Bacteriality

Exploring chronic disease

Category: cognitive dysfunction

Several years ago this finance lawyer and mother of two was so debilitated both physically and mentally that she thought it unlikely that she’d live to see her children go to high school. Today, after five years on Autoimmunity Research Foundation’s Marshall Protocol, almost all of her symptoms have resolved and she has rejoined the world – picking up many of her old activities including tennis lessons. Meet JST.

During my teenage years but it took another twenty years or so before I was to become chronically ill and debilitated.

Describe the progression of your disease

While I was at high school I had odd bouts of ill health including chronic tonsillitis and sinusitis. In 1979, while at university, I suffered an episode of sudden fatigue and paralysis in both legs which disabled me for about three weeks. I was not seen by a specialist and it was concluded that I was suffering from “hysteria.”

I was generally healthy until the early 90s when for no apparent reason I began to suffer periods of intermittent fatigue, difficulty in articulating myself, and a collection of seemingly unconnected and disparate symptoms like mild asthma, abdominal pain, weight loss, amenorrhea, malaise, and dizziness. I had an absorbing and challenging professional job, but found it increasingly difficult to perform my work. During my first pregnancy most of my symptoms surprisingly resolved and I thought I had recovered.[1] After a severe chest infection in 1993 the intermittent fatigue became unrelenting. I resigned from my job and did part-time pro-bono work while awaiting the birth of my second child. To my dismay, I had to give even that work up when I found myself completely out of breath just walking to the station.

My symptoms improved somewhat again during my second pregnancy but I began to feel very ill indeed post partum. I developed a host of new symptoms – severe photosensitivity, compression-like headaches, tinnitus, changes in proprioreception, blackouts, hair loss, mild fever, night sweats, anxiety, edema, abdominal pain and discomfort, and, swollen lymph nodes in the neck. In 1997, I decided to consult a general hospital and an ultrasound scan revealed enlarged abdominal lymph nodes. Sarcoidosis was diagnosed on the basis of a cervical lymph node biopsy and confirmed via chest X-ray, BAL (Bronchoalveolar lavage), lung biopsies and a thoracic CT scan. Because my Angiotensin Converting Enzyme assay (commonly used as a marker of Sarcoid inflammation) was only slightly above “normal” and I did not have overt organ damage, the pulmonologist whose care I was under decided to take a “wait and see” approach.

Determined to try and preserve as much function as possible, I walked everywhere but over the next couple of years became increasingly short of breath, the fatigue grew even more profound, and swollen lymph nodes and inflamed joints kept me in chronic low grade pain. Sitting crippled by fatigue in an armchair late in the afternoon while my infant children ran riot around me, I would often wonder why I was not out sailing the world single-handed or climbing mountains like the anecdotal super-patients of the sarcoidosis specialist’s home pages.

During 1999 my headache became more prominent; I developed problems with my sense of balance and position and experienced loss of motor function and peripheral sensation in my arms and legs. I first noticed this in my hands which became very weak and clumsy. I dropped and broke many things. Eventually my fingers became too weak to even operate an ATM key pad. I lost my opposable thumbs so could not do simple things like get change out of my purse.

My legs became leaden and clumsy and I began to trip over my feet. Myasthenia and spasticity obliged me to use elbow crutches or a cane to walk most of the time. To explain how this feels to someone who has not experienced it, imagine having both legs in plaster casts to the thighs with one’s knees cast at 140 degrees. Life and my legs were a drag.

What JST looked like without the palsy. She gets some palsy symptoms when very tired. Rings under her eyes come back when she takes one of the phase III antibiotics, although the rings are getting lighter as time goes by.Later in 1999 I was admitted to hospital with severe muscular weakness and spasticity in all four limbs barely able to move from the neck down. MR imaging failed to reveal any gross pathology but a diagnosis of sarcoid inflammation of the spinal cord was made via clinical examination. I spent a total of five weeks in hospital, but worse still was being separated from my children for nearly three months as they had to be sent back to New Zealand. I declined methylprednisolone pulse therapy. After a poor response to 10mg/day, I agreed to 50mg/day of the oral corticosteroid prednisolone. After discharge I was kept on varying dosages of prednisolone for 3 years. Prognosis for Sarcoidosis of spinal cord at the time was that 70% patients “deteriorated”. I made arrangements with my lawyers in anticipation that I too would deteriorate, lose cognitive function, and be unlikely to live to see my children go to high school.

