Monday 23 July 2012

OPTIMIZING OUR PROBIOTICS WITH DIETARY CARBOHYDRATE CHOICES TOM GRIER


Optimizing Our Probiotics With Dietary Carbohydrate Choices 

by Tom Grier 

Recently after the July floods in Hermantown, MN near Duluth,many people in the region experienced severe diarrhea, possibly from the contamination of well water.
 
None suffered from this condition more so than our singer in our band. 


For over a week she took her probiotic capsules only to find each day her condition seemed to get worse.
 
Medically trained she knew taking her probiotic with milk would give something for the Acidophillus and Bifidobacteria bacteria to grow on.
 
Unfortunately she was severely lactose and gluten intolerant and felt milk or grains would worsen her condition. 

Not knowing what else to do she adhered to the medically recommended diet for severe dysentery known as theBRATs diet.   (Bananas, Rice, Apples, Toast)
  
She felt she had few dietary choices that would help, but with a little research she soon discovered that what her diet needed wasn’t dairy products or wheat; but rather a special class of carbohydrates:
 
Specifically oligosaccharides.

Definitions: 

Oligosacharide - 3-10 simple sugars linked together and found in natural foods. 

Lactobacillus acidophilus
(Latin meaning acid-loving milk-bacterium) is an aerobicbacterium that ferments sugars into lactic acid, and grows readily at rather low/acidic pH values (below pH 5.0) and has an optimum growth temperature of around 37 °C (99 °F), and is used in the production of acidophilus-type yogurt.
(Source - Wikipedia) 

Bifidobacterium is a genus of Gram-positive, non-motileanaerobic bacteria. They are inhabitants of the gastrointestinal tract, vagina, and mouths (B. dentium) of mammals.
 
Bifidobacteria are one of the major genera of bacteria that make up the colon flora in mammals. Some bifidobacteria are used asprobiotics.
 
(Before the 1960s, Bifidobacterium species were collectively referred to as "Lactobacillus bifidus".) (Wikipedia) 

Most digestion takes place in the upper intestine where the predominant digestive bacteria is the aerobic Lactobacillus acidophillus.

These bacteria also help supply us with vitamin-K for blood clotting which our bodies cannot produce without L. acidophillus. 


In the lower-intestine/colon, anaerobic bifidobacteria finish most of the digestive processes. It is in the colon where diarrhea must be controlled. 

Why Carbohydrates are important in our GI Tract 

Not long ago we were all taught that there were just two kinds of carbohydrates: Sugars and Starches. 

Simple sugars were just one or two six carbon rings linked to each other.
Sucrose or table sugar is a disaccharide made of glucose and fructose.

      Glucose  Sucrose (Glucose + Fructose) 

Carbohydrates such as starches, were long chains of simple sugars strung together like a chain, or linked in a fashion resembling a tree branch and we called them complexed-carbohydrates. 
 
Then we were told about another class of carbs that didn’t count much because they were mostly undigestible, and we called them fibers or insoluble-fibers.
 
Later in the 1970s,  we learned that dietary fiber lowered the risk of colon cancer.
 
Then we discovered soluble-fibers, and learned that they lowered our cholesterol. 
 
As it turns out, this class of complex-carbohydrates known as dietary fiber is important to our GI health, not just because of cancer and cholesterol but because of how they are digested. 
 
The term complex-carbohydrates may becoming an obsolete term because we now know that some complex-carbs raise blood sugar faster than many sugars.
 
And many simple sugars play roles we never dreamed of beyond just giving us energy/calories. 
 
Most starches are only partially digested in the upper intestine.
 
The starches then complete the digestion process in the colon, where the break-down products play a vital role in the health of the colon.  
 
Some starches especially resistant starches are fermented in the colon and produce a fat that our body needs called short-chain-fatty-acids, SCFAs, which cannot easily be obtained in our diet.
 
 (Pretty cool huh! A carbohydrate that becomes a fat in the gut because of our probiotic anaerobic bacteria!)
 
One SCFA is butyrate which protects our colon cells from genetic damage and cancer. 

Between the simple sugars and the starches (polysaccharides),is a middle class of carbohydrates known as theoligosaccharides.
 
