Combined Antibiotic Protocol for MS - Begin Here

A forum for the discussion of antibiotics as a potential therapy for MS

Combined Antibiotic Protocol for MS - Begin Here

Postby notasperfectasyou » Wed Jan 07, 2009 2:52 pm

There is a lot of info here, there and everywhere. I'm putting this post up as a very basic place to start. I realize that my TIMS thread is now so long, it's likely cumbersome for someone to follow if they just want to find a starting point. I simply want to cover what I think are the obvious things someone with no prior knowledge of the ABX protocol would want to know.

Has this really helped anyone?

Yes. One of the best documented cases is that of Sarah Longlands. You may want to read a summary of her account titled "Ignoring the evidence" that was published in 2005 in Hospital Doctor.

Was this developed by doctors?

Yes. There are three doctors who are credited with developing the Combined Antibiotic Protocol (CAP). They continue to work on improving the CAP; David Wheldon, Subramaniam Sriram and Charles Stratton.

Besides TIMS, where can I learn more about CAP for MS?

The very best site for info about CAP is CPn Help. Be sure to first read either "Getting Started" or "CPn Handbook" (links at top of the page). "Getting Started" is more basic and "CPn Handbook" is more thorough, but both are definitely the best place to begin.

Last edited by notasperfectasyou on Thu Jan 08, 2009 8:42 pm, edited 1 time in total.
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Postby Anecdote » Thu Jan 08, 2009 10:30 am

Neat idea, Ken and something which I had been meaning to do myself. One thing, though: it would be more accurate to put Stratton and Sriram before David, who only found out about CAP from them when I needed help and quick!

Sarah :wink:
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby notasperfectasyou » Thu Jan 08, 2009 10:59 am

I went by volume of information I have read. As an accountant, I've learned to make judgments this way. More seriously, I've taken the thread I started at cpn about othersites a step further with some refreshing results. Surprisingly for me, I'm experiencing a balance that Lori suggested a long time ago about trying to disprove the effect. Not that I'm trying to do that, but in messaging with others who don't know about this, I've learned not to take the word cure lightly. This also made me really think about how to introduce this to others and David's article about your diagnosis won. It really is a great summary for folks to read first. I wanted it to be more accessible.
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ABX Links

Postby notasperfectasyou » Mon Feb 02, 2009 9:01 am

A Beginners Guide to Combined Antibiotic Protocol for Multiple Sclerosis: Questions, Answers and Peer Reviewed Support

One of the problems with learning about various Multiple Sclerosis theories is the perception that they are in conflict with what we already know about MS. Another problem is that we often get non-authoritative or somewhat questionable support for explanations we are offered. I have assembled the following questions and answers in an effort to help others who are interested in Multiple Sclerosis to understand the reasoning behind the Combined Antibiotic Protocol and how bacterial theory can be compatible with autoimmune theory. Each link (with few exceptions) should take you to a COMPLETE peer reviewed article from a medical journal that supports the answers provided. Please let me know about any new questions you think should be included, bad links or ideas to improve the post. It is notable that there are a LOT more articles that might even be better than those I have referenced, however, I have tried to only use resources that are free, complete and authoritative.


Q: Isn’t apoptosis supposed to protect my body from bacterial infection?
A: Yes, but it doesn’t always work. Your cells are pre-programmed to self-destruct when they become infected through a process called apoptosis. When infected by Chlamydia Pneumoniae, many human cells, including immune system cells, become hosts for the bacteria instead of working to destroy the bacteria. To be absolutely clear, CPn bacteria cell - living within your body's cell. It has even been shown that CPn infected host cells can proliferate via mitosis, creating more infected host cells.

