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zaterdag 24 maart 2012

Eliminate neurotoxins from Lyme with selenium

"Our research also suggested that toxins from tick-borne pathogens such as Borrelia burgdorferi (Lyme disease organism) and Babesia microti may cause chronic illness even after the spirochetes or intracellular protozoa (also called apicomplexans) have been killed by antibiotics. People who cannot naturally eliminate biotoxins develop chronic illness.


Selenium and Disease defense: how the immune system works

Selenium has a pivotal role in disease defense because it is critical to both the innate and adaptive arms of the immune system. It is present in the form of the antioxidant enzyme glutathione peroxidase (GPx) in scavenger white blood cells called macrophages that ingest and destroy invading pathogens as part of innate immune defense. When these cells ingest pathogens, they project parts of the invaders (called antigens) on their own cell surfaces to alert the T and B-cells.

T-cells and B-cells form the basis of adaptive or acquired immunity. T-cells are the effectors of ‘cell-mediated’ immunity, while B-cells produce antibodies. T-cells are the ‘helper’ cells of the immune system, and without them none of the various parts of the immune system, including antibody-mediated defense, operates efficiently.

There are two kinds of T-cells: CD4 cells (sometimes called T-helper cells) and CD8 cells, or ‘killer’ T-cells. CD4 cells ‘see’ the antigens displayed on macrophages and then alert and direct the rest of the immune system including killer T cells, neutrophils and antibody-producing B cells to neutralize the attacker.

T- and B-cells, along with macrophages and neutrophils of the innate immune system, contain selenium in its antioxidant enzyme form. Macrophages and neutrophils lose their ability to “kill” pathogens when selenium is deficient; and T-cell numbers (and effectiveness) decline. Both factors contribute to an association between selenium deficiency and greater susceptibility to disease.

1) have your levels of selenium checked
2) supplement if necessary and check levels again
3) after 4-6 months, keep maintenance dose

donderdag 22 maart 2012

Spontaneous remission is a myth

The chronic inflammatory diseases treated by the Marshall Protocol (MP) never go away on their own. It’s not that patients with Th1 disease can’t and won’t go through periods where they might feel better. Unfortunately, these periods are usually a sign that the immune system has become severely compromised.

Whether temporary “remission” is driven by immunosuppressive drugs like corticosteroids, a high intake of vitamin D, excessive sun exposure, or simply the accumulation of a bacterial load that is so high that the VDR is almost completely shut down by bacterial ligands – these periods are times when the Th1 pathogens are alive and well, spreading, and surely infecting other tissues. This unchecked infection leads to illnesses that will only be discovered later in life such as arthritis, heart disease, decreasing kidney function, diabetes, cancer and even the diseases of aging. But during the “remission period,” when the immune system is not capable of killing the pathogens, there is no corresponding inflammatory response that would be occurring if the body was mounting a defense against the infection. This causes the patient to feel a sense of temporary relief during immune suppression that is often mistaken for “wellness.”

Relapsing/remitting nature of infection

One of the important factors in why symptoms of illness relapses and remits is that infections relapse and remit. For example, Staphylococcus aureus is a major human pathogen which plays a role in deep tissue infections, osteomyelitis, and chronic lung infections. A key characteristic of these infections is that relapses can occur months or years after an apparent cure. These relapses, Dr. Bettina Löffler and her team from the Institut für Medizinische Mikrobiologie in Münster, Germany, believe are due to phenotype switching, a change in the bacterial behaviour. After infection and invasion of the patient's host cells, the bacteria form small colony variants (SCVs), tiny bacterial subpopulations that can evade the immune system as well as many antibiotics and grow slowly. 21268281

Microbes ability to easily switch between forms explains both their persistence and the variability in patients' symptom presentation from one time point to another.

Research with insufficient follow up

As it happens, members of the medical community who put credence in spontaneous remission tend to base their information on studies that are notoriously poor at following subjects for long periods of time – periods of time that would allow researchers to take note of the declines that occur after bacteria have spread and any temporary periods of palliation have subsided. These studies would have to last for at least 5-10 years, with endpoints assessing systemic illness. Such studies would surely find that disease symptoms persist even in those people who had once experienced temporary periods of relief.

There has somehow been a misconception that remission could last a lifetime. In reality, remission is accompanied by recurrence and relapses.