 Oligosaccharides are made of chains of 3-10 simple sugars and can be found naturally in many plants; they often have a slight sweetness and have been described by food scientists as having a pleasant mouth-feel, and are now common food additives for texture and fiber. 

Natural sources of oligosaccharides include:
 onions, leeks, garlic, most legumes (beans, lentils, and peas) wheat, asparagus, and chicory (labeled as inulin on food labels), and al dente pasta. 

Why are these foods good to consume with your probiotics? 

Recently this class of foods have been referred to as pre-biotics, because they feed the bacteria we need to digest our food.
 
Unfortunately Americans get about 1/3 the levels of oligosaccharides in their diet as Europeans, or what is consumed in a typical Mediterranean diet. 
 
 Because the upper intestine has a hard time breaking down this class of carbs, almost 90 % escapes to the colon where oligosaccharides reach their full pre-biotic potential. 
 
A prebiotic supports the health of probiotics! 

So now you can see how taking a probiotic does little good for your intestinal track if you don’t support the probiotic bacteria with proper nutrition. 

Up until the 21st century we used to think nutritional support of our gut bacteria was as simple as drinking a glass of milk. 

In addition to the oligosaccharides, another class of prebiotic is emerging.
 
Both resistant starches and fermentable fiber are two carbohydrates that also add to our colon’s good health.
 
You might know resistant starches by their signature sound and smell as a by product of digestion in the colon is methane gas. 
 
The digestion of fermentable fiber in the colon also produces more beneficial by-products including:
 
short-chain-fatty-acids, and some B-vitamins, and recapture dietary magnesium and calcium that would have been excreted.
 
So as we feed our probiotic bacteria with these alternative food sources we also reap the benefits of:
 
lower cholesterol, lower triglycerides, improved insulin sensitivity, and improved immune system function. 

If you have diarrhea from antibiotic use and are taking probiotic capsules or probiotic yogurts, and kefirs, then the following foods may help support the probiotics and improve the health of your intestinal tract.

Bon Appetite 

BRAT diet:  Bananas, Rice, Apples, Toast.
 
Bananas may be more effective when they are green, and use low-fiber or white bread for toast.
 
Other foods to eat during episodes of diarrhea include
 
crackers, pretzels, apricots, applesauce, mashed potatoes, noodles, cream of wheat or cream of rice, smooth peanut butter, eggs prepared any way but fried, skinless poultry, mild white fish, lean beef, low-fat cottage cheese, and canned vegetables.
 
 It is best to eat small, frequent snacks and meals instead of larger meals.
 
Beans, peas, lentils, wheat, rice (Creme of Rice hot cereal seems to work best)  
 

Foods to Avoid

* Greasy, deep-fried, fatty foods, and rich saucesbecause these may worsen diarrhea. 
 
* Sugary or very spicy foods may also be bothersome. 

* Sugar-free gums and candies usually contain sugar alcohols (sweeteners) that may cause diarrhea.  

* Large meals with large amounts of protein and Fats. 

Saturday 21 July 2012

LYME DISEASE INCREASE IN CANADA

More in the news about Lyme disease in Canada


Janet Sperling a University of Alberta entomologist, and co-author of a submission to The Canadian Entomologist on the presence of Lyme disease ticks in Alberta, was interviewed on Alberta Prime Time link to the interview here 


A five year study is showing that Alberta is not safe from a species of tick that carries Lyme disease — news article here 


Researcher warns heavy rains increase risk of Lyme-carrying ticks across Alberta. Ticks “like it moist,” said George Chaconas, a University of Calgary professor who holds the Canada research chair in the Molecular Biology of Lyme Borreliosis. “They don’t like it dry.” here


Research published in The Canadian Entomologist

Volume 141, Number 6, November/December 2009ISSN 1918-3240

Lyme borreliosis in Canada: biological diversity and diagnostic complexity from an entomological perspective Janet L.H. Sperling and Felix A.H. Sperling



