Quorum Sensing, bacteria, and pigment morphology

So the conundrum that I have been faced with is that even though the eczema isolated Staph has been associated with fungus it is not a fungus.  Staph is not dimorphic in shape with milk and egg (casien and ovalbumin) rather it becomes cloaked with yellow pigment hence the name goldenrod.  I looked first to see if gluten and casein could be functioning as serpins triggering not a shape morphology change but a pigment production. What I found was Quorum sensing. In response to an increase in bacteria population bacterias release quorum molecules which induce serine proteases, antibiotics, and pigments. This new quorum induced state is always described as a more virulent species of the bacteria.

so I am now pondering...is this what is happening in staph? similar to a fungus shifting between a dormant mold state to a spewing yeast state does a staph shift from a quiet state to a quorum virulent state where it spews proteases and cloaks itself in colored pigment? are these comparable states? Staph makes the golden pigment when plated on egg.

Here are examples:
The tail rot in fish is caused by Aeromonas salmonicida  secretes a serpin in response to quorum factors.
The potato pathogen Pectobacterium carotovorum expressed Evr and orange pigment in response to quorum sensing.

Hmm Maybe I am again going to far out on a limb but something is there.  Children may develop the immune reaction to milk and egg because the staph in the eczema reacts to the them...with a quorum like response? Is this possible? I am still trying to piece things together.

Kids have milk and egg allergies with eczema. Staph makes the pigment with milk and egg.


Angela Biggs

Ashley's Peanut allergy

When my daughter Ashley was a baby she caught eczema from some neighbors' children.  I say caught because eczema does not run in my family or my husbands' and these neighbors had eczema from head to toe.  To me it was too much of a coincidence.  The doctors at the time told me that eczema was just a form of sensitive skin and not contagious.  In my opinion i was slowly watching it spread from her hand up her arm and onto part of her face.  At one point i had traced with ball point pen the area and watched it slowly become larger. Not only that I had noticed that it seemed to fax and wane when it was visible. When I noticed the milk sensitive nature of the eczema patches, appearing after she had some,  the doctor said yes lots of kids with eczema are sensitive or even allergic to milk and eggs. 

Then at ten months Ashley touched or should I say grabbed her brother's peanut butter banana. The reaction was immediate.  The areas of eczema and only those areas became raised and filled with some kind of white liquid.  When the liquid disappeared an anaphylatic reaction began.  Ashley started swelling in response to this white liquid.  I rushed her to the emergency room frantically explaining that the reaction was connected to her eczema. rash.  The ER physicians looked me straight in the eye and said that peanut allergies are not associated with eczema.  24 hours later i did a search online and found a British Journal of medicine publication associating peanut allergy with eczema.

From then on i decided to go with my gut.  I started to research the possible culprits for the infection.  Infections drop toxins in microbial warfare. That's how we initially developed antibiotics, penicilin was released by one bacteria to kill another.  My notion was that the eczema infection saw the aflotoxin in the peanut butter and thought a mold was encroaching on it's territory. Ashley's anaphylatic reaction was to the toxin.

I found two possibilities: a staph infection or a malassezia fungal infection based on papers i found on pubmed. I then tried to understand the milk sensitive to these infections.  How could milk or egg make the ezcema visable?

I thought back over similar patterns. When I had studied type 1 diabetes I had read it had been associated with both candida and celiac disease.  Celiac disease was wheat and milk senstive.  Then i remembered researching autism because my son had been a late talker. Although I had ruled autism out for my son i had learned that autism had  intestinal issues, vaccine issues, and  there had been a couple that claimed they had cured their son with a gluten and casein free diet.

What if the infections were causing an immune response when exposed to wheat, milk, or egg? what was it about gluten, casein, and ovalbumin that would cause the infections to react?  I found an Italian paper talking about the induction of antibodies by gluten.  I started to wonder if the immune system was only seeing the infection when gluten was there.

Then one day I read an article about golf courses using corn gluten to inhibit the growth of crabgrass. I immediately looked up the original paper.  Not only did the corn gluten block the ability of the grass seed to sprout roots but the original experiment was looking at a parasitic grass fungus.  On the corn gluten the fungus had failed to thrive.  Corn gluten had not only blocked the seed roots but the fungal parasitic roots! or at least that is how I interrupted the paper.

I had a eureka moment. If the root morphology was blocked a fungus might shift to a yeast morphology.  The infections were dimorphic.  Mold to yeast...yeast to mold.  Appearing and disappearing to the immune system.

So what ever infection Ashley had it was shifting morphologies when she had egg or milk. ( that was a guess at the time which was wrong but why I did this)  I pushed the pediatrician to give me the antifungal loprox.  Since most antifungals work on the cholesterol which would be in higher quantities in the mold form, roots have more structure therefore more cholesterol in the membrane..i chose to take her off milk and egg during the loprox treatment.  I can't remember exactly how many days i treated her..i used up the loprox in less then a month, but she has never had eczema since then.

