Tinkering with the Immune System: Harmony is the Goal, But Can We Find It?

As we continue our discussions of the immune system dysfunction we are blaming for so much misery (Autism, Alzheimer’s, Inflammatory Bowel Disease, Diabetes, etc), I feel it is very important for you to understand we are messing with Mother Nature. We accept she is messing with us and we want to mess back, but finding that balance is more challenging than keeping blood sugar balanced for an insulin dependent teenager (and believe me – that is challenging).

DON”T MESS WITH MOTHER NATURE?

image

This is the work of Jonathan Wong – Very talented Artist

She looks a little scary in this depiction and that is the impression I wanted. Now let’s take a closer look at what we want to mess with.

http://www.ncbi.nlm.nih.gov/pubmed/19707398  links to the full open access paper I will discuss.

image

Now take a closer look at the left side of the diagram.  See the macrophage? There is an arrow to an activated macrophage which in turn makes TNF alpha. So that is easy enough. Oh. but wait we have a problem.  In cancer you would seem to want lots of TNF alpha to kill cancer cells but it doesn’t work.  In fact, high TNF alpha means high neopterin (an important biomarker) and the higher the neopterin the worse the prognosis.  That is also true for HIV infection: higher neopterin means higher TNF alpha and a worse prognosis.  So what’s up?

“Neopterin is produced by human macrophages/monocytes when stimulated with interferon-gamma. Production of neopterin is found in serum, cerebrospinal fluid (CSF) and urine of patients with infections by viruses, intracellular bacteria and parasites, autoimmune diseases, malignant tumors and patients in allograft rejection episodes.”  full paper online open access.  [Gut Pathog. 2010 Aug 22;2(1):9.]   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2939532/?tool=pubmed

Now I have get you back to nagalase: alpha-N-acetylgalactosaminidase.  This enzyme prevents the Vitamin D3 receptor from being activated on the surface of macrophages and with that they cannot properly activate.  I don’t think we fully understand the function of the GcMAF receptor. Nagalase levels are high at the same time that neopterin is elevated. It would seem that shouldn’t be true if GcMAF was initiator of macrophage activation. It must be a bit more downstream from neopterin.  To me, the likely scenario is that TNF sends the signal and part of the activation takes place – hence high neopterin and lots of macrophages, but as a result of nagalase activity the Vitamin D3 receptor looses its active site.  But something about adding Gc MAF back into the system allows macrophages to kill cancer cells and rid the body of HIV: as noted in my discussion 2 days ago. 

So my suggestion is some combination of GcMAF and perhaps Etanercept (Enbrel) may be able to bring us some rather tricky balance to Mother Nature’s combat zone.  But a Warning here – as far as I know no one has ever done this.

About Dr Bradstreet
Dr Bradstreet is a graduate of the University of South Florida College of Medicine and received his residency training at Wilford Hall USAF Medical Center. He is a Fellow of the American Academy of Family Physicians. He is an Adjunct Professor at the Southwest College of Naturopathic Medicine in Arizona. He is extensively published in the peer-reviewed literature on subjects of autism, oxidative stress, mitochondrial disorders, virology, hyperbaric oxygen, and toxicology (especially heavy metal chelation). He is trained in the the isolation and use of stem cells.

29 Responses to Tinkering with the Immune System: Harmony is the Goal, But Can We Find It?

  1. cindymoore75 says:

    This likely scenario of yours seems right….But, can it be that it’s not downstream from neopterin, that macrophages are activated, they produce neopterin, but because of the nagalase which prevents making of GcMAF they’re activated wrongly so they don’t kill cancer cells and viruses…but instead produce autoimmunity?

    • I think we are saying mostly the same thing. Autoimmunity is complex. Most models of autoimmunity involve B cell antibodies which are indirectly linked into this system. But we are at the frontiers of our understanding about this process with nagalase and the Vit D3 receptor.

  2. Karin says:

    I see it as a complex self-repairable, self-regulated machinery, able to deal on its own with all kinds of immune challenges. Something has contaminated the core of this machine and made it dysfunctional (one hypothesis would be a retrovirus).