Abstract: Lyme borreliosis (LB), also known as Lyme disease, is emerging as a serious tickborne illness across Canada. More than three decades of research on LB in North America and Europe have provided a large, complex body of research involving well-documented difficulties at several levels. However, entomologists are well situated to contribute to resolving some of these challenges. The central pathogen in LB, the spirochete Borrelia burgdorferi Johnson et al., includes numerous genospecies and strains that are associated with different disease symptoms and distributions. The primary vectors of LB are ticks of various Ixodes Latreille species (Acari: Ixodida: Ixodidae), but questions linger concerning the status of a number of other arthropods that may be infected with B. burgdorferi but do not transmit it biologically. A variety of vertebrates may serve as reservoirs for LB, but differences in their ability to transmit LB are not well understood at the community level. Persistent cystic forms of and immune system evasion by B. burgdorferi contribute to extraordinary challenges in diagnosing LB. Multiple trade-offs constrain the effectiveness of assays like ELISA, Western blot, polymerase chain reaction, and microscopic visualization of the spirochetes. Consequently, opportunities abound for entomologists to contribute to documenting the diversity of the players and their interactions in this devilishly complex disease.



Janet's son featured in a TV program on Lyme Disease here note the program was in two parts.


An earlier post about a news article interviewing Janet  here 

Friday 20 July 2012

RAISING AWARENESS OF LYME DISEASE


I started this blog 12 November 2009 my first post a translation of some Brorson research here 

 Frustrated at the lack of awareness in the UK about Lyme disease and the lack of media attention I decided to use this blog to help raise awareness as well as being a useful resource for me to find information on Lyme Disease.

The search box helps but flipcard top right hand column is also a useful tool.

 In less than three years I have had over 90000 page views.

I am pleased to see that it is making some small difference in helping to raise awareness.

A review of the stats information on this blog shows


Pageviews today
261
Pageviews yesterday
262
Pageviews last month
6,659
Pageviews all time history
90,061





Tuesday 17 July 2012

GLOBAL CHALLENGES IN DIAGNOSING AND MANAGING LYME DISEASE


Global Challenges in Diagnosing and Managing Lyme Disease—Closing Knowledge Gaps here  THIS LINK NO LONGER WORKS BUT SEE BELOW


Subcommittee on Africa, Global Health, and Human Rights
Chaired by Christopher H. Smith (R-NJ)

witnesses
  • Stephen W. Barthold, Ph.D.
    Distinguished Professor
    Department of Pathology, Microbiology and Immunology
    Center of Comparative Medicine, School of Veterinary Medicine University of California, Davis
  • Raphael Stricker, M.D.
    Vice President
    International Lyme and Associated Diseases Society
  • Mark Eshoo, Ph.D.
    Director, New Technology Development
    Abbott
  • Ms. Patricia Smith
    President
    Lyme Disease Association
  • Mr. Evan White
    Lyme Disease Patient
  • Ms. Stella Huyshe-Shires
    Chair
    Lyme Disease Action

    I have just been listening to this live.  It is available to watch again as are the written testaments, Dr Steven Barthold's is definitely one to look out for.
    Lyme Disease Action have some comprehensive links here  


    Meanwhile just a few notes I made plus many more posted by Lyme disease.org on Facebook here 

    Barthold: dormant, non-dividing bacteria are tolerant of antibiotics. During persistent infection there is a 10-fold reduction in number of bacteria but they are not dividing, so antibiotics can't hurt them.

     100% of animals remain infected after antibiotics--- described as debris but it is often metabolically viable organisms.

    12 months after treatment we see widescale prevalence of spirochetes but it remains to be determined the role of this persistence --not everyone is showing symptoms.

     Biofilms - universal mechanism for bacteria, virus and fungus throughout the world for microbial communities. Borrelia - persistent infection --- reduction in host/animal ( with antibiotics?)- go dormant (not necessarily in bio film) - antibiotics can't touch.

    If you just enlarge the pot of funding, and you award the money to the same old school club of people who feed off Lyme disease, we won't get anywhere. If NIH is willing, they should put out a call for applications [for research] that is more focussed on biology.

    Dr. Stricker: About 70% of my patients will get better with long-term antibiotics. This is very rewarding for a physician and helps me to ignore the politics and just go ahead and treat them.

    In his investigation, the CT Attorney General found that a group of about 14 individuals within the IDSA were responsible for making decisions about Lyme disease, and the rest of the 9,000 member organization follows their lead. This has been hugely problematic.

    I have a mentoring program for physicians but it's hard to find doctors who are want to do it. The controversy around Lyme disease has had a chilling effect on developing doctors who want to learn about how to deal with Lyme disease. 