I have to admit that the infection could have been staph and not malassezia.  I think Loprox would have killed either.

When they do skin scrapings here at National Jewish they find staph.  Staph makes a yellow pigment on egg or milk....the golden rod look is from being plated on egg.  I am leaning toward the infection to have been a form of staph.

Although the eczema was gone from Ashley's skin for years the peanut allergy persisted.  I had a RAST test done every year on Ashley and tracked her antibodies.  The only time the antibodies went up, ironically, was when she had been bitten by fire ants and had a reaction to them in Florida.  Who doesn't react to fire ant toxin? (First allergy in Thornton has her records and I told National Jewish they could have them)

Over time the antibody levels dropped and dropped.  I kept her away from peanuts completely, nothing in the house ever. At 9 years old Ashley accidently was exposed to candy with peanuts. She had no reaction at all.  6 months later the allergist based on her low Rast score agreed to a challenge in the office.  Ashley has officially been labeled as one of the lucky few who have "outgrown" her peanut allergy. My daughter can eat peanuts and all she gets is a slight stomach ache.


I am going to stop at this point. There is a lot for a reader to digest. I hope you could follow me.
Angela

omega fats are not just insulation for nerves

Give a man a fish he eats for a day.  Teach a man to fish he eats for a lifetime….and he lives longer. 

Recent studies have inferred that omega fats and vitamin E do not protect against Alzheimer’s disease.  However it is my opinion that these studies were conducted incorrectly since these supplements were not given together.  “Researchers” have suggested that vitamin E stabilizes the omega fat phospholipid membranes  instead of cholesterol.    Therefore I believe vitamin E and omega fats work synergistically in the critical regions of the nerve: the synapse and the inner mitochondrial membrane.

If we look at key players we can see how nerves normally function and how these 2 regions are central. 

APOE is an omega fat and vitamin E delivery man to the synapse.  As we age less vitamin E is found at the synapse and we struggle to remember.  APOE4 has been associated with an increased risk for Alzheimer's disease. It would be interesting to know if APOE4 delivers less vitamin E.

 Amyloid is a serine protease which could be a microtubule builder at the synapse membrane. (like the serine protease Htra1 building microtubules)   If the amount of omega fats at the synapse decreased or become unstable without vitamin E does less APP (amyloid)  exist in the synpase? Does more amyloid end up in the mitochondria or secreted to form plaques?

Looking specifically at the omega fats of the mitochondria is there a connection between the functionality of the mitochondria and the fats? The mitochondria must be able to move to the synapse on the microtubules.   Tau is a mitochondria zone controller.  Tau binds to the microtubule that the mitochondria travels on locking it into regions of travel.  Most vitamin E ends up in the mitochondrial inner membrane; as we age less and less vitamin E exists at the synapse.   Does this destabilize the membranes?  These 2 regions are critically intertwined in function.

 It is my hope that if we recognize the similarities of these omega phospholipid regions we will understand how the failure of one region could affect the other.  They may compete for vitamin E. They may compete for omega fats. They have the same free radical susceptibility.  They may even be confused and mixed up during dysfunction thus end up with each other’s  proteins.   

separating the autoimmune diseases

I  have been trying to create reasonable groups of autoimmune diseases and associate them with different dimorphic infections. I will modify this over time and these associations are not proven just vague guesses to start the process of research

Celiac disease: unknown infection
wheat  & milk

type 1 diabetes: several types one associated with Candida which is dimorphic
(when i have suspects i will attempt to divide this up)
wheat and milk

schizophrenia: T. gondi 
wheat and milk

ulcerative colitis: currently looking at C. diff and c.sorredilli
milk and egg...daisy family allergy (chamomile which is the holistic remedy?)
erythema mulitforme

eczema:  staph
milk and egg....peanut allergy
white hives

Autism:
wheat and milk
red hives

Exercise induced asthma: ?
gluten

Psoriasis: mycobacteria
gluten and casein

Asperger's ?  a pigment involved infection?
vitiligo, restless leg syndrome
milk? 
Epstein barr? (mono)

Nerves as roots

To test the mechanism of the serpin off growth and serine protease on I was having difficulty with fungus.   I couldn't find serpins in them.  I did find a paper evaluating the content of mediums used to grow fungus.  Mediums containing fish seemed to grow in a more thready root-like shape  whereas other mediums containing gluten caused a rounder morphology.  I did not find a documented mechanism of hyphal root growth of fungus specifically controlled by serpins.

What I was hoping to find was that fungal infections would change morphologies. If a serpin was present the mold -root growth would hault and it would switch to a  yeast morphology instead.  I was hoping to find the pathway already documented.  I couldn't even find serpins.  I started researching the evolution of serpins and it was not until eukaryotes appeared that serpins became abundant in the genetic code.  I am hoping that with so many serpins to choose from in eukaryotes that my growth pathway would be conserved in several.  That I could find the growth on and off growth mechanism of serpins in eukaryotes.  I decided to look for this in people.