Lancellotti, Marcelo et al. 2006 Bacteria-induced apoptosis: an approach to bacterial pathogenesis
Geng, Yuemei et al. 2000 Chlamydia pneumoniae Inhibits Apoptosis in Human Peripheral Blood Mononuclear Cells Through Induction of IL-10
Rajalingam, Krishnaraj et al. 2001 Epithelial Cells Infected with Chlamydophila pneumoniae (Chlamydia pneumoniae) Are Resistant to Apoptosis
Fischer, Silke et al. 2004 Protection against CD95-Induced Apoptosis by Chlamydial Infection at a Mitochondrial Step
Fischer, Silke et al. 2004 Chlamydia Inhibit Host Cell Apoptosis by Degradation of Proapoptotic BH3-only Proteins
Green, Whitney et al. 2004 Chlamydia-Infected Cells Continue To Undergo Mitosis and Resist Induction of Apoptosis
Sasu, Sebastian et al. 2001 Chlamydia pneumoniae and Chlamydial Heat Shock Protein 60 Stimulate Proliferation of Human Vascular Smooth Muscle Cells via Toll-Like Receptor 4 and p44/p42 Mitogen-Activated Protein Kinase Activation

Q: Do my cells function differently after they become hosts for Chlamydia Pneumoniae?
A: Yes. Cellular expression can be dramatically altered. Genes related to apoptosis, the cell cycle and host metabolism are permanently differentially regulated by Chlamydia Pneumoniae. Chlamydia Pneumoniae has been shown to remain transcriptionally active while hosted by immune system cells. Infected human host cells have been found to significantly increase the release of interleukin (IL) 1b, IL-6, IL-8, IL-12, tumor necrosis factor alpha (TNF-a), intercellular cell adhesion molecule 1(ICAM-1/CD54) and gamma interferon (IFN-y). These cytokines stimulate the immune system. In addition CPn activates nuclear factor kappa B (NF-kB) and down regulates major histocompatibility complex class I molecules (MHC-1).

Eickhoff, Meike et al. 2007 Host Cell Responses to Chlamydia pneumoniae in Gamma Interferon-Induced Persistence Overlap Those of Productive Infection and Are Linked to Genes Involved in Apoptosis, Cell Cycle, and Metabolism
Krull, Matthias et al. 2004 Differences in Cell Activation by Chlamydophila pneumoniae and Chlamydia trachomatis Infection in Human Endothelial Cells
Rupp, Jan et al. 2009 Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages
Gencay, Mikael et al. 2003 Chlamydia pneumoniae Activates Epithelial Cell Proliferation via NF-κB and the Glucocorticoid Receptor
Yang, Jun et al. 2003 Induction of Proinflammatory Cytokines in Human Lung Epithelial Cells during Chlamydia pneumoniae Infection
Yamaguchi, Hiroyuki et al. 2002 Chlamydia pneumoniae Infection Induces Differentiation of Monocytes into Macrophages
Rodel, Jurgen et al. 2000 Production of Basic Fibroblast Growth Factor and Interleukin 6 by Human Smooth Muscle Cells following Infection with Chlamydia pneumoniae
Gaydos, Charlotte 2000 Growth in Vascular Cells and Cytokine Production by Chlamydia pneumoniae


Q: Has anyone actually demonstrated a relationship between CPn bacteria and MS?
A: Yes, an excellent article was published in 1999 that effectively says that lots of folks with MS also have the CPn bacteria and the prevalence of the bacteria in folks with MS is significantly greater than average.

Sriram, Subramaniam et al. 1999 Chlamydia pneumoniae Infection of the Central Nervous System in Multiple Sclerosis.

Q: Has CPn bacteria been identified in the central nervous system?
A: Yes, in fact CPn DNA has been identified in the brain and cerebrospinal fluid.

Sriram, Subramaniam et al. 2005 Detection of chlamydial bodies and antigens in the central nervous system of patients with multiple sclerosis
Contini, Carlo et al. 2008 Chlamydophila pneumoniae DNA and mRNA transcript levels in peripheral blood mononuclear cells and cerebrospinal fluid of patients with multiple sclerosis
Itzhaki, Ruth et al. 2004 Infiltration of the brain by pathogens causes Alzheimer’s disease
Tang, Yi-Wei et al. 2009 Qualitative and Quantitative Detection of Chlamydophila pneumoniae DNA in Cerebrospinal Fluid from Multiple Sclerosis Patients and Controls

Q: Can Chlamydia pneumoniae infect cellular hosts within the CNS?
A: Yes, it has been demonstrated that CPn can infect and reproduce in microglial cells. Furthermore, CPn can sustain a chronic infection in neuronal cells by interfering with apoptosis.