Short term memory problems and language difficulties, particularly with Japanese – which is a language I acquired as an adult – made life unbearable. I struggled to make myself understood at the most elementary level and would be misunderstood or treated like a child because I was unable to articulate my thoughts or feelings spontaneously. This was so humiliating that I began to consciously avoid interacting with people. I was completely overwhelmed trying to look after two young children and constantly anxious and very short tempered. Varying doses of the oral steroids left me disconnected and confused. I would do things like turn up at the supermarket counter with insufficient money in my purse, make terrible mistakes in ordering things and was forever losing important documents. Opportune infections caused a continuum of relapses that I never fully recovered from. I lived one day at a time not knowing whether when I got out of bed in the morning I would be able to walk or use my arms.

It was impossible to commit to anything more than a few hours ahead. Central Tokyo, with its aggressive traffic and poor infrastructure, was a nightmare for a disabled person. I spent most of the day asleep but no matter how much I slept it never relieved the fatigue. As my deterioration was slow and subtle those around me didn’t really notice it. It was only when I went back to New Zealand and my mother gasped when she met me at the airport that I realized how much I had changed.

Spasticity in JST’s hand. JST’s comment: “At a glance my hand looks normal, but if you try to actually mimick the position and angles of my fingers you will find yourself with a very distorted hand, Now that my muscles are only slightly hyper-reflexive I am no longer able to recreate the observed distortion. My feet were very spastic too at times, but I don’t have a photograph.”

For three years I half lived through a nightmare roller coaster of exacerbations and short lived partial remissions. Every step I made was a conscious effort and it seemed that all my concentration and energy went into fighting intransigent muscles. The side effects of prednisolone were horrible but every attempt to wean from it failed. I was hirsute, bloated, disconnected, and somewhere between ornery and psychotic most of the time. Ever more crippled by fatigue and cognitive dysfunction I withdrew completely and seldom left the house. The toll on my family was immense. It was as if I became the insect of Kafka’s metamorphosis.

What are your symptoms like now?

I seldom think about them.

My spinal cord inflammation has resolved to the extent that I can take tennis coaching twice a week. I have residual spasticity but it is barely discernable except to the trained eye. This is good evidence I believe, of the ability of the CNS to heal. Despite being less supple I feel as if I can run and hit the ball way better and stronger than I did fifteen years ago. I concede though that this may be related in part to having replaced my wooden racquet with a state-of-the art carbon fibre one! The aerobic exercise seems to improve my energy levels and rather than causing me to become fatigued upon exertion; I feel better for it – something that would have been unimaginable even a couple of years ago. Recently I was also quite astonished when someone remarked on the muscle tone in my arms.

Last February I took my open water scuba divers license again after a gap of 20 years and this past New Year’s Day had the time of my life sailing a Laser.

I have rejoined the world cognitively and socially. I am able to read and write again. Once a month I attend a group to read Shakespeare which has been a lot of fun. Last year I surprised a professional association of which I had been an inaugural member in the early 1990s by rejoining after 12 years. Although I did post graduate legal studies in Japanese, disuse of the language during my illness completely eroded my confidence in using it. Recently, I gained the courage to go back to language school for a stringent refresher course. This has enabled me to begin writing in Japanese and feel comfortable about interacting with people again.

I need to be a little careful about conserving my energy as I still get a little tired after taking my medication. Sometimes a recrudescence of symptoms in response to treatment will make me feel unwell for a day or so but these are nothing like the massive IP episodes of the early days. I am hopeful that they will soon resolve and I shall be able to take on professional commitments again.

That is a difficult question. Like everybody else my age, I would like to be a 20 year old again. As there are few precedents for a full recovery from chronic inflammatory disease, I am really having to define my own clinical endpoints. My symptoms fluctuate between 75% and 95% of normal (as compared to between 25% and 75% for the preceding 9 years). My neurological deficits are minimal and it is over a year since I have needed to use a walking aid for any reason. That is a huge milestone for me. I can run to tennis in the mornings, do a solid hour and half coaching then walk back. My bloodwork is very good now barring a couple of anomalies that indicate residual but resolving infection. ACE is down to 15.5 U/l from a peak of 35.6 U/l. Chest x-ray is normal. Lung function tests are completely normal (% predicted: VC140%; FVC141%; FEV1.0 124%;DLCO 108%) with room for further improvement. ECG which showed an ST depression prior to ARB therapy is now normal other than a slight shortening of the PR interval; I no longer suffer from heat failure symptoms (orthopnea, syncope, lightheadedness, exercise intolerance) or arrhythmia. Myasthenia as evidenced by a muscle waning decrement of 30% under Repetitive Nerve Stimulation has resolved. Lateral L2-L4 BMD (bone mineral density) has gone up from a T score of -2.47 (09/00) to -1.09 (04/07) and Z score from -2.11(09/00) to -0.23 (04/07) which I think is pretty good given that the 2007 tests were done before I began high impact sports again. For the first time in my life, I no longer have any nasal congestion and an irritating nasal polyp I had for 15 years has disappeared. Headaches are a thing of the past. I still get the odd bout of fatigue but it is seldom for long. I am generally able to articulate myself in both English and Japanese, I enjoy reading and my short term memory has improved significantly. Most fascinatingly and delightfully I am gradually regaining the memories of people and events from the ten or so years prior to CNS involvement that appeared to have been lost.