Trevor Marshall, PhD


Researchers at Jefferson Medical Center in Philadelphia found a 74% relapse rate in sarcoidosis patients with treatment-induced remission, while only 60% of patients identified as having a favorable prognosis actually sustained remission over 130 months.1

Many argue that the most accurate study of sarcoidosis to date is the 2003 NIH ACCESS study, which followed 215 sarcoidosis patients for two years - a period during which it is sometimes mistakenly thought that the disease can go into remission. The study found that measures of sarcoidosis severity remained unchanged over the two-year period, despite the fact that many patients were using corticosteroids and other drugs.

In fact, in the NIH ACCESS study there were no documented cases of spontaneous remission. Even in the positive-sounding “improved” category for clinical markers, the percentages described were at best “improved”, not “substantially better” and certainly not “cured.” An indication of lack of substantial improvement in the improved group is the fact that there were essentially no change in use of corticosteroid therapy during the two year period. The study also concluded that most patients with persistent sarcoidosis at two years were “unlikely to have resolution of the illness” and that “end-stage pulmonary sarcoidosis usually develops over one or two decades.”

In simple terms, the study found that not one patient recovered over a two year period, and that any patient to remain ill with sarcoidosis for two years is likely to die from the disease over the following ten to twenty years.

What is cure?

It has also been argued that there is a gap between how patients themselves and members of the medical community perceive success and improvement, as well as their concept of cure. The medical community has a tendency to be satisfied by results that show a patient has stabilized thanks to a particular medication, without taking into account systemic effects of disease, such as fatigue and pain, which are often excluded as endpoints.

A 2005 article on gene therapy described patients who had undergone treatment as “basically cured” – even though three had developed leukemia and one died.

The above example is a misuse of the word “cure.” For one thing, an actual cure results from a treatment that allows all participants to become well, no side effects or long-term harm included. Did the above study check in with its subjects a decade down the road in order to access their health years later? Probably not. But if they did, the subjects were probably symptomatic again, as gene therapy has not yet been adopted as an effective way to treat disease.

The public often isn’t satisfied with the medical community’s perception of a “cure,” which is why so many patients have left mainstream medicine – searching for solutions among doctors that practice alternative medicine or even among psychotherapists.

Unfortunately, for chronically ill patients, commercial culture and the media have combined to progressively define down what “better” means—so much so that assessing the significance of any new “breakthrough” becomes difficult, at best.

How is the Marshall Protocol different?

The MP is different. It is an attempt to address the underlying cause of Th1 disease – the bacteria causing symptoms in the first place. And unless these bacteria are targeted and killed, Th1 diseases do not go away. Indeed, if they went away on their own, why would there be hundreds of forums on the Internet where people with chronic disease discuss what it’s like to live a life full of relapses and pain?

Notes and comments
Legacy content


1. Gottlieb JE, Israel HL, Steiner RM, Triolo J, Patrick H Outcome in sarcoidosis. The relationship of relapse to corticosteroid therapy. Chest. 1997;111:623-31.

Strepto infection in childhood can lead to OCD

Obsessive compulsive disorder and childhood infections like strep –

A 2010 team of researchers developed a new animal model to show how exposure to strep affects the brain and leads to a number of physical and mental ailments. According to one of the collaborators, Daphna Joel,
“It's almost impossible to show how strep can lead to OCD in humans ― almost all of us, even very young children, have been exposed to the bacterium at one time or another. But childhood seems to provide a distinct window of opportunity for the disorder to take root through strep infection. This work was presented at a 2010 meeting and is expected to be published at the beginning of 2011.


zaterdag 17 maart 2012

Protocols that can make a difference

The Marshall Protocol:

The Yasko Protocol:

Yasko files: (login required)
Yasko website:
Yasko CFS group:
Yasko CH3 forum:

The Richard A. Van Konynenburg Protocol:

To be done under supervision of your doctor.

donderdag 8 maart 2012

Vitamin D receptor gene methylation is associated with disease susceptibility

Could it be a coincidence I had tuberculosis as a child and then developed lupus as a teenager, ME as years went by and now arthritis?
What if dysfunctional methylation leads to disease?

Hum Immunol. 2011 Mar;72(3):262-8. Epub 2010 Dec 16.

Vitamin D receptor gene methylation is associated with ethnicity, tuberculosis, and TaqI polymorphism.

Andraos C, Koorsen G, Knight JC, Bornman L.

Department of Biochemistry, University of Johannesburg, Auckland Park, South Africa.