Ikejima, Hideaki et al. 2006 Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease
Appelt, Denah et al. 2008 Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae

Q: Have there been any studies that show how CPn infection can get out of the lungs?
A: Yes. It has been shown that infected Alveolar Macrophages can transmigrate through the mucosal barrier, thus giving Chlamydia Pneumoniae access to the lymphatic and systemic circulatory systems. It is also notable that Neutrophil Granulocytes (one of the first immune system cells to encounter CPn in the lungs) can host and incubate Chlamydia Pneumoniae.

Gieffers, Jens et al. 2004 Phagocytes transmit Chlamydia pneumoniae from the lungs to the vasculature
Blasi, Francesco et al. 2004 Chlamydia pneumoniae: crossing the barriers?
Van Zandbergen, Ger et al. 2004 Chlamydia pneumoniae Multiply in Neutrophil Granulocytes and Delay Their Spontaneous Apoptosis
Rodriguez, Nuria et al. 2005 Polymorphonuclear Neutrophils Improve Replication of Chlamydia pneumoniae In Vivo upon MyD88-Dependent Attraction

Q: Are there any studies that show the beneficial effect of antibiotics on MS?
A: Yes, there have been several studies that link antibiotics to improvement in patients with MS.

Brundula, Veronika et al. 2002 Targeting leukocyte MMPs and transmigration: Minocycline as a potential therapy for multiple sclerosis
Minagar, Alireza et al. 2007 Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis

Q: A lot of folks are just taking Minocycline, why are multiple antibiotics required in the protocol?
A: While Minocycline is a tetracycline that can work against CPn, it cannot kill CPn in all three phases of its life cycle: elementary body, reticulate body and cryptic form. Rifampin in combination with Azithromycin has been found to be more effective than single antibiotic therapy.

Wolf, Katerina et al. 1999 Effect of Azithromycin plus Rifampin versus That of Azithromycin Alone on the Eradication of Chlamydia pneumoniae from Lung Tissue in Experimental Pneumonitis.

However duel therapy does not eliminate CPn in its cryptic form, which is also referred to as persistent, nonreplicating, aberrant and refractory. The addition of a third antibiotic is needed to completely eliminate CPn bacteria from the body.

Gieffers, Jens et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment
Hogan, Richard et al. 2004 Chlamydial Persistence: beyond the Biphasic Paradigm
Mukhopadhyay, Sanghamitra et al. 2006 Protein Expression Profiles of Chlamydia pneumoniae in Models of Persistence versus Those of Heat Shock Stress Response

Q: When taking antibiotics, does dosage really matter?
A: Yes, not following dosage frequency and amounts can induce persistence.
Gieffers, Jens et al. 2004 First-Choice Antibiotics at Subinhibitory Concentrations Induce Persistence of Chlamydia pneumoniae.


Q: Does the way MMP-9 has been implicated in MS correlate with CPn infection?
A: Yes it does. Increased MMP-9 expression has been demonstrated in MS and MMP-9 has been shown to disrupt myelin and cause demyelination. Chlamydia Pneumoniae has been found to stimulate the production of MMP-9 in macrophages.

Leppert, David et al. 1998 Matrix metalloproteinase-9 (gelatinase B) is selectively elevated in CSF during relapses and stable phases of multiple sclerosis
Yong, V. Wee et al. 2001 Metalloproteinases in Biology and Pathology of the Nervous System
Vehmaan-Kreula, Pirjo et al. 2001 Chlamydia pneumoniae Proteins Induce Secretion of the 92-kDa Gelatinase by Human Monocyte–Derived Macrophages

Q: Does the way IL-6 has been implicated in MS correlate with CPn infection?
A: Yes it does. CPn infection is known to upregulate IL-6 and IL-6 is known to be proinflammatory in MS. In an MS related illness, Transverse Myelitis, there is evidence that IL-6 causes demyelination and axonal injury.