In time, I hope to be able to proclaim of sarcoidosis, as did fellow New Zealander, the late Sir Edmund Hillary after conquering Mt. Everest… that I have “knocked the bastard off!”

ACE (Angiotensin Converting Enzyme) is a marker that reflects the severity of inflammatory diseases such as sarcoidosis. In JST’s case, you can see her ACE was high when starting the treatment and also flared during bacterial killing, but in the end has fallen and continues to fall.

What was your immunopathology like? Was it very strong or easy to control? How did you manage it?

My immunopathology (bacterial die-off reaction) was severe at times and hard to manage psychologically. It typically involved sudden severe weakness and loss of motor function, sometimes in a single limb (I once had to finish a bowl of noodles using chopsticks in my left hand!), in opposing limbs and occasionally in all four limbs rendering me bed-bound until it subsided.

This was particularly so while the MP antibiotic regimen was being developed. There were no set dosages then and the necessity for maintaining sub-inhibitory concentrations on a pulsed schedule was not yet fully understood. I moreover did not have the benefit of Olmesartan in the early stages (it was not yet available in Japan) so had a very difficult time managing the immunopathology (IP). However, after I began suffering from symptoms indicating cardiac inflammation, I was prescribed an ARB called Valsartan. To my amazement, around five days after starting it, the symptoms all but resolved. Not quite believing that Valsartan could have had such an effect, I decided to take a self-appointed “holiday” from the drug a couple of weeks later. Ten hours after missing my dose, the symptoms returned in full force. I resumed the Valsartan and to my relief the symptoms began to resolve some hours later. This convinced me of the phenomenal power of ARBs to alleviate inflammation and without any side effects. I never looked back. Soon after, I was finally able to switch from Valsartan to Benicar. I noticed even more improvement once on Benicar and what are now the standard MP antibiotics.

Top: After taking a break from the MP in May of 2004, JST developed edema (swelling) in her foot. Her eyes, face, belly, and hands all swelled at the time.
Bottom: The edema went away six days after she resumed taking Benicar.

For the first year and a half on the MP however, I had quite a rocky time. I experienced an endless and incoherent parade of old and new symptoms and what seemed like no real change. A small increase in inflammation in the central nervous system is capable of deranging the function in very different areas of the body so even when transient it can be quite disconcerting. But about nine months into MP Phase II, I suddenly began to notice slight improvements in function and from there on my IP became more stable and my gains sustained.

To date however, no matter how severe my IP, I have been able to manage it by adjusting the timing, amount or constitution of my antibiotic therapy and by increasing my Benicar dosing. This has necessitated some very detailed and timely advice from the MP staff and a huge dose of courage at times but it has invariably worked.

What was the hardest part about doing the MP?

Believing that I was getting better. I had never really thought of myself as “sick,” just a normally healthy person with some irritating problems that I needed to get rid of and quickly. I wanted a magic bullet which the MP is not. It takes time and you have to persevere.

How did you learn about the MP?

In 2002 I had a three-month remission following a course of an antibiotic prescribed for an opportune infection. As this was the second time I had noticed an improvement in my condition after a short course of an antibiotic, I decided to investigate whether there was any connection between my perceived remission and the etiology of sarcoidosis. I typed in “Sarcoidosis” and “remission” and found Sarcinfo.com – the precursor website to what is now the Marshall Protocol study site.

What made you decide to do the treatment?