    Now we only have access to a few test points to assess how the machinery is functioning, and we only have access to a few wheels of the machinery that we can tweak. The problem is that by tweaking one of these surface wheels, we might set up a chain reaction affecting the function of many other wheels, and the end result might be difficult to predict, because it will all depend on how dysfunctional the system is, on each individual specificities, etc…

    Ideally, we should be going as close as possible to the root cause of the dysfunction, and remove it, or at least handcuff it. That would be the most likely to restore the original ability of the whole machinery to self-repair and self-adjust. But even if we can’t do that, the more we understand about the root cause and about the ways it affects the machinery, the more we would be able to find ways to counteract these negative forces close to their source, and the less likely we would be to dysregulate the whole system even more.

    That’s why I think it is still critical to find exactly what is the root cause, what is at the origin of the dysfunction, so we can hit the nail on the head.

    I personally think there is one single root cause responsible for the recent autism epidemic, with a variety of secondary factors. We need to find what this root cause of immune dysfunction is, to stop its spread in the population and find effective treatments. I said it before but I personally think the hypothesis that makes the most sense is an infectious human retrovirus causing an acquired immune dysfunction syndrome.

    • Karin, great comments and I obviously agree with the general concept. I don’t know how much of the blog you have seen but last week I was writing about the likely underlying viral persistence as the driving force. That is why some agent GcMAF or something that can tell the immune system where to find its enemies is going to be critical to success. I believe the work of Persico points to multiple polyomaviruses (JC, BK, SV40) as well.

      So if we say persistent pathogens: almost assuredly viral, but spirochetes (Lyme) can cause persistent infections as can other strange bacteria, we will probably be closer to the truth.

      It appears to me that at least one mechanism of pathogen persistence is their ability to induce the infected cell to produce nagalase.

      We may be able to target nagalase in many ways. I will post some more thinking on this soon. In the meantime I very much appreciate the feedback and forum for discussing this. And I think creating this blog was one of my best ideas in recent years. It is very helpful to me to in many ways so thank you all for your interest, enthusiasm and support..

      • Susan says:

        In a quick Google search of what citations would be returned for “autism” and “virus”, I found a couple citations to be interesting. In 1998, researchers at the University of Michigan were already finding that autism may be caused by an immune system response to viruses (article was published in October 1998 issue of Clinical Immunology and Immunopathology). They generally theorized that early exposure to a virus prompts the body into an immune response that goes awry — in addition to producing antibodies against the virus, the body also makes antibodies against itself. They found that virus antibody levels were about the same in autistic and non-autistic children, but the majority of autistic chilren also had brain autoantibodies. They theorized that an autoimmune response interferes with the development of myelin such that nerve fibers won’t work as they should which could explain the brain abnormalities associated with autism.

        Fast foward 11 years to October 2009, and researchers at the Whittemore Peterson Institute found that 40% of a small group of children with autism were positive for XMRV (published in Science)which researchers indicated can lie dormant in people until it is turned on by other factors including response to the presence of cytokines. The lead author provided an explanation which seemed to explain what I feel happened to my son –she stated why vaccines would lead to autism in some children. XRMV viruses live and replicate in lymphocytes, the immune response cells, and B and T cells. When a vaccine is given, it sends B and T cells into overdrive, which is to be expected. But, if you’re harboring a virus, it’s replicated many times over, and the balance is broken between immune response and the virus. In summary, the virus was amplified by the vaccine and set off a disease that your immune system no longer can control along with other infections and created an immune deficiency.

        These articles may explain the “why” of autism, but what I still wonder is have these viruses been with us for some time such that the end result of autism wasn’t previously triggered because of the fewer number of vaccines or other agents? Or are the presence of these viruses a new development, and if so, how did this occur?

        If we can successfully regulate macrophages and TNF-alpha through the use of Embrel and GcMAF, can we still repair the myelin damage and other tissue damage that like occurred as well?

  3. Kent Heckenlively says:

    Dr. Bradstreet:

    What do you think of a combination of actos, spironolactone, and GcMAF?