    Ms. Stella Huyshe-Shires of Lyme Disease Action in the UK said IDSA guidelines are influencing UK doctors. 
    If patients have visible arthritis, they may be able to get more treatment, "but if you have invisible pain, you can't," she said.

     European guidelines are based on the IDSA guidelines, but are more clear on stating where the evidence is uncertain and note where studies have not been done.

    In the UK, even after the civil investigation, no one thought it necessary to question the IDSA guidelines, even though the IDSA's own panel had recommended changes.

    LDA President Pat Smith: Other diseases have advisory committees and nobody says anything bad about them. The government can do this. It's not even difficult or expensive.

     When my daughter was ill, people said she just wanted to avoid school. What 15 year old wants to stay home with her mother for 4 years? What mother wants her 15 year old to be home for 4 years?

    Pat Smith also spoke eloquently about the problems of having children treated, with doctors and Social Services accusing  parents of Munchhausen's by proxy (even when a physician had diagnosed the child) and children being taken into care of the authorities. As crazy as this sounds it also happens here in the UK.

    Evan White gave an account of his struggles for diagnosis and treatment and his successful recovery. His successes in life indicating what can be achieved if only people are treated appropriately.

    Excellent presentations by all those involved the marked absence of IDSA, NIH and CDC from this hearing despite invitations, clearly shows a lack of will to help so many sick patients.

    The Testimony statements can be accessed through Lyme Disease Action website First and Second recording here

     First video http://www.ustream.tv/recorded/24058724 
            Second Video http://www.ustream.tv/recorded/24060689  