Dasgupta, Subhajit et al. 2003 Role of Very-late Antigen-4 (VLA-4) in Myelin Basic Protein-primed T Cell Contact-induced Expression of Proinflammatory Cytokines in Microglial Cells
Kaplin, Adam et al. 2005 IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis
Johnston, S. Claiborne et al. 2005 Chlamydia pneumoniae Burden in Carotid Arteries Is Associated With Upregulation of Plaque Interleukin-6 and Elevated C-Reactive Protein in Serum

Q: Does the way ICAM-1 has been implicated in MS correlate with CPn infection?
A: Yes. ICAM-1 is barely detectable in the normal brain. However, increased expression of ICAM-1 has been shown on endothelial cells, microglia and astrocytes in active MS. More specifically, ICAM-1 has been shown to be crucial for leukocyte infiltration into the brain, and the process of migration across the brain endothelial layer can accelerate the breakdown of the blood brain barrier. Several lines of evidence indicate that ICAM-1 acts as a docking molecule for lymphocytes before migration. ICAM-1 further facilitates transmigration through the CNS endothelium by rearrangement of the endothelial actin cytoskeleton, meaning ICAM-1 stimulates the altering of the impermeable tight junctions of the blood brain barrier. Chlamydia Pneumoniae can infect human endothelial cells where it induces the expression of ICAM-1, which has also been linked to monocyte migration.

Etienne-Manneville, Sandrine et al. 2000 ICAM-1-Coupled Cytoskeletal Rearrangements and Transendothelial Lymphocyte Migration Involve Intracellular Calcium Signaling in Brain Endothelial Cell Lines
Bullard, Daniel et al. 2007 Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis
Dai, Jianfeng et al. 2008 ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System
Adamson, Peter et al. 1999 Lymphocyte Migration Through Brain Endothelial Cell Monolayers Involves Signaling Through Endothelial ICAM-1 Via a Rho-Dependent Pathway
Buul, Jaap et al. 2004 Signaling in Leukocyte Transendothelial Migration
Lawson, Charlotte et al. 2009 ICAM-1 signaling in endothelial cells
Kol, Amir et al. 1999 Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages
Vielma, Silvana et al. 2003 Chlamydophila pneumoniae Induces ICAM-1 Expression in Human Aortic Endothelial Cells via Protein Kinase C–Dependent Activation of Nuclear Factor- B

Q: Does the way Immunoglobulin G antibodies (IgG) have been implicated in MS correlate with CPn infection?
A: Yes. The detection of elevated IgG in Cerebral Spinal Fluid (CSF) via oligoclonal bands has an extensive association with the diagnosis of MS by lumbar puncture. In fact, unique antibody patterns have been associated with the different types of MS and IgG from MS patients may provoke T-cell response. Likewise, anti-Chlamydia Pneumoniae antibodies (IgG) have been associated with MS. These have been identified in the CSF of MS patients and been shown to have greater gene transcription. Interestingly, it has also been shown that CPn infection can lead to an accumulation of IgG within an infected cell, which potentially correlates with increased IgG populations in patients with a longer history of MS.