    My daughter has a 6-fold elevation of TNF-alpha, (and is hitting puberty) so it seems I’d want to first lower TNF-alpha, address the hormone surges which are prompting replication of XMRV and HHV-6, type B (both confirmed by the Whittemore-Peterson Institute), then a healthy serving of GcMAF to get the vitamin D receptor working.

    She is also receiving IV glutathione and vitamin C.

    All the best,
    Kent.

  4. marilina says:

    I read: “In fact, high TNF alpha means high neopterin”

    question: the opposite, (high neopterins >>> high TNF-alfa) is also ALWAYS true?

    and TNF-alfa levels are linked someway with high or low NK-lymphocytes levels?

  5. Nagalase. It’s used in lysosomes to take sugars off proteins. It’s produced by fetuses or mayhap placenta to prevent GcMAF and thus prevent activated macrophages. You do not want activated macrophages when you want to stay pregnant.

    Some viruses produce nagalase which protects the infected cells from activated macrophages. Cancers produce nagalase, perhaps because the ones that do not are consumed by activated macrophages before they get big enough for doctors to detect them. Higher than base levels in serum (always?) indicate some condition you would like to remove, though sometimes only after nine months of gestation.

    Is there an easy, quick, cheap test for nagalase?

    Nobuto Yamamoto thinks nagalase prevents GcMAF by removing all three sugars from VDBP (Gc) but mass spectrometer studies of serum from cancer patients say there remains plenty of fully glycosylated Gc. Your remarks seem to suggest a different mechanism, which is a detail I want to know more about.

    Yamamoto’s clinical trials of GcMAF all showed very consistent drops in nagalase levels at least every two weeks of treatment. This gives very early indication that the GcMAF is working.

    The web site GcMAF.eu gives some evidence that two or more classes of patients do not benefit from GcMAF, ether for genetic reasons or for being too sick to walk for forty-five minutes or so each day.

    Perhaps those patients would benefit from the Leukocyte InFusion Therapy, LIFT, developed by Dr. Zheng Cui of Wake Forest Baptist Medical Center and now in clinical trial at the South Florida Bone marrow and Stem Cell Transplant Institute. He developed a method of measuring the cancer killing activity of white blood cells, macrophages, neutrophils, and perhaps natural killer cells. This let him discover that 10-15 percent of us humans have blood that attacks cancer (at least 25 different kinds of it) in the summer time.

    Now I hear that Russian doctors use in vitro colonies of macrophages instead of antibiotics. How can we who have failed to learn their language get the advantage of their understandings about this complex topic?

    Speaking of medicine in other countries, I was amazed to learn that the French physician Jean Sterne, published the first clinical trial of metformin as a treatment for diabetes in 1957, It was introduced to the United Kingdom in 1958, Canada in 1972, and the United States in 1995, cf Wikipedia.

    How can we reduce these long delays in moving the effective treatments across mere political boundaries? I guess we could just encourage more medical tourism in the meantime, but that seems needlessly inefficient.

    • We are testing Nagalase through a lab in Holland. The test costs and 50 euros. Typically, the delay in moving effective treatment into practice is based on economics. In general, a very expensive treatment finds resistance from the payors: Governments, Insurers, etc. On the other hand, natural or inexpensive treatments which cannot be patented (like GcMAF) are often ignored by medicine since there is no profit to be had in recommending the treatment. Cancer in the US and Europe is big business. GcMAF would likely wipe out many cancer centers if it was widely implemented.

    • More on this – I suspect but cannot prove that nagalase prevents “target acquisition” by the immune cells. This is as much to say that the effect of nagalase is a proximity defense mechanism for cancer cells. The highest levels of nagalase would be in direct proximity to the producing cell. So as immune cells move in for the “kill” they would encounter the highest levels of nagalase and effectively become blind to the cancer cells (assuming my theory is correct). I believe we will find the glycosolated GcMAF receptor is involved in both activation as well as targeting. I will be happy to try to answer more direct questions on this subject but I am a stuck with weak literature in this area of our understanding of GcMAF. Clearly we need more research to help clarify this endgame in the struggle between cancer cells and our defenses.