Friday 13 July 2012

PROTOMYXZOA RHEUMATICA IMPLICATED IN CHRONIC ILLNESSES


Listen to internet radio with Focus on Health on Blog Talk Radio


1 Step Blood Test Discovers Protozoa under Biofilm Structure

by Focus on Health

in Health
Thanks to Better Health Guy for the following  here
Steve Fry MD

  • Presented on FL1953 which is now called Protomyxzoa rheumatica.
  • Has found Ivermectin, Flagyl, and a low-fat diet to be helpful.
  • Studies that have been done on Multiple Sclerosis patients show that patients live longer when on low-fat diets.
  • Likes testing from Infectolab from Dr. Armin Schwarzbach for Chlamydia and Mycoplasma.
  • Biofilm is an aggregate of microorganisms in which cells adhere to each other or to a surface.  Bacterial biofilms are a structured community of bacterial cells enclosed in a self-produced matrix according to Bill Costerton, a world leader in biofilm research.
  • Lipids (fats) play a role in biofilms.
  • Biofilms impact teeth, drinking water, paper manufacturing, ship hulls, medical implants, food processing, cooling towers, oil recovery, and much more.
  • Iron, calcium, and magnesium all play a role in biofilm formation; be careful about the minerals that you use as these may add to the biofilms.
  • There are 1,000 organisms in normal oral flora found in biofilms.
  • Biofilms consist of extracellular DNA, proteins, and polysaccharides.
  • Biofilms are microbial cells and EPS (extracellular polymeric substances).  EPS may be 50-90% of the biolfilm.
  • Microbes are quorum sensing – biofilm communities talk to each other.  Decision making is made by decentralized groups to coordinate behavior.  This is used to coordinate gene expression.
  • When microbes come together in a group, it becomes a more complex entity.
  • Biofilms play a role in many diseases including ear/nose/throat, dental, respiratory, urology, orthopedic, chronic wounds, medical devices, catheters, chronic inflammation and osteonecrosis.
  • Many areas of disease in the body are related to biofilms.  Coronary artery disease, MS, ALS all have association with biofilm communities.
  • 46/50 children with otitis media (ear infection) had biofilms.  Chronic rhinosinusitis is a combination of  biofilms and several microbes.
  • Biofilm plays a role in cystic fibrosis.
  • Nanobacteria can be a cause for kidney stones and generates biofilm.
  • In chronic wounds, bacteria is protected from systemic antibiotics and host defenses by biofilms which makes infection difficult to clear.
  • Actinomyces, Acinetobacter, Treponema, and others are found in dental biofilms.
  • Pseudomonas aeruginosa is a bacteria that is a profound biofilm former.
  • Biofilm infections are difficult to eradicate.
  • The immune system recognizes the infection, but it cannot eradicate it.
  • Items that have been researched in biofilm treatment: Manuka honey, enzymes, multiple antibiotics, bismuth thiols, restricting metals, botanicals, mechanical removal, and EDTA to help chelate magnesium.   Magnesium is a main stabilizing force in biofilms.
  • Other substances that are of interest to biofilm researchers include: Lactoferrin, Xylitol, Gallium, Dispersin, Farnesol, RNAIII inhibiting peptide, and Furanone C30.
  • Corneal eye disease may be Acanthamoeba infection (protozoan).
  • Protomyxzoa rheumatica (FL1953) is an Apicomplexa.
  • CCSVI is a very hot topic but is also quite controversial.  One has to suspect biofilm communities.
  • Organisms living in biofilm communities are usually not culturable.
  • Biofilms are the rule, not exception.  They are ubiquitous.
  • Book – "Biofilm Primer" by Bill Costerton.
  • There is a Center for Biofilm Engineering at Montana State University - http://www.biofilm.montana.edu/
  • Silver is a well known biofilm inhibitor.
  • Ozone is used in industry to reduce biofilms.  Not sure if it works in humans, but may break up biofilm communities.
  • Fry Labs does microscopy, serology, and molecular diagnostics.
  • Protomyxzoa is an inflammatory trigger and vascular pathogen.
  • Louis Pasteur believed that all diseases are caused by infections.
  • Some autoimmune conditions include Graves, Hashimoto’s, Insulin-Dependent Diabetes Mellitus, Insulin Requiring Diabetes Mellitus, Multiple Sclerosis, Myasthenia Gravis, ALS, Systemic Lupus Erythematosus, Rheumatoid Arthritis, Sjogren's.
  • Thomas McPherson Brown suggested that autoimmune disease is infectious in nature; primarily Mycoplasma.  The book “The Arthritis Breakthrough” was written by Brown in 1992.
  • Fry has seen Protomyxzoa and biofilm in CFS, Fibromyalgia, Scleroderma, Rheumatoid Arthritis, Lupus, Multiple Sclerosis, ALS, Parkinson’s, Autism, and other conditions.
  • In their smear testing, they originally identified Hemobartonella which included Hemoplasma. Today, they suggest that Epierythrocytic bacteria is a better term.  They rarely find actual Bartonella when doing PCR testing but have found cousins.
  • Even a single organism can protect itself with biofilm.
  • People with parasitic infections are immunocompromised.
  • They have found a host of different types of bacteria in biofilms – Ralstonia, Acinetobacter (commonly seen in many patients).
  • Protomyxzoa is a slime forming protozoa.  It produces biofilm.
  • In ALS, 6 of 6 tested had Protomyxzoa.  5 of 6 tested has Ralstonia which is also a biofilm former.  They see profound biofilm communities.
  • When one is infected with Plasmodium as a child, it reduces later incidence of Multiple Sclerosis.  The efficacy of quinine in the treatment of MS supports this connection.
  • They are able to culture Protomyxzoa now.  The entire thing becomes like gelatin and they cannot get it off the microtiter plates.
  • They have seen filaments as long as 3 or 4 inches in some blood samples.  When sticky stuff is coming out during a blood draw, it may not be a clot, but may be a filament or biofilm.
  • In CCSVI, filaments of Protomyxzoa may be involved.  It is a vascular disease and may lead to inflammation of the vessel or vasculitis.
  • Protomyxzoa has been isolated from Culex tarsalis and Culex quinquefasciatus mosquitoes.  81% by PCR carried Protomyxzoa.
  • Dogs have Protomyxzoa more than cats and the older the dog, the more likely they are to have Protomyxzoa.
  • Diseases are infectious and a biofilm forming protozoan could be at the heart of the problem.
  • Treatment may include Tetracyclines, Plaquenil, Flagyl, herbs, enzymes, McDougall diet, and mechanical interventions such as CCSVI venoplasty.
  • One should generally not consume arginine, folic acid, or magnesium as these may strengthen the protozoan and thus the biofilm.
  • As for folic acid supplementation, some breads have 5% folic acid by weight.  Folic acid may increase cancer risk.  Protozoans love folic acid.
  • For autoimmune conditions, antimalarials, antibiotics, anti-protozoals, anti-fungals, anti-biofilm agents, biologics, and dietary modifications may be beneficial.
  • Enbrel may be helpful in some for reducing the inflammatory response.
  • Fry Labs is now working on drug sensitivity studies.
  • CCSVI treatment includes a mechanical clearing or balloon procedure.  It runs about 10K.  There was reportedly one death from a CCSVI procedure.
  • Stents do not do very well in veins.
  • From the Hubbard Study, about 1/3 feel worse, 1/3 feel nothing, and 1/3 get better with some significantly better.  One bedridden runner was running again after the procedure.
  • Protozoans love lipids (fats).  The McDougall diet is used as part of treatment.  Doxycycline and tetracyclines may target the fatty acid synthesis machinery.
  • Toxoplasmosis is also dependent on fats.
  • Protomyxzoa grows 100 times faster with fats than without.
  • There is a reduction in relative biofilms with the McDougall diet.
  • In some people where they had seen the organism and biofilms, they could not find the organism after being on the McDougall diet.  Unfortunately, after starting to eat higher fat content, the microbe was again present and visible.
  • They did a test in people with Protomyxzoa using a 12.5 day water fast and levels of Protomyxzoa dropped to undetectable.  Within 2 days of eating again, it was back.
  • Protomyxzoa is found in CFS, Fibromyalgia, Rheumatoid Arthritis, Lupus, Crohn’s, MS, Parkinson’s, ALS, Autism, Scleroderma, and others.
  • Protomyxzoa is Public Enemy #1.
  • Protomyxzoa loves fat.  It is complex.  It is drug-resistant.
  • Antiprotozoals or anthelmintics may be good options.
  • Roy Swank Diet – 0 people on a regular diet lived with MS for 30 years.  In those on low fat diets, all but 1 was still alive.
  • Protomyxzoa leads to vascular disease and chronic inflammation.  There are coagulation impairments and retrograde venous blood flow.
  • Many systemic diseases can be explained as vascular phenomenon.
  • Protomyxzoa is likely transmitted by mosquitoes.  Ticks are being analyzed.
  • The protozoan is believed to be the foundation pathogen.
  • It is not an intracellular bug; it is a big bug.  Likely exists more on the surface of the RBC, not inside.
  • Patients often get worse when on magnesium.  He does not support the use of topical magnesium either.
  • Bismuth may play a role as a biofilm inhibitor.
  • Omega fats from chicken and plants are probably the best.
  • Interestingly, it may be that magnesium is sequestered in the body and not always low as magnesium levels seem to go back to normal when the Protomyxzoa is treated.
  • Dr. Fry previously had a success rate of over 70% with his patients.  Since introducing dietary modifications, this has now gone to over 90%.
  • http://www.frylabs.com
For information about the work of Dr Brown which Dr Fry refers to see The Roadback Foundation here  and an earlier post here  with a video of Dr Brown and his work.