Ezio Paolino et al. 1996 A prospective study on the predictive value of CSF oligoclonal bands and MRI in acute isolated neurological syndromes for subsequent progression to multiple sclerosis
Francisco Quintana et al. 2008 Antigen microarrays identify unique serum autoantibody signatures in clinical and pathologic subtypes of multiple sclerosis
Holmoy, Trygve et al. 2003 T cells from multiple sclerosis patients recognize immunoglobulin G from cerebrospinal fluid (abstract only)
Enrico, Fainardi et al. 2008 Under the microscope: focus on Chlamydia pneumoniae infection and multiple sclerosis (abstract only)
Dong-Si, Tuan et al. 2004 Increased prevalence of and gene transcription by Chlamydia pneumoniae in cerebrospinal fluid of patients with relapsing-remitting multiple sclerosis
Yao, Song-Yi et al. 2001 CSF oligoclonal bands in MS include antibodies against Chlamydophila antigens
Pollack, David et al. 2008 Uptake and intra-inclusion accumulation of exogenous immunoglobulin by Chlamydia-infected cells
Owens, Gregory et al. 2003 Single-cell repertoire analysis demonstrates that clonal expansion is a prominent feature of the B cell response in multiple sclerosis cerebrospinal fluid

Q: Does the way IFN-y {gamma} has been implicated in MS correlate with CPn infection?
A: Yes it does. IFN-y has been associated with exacerbations and oligodenrocyte death. It has been shown that IFN-y expression plays a central role in the bodys effort to control Chlamydia Pneumoniae infection.

Panitch, Hillel et al. 1987 Treatment of multiple sclerosis with gamma interferon
Mana, Paula et al. 2006 Deleterious Role of IFN in a Toxic Model of Central Nervous System Demyelination
Rottenberg, Martin et al. 2000 Regulation and Role of IFN-y in the Innate Resistance to Infection with Chlamydia pneumoniae

Q: Monocytes have been implicated in MS. How does this relate to CPn infection?
A: Monocytes have been found to migrate across the blood brain barrier and contribute to inflammation. Some benefits associated with MS therapies have been linked to their targeting monocytes. Monocytes are easily infected with CPn and can disseminate CPn within systemic circulation.

Bar-Or, Amit et al. 2003 Analyses of all matrix metalloproteinase members in leukocytes emphasize monocytes as major inflammatory mediators in multiple sclerosis
Kopadze, Ted et al. 2006 Inhibition by Mitoxantrone of In Vitro Migration of Immunocompetent Cells: A Possible Mechanism for Therapeutic Efficacy in the Treatment of Multiple Sclerosis
Minagar, Alireza et al. 2008 Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis: An Open-Label Trial
Burger, Danielle et al. 2009 Glatiramer acetate increases IL-1 receptor antagonist but decreases T cell-induced IL-1β in human monocytes and multiple sclerosis
Hakki, Amal et al. 2007 Chlamydia pneumoniae infection modulates cytokine production by human T lymphocytes and monocytes
Gieffers, Jens et al. 2001 Chlamydia pneumoniae Infection in Circulating Human Monocytes Is Refractory to Antibiotic Treatment

Q: Besides monocytes, do other immune system cells have behavior that correlates between MS and CPn infection?
A: Lymphocytes are also a major group of immune system cells that exhibit potentially corroborating behavior in MS and CPn infection. T-Lymphocyte and B-Lymphocyte migration through the brain endothelium/blood brain barrier has been associated with Multiple Sclerosis. Chlamydia Pneumoniae has been shown to infect and multiply in Lymphocytes. CPn infected Lymphocytes have been shown to be resistant to some antibiotic therapies.

Alter, Andrea et al. 2003 Determinants of Human B Cell Migration Across Brain Endothelial Cells
Prat, Alexandre et al. 2002 Migration of Multiple Sclerosis Lymphocytes Through Brain Endothelium
Haranaga, Shusaku et al. 2001 Chlamydia pneumoniae Infects and Multiplies in Lymphocytes In Vitro
Yamaguchi, Hiroyuki et al. 2003 Chlamydia pneumoniae Resists Antibiotics in Lymphocytes


Q: Has it been proven that MS is an autoimmune illness?
A: No. While science has pursued autoimmune theory for decades, it has yet to be proven that the underlying cause of MS is initiated or perpetuated through autoimmunity.
Chaudhuri, Abhijit et al. 2005 Multiple sclerosis: looking beyond autoimmunity
Last edited by notasperfectasyou on Wed Apr 28, 2010 5:47 pm, edited 68 times in total.
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Postby furch » Fri Mar 06, 2009 5:10 am

VERY cool collection of articles, thanks a million!:)

This one: "Chlamydial Persistence: beyond the Biphasic Paradigm" was especially interesting, explaining the life cycle of the chalmydia bacteria and the ability to persist undetected.