      • louise says:

        Hi Dr Bradstreet
        Are you following the work of a certain Belgian doctor who is using GcMaf to treat CFIDS patients?
        Also, any concerns about GcMaf causing IRIS, & presumably increasing TNF-alpha, which could have negative consequences for methionine synthase?
        Also, I measured TNF-alpha in the blood thru VIPdx. It was in range but given what you said at Autism One about the differences in levels of TNF-a in CSF & blood, I wonder whether that test has any value at all.
        Any thoughts?
        You say you are testing thru ELN. I assume you are testing blood and not CSF?
        Thanks
        Louise

      • I am measuring neopterin in the urine as an amplified reflection of TNF alpha effects. I use Lab Phillippe Auguste in Paris. I use ELN for nagalase testing. IRIS in ASD is unlikely since the immune system is not as severely compromised as AIDS. I go slowly with GcMAF and so far the general feedback is overwhelmingly positive using the titration schedule I favor. I too am concerned about excess TNF alpha but I think at some point the body needs to win its battle with the pathogen and end the ongoing struggle. I do not measure TNF alpha. I do not trust the results with our presently available methods :shipping etc.

  6. Amy says:

    Dr. Bradstreet,

    Did you see the below article about the man cured of HIV through his bone marrow stem cell transplant? Do you think a similar treatment could help our kids (in our lifetime)?

    http://news.yahoo.com/s/yblog_thelookout/20110603/us_yblog_thelookout/first-man-functionally-cured-of-hiv

    Since HIV was discovered 30 years ago this week, 30 million people have died from the disease, and it continues to spread at the rate of 7,000 people per day globally, the UN says.

    There’s not much good news when it comes to this devastating virus. But that is perhaps why the story of the man scientists call the “Berlin patient” is so remarkable and has generated so much excitement among the HIV advocacy community.

    Timothy Ray Brown suffered from both leukemia and HIV when he received a bone marrow stem cell transplant in Berlin, Germany in 2007. The transplant came from a man who was immune to HIV, which scientists say about 1 percent of Caucasians are. (According to San Francisco’s CBS affiliate, the trait may be passed down from ancestors who became immune to the plague centuries ago. This Wired story says it was more likely passed down from people who became immune to a smallpox-like disease.)

    What happened next has stunned the dozens of scientists who are closely monitoring Brown: His HIV went away.

    “He has no replicating virus and he isn’t taking any medication. And he will now probably never have any problems with HIV,” his doctor Gero Huetter told Reuters. Brown now lives in the Bay Area, and suffers from some mild neurological difficulties after the operation. “It makes me very happy,” he says of the incredible cure.

    The development of anti-retroviral drugs in the 1990s was the first sign of hope in the epidemic, transforming the disease from a sudden killer to a more manageable illness that could be lived with for decades. But still, the miraculous cocktail of drugs is expensive, costing $13 billion a year in developing countries alone, according to Reuters. That figure is expected to triple in 20 years–raising the worry that more sick people will not be able to afford treatment.

    Although Brown’s story is remarkable, scientists were quick to point out that bone marrow transplants can be fatal, and there’s no way Brown’s treatment could be applied to the 33.3 million people around the world living with HIV. The discovery does encourage “cure research,” according to Dr. Jay Levy, who co-discovered HIV thirty years ago, something that many people did not even think was possible years ago.

  7. Vanessa Li says:

    Hi Dr Bradstreet,

    Could you please explain why you recommend etanercept with Gcmaf? Thank you so much.

    • Hi, To be clear I do not recommend entanercept but the concept of taking out TNF alpha is very intriguing. GcMAF is the only apparent way to clear certain viruses and it is safe way to clear cancer based on the research of Yamamoto.

