://www.irondisorders.org/Disorders/about.asp see chapter absorption
Iron is so important that without it all life would cease to exist. Every living thing: plants, animals, human beings, bacteria (good and bad) and yes, even cancer cells all need iron to survive and grow.
Free iron can also provide nourishment for bacteria such as Yersinia, Listeria and Vibrio. These bacteria are harmless for people with normal iron levels, but when transferrin is highly saturated with iron Yersinia, , Listeria, and Vibrio, contained in raw shellfish such as oysters, can lead to septicemia (definition will include symptoms). Death by septicemia can occur within hours if a person has very high body iron levels. People with high iron should always take care not to eat raw shellfish or walk barefoot on a beach where they might step on an infected shells.
Some microorganisms are skilled in other ways in obtaining iron from human hosts. Staph, for example can break open red blood cells and extract the iron it needs. Another pathogen, the protozoan that causes malaria, can get into the red blood cell to obtain iron necessary to thrive. And finally, there are bacteria such as the one that causes tuberculosis, that grow best inside macrophages that are iron loaded.
Macrophages are white blood cells that protect us against disease; they scavenge for harmful invaders that enter our bloodstream. When the macrophage is called into action, it engulfs the bacteria or harmful debris and traps it so that it cannot thrive and spread disease in the human host. Iron-loaded macrophages are helpless to defend us against opportunistic infection and disease. Overwhelmed with an iron these macrophages can migrate to other parts of the body and release free iron to that organ. An example is iron-loaded alveolar (lung macrophages) that migrate to the bladder and increase the risk of bladder disease. For this reason, people who smoke are at risk for many diseases, especially cancer. Cancer cells thrive on iron.
Maybe the following articles are of interest.
Hepcidin mediates "anemia of chronic disease" and is reason iron supplements won't help
http://www.medscape.com/viewarticle/538033
Iron feeds joint inflammation
"The importance of recognizing that iron is phlogistic, ie, proinflammatory, is that such recognition helps us to understand that in giving iron to patients with inflammatory joint disease, we supply the means for increasing the inflammation," McGrath tells rheumawire . "When we give iron, we supply the macrophage, the cell making up much of the diseased proliferating synovium, with the means to do damage to bone and cartilage. That's because giving iron increases hepcidin, which increases the sequestration of iron in the macrophage, where iron facilitates the Fenton reaction, resulting in the production of toxic oxygen radicals. These toxic oxygen radicals increase the capacity of the macrophage to damage cartilage and bone. Unless patients are truly iron deficient, we probably should not be giving iron to them at all."
"Although there may be plenty of iron in the body, it is unavailable for the production of red blood cells, so patients develop iron-deficiency anemia," McGrath says. "When physicians check for iron loss or for poor iron intake, there is none. They may then check the bone marrow and find plenty of iron. Despite this, many physicians will go ahead and give iron, believing that it can do no harm. I believe it can."
Dysregulation of hepcidin or its receptor ferroportin results in a spectrum of iron disorders:
http://flipper.diff.org/app/pathways/info/869
In inflammatory disorders and infections, cytokine induced hepcidin exces contributes to development of anemia of inflammation , characterized by hypoferremia and anemia despite adequate iron stores.
IRON AND MICROBIAL INFECTION
http://fst.snu.ac.kr/~shchoi/Lecture/2008%20Food%20Biotech/1a.%20Iron-Virl-NatRev%20(THA).pdf
The use of iron as a cofactor in basic metabolic pathways is essential to both pathogenic microorganisms and their hosts. It is also a pivotal component of the innate immune response through its role in the generation of toxic oxygen and nitrogen intermediates. During evolution, the shared requirement of micro- and macroorganisms for this important nutrient has shaped the pathogen–host relationship. Here, we discuss how pathogens compete with the host for iron, and also how the host uses iron to counteract this threat.
The pathogen
Iron is an important growth factor for pathogenic bacteria, with the exception of the LYME DISEASE agent, Borrelia burgdorferi,which persists in environments with very low concentrations of iron19.This is because of the selective loss of loci that encode iron-dependent proteins from the genome of B. burgdorferi. Iron concentrations of 10–6 to10–7 M are required by most microorganisms for various metabolic processes that are crucial for microbial replication, including electron transport, glycolysis,DNA synthesis and defence against toxic ROI 20. Specialized iron-uptake systems have been identified in most bacterial species studied so far, and these allow microorganisms to compete for this vital element within mixed microbial communities in the environment.
....Iron overload in the host, owing to nutritional, hereditary or therapeutic reasons, exacerbates several infectious diseases, including yersiniosis, salmonellosis, tuberculosis and AIDS........... Clinical studies of prophylactic iron supplementation to treat anaemia also showed a direct correlation between iron uptake and an increased risk of these infections, as well as tuberculosis...
Susceptibility of iron-loaded Borelia burgdorferi to killing by hydrogen peroxide and human polymorphonuclear leucocytes
http://www.ncbi.nlm.nih.gov/pubmed/1874405
Borrelia burgdorferi grew more slowly in iron-depleted than in iron-sufficient media. The addition of increasing concentrations of iron stimulated borrelial growth and resulted in the intracellular accumulation of this element. Compared with iron-starved borrelia, iron-enriched organisms showed enhanced sensitivity to hydrogen peroxide. Intracellular iron-content did not, however, influence susceptibility to killing by human polymorphonuclear leucocytes [corrected].
Diesel
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Vit.B12 Hydroxo-cobalamin injection dependant 1995 Sublingual Methyl-cobalamin and Adenosyl-cobalamin tabl. 2008
Osteoporosis 2007 True knowledge exists in knowing that you know nothing
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TikBitten
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Posted: Mon Jan 11th, 2010 21:28 |
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Diesel wrote: Iron is an important growth factor for pathogenic bacteria, with the exception of the LYME DISEASE agent, Borrelia burgdorferi,which persists in environments with very low concentrations of iron19...
Not sure how it plays into the interwoven microbiome of Th1 disease but, the mineral of choice of Borrelia.burgdorferi is Magnesium NOT iron. Any insight into this, especially with regard to MP diet and ABXs?
TB
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Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09
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keithw
Member in Phase 2
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Posted: Tue Jan 12th, 2010 01:15 |
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Diesel, I am not sure how MP relates to this article.
My understanding is that MP will prevent many of these problems if they are caught early enough.
However, for chronic sufferers other people have this problem well in hand, and unsurprisingly they are also biomedical engineers.
The people at Artemisia biomedical make a living from iron based pathogens, See below.
http://www.artbiomedical.com/home.html
This is a bad time to be an oncologist.
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SLE, CNS vasculitis, avascular necrosis, arthritis both shoulders | 25D35 (May09) | WeanPredMay09 Ph1Aug09 Ph2Nov09 Ph3Feb10 | 25D18 (Mar10)
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