 Which brings us to the end of the last blog focusing on maspin the breast cancer serpin.  When maspin is lost it causes the uncontrolled growth of cancer.  Yet a breast cell is not root like. Nerves on the other had are very root like. Nerves had a documented serpin called neuroserpin which did appear to be somehow involved with growth inhibition.  So i then started to look for a serine protease in nerves. I went looking for an on switch for nerve growth.  Interestingly the APP protein that becomes the amyloid plaque in Alzheimer's has no known normal function. The app protein is associated with nerve axon tips and has a serine protease in it.  So I started an entirely new theory using the same mechanism.  I am now hoping to find that the APP protein causes nerve growth and perhaps even how it does.  I am currently looking at HtlrA as a serine protease that helps extend microtubules the intracellular scaffold. Perhaps this is how the APP protein sitting in the membrane at the tip of the nerve's axon causes nerve root to extend toward other nerves. Possible?  

I apologize that I think so densely and cover so much material  so quickly.  I hope someone out there can follow me.  Perhaps over time with more blogging i will learn to expand and extrapolate on each idea enough that people will understand.  Does anyone out there follow me yet? Does anyone understand what  I am saying?

Angela Biggs

Organic Gardening

Gluten, casein, and ovalbumin were 3 proteins capable of inducing antibodies but how?
If they were functioning as serpins like the human maspin which is involved with breast cancer then they might be involved with growth.  Maspin is a serpin which when lost causes breast cancer to grow out of control.  So i began to think about these serpins as growth inhibitors and doing searches online.  I ran across an article about corn gluten inhibiting the growth of crab grass.  When i looked up the original article by Ohio state I discovered that the original experiment was looking at a parasitic grass fungus.  Grass seed grown on the corn meal failed to germinate and the fungus failed to be parasitic.  The researchers conducting the experiment focused on the inhibition of the grass roots specifically and started to sell the corn gluten as an organic crab grass treatment for golfcourses.  In my mind I realized if the gluten haulted the grass roots it might hault the fungus roots too which would explain why it failed to thrive.
Then I remembered that to prevent powdery mildew the organic method was to spray  milk on the leaves.  Was it possible that milk casein haulted powdery mildew roots in the same manner that corn gluten haulted root growth?

This year i conducted a very relaxed experiment with my kids, not a very scientific one.  I decided to grow grass seed in paper cups but expose some to wheat gluten and milk everyday.  Only the controls grew grass for my children.  Now I could not say the effect was just casein because any of the other proteins in milk could be involved.  I still suspected that gluten was actually something similar to a gluten serpin because the amino acid sequence was right but i had enough evidence now that i felt i was on the right track.

Taking the root idea back to the human maspin...well breast cells don't really have a root.  Then it dawned on me the cells in the body that grow the most like a root are nerves.  When I looked up what was know about nerves i realized that there was a neuroserpin which did in some way hault growth but that the entire area was hazy.  I hadn't seen an "on serine protease" for the Maspin. Could I see one for neuroserpin?
I have covered a lot in a short period of time here. Can anyone out there follow my logic about serpins and roots?
Angela Biggs

Milk, wheat, and eggs

see update on bottom...this hypothesis was wrong 

I have hesitated to start a blog but my lack of progress, writing in isolation, has made me realize I should at least try this format.

I have been trying to make sense of the patterns I see. I have been trying to develop reasonable theories to explain what i am seeing.

I have a theory that I developed involving serpins and serine proteases in the development of autoimmune disease. There are so many autoimmune diseases let me say that my theory rests in the area of overlap.  What they have in common. What i noticed first were the common triggers : wheat, egg, and milk.  How many autoimmune diseases can you associate with these?  Here's a start: celiac disease, type 1 diabetes, autism, ulcerative colitis, schizophrenia, crohn's, psoriasis, and eczema. Yes i am including eczema which has tradtionally been considered an allergy. I think allergies as an immune system error need to be included especially when the top allergies are: milk wheat, and eggs.
My instinct says something is going on here.  This is not just a leaky gut issue.  What do these trigger proteins have in common? How do they trigger the immune system? What are we missing here?
The protiens in milk, wheat, and eggs that have the most antibodies reacting are casein, gluten, and ovalbumin. Ovalbumin is a serine protease inhibitor, serpin for short. Which then leads us to the question how could a serpin trigger the immune system?
And gluten which is not a serpin...must look like one because we can see in Celiac disease the induction of antibodies.  Some forms of Celiac disease has been associated with Candida, is that relevant?
Eczema is milk and egg senstive and look worse when those foods are eaten. (i know my daughter had this)  The only infection found associated with eczema has been a form of staph not candida.  So we have different diseases with different culprits and we can't prove the infections are involved however I suspect the triggering mechanism might be the same.

I have more theory...but I will stop here. What do you think? Am I crazy? Do you see what I see?
Angela

After years of looking at the diseases that are gluten sensitive I have found that they are all barrier crossing infections. Infections that have the ability to cross the intestine or the blood brain barrier. The gluten crosses using the holes made by these infections and over stimulates the immune system.