Sunday 1 July 2012

ONE CAUSE OF ALZHEIMER'S DISEASE AND OTHER NEUROLOGICAL DISEASES - ALS, MOTOR NEURONE, MULTIPLE SCLEROSIS, PARKINSON'S







Dr Alan MacDonald has been posting some excellent and informative posts on Lymenet Europe of late


Many patients with Chronic lyme Disease will remember Dr MacDonald from scenes in Under our skin As you can see in the above video Borrelia has not just been found in patients with Alzheimer's but also patients with other Neurological Diseases - ALS, Motor Neurone, Multiple Sclerosis and Parkinson's.


According to Under Our Skin news clip Dr MacDonald became ill with an Alzheimer's like illness and had to retire. He says on the Lymenet forum that he is doing well providing he is on medication, clearly reading his posts there is not a lot wrong with his cognitive abilities and I was delighted to read the following.


'My research was interrupted by several years when I was ill. I have now returned to limited Alzheimer's disease Research as an Affiliated Researcher at the Harvard University McLean Brain Bank.'


Taken from the comment below:-


I am glad that you asked:
Dr Judith Miklossy has always worked independently commencing her studies on Neuroborreliosis and Alzheimer's Disease in 1993 with her initial publication in Neuroreport.
She is presentlythe President of a Foundation which is devoted to Alzheimer's research and connections
to neuroborreliosis. She operates her own website, which contains her credentials and her biblography.