The Vitamin D receptor (VDR) gene encodes a transcription factor which, on activation by vitamin D, modulates diverse biologic processes, including calcium homeostasis and immune function. Genetic variation involving VDR shows striking differences in allele frequency between populations and has been associated with disease susceptibility, including tuberculosis and autoimmunity, although results have often been conflicting.
We hypothesized that methylation of VDR may be population specific and that the combination of differential methylation and genetic variation may characterize tuberculosis (TB) predisposition. We use bisulfite conversion and/or pyrosequencing to analyze the methylation status of 17 CpGs of VDR and to genotype 7 SNPs in the 3' CpG Island (CpG island [CGI] 1060), including the commonly studied SNPs ApaI (rs7975232) and TaqI (rs731236).
We show that, for lymphoblastoid cell lines from two ethnically diverse populations (Yoruba from HapMap, n = 30 and Caucasians, n = 30) together with TB cases (n = 32) and controls (n = 29) from the Venda population of South Africa, there are methylation variable positions in the 3' end that significantly distinguish ethnicity (9/17 CpGs) and TB status (3/17 CpGs).
Moreover, methylation status shows complex association with TaqI genotype highlighting the need to consider both genetic and epigenetic variants in genetic studies of VDR association with disease.

Copyright © 2011 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.


zaterdag 3 maart 2012

Cholesterol drug can be responsible for permanent impairment of memory

It seems I'm not the only one who suffered total black-outs from this drug.

All statins in use today can be associated with cognitive side effects such as amnesia, forgetfulness, confusion and disorientation. The mechanism of action seems to be excessive reduction in the bio-availability of cholesterol for proper brain function.

For some reason Lipitor "does this better" than the others just as Baycol caused rhabdomyolysis so much more than the other statins that it had to be removed from the market. But, in truth, all the statins can cause this dreaded muscle breakdown.

Associated with this distortion of memory is a tendency for prolonged, even permanent impairment of the process of short-term memory with the use of Lipitor. We have a growing list of these reports where former breadwinners have been reduced to dependents and the entire family structure has been drastically altered.

The following are but a few examples of this legacy of Lipitor - atorvastatin - sent to me by readers.

1) Three weeks ago I had an eight-hour episode of TGA. I had been on Lipitor and Lisinopril for about six weeks prior. I have stopped both medications for the time being until I get back to normal. Even after stopping the Lipitor I was disoriented (especially in the morning) and "just wasn't feeling right (poorly described by a physician).

2) Four months ago I was put on Lipitor to reduce my bad cholesterol to 100. Suddenly I found I could not handle basic math or remember how to spell. It became so bad that I was in a constant fog. I should tell you I spent most of my career in Silicon Valley writing specifications for software and hold a patent on expert system technology. I had an MRI to rule out a brain tumor or stroke. Since the only thing that had changed was the addition of Lipitor I stopped taking it. Five weeks later I am still having problems spelling and frequently forget things.

3) We have recently taken my mother off of the Statins because she is suffering from memory loss. Ten days after removing her from Statins, her doctor sent her for neuropsych testing and a CT scan. CT results are still pending. The neuropsychologist diagnosed Alzheimer's disease and referred her back to her internist to begin cholinesterase inhibitors. We believe that this is a premature diagnosis, as her memory loss has not progressed beyond the initial stages observed over 2.5 years ago and that she has only been off Statins for ten days when she was tested. She has been on statin therapy for nine years.

4) I was put on Lipitor when Mevacor didn't appear to be doing its job. I was started on Mevacor at approximately 30 years of age....I'm 49 now. The Lipitor was started approximately two years ago...I'd have to have the Doctor's office check as I can't really remember when I was switched! I noticed my memory was getting bad and every doctor I saw blamed it on menopause and / or my fibromyalgia.

Within the past few months however, new and frightening symptoms appeared. While talking to friends, out shopping or just sitting home and watching television I would have the strangest and most unsettling sensation that I didn't know who I was. It would last for seconds and felt so odd- like an out of body experience...who was this person talking...oh, it must be me.

I was always a voracious reader and now it's so hard for me to concentrate and remember things that I've all but given up reading. Crossword puzzles were a favorite pastime. Now I have a hard time carrying on a conversation since I stutter and ummm and uhhh trying to think of a word or name. Names of old friends escape me and sometimes I can't recall if I've done something just seconds after I've done it.

The muscles in my forearms began to be so sore I found it difficult to take a half-gallon container of soymilk out of the fridge, and pushing the button on the remote to change channels actually hurt. I was terrified that I had Alzheimer's, or worse yet a brain tumor. I was prepared to ask my Doctor for a CT scan or MRI to rule out that possibility when I received the e-newsletter and discovered the root of my problem. I immediately discontinued my Lipitor.

When I showed my physician the information I had gathered about Statins she was very interested as her own husband is on 20mg of Lipitor and had been complaining of memory problems and brain fog! She said she had no idea the two were linked.