When I received the diagnosis of sarcoidosis, my father who is a pathologist, had remarked to me that tuberculosis, leprosy, and other granulomatous diseases looked quite similar to sarcoidosis under the microscope so, it was quite conceivable that Sarcoidosis also had an infectious etiology. That insight remained my guiding light. I had already observed two brief remissions after taking antibiotics for opportune infections and was sure that there was a correlation. The role of the vitamin D receptor in chronic inflammation was a great revelation however. While in hospital, I had begun to think that the inexplicable and sometimes severe fluctuations in my symptoms might be hormonal. I even bought a monograph about hormones, however Vitamin D was mentioned only in relation to its role in calcium metabolism so I didn’t make the connection. Later, when I read the Marshalls’ “Angiotensin Hypothesis,” it was like finding the missing piece to a 1000-piece jigsaw puzzle.[2]

I had my 1-25-D/25-D ratio measured and it came out at 4:1 (normally the ratio should be around 1:1.1). Not only did I have an excess of this chemical in my body, it was a steroid hormone that was interfering with the activity of my immune system. Finally I had found a plausible explanation for many of my bizarre and often transient symptoms. My doctor was also persuaded on the basis of my D metabolite test results to prescribe the MP prototype antibiotic therapy on the condition that I persevere with any antibiotic chosen for a minimum of three months.

What was it like to be one of the first people to start the MP?

I felt like an intrepid explorer. I was strongly convinced of the science behind the MP and always kept in mind Pasteur’s dilemma when he decided to treat Joseph Meister for rabies. I had two young children who needed a mother. There was a small chance that the medications might adversely affect me, however the alternative was a half of a life on steroids and a cornucopia of toxic palliative drugs that would do nothing to alter the course of the disease.

Although I had little or no access to information in Japan, the support I received through Sarcinfo and the extraordinary generosity and vision of the American people in making the website PubMed freely available online enabled me to become the arbiter of my own destiny. I was able to make informed choices and to participate in an international clinical trial through the Marshall Protocol study site that I would never otherwise have been considered for. I was more than happy to participate in this experiment, if, as a result, even one person could be spared the misery I had endured.

As the protocol developed and positive responses to the therapy filtered in however, the magnitude of Trevor Marshall’s vision became apparent. Not just a few sarcoidosis patients but many, many patients suffering from a wide range of chronic diseases stood to benefit from the therapy. The feeling was one of exhilaration.

Describe your experience with light. Were you very sensitive at first? How much light can you tolerate now?

During my early days on the MP, I was extremely sensitive to light and had frequent transient black-outs while working under the fluorescent lighting of my kitchen bench. When the blackouts began to occur while I was driving, I stopped driving. Flickering light from any source would make me anxious and irritable and I always wore sunglasses outside because I found looking into sunlight so painful.

Interestingly, I always felt very peaceful when wearing goggles while skiing and it wasn’t until I first bought a pair of NoIR glasses that I understood why. The relief they provided, and still provide is immense. I have largely lost my photosensitivity but still wear the glasses outside as a matter of habit and precaution. Today patients on the MP are required to block light with NoIR glasses until photosensitivity subsides.

How does your doctor feel about your progress?

My physicians have been very supportive. The prognosis for sarcoidosis of the central nervous system is not very good so I would say that my progress has been greeted with “cautious optimism.” One has to remember that neurologists are not particularly used to seeing patients go from crutches to the tennis court.

What advice do you have for new patients on the MP or current patients?

Think Big!

Be knowledgeable and courageous about beginning the MP. My life would have been very different had the MP been available ten years ago. I “lost” what should have been the best ten years of my life.

Read. Understand your clinical condition and the science underpinning the MP as best you can so that you can understand how a temporary exacerbation of symptoms appearing as IP might affect you. Keep good records. I keep two Excel databases:

1. a daily “Drugs vs Symptoms daily monitor”

2. blood test results which I graph to show trends

I keep copies of all diagnostic tests undergone and (no matter how unpleasant this may seem) get people to take digital photographs and occasionally videos of my symptoms.

What lies ahead?

To return to my professional work very soon I hope.

To be able to follow my dreams again – “Last seen sailing an RS800”?

Not to need another doctor’s appointment for the next 35 years.

Interested in doing the Marshall Protocol yourself? Visit curemyth1.org and your questions will be answered free of charge by experienced patient advocates that volunteer for the non-profit organization that runs the treatment. (Th1 is a name currently given to diseases caused by L-form bacteria, hence the name cure my Th1)

 

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  • Filed under: cognitive dysfunction, interview (patient), marshall protocol
  • What’s the latest news among people taking statins, or drugs that are marketed as cholesterol lowering agents? Pfizer Inc.’s Lipitor, the world’s best-selling statin, with revenues of $12.6 billion in 2007, causes some women to experience what researchers are referring to as serious cognitive side effects, reports reports The Wall Street Journal.