"In mice infected with either C. trachomatis (125) or C. pneumoniae (67), infections that had become asymptomatic reactivated to productive infections after treatment with cortisone."

scary, given that this is standard acute procedure with ms-attacks...

Seems the pleomorphic nature of bacteria is indisputable?! are there still any monomorphists?

if anyone is interested here is another recent article from a bulgarian bacteria-researcher, nadya markova.
Formation of Persisting Cell Wall Deficient Forms of Mycobacterium bovis BCG during Interaction with Peritoneal Macrophages in Guinea Pigs

her blog here:
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Postby notasperfectasyou » Fri Mar 06, 2009 9:49 pm

I'm glad you found this "very cool".

In one day 200 views since your post. I'd love for some of the folks reading this to share their interest in ABX.

Q: Has anyone demonstrated that Multiple Sclerosis can spread as an infection does?
A: Yes, Epidemiologic evidence, in particular that from the Faroe Islands, suggests a systemic infectious cause. Kurtzke, John 1993 Epidemiologic Evidence for Multiple Sclerosis as an Infection
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Postby CuriousRobot » Mon Jan 10, 2011 7:35 am

Nice work.
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combination therapy

Postby kda » Sat Jan 29, 2011 8:42 am

Ken, your wife is so lucky to have such a dedicated, intelligent, in-house support system!

I am currently taking Avonex - as are so many out there. I was wondering if you thought there would be any harm in using this antibiotic regime along with Avonex? I don't think my neuro would be very open to this 'new' way of thinking of the disease without a lot of evidence backing it up.

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Re: Combined Antibiotic Protocol for MS - Begin Here

Postby Brightspot » Mon Dec 03, 2012 2:23 pm

Thanks Ken, for all of your work creating this great introduction and assembling the links!! It is great.
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Re: Combined Antibiotic Protocol for MS - Begin Here

Postby Ruthless67 » Wed Jan 23, 2013 10:21 pm

I thought this was a good description of CPN

Chlamydia pneumonia Responsible for Atherosclerosis
Posted on August 22, 2012

Chlamydia also are intracellular pathogens, meaning that they can only grow and reproduce inside of another cell.
Cholesterol connection
One of the keys lies in the macrophages’ cell walls, which store cholesterol and usually tightly control it.
But when it’s infected with C. pneumoniae, the microbe traffics cholesterol from the macrophage cell membrane to its own, causing a change in the macrophage that makes it rigid and unable to move.
The bacterium also disturbs the macrophage’s production of toxins in a process that transforms them into “signaling molecules,” which support functions that keep the bacterium alive.
“C. pneumoniae really wants to hijack the cell functions for its own use, like a parasite would,” he says. “The macrophage, though, wants to kill Chlamydia, but its killing ability has been converted to signaling.”
This is the reason the infection becomes chronic, Azenabor says. “Because of signaling, everything else in the human cell is still fine except for the altered toxins, so the bacteria can reproduce in a short time.”
As the macrophages become immobile, they accumulate in the blood vessel walls, setting the stage for atherosclerosis.

Infection and pregnancy

How is Chlamydia trachomatis, the species that causes a sexually transmitted disease, involved in the occurrence of spontaneous abortions or miscarriages?
Trophoblasts act like macrophages in many ways, and their functions are mediated by the hormones estrogen and progesterone. And cholesterol is the molecule used to produce those hormones.
Azenabor’s research shows that, like its cousin, C. trachomatis does take cholesterol from the trophoblast, and it also reproduces once inside the cell.
“It’s the same old story,” says Azenabor. “Only this time the attacked cell is a trophoblast instead of a macrophage, and the depleted cholesterol hinders production of estrogen and progesterone instead of altering toxin production.”
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