  8. stefano says:

    hi, first of all i am super pleased about your blog and share of information

    i am using gcmaf.eu for hbv after i have found my naglase at the very high level of 6.7 with several signs of immune depression but high cd4 counts (countless flu, candida infection in mouth that i still ahve even if rare, cuts getting infected for months)…..
    it has decreased to 3.3 at about 10 weeks but too little hbsag decrease for now

    i have seen many studies with proof that hbsag antigen has a receptor on macrophages and dentric cell probably used to inactivate them, looks a different strategy than nagalse?

    how can we link nagalase to hbv and macrophages/dentric cells inactivity on hbv from experience with other viruses?

    i also saw that hbv before starting liver infection goes or infect bone marrow, macrophages and maybe dentric cells too,

    any thought about the way hbv hijcks immune system?is it just similar to hiv?

  9. stefano says:

    another thing i cannot link with my little knowledge of biology

    i have found an old article about bone marrow transplant and abnormal nagalase getting to normal range just with the transplant

    can this help think about new link between nagalase and immune system or just something we cant explain yet?

    • Most likely the nagalase was elevated due to cancer and the BMT was the end game of the treatment for that cancer and the negative nagalase was used by the team to confirm disease free status.

  10. stefano says:

    by the way the general effect of gcmaf is…immune system works great since a couple of weeks on gcmaf and candida is extremely weak and rare now

    flu and sore throat improved with just d3 supplements and are now totally unknown to me

  11. Melissa A says:

    I am a Cancer patient. I am 36 years old and was diagnosed 10 months ago with stage 3 breast Cancer. After receiving 2 treatments of the dreadful chemotherapy (it was against my beliefs in the first place), i prayed to God and asked for the chemo to stop, create a miracle. three days later I lost my insurance, miracle received! I began a complete herbal detoxifiction that consisted or hydrotherapy, juicing (enzymes), raw food (more enzymes) and added some other components. After 3 months I was tested via CT scan, no mention of the tumor (which was last measured at 7.6cm) yet it was palpable. I recently accepted that I could not push out the tumor on my own and agreed to a bilater mastectomy, my recovery has been so fast and I know it is largely due to the fact that my immune system recieved the boost it needed. Here is my question and bare with me bc my background in in business not endocrinology, although I am learning fast.
    I added to my regimin Curcumin (Tumeric) with Bioperine for soluability at 2000mg a day for one month. Can the properties of this herb be of any help to this equation? In a recent study issued by Sloan Ketterin and MD Andeson, Curcumin has been found to not only kill the cancer cell, while not effecting the other healthy cells but has the ability to communicate and force a reversal of the wouldbe formation of cancer cells. Is there a characteristic in the curcumin that is forcing the immune system to revert and push through such a response? can this help GcMAF?

    I am pushing on and am determined to be apart of the real CURE.

    • I am very optimistic about GcMAF and you can red more about that on my blog by searching g\GcMAF and also about curcumin = great stuff and the right curcumin is terrific – just like the right GcMAF. There is a lot of hope.

  12. debbie says:

    I have CFIDS FIBRO and Just did my 3rd injection of gcmaf. 1st dose was .25 ml. Felt pretty bad so went to. .1.ml for 2nd shot. Still felt bad so 3rd week skipped dose. 4th week di. .1/1 ml. Feeling better but has activated several chronic infections but very mild and brief. Taking vit d3 5000 IU and compounded cortisol. Sr 10 mg for adrenal fatigue and just started. Cytomel .05 1/2 tablet to see if I can tolerate this time. Also taking seriphos at bedtime for the insomnia which is severe since starting gcmaf. Also taking seacure ( a fermented white fish protein 2 capsules and curcumin. Are all these ok to take with the gcmaf? Sorry but I know there is limited knowledge at this point but hoping you could help. Thanks
    Debbie

    • Debbie – it is not possible to provide specific medical advice via a blog. I am using different techniques with GcMAF (like homeopathic dilutions) in the CFIDS population as your story is not unusual. If desirable you may contact my office to arrange a consultation.

  13. I am really inspired together with your writing skills and also with the format for your blog. Is that this a paid topic or did you modify it yourself? Anyway keep up the nice quality writing, it is rare to peer a nice weblog like this one nowadays..

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