    “This drug makes women stupid,” Orli Etingin, vice chairman of medicine at NewYork-Presbyterian Hospital, declared at a recent luncheon discussion sponsored by Project A.L.S. to raise awareness of gender issues and the brain. Dr. Etingin, who is also founder and director of the Iris Cantor Women’s Health Center in New York, told those present about a typical patient in her 40s, who after taking Lipitor was unable to concentrate or recall words. Tests found nothing amiss, but when the woman stopped taking Lipitor, the symptoms vanished. When she resumed taking Lipitor, they returned.

    “I’ve seen this in maybe two dozen patients,” Dr. Etingin said later, adding that they did better on other statins. “This is just observational, of course. We really need more studies, particularly on cognitive effects and women.”

    Gayatri Devi, an associate professor of neurology and psychiatry at New York University School of Medicine, says she’s seen at least six patients whose memory problems were traceable to statins in 12 years of practice. “The changes started to occur within six weeks of starting the statin, and the cognitive abilities returned very quickly when they went off,” says Dr. Devi. “It’s just a handful of patients, but for them, it made a huge difference.”

    Researchers at the University of California at San Diego are nearing completion of a randomized controlled trial examining the effects of statins on thinking, mood, behavior, and quality of life. As part of a separate project the team is also collecting anecdotal experiences of patients, good and bad, on statins. They’ve found that in about 5000 people to date, memory problems are the second most common side effect, after muscle aches.

    “We have some compelling cases,” says Beatrice Golomb, the study’s lead researcher. One case is that of 69-year-old Jane Brunzie, a San Diego woman who after taking a statin became so forgetful that her daughter sought to put her under care for Alzheimer’s and refused to let her babysit for her 9-year-old granddaughter. Then Brunzie stopped taking the statin. “Literally, within eight days, I was back to normal — it was that dramatic,” says Brunzie.

    Doctors put her on different statins three more times. “They’d say, ‘Here, try these samples.’ Doctors don’t want to give up on it,” she says. “Within a few days of starting another one, I’d start losing my words again,” says Mrs. Brunzie, who has gone back to volunteering at the local elementary school she loves.

    “I feel very blessed — I got about 99% of my memory back,” she adds. “But I worry about people like me who are starting to lose their words who may think they have just normal aging and it may not be.”

    There’s no doubt that some women who take Lipitor, also called atorvastatin, are experiencing increased mental problems. But is their loss of cognitive function an unexplainable side effect of the drug, or is something else going on?

    That something else may very well be immunopathology – or the immune system’s response to bacterial death. Women who are prescribed statins are almost certainly infected with L-form bacteria, as the pathogens and other biofilm bacteria (collectively called the Th1 pathogens) are responsible for causing the inflammation that leads to high cholesterol.

    As patient reports from the Marshall Protocol site confirm, the Th1 pathogens seldom infect only one area of the body, and everyone in the population acquires them as they age. This means that many women prescribed statins for high cholesterol very likely have these bacteria in their brains as well.

    Aside from mild episodes of brain fog or memory loss, most women on statins are probably unaware of the that fact their brains may harbor Th1 pathogens, largely because it’s not until these bacteria are killed that the host becomes acutely aware of their presence.

    When the immune system targets the Th1 pathogens, it releases a host of inflammatory molecules in response to their death, which along with the toxins released by the bacteria as they die, and the debri from the cell they once inhabited, cause a rise in symptoms in the area in which the bacteria are been killed (immunopathology).

    Interestingly, biomedical researcher Trevor Marshall’s recent molecular modeling research has made it abundantly clear that while statins do lower cholesterol, their main actions on the body come not from their cholesterol lowering properties but from the fact that they bind the nuclear receptors – a class of receptors intrically connected to the activity of the innate immune system. These receptors include the Vitamin D Receptor, the glucocorticoid receptor, and the alpha and beta thyroid receptors.

    These are the same receptors activated by Benicar – the ARB medication used by patients on the Marshall Protocol; the medication that activates and enables the innate immune system. In fact, drugs such as Benicar that bind and activate the nuclear receptors can be so effective at turning on the innate immune system that they enable some people to kill the Th1 pathogens even without the help of antibiotics.

