Now for something complete different – 2 : Parkinson's Disease

I have been requested to look at the possibility that Parkinson’s Disease (PD) may also be a stable dysfunction gut bacteria. We know from PubMed, the biodiversity of gut bacteria decreases with age. We also read that neurological and behavior changes can be associated with variation in gut bacteria…. So the concept is worth running up the flag pole!

Doing a little searching, we find:

  • [May 2011] Helicobacter pylori is associated with Parkinson’s Ref 1,2 – it is interesting to note that this only occurred with middle-aged mice. Does not occur with younger mice.
  • There is an ongoing trial “. The investigators are studying changes in the normal population of gut flora and in intestinal permeability and their associations with early Parkinson’s Disease.”
  • [2011] Parkinson’s patients are 8 times more likely to have small intestinal bacterial overgrowth
  • [2011]  Parkinson’s patients have abnormal intestinal permeability.

Buried on the internet, was a very interesting paper, “Bacterial Neurotoxicity and Parkinson’s Disease” written as a result of a grant from National Institutes of Environmental Health Sciences. In summary, it states

“high prevalence of PD found in people who work in the soil or drink well water, these patients may be exposed to factors excreted by  soil bacteria”

The paper Identified two bacteria that “fit the bill”

  • Streptomyces lividans
  • Streptomyces venezuelae

This study is cited in Parkinson’s Disease and Movement Disorders: Laboratory Management and … By Joseph J. Jankovic, Eduardo Tolosa, 2007. A further 2009 study is available on PubMed.

However, Streptomyces platensis produces lergotrile, which alleviate tremors in PD. In other words, there appear to be both friend and foe within the same family. Streptomyces avelmitilis also appears to be helpful according to a 2009 study.

One logical exploration is to examine antibiotics that kill Streptomyces. Unfortunately, this family of over 500 species is often used to produce antibiotics and are rarely associated with infections. They produce over two-thirds of the clinically useful antibiotics of natural origin.

The only recognized infections are due to:

  • Streptomyces somaliensis
  • Streptomyces sudanensis

There is a little treatment information available for other species in this family:

  • novobiocin [One study suggesting usefulness], gentamycin [no studies] and doxycycline [2011 Study]
    • Doxycycline appears to produce positive results in several studies, 1, 2. the related monocycline is an established neuroprotective.
  • Rifampicin [1989 Study] – also a neuroprotective and suggested for PD in multiple papers
  • amikacin and linezolid [2008 Study] – in this case, a brain abscess was caused by this bacteria. No studies of either with PD.

Bottom Line

Studies are in progress to determine how gut bacteria is altered. Evidence indicate that it is.  Helicobacter pylori is an easy one to test for and treat when found. There is a only one ghostly finger point at a specific bacteria family: Streptomyces, a family that is usually deemed to be very friendly and gives us many antibiotics. Of course, there may be a dark side to this family, a few species that may produce toxins that results in PD instead of unhealthy bacteria. There are a few antibiotics identified above which could help — but no human studies have been done….

Doxycycline/minocycline and rifampicin are two likely candidates on the basis of both being neuroprotectives alone.

 Doxycycline/minocycline and rifampicin are two likely candidates on the basis of both being neuroprotectives alone. Minocycline is not negatively spoken of in this 2006 News Article. Cochrane reported in 2011: “One of the trials reported a significant increase in levodopa absorption and improvement in motor symptoms when antibiotics were used to eradicate H pylori.” — it is unclear if this improvement would also been seen with PD patients are do not have H pylori.
Thus PD as an illness that may have a significant co-factor being dysfunctional gut-bacteria (possibly with Streptomyces species) appears to be a viable hypothesis. As mentioned in earlier posts, the use of Lactobacillus probiotics are unlikely to be of help.
PD are high in Iron (like CFS patients are low in B12). This may point to a specific bacteria overgrowth (or undergrowth of those that retain surplus iron) – which one(s) are significant for iron in the human gut appears to be unknown, although this1968 paper could provide some insight (or not).

 

The probiotic sensitive CFS patient

Eleven years ago there were four of us that started treatment for CFS using a combined Jadin-Rickettsia and Berg-Coagulation protocol.  Three of the four went into full remission, the fourth did not.  This agrees with studies reporting a 70-85% success rate. Of the three that recovered, one had a IBS diagnosis that progressed into a Crohn’s diagnosis.

Clearly, the treatment was a “near miss”. There was some aspect that was significant but unknown. It did not always come into play for every patient — but for 25% of patients it does. These failures resulted in me keeping an eye on CFS research and treatment over the last 10 year — trying to find and understand the missing piece.  I do not know the entire missing piece, but I suspect the the gut bacteria dysfunction is a significant part of it.

Both of the failures cited above have started on the correcting the gut-flora approach, with very positive results so far. One of these is very probiotic sensitive.

The Probiotics Sensitive

The individual cited above, was able to eat yogurt. She had a severe, debilitating from taking almost any probiotics. Slowly trying different single strain probiotics, we found one that worked, Lactobacillus Reuteri.  Yes, she herxed from taking it but found that she had increased energy afterwards (which may be due to increase B12 production). This was an acceptable trade off — so she is continuing taking Reuteri.

How long to take Reuteri? The answer is actually very simple: “Until she no longer herxs”. Once that occurs, then it is time to see what probiotic she is able to tolerate next.  It is a slow process. There is no benefit from killing off the bad bacteria if there are not good ones ready to muscle into the space generated.

She has been gluten sensitive, so 100% rye bread has been avoided — however,at some time, I would like her to try german made, 100% rye bread. Why? because it appears to be the best FOS for encouraging good bacteria. I speculate that gluten sensitivity may be also be due to gut bacteria dysfunction.