I have always worrked independently commencing my Studies of Alzheimer's disease and connections
between Neuroborreliosis and Alzheimer's disease in 1986 with my publication in the Journal of the American Medical Association "Borrelia inthe Brains of patiens dying with Dementia", followed by the 1987
article "Concurrent Neocortical Borreliosis and Alzheimer's Disease" published in Human Pathology,
and then"Concurrent Neocortical borreliosis and Alzheimer's Disease - Description of a spirochetal cyst form", in 1988 in the Annalsof the New York Academy of Sciences.


Although Dr Miklossy and I have a close friendship, we beleive that maintaining independent
research Laboratories ( In New York and in Switzerland) is the ideal pathway to establish 
a bibliographic base of independently produced papers to support th concept of an infectious
pathway to future development of some ( but not all) cases of Alzheimer's Disease.


I have never been a reviewer nor referee for the peer review of any of Judith's papers.
Judith has never been a reviewer or referee for the peer review of any of my papers.


My Last published works were reviewed and accepted for presentation at the Alzheimer's Disease
and Related Disorders International conference in 2006 Madrid Spain. My research was interrupted by
several years when I was ill. I have now returned to limited Alzheimer's disease Research as an Affiliated
Researcher at the Harvard University McLean Brain Bank.


What commonalities have been gleaned by two independent investigators working on the Chronic
Neuroborreliosis /Alzheimer's disease connection:
1. Identification of Borrelia burgdorferi spirochetes in Autopsy Alzheimer's brain tissue by
Silver staining ( Miklossy+ MacDonald+)
2. Culture of Autopsy Alzheimer's Brain tissue to yield growth of Borrelia burgdorferi spirochetes
(Miklossy + MacDonald +)
3. Idenification of argyrophilic plaques in Autopsy General Paresis brain tissue 
which are exactly the same size, density and distribution as argyrophilic plaques in
Alzheimer's disease autopsy tissue ( Miklossy + MacDonald +)
4. Identification of bacterial peptidoglycan staining in Alzheimer's plaques
(Miklossy + MacDonald -not studied)
5. Indentification of Intracellular borrelia burgdorferi spirochetes within diseases neurons
inautopsy Alzheimer's Brain tissue ( Miklosssy + macDonald+)
6. Identification of the role of the granular form of borrelia burgdorferi as a contributor to
the classical finding of "granuolo-vacuolar" degeneration of Neurons in Alzheimer's disease
(Miklossy +( immunohistochemistry) MacDonald + (In Situ DNA hybridization))
7. The use of highly specific molecular beacons to pick up evidence of Borrelia burgdorferi DNA
sequences in Alzheimer's disease Plaques ( MacDoanld +)
8. The use of PCR performed on total Alzheimer's frozen brain tissue from the Harvard Brain Bank
to amplify borrelia specific DNA sequences from Orf BB0147 and to confirm the DNA structure
by DNA sequence analysis of PCR amplified products. (MacDonald +)


We seek to analyze Cerebrospinal fluid from Alzheimer's Disease patients for the following:
a. Borrelia burgdorferi Specific DNA
b. Whole proteome analysis using Dr Steven Schutzer's MASS spectroscopy analysis
protocol which was published in PlosONE. Dr Schutzer's program is able to
reliably distinguish CSF specimens from Chronic Lyme Disease patients
and to separate such patients from those with Chronic Fatique (notlyme),
Based on State of the art Proteome analysis via Mass Spectrographic Analysis.
Respectfully,
Alan B.MacDonald MD
PS: Ifyou have a moment,please read Dr Hideyo Noguchi and J E.Moore's paper in the Journal of Experimental Medicine from their lab at the Rockefeller Research Institute in New York City
(Link: http://jem.rupress.org/content/17/2/232.full.pdf+html ) and you will read about the "politics of Paresis" which prompted heated debates between Noguchi and Professor Max Nonne.


Lymenet Europe forum here


Dr Alan Macdonald was the first person to find Borrelia spirochetes in the brains of patients who had diesd from Alzheimer's I have posted before about him and his work here 





Dr MacDonald is the first person I have heard of diagnosed with an Alzheimer's type illness retired from work who has sufficiently recovered to return to work, albeit limited and for that work - to be research into Alzheimer's Disease this most important research area.