    Despite the fact that Lipitor doesn’t bind the VDR directly, it still affects, and could very likely activate, the immune system because it binds both the glucocorticoid and thyroid receptors with a very high affinity in both cases. Could this mean that those women who experience a rise in cognitive symptoms from Lipitor are simply feeling the effects of bacterial die-off in the brain as the statin allows their immune system to target pathogens in that area more effectively?

    Brain fog, memory loss, inability to process and retain information, loss of problem solving skills, and significant drops in other areas of cognitive function are certainly observed among women who begin to kill bacteria on the Marshall Protocol.

    If this is the case, then those women to experience cognitive side effects from Lipitor would be best off starting the Marshall Protocol – using Benicar and the MP antibiotics to fully eliminate Th1 pathogens in the brain. Of course, until the ability of statins to activate the nuclear receptors and the presence of the Th1 pathogens is accepted by mainstream medicine, women like Jean Brunzie will remain perplexed as to how a simple cholesterol lowering medication could so profoundly effect their mood, memory, and ability to think.

  • Comments Off on Mysterious side effects or bacterial death?
  • Filed under: cognitive dysfunction, News Flash, statins
  • Lost your keys again? Recent research confirms that whether or not you have been diagnosed with dementia you can probably blame L-form bacteria for your substandard memory. Researchers at Rush University Medical Center in Chicago who conduced a recent study on aging and memory were surprised to find that most older adults have significant brain pathology (disease), regardless of the presence or absence of outward signs of dementia.[1]

    The results of this study jive with the work of researchers such as Dr. Trevor Marshall who, while investigating the manner in which L-form bacteria affect people as age, have found that few, if any, people are spared from the actions of these pathogens as they reach their later years.

    L-form bacteria are hardy survivors – they cannot be killed by pasteurization or chlorination, nor can they be eliminated by filtering processes or tecniques that purify injectible medicines. They are even found in dry soil. Not to mention that fact that the ubiquitous use of corticosteroid medications, and supplements such as vitamin D (which is itself a corticosteroid), has reduced the immune function of most of the population to the point where L-form bacteria can survive and spread with ease.

    Once in the body, these pathogens create ligands which dysregulate the Vitamin D Receptor – slowing the activity of the innate immune system and the antimicrobial peptides, causing the host to further succumb to the actions of these cell-wall-less forms.

    Some people eventually fall ill with recognized mental diseases such as Alzheimers and dementia – diseases which have recently been linked to L-form bacteria. But in the majority of cases, the cognitive decline seen amongst the elderly is simply considered a “normal” part of the aging process. This begs the question – are these people suffering needlessly, and if so, do they have signs of brain damage which indicate that they too could benefit from therapy aimed at killing L-form bacteria?

    Indeed, this seems to be the case. The Rush team, under the direction of Dr. Julie A. Schneider, evaluated the spectrum of abnormalities found in the brains of 141 older adults, with and without clinically evident dementia. They found that at the time of death, only 20 persons (14.2 percent) were free of brain disease.

    The diseases most commonly detected were Alzheimer’s disease pathology and cerebral infarcts (strokes), followed by Alzheimer’s disease and Lewy body disease.

    The researchers found that the only way to distinguish persons with dementia (i.e., memory and other cognitive impairments) from “healthy” subjects was the fact that dementia patients tended to have more than one type of pathology in their brain causing impairment, whereas “healthy” subjects tended to have signs of only one disease.

    However older persons without dementia frequently had brain disease, most commonly Alzheimer’s-like disease, but also multiple other abnormalities. Having more than one disease in the brain significantly increased the likelihood that symptoms of dementia will be present.

    “Older persons can often handle one pathology in their brain, but the burden of more than one pathology may tip them over the threshold of clinical dementia,” argues Schneider.

    In the end, the results show that nearly the entire population suffers from brain damage as they age, including people deemed as “normal” by mainstream medicine. It’s proof positive that the vast majority population is infected with L-form bacteria and that as the Marshall Protocol gains acceptance, and L-form bacteria are killed, mental decline may no longer become a hallmark of the aging process.

    REFERENCES

    1. Schneider, J. A., Arvanitakis, Z., Bang, W., & Bennett, D. A. (2007). Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology, 69(24), 2197-204. []
  • Comments Off on Study shows that most older adults have signs of brain damage
  • Filed under: cognitive dysfunction, News Flash
  • About Amy Proal

    Amy and Zeus

    Amy Proal graduated from Georgetown University in 2005 with a degree in biology. While at Georgetown, she wrote her senior thesis on Chronic Fatigue Syndrome and the Marshall Protocol.