Now for something completely different: Crohn’s Disease

I was recently asked, “Does this work for other autoimmune diseases? For example Crohn’s?”. Since this person has Crohn’s, I will work the approach for Crohn’s.

First we need to know the microflora shift

With some effort on PubMed, I found the following description of the changes seen:

Clearly this is a very different microflora than CFS. As I mentioned in an early post, studies have found that microflora is almost a finger print for infections and likely diseases and syndromes.

Fixing the microflora

The art of fixing the microflora is still immature. The following are suggestions to address the above that are herbs with PubMed study backing them. A skilled herbalist may know of additional ones (and you should press them to supply PubMed articles supporting their recommendations). As always, discuss with your knowledgeable medical professional before starting.

  • Mutaflor (E.Coli Nissle) to address the invasive E.Coli because it usually push them aside. This could be done with alternative pulses to reduce the total E.Coli population (i.e. kill many, repopulate with Mutaflor).
  • Bacteriode Fragilis: inhibited by Rheum officinale
  • Peptostreptococcus: Chitosan appears to inhibit this according to a 2011 study. This is available as a supplement:

    One 2012 study found that bacteria do develop resistance to herbs. The effectiveness of a “herb” also depend on local variations of the plants, so changing manufacturers/suppliers for each herb is recommended.

    The bacteria that dominates

    A 2007 study found a very clear pattern: “Of all invasive bacterial strains in Crohn’s Disease, 98.9% were identified as E. coli as opposed to 42.1% in  ulcerative colitis and 2.1% in normal controls.”

    Reading on antibiotics against E.Coli, there are many species that are resistant to many of the antibitotics used, or the antibiotics that is effective has nasty side effect, for example: Gentamicin.  The use of rotating herbs (2 at a time) that are known to be effective against E.Coli (with biofilm breakers) followed by Mutaflor, appears to be an approach that deserves investigation.

     

Now for something completely different: Crohn's Disease

I was recently asked, “Does this work for other autoimmune diseases? For example Crohn’s?”. Since this person has Crohn’s, I will work the approach for Crohn’s.

First we need to know the microflora shift

With some effort on PubMed, I found the following description of the changes seen:

Clearly this is a very different microflora than CFS. As I mentioned in an early post, studies have found that microflora is almost a finger print for infections and likely diseases and syndromes.

Fixing the microflora

The art of fixing the microflora is still immature. The following are suggestions to address the above that are herbs with PubMed study backing them. A skilled herbalist may know of additional ones (and you should press them to supply PubMed articles supporting their recommendations). As always, discuss with your knowledgeable medical professional before starting.

  • Mutaflor (E.Coli Nissle) to address the invasive E.Coli because it usually push them aside. This could be done with alternative pulses to reduce the total E.Coli population (i.e. kill many, repopulate with Mutaflor).
  • Bacteriode Fragilis: inhibited by Rheum officinale
  • Peptostreptococcus: Chitosan appears to inhibit this according to a 2011 study. This is available as a supplement:

    One 2012 study found that bacteria do develop resistance to herbs. The effectiveness of a “herb” also depend on local variations of the plants, so changing manufacturers/suppliers for each herb is recommended.

    The bacteria that dominates

    A 2007 study found a very clear pattern: “Of all invasive bacterial strains in Crohn’s Disease, 98.9% were identified as E. coli as opposed to 42.1% in  ulcerative colitis and 2.1% in normal controls.”

    Reading on antibiotics against E.Coli, there are many species that are resistant to many of the antibitotics used, or the antibiotics that is effective has nasty side effect, for example: Gentamicin.  The use of rotating herbs (2 at a time) that are known to be effective against E.Coli (with biofilm breakers) followed by Mutaflor, appears to be an approach that deserves investigation.

     

To kill the bad and then seed the good? Or ?

A CFS correspondent asked me the question whether she should start killing stuff off first and then take appropriate probiotics OR should she take the probiotics, then kill off the bad stuff and then take more good stuff. I had been reflecting on this over the last week and my thoughts are below.

I do not intend to go biblical on my readers, but the following seems appropriate to understand the CFS demon…

When an bad demon comes out of a person, it goes through arid places seeking rest and does not find it. Then it says, ‘I will return to the house I left.’ When it arrives, it finds the house unoccupied, swept clean and put in order.  Then it goes and takes with it seven other demons more wicked than itself, and they go in and live there. And the final condition of that person is worse than the first.  Matt 12:43-46

Bacteria has a resister behavior. A resister is a cell that goes dormant. Since most antibiotics interferes with the reproduction process, these sleep through it. The numbers are small, typically 0.05% of the population.  There may also be mutations that are resistant.

If you kill the bad bacteria first, and leave an empty gut, resisters finds an ideal environment and proceed to fill the void. The resistant mutations will become a larger percentage of the population. You could end up with a worst situation!

The better approach is to populate with the good bacteria, using therapeutic dosages. Some of these will be resisters too.  To give a real experience: when I started Amoxicillian and then the Tulsi,Neem, Haritaki combination, I knew that these would likely kill off the Mutaflor that I had already taken. Nothing like spending good money on probiotics that you then kill! To my surprise (and delight), while I started to have niacin flushes again (which disappears with Mutaflor) because of less NADH being produced, the flushes were very mild — so it appears a significant amount of Mutaflor survived….

So, my conclusion is that you want to do at least two weeks of all of the good probiotics (at therapeutic dosages) before you start killing off the bad ones. You need to have a few saints ready to occupy your gut immediately after clearing the demons.

My next post will deal with a problem that some CFS patients may have from taking probiotics.  Mutaflor is “nasty” in terms of herx.  Some CFS patients have problem with almost all